Pain Management
Pain Management SECOND EDITION
Steven D. Waldman, MD, JD
Clinical Professor of Anesthesiology Professor of Medical Humanities and Bioethics University of Missouri–Kansas City School of Medicine Kansas City, Missouri
1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 PAIN MANAGEMENT
ISBN: 978-1-4377-0721-2
Copyright © 2011, 2007 by Saunders, an imprint of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher's permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).
Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods, they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence, or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Pain management / [edited by] Steven D. Waldman. -- 2nd ed. p. cm. Includes bibliographical references and index. ISBN 978-1-4377-0721-2 (hardcover : alk. paper) 1. Pain--Treatment. I. Waldman, Steven D. RB127.P332284 2011 616'.0472--dc22
Acquisitions Editor: Pamela Hetherington Senior Developmental Editor: Lucia Gunzel Publishing Services Manager: Anne Altepeter Team Manager: Radhika Pallamparthy Senior Project Manager: Doug Turner Project Manager: Vijay Vincent Designer: Louis Forgione Producer: Kitty Lasinski Printed in the United States of America Last digit is the print number: 9 8 7 6 5 4 3 2 1
2011009894
To my children: David for his caring nature and amazing work ethic, Corey for his integrity and determination, Jennifer for her intellect and compassion, and Reid for his ambition and unabashed joie de vivre. Steven D. Waldman Summer 2010
Contributors Salahadin Abdi, MD, PhD
Bassem Asaad, MD
David Borenstein, MD
Vice Chair and Chief of Pain Medicine Department of Anesthesia, Critical Care, and Pain Medicine Beth Israel Deaconess Medical Center; Associate Professor Harvard Medical School Boston, Massachusetts
Assistant Professor Department of Anesthesiology Stony Brook University Stony Brook, New York
Clinical Professor of Medicine George Washington University Medical Center Washington, District of Columbia
Bernard M. Abrams, MD, BS Clinical Professor Department of Neurology University of Missouri–Kansas City School of Medicine Kansas City, Missouri; Medical Director Dannemiller, San Antonio, Texas
Vimal Akhouri, MD, MBBS Instructor Department of Anesthesia Harvard Medical School; Staff Department of Anesthesia, Critical Care, and Pain Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts
J. Antonio Aldrete, MD, MS Professor Emeritus Department of Anesthesiology University of Alabama at Birmingham; President and Founder Arachnoiditis Foundation, Inc. Birmingham, Alabama
Frank Andrasik, PhD Distinguished Professor and Chair Department of Psychology University of Memphis Memphis, Tennessee
Sanjib Das Adhikary, MD Assistant Professor Department of Anesthesiology Penn State College of Medicine Milton S. Hershey Medical Center Hershey, Pennsylvania
Sairam L. Atluri, MD Director Tri-State Spine Care Institute Cincinnati, Ohio
Zahid H. Bajwa, MD Secretary American Academy of Pain Medicine; Director Education and Clinical Pain Research Beth Israel Deaconess Medical Center; Assistant Professor Department of Anesthesia Harvard Medical School Boston, Massachusetts
Samir K. Ballas, MD, FACP Professor Departments of Medicine and Pediatrics Thomas Jefferson University Philadelphia, Pennsylvania
David P. Bankston, MD Consultant in Pain Management Overland Park, Kansas
Ralf Baron, MD Head Division of Neurological Pain Research and Therapy Department of Neurology University Hospital Schleswig-Holstein, Campus Kiel Kiel, Germany
Andreas Binder, MD Consultant Neurologist Division of Neurological Pain Research and Therapy Department of Neurology University Hospital Schleswig-Holstein, Campus Kiel Kiel, Germany
Hifz Aniq, MBBS, FRCR
Nikolai Bogduk, MD, PhD, DSc, FAFRM, FFPM (ANZCA)
Honorary Lecturer Mersey School of Radiology University of Liverpool; Consultant Radiologist Radiology Department Royal Liverpool University Hospitals Trust Liverpool, United Kingdom
(Conjoint) Professor of Pain Medicine University of Newcastle; Director Department of Clinical Research Newcastle Bone and Joint Institute Royal Newcastle Centre Newcastle, Australia
vi
Mark V. Boswell, MD, PhD, MBA Professor and Chair Department of Anesthesiology University of Louisville School of Medicine Louisville, Kentucky
Geoffrey M. Bove, DC, PhD Associate Professor College of Osteopathic Medicine University of New England Biddeford, Maine
Fadi Braiteh, MD Director, Phase I Program Medical Oncology Comprehensive Cancer Centers of Nevada Las Vegas, Nevada
Eduardo Bruera, MD Professor and Chair Department of Palliative Care and Rehabilitation Medicine The University of Texas M.D. Anderson Cancer Center Houston, Texas
Allen Burton, MD Professor and Chair Department of Pain Medicine The University of Texas M.D. Anderson Cancer Center Houston, Texas
Roger Cady, MD Founder Primary Care Network and Headache Care Center; Adjunct Professor Missouri State University Springfield, Missouri; Associate Executive Chair National Headache Foundation Chicago, Illinois
Robert Campbell, MB, ChB, FRCR Honorary Clinical Lecturer University of Liverpool; Consultant Musculoskeletal Radiologist Department of Radiology Royal Liverpool University Hospitals Trust Liverpool, United Kingdom
Contributors
vii
Kenneth D. Candido, MD
Paul Creamer, MD, FRCP
Maxim Savillion Eckmann, MD
Chairman Department of Anesthesiology Advocate Illinois Masonic Medical Center; Professor of Clinical Anesthesiology University of Illinois College of Medicine Chicago, Illinois
Senior Clinical Lecturer University of Bristol Medical School; Consultant Rheumatologist Department of Rheumatology Southmead Hospital North Bristol NHS Healthcare Trust Bristol, United Kingdom
Assistant Professor Director of Acute Pain Service Department of Anesthesiology The University of Texas Health Science Center at San Antonio San Antonio, Texas
Sukded Datta, MD, DABPM, FIPP, DABIPP
Assistant Professor Department of Neurological Surgery Division of Neuro-oncologic Neurosurgery and Stereotactic Radiosurgery; Co-Director Center for Minimally Invasive Cranial Base Surgery and Endoscopic Neurosurgery Thomas Jefferson University Philadelphia, Pennsylvania
Joseph S. Chiang, MD Professor Department of Anesthesiology The University of Texas M.D. Anderson Cancer Center Houston, Texas
Martin K. Childers, DO, PhD Professor Department of Neurology Wake Forest University Health Sciences; Investigator Institute for Regenerative Medicine Wake Forest University School of Medicine Winston-Salem, North Carolina
Saima Chohan, MD Assistant Professor Department of Medicine Section of Rheumatology University of Chicago Chicago, Illinois
Philip G. Conaghan, MB, BS, PhD, FRACP, FRCP Professor Department of Musculoskeletal Medicine Section of Musculoskeletal Disease University of Leeds; Deputy Director NIHR Leeds Musculoskeletal Biomedical Research Unit Leeds Teaching Hospitals NHS Trust Leeds, United Kingdom
Darin J. Correll, MD Assistant Professor Department of Anesthesia Harvard Medical School; Director Acute Postoperative Pain Management Service; Administrative Director of Resident Education Department of Anesthesiology, Perioperative, and Pain Medicine Brigham and Women's Hospital Boston, Massachusetts
Scott C. Cozad, MD Radiation Oncologist Liberty Radiation Oncology Center; Clinical Assistant Professor University of Kansas Medical Center Kansas City, Missouri
Edward V. Craig, MD Attending Surgeon Hospital for Special Surgery; Professor of Clinical Orthopedic Surgery Cornell Medical School New York, New York
Director Vanderbilt University Interventional Pain Program; Assistant Professor Department of Anesthesiology Vanderbilt University Medical Center Nashville, Tennessee
Miles R. Day, MD Professor and Medical Director International Pain Center Department of Anesthesiology and Pain Management Texas Tech University Health Sciences Center Lubbock, Texas
Debra Ann Deangelo, DO Partner Pain Management Specialists Hanover, Pennsylvania
Timothy R. Deer, MD
James J. Evans, MD
Frank J.E. Falco, MD Clinical Assistant Professor Temple University Medical School Philadelphia, Pennsylvania; Medical Director Midatlantic Spine Newark, Delaware
Kathleen Farmer, PsyD Co-Founder and Psychologist Headache Care Center Springfield, Missouri
President and Chief Executive Officer Center for Pain Relief; Clinical Professor Department of Anesthesiology West Virginia University School of Medicine Charleston, West Virginia
Colleen M. Fitzgerald, MD
Seymour Diamond, MD
Co-Director Diamond Headache Clinic Chicago, Illinois; Clinical Assistant Professor Department of Family Medicine Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago, Illinois; Director Headache Medicine Research Baylor University Medical Center; Clinical Director Department of Headache Medicine Baylor Neuroscience Center Baylor University Medical Center Dallas, Texas
Director Emeritus and Founder Diamond Headache Clinic Chicago, Illinois; Adjunct Professor Department of Cellular and Molecular Pharmacology; Clinical Professor Department of Family Medicine Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago, Illinois; Lecturer Department of Family Medicine (Neurology) Stritch School of Medicine Loyola University Chicago Maywood, Illinois
Anthony Dickenson, PhD, BSc Professor Department of Neuroscience, Physiology, Pharmacology University College London London, United Kingdom
Charles D. Donohoe, MD Associate Clinical Professor Department of Neurology University of Missouri–Kansas City School of Medicine Kansas City, Missouri
Physical Medicine and Rehabilitation Specialist Rehabilitation Institute of Chicago Chicago, Illinois
Frederick G. Freitag, DO
M. Kay Garcia, MSN, MSOM, DrPH Adjunct Associate Professor American College of Acupuncture and Oriental Medicine; Advanced Practice Nurse/Acupuncturist Department of Integrative Medicine The University of Texas M.D. Anderson Cancer Center Houston, Texas
viii
Contributors
F. Michael Gloth III, MD
Howard Hall, PhD, PsyD, BCB
Joel Katz, PhD
Corporate Medical Director Mid-Atlantic Healthcare Timonium, Maryland; Associate Professor Department of Medicine Johns Hopkins University School of Medicine; Adjunct Associate Professor Department of Epidemiology and Preventive Medicine University of Maryland School of Epidemiology and Preventive Medicine Baltimore, Maryland
Associate Professor Department of Pediatrics Case Medical Center Rainbow Babies and Children's Hospital Cleveland, Ohio
Professor and Canada Research Chair in Health Psychology Department of Psychology York University; Professor Department of Anesthesia University of Toronto; Director Acute Pain Research Unit Department of Anesthesia and Pain Management Toronto General Hospital Toronto, Canada
Vitaly Gordin, MD Associate Professor Department of Anesthesiology Director Pain Medicine Clinic; Medical Director Spine Center; Co-Director Pain Medicine Fellowship Program Penn State College of Medicine Milton S. Hershey Medical Center Hershey, Pennsylvania
Martin Grabois, MD Professor and Chair Department of Physical Medicine and Rehabilitation Baylor College of Medicine; Adjunct Professor Department of Physical Medicine and Rehabilitation University of Texas Health Science Center at Houston; Professor Department of Anesthesiology Baylor College of Medicine Houston, Texas
Mark A. Greenfield, MD The Headache and Pain Center Leawood, Kansas
H. Michael Guo, MD, PhD Assistant Professor Director, Neurorehabilitation Fellowship Program Section of Physical Medicine and Rehabilitation Wake Forest University Baptist Medical Center Winston-Salem, North Carolina
Brian Hainline, MD Clinical Associate Professor Department of Neurology New York University School of Medicine New York, New York; Chief Department of Neurology and Integrative Pain Medicine ProHEALTH Care Associates Lake Success, New York
Brian L. Hazleman, MA, MB, FRCP Associate Lecturer Department of Medicine; Fellow Corpus Christi College University of Cambridge; Visiting Consultant Rheumatology Research Unit Addenbrooke's Hospital Cambridge, United Kingdom
James E. Heavner, DVM, PhD
Yoshiharu Kawaguchi, MD, PhD Associate Professor Department of Orthopaedic Surgery University of Toyama Toyama City, Japan
Professor Department of Anesthesiology and Cell Physiology and Molecular Biophysics School of Medicine Anesthesiology and Pain Research Texas Tech University Health Sciences Center Lubbock, Texas
Richard M. Keating, MD
D. Ross Henshaw, MD
Bruce L. Kidd, MD, DM
Director Sports Medicine Program Section of Orthopedic Surgery Danbury Hospital Danbury, Connecticut
Bernard H. Hsu, MD Assistant Clinical Professor Department of Anesthesiology School of Medicine and Biomedical Sciences State University of New York at Buffalo Buffalo, New York
Takashi Igarashi, MD Associate Professor Department of Anesthesiology and Critical Care Medicine Jichi Medical University School of Medicine Shimotsuke, Japan
Jeffrey W. Janata, PhD Associate Professor Departments of Psychiatry and Anesthesiology University Hospitals Case Medical Center; Director Behavioral Medicine Program Case Western Reserve University School of Medicine Cleveland, Ohio
Ravish Kapoor, MD Resident Department of Anesthesiology Penn State College of Medicine Milton S. Hershey Medical Center Hershey, Pennsylvania
Professor Department of Medicine Section of Rheumatology University of Chicago Pritzker School of Medicine Chicago, Illinois
Professor William Harvey Research Institute Bart's and the London Queen Mary School of Medicine and Dentistry London, United Kingdom
Katherine A. Kidder, OT, MBA Executive Director Society for Pain Practice Management Leawood, Kansas
Paul T. King, MD, PhD, FRACP Respiratory Physician Department of Respiratory and Sleep Medicine; Senior Lecturer Department of Medicine Monash University Monash Medical Centre Melbourne, Australia
Nicholas Kormylo, MD Assistant Clinical Professor Department of Anesthesiology University of California, San Diego La Jolla, California
Dhanalakshmi Koyyalagunta, MD Associate Professor Department of Pain Medicine The University of Texas M.D. Anderson Cancer Center Houston, Texas
Milton H. Landers, DO, PhD Associate Clinical Professor Department of Anesthesiology University of Kansas–Wichita School of Medicine; Pain Clinician Pain Management Associates Wichita, Kansas
Contributors
Erin F. Lawson, MD
Laxmaiah Manchikanti, MD
Richard B. Patt, MD
Assistant Professor Department of Anesthesiology Division of Pain Medicine University of California, San Diego La Jolla, California
Medical Director Pain Management Center Paducah, Kentucky; Associate Clinical Professor Department of Anesthesiology and Perioperative Medicine University of Louisville Louisville, Kentucky
President and Chief Medical Officer Patt Center for Pain Management Houston, Texas
Mark J. Lema, MD, PhD Professor and Chair Department of Anesthesiology School of Medicine and Biomedical Sciences State University of New York at Buffalo; Chair Division of Anesthesiology Roswell Park Cancer Institute Buffalo, New York
Jennifer B. Levin, PhD Assistant Professor Department of Psychiatry Case Western Reserve School of Medicine; Clinical Psychologist University Hospitals Case Medical Center Cleveland, Ohio
John Liu, MD Associate Professor Department of Neurosurgery Northwestern University Feinberg School of Medicine Chicago, Illinois
Mirjana Lovrincevic, MD Associate Professor Department of Clinical Anesthesiology and Oncology Roswell Park Cancer Institute; Clinical Assistant Professor Department of Anesthesiology School of Medicine and Biomedical Sciences State University of New York at Buffalo Buffalo, New York
Z. David Luo, MD Associate Professor Department of Anesthesiology School of Medicine University of California, Irvine Irvine, California
John A. Lyftogt, MD, MRNZCGP Senior Medical Officer Active Health Clinic QEII Sports Stadium Christchurch, New Zealand
James A. MacDonald, MD Assistant Professor Department of Neurology Wake Forest University Baptist Medical Center Winston-Salem, North Carolina
Mark N. Malinowski, DO, DABA Medical Director Center for Pain Management Wood County Hospital Bowling Green, Ohio
Danesh Mazloomdoost, MD Medical Director Paradigm Pain Management Medicine Lexington, Kentucky
Brian McGuirk, MB, BS, DPH, FAFOEM
†
Senior Staff Specialist Occupational and Musculoskeletal Medicine Newcastle Bone and Joint Institute Royal Newcastle Centre Newcastle, Australia
Ronald Melzack, PhD Professor Emeritus Department of Psychology McGill University Montreal, Canada
Jeffrey P. Meyer, MD President and Chief Executive Officer Midwest Pain Consultants Oklahoma City, Oklahoma
George R. Nissan, DO Clinical Assistant Professor Department of Medicine Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago, Illinois; Co-Director Diamond Headache Clinic Chicago, Illinois
John L. Pappas, MD Chief Department of Anesthesiology Beaumont Hospital; Medical Director Division of Pain Medicine Department of Anesthesiology Beaumont Hospitals Troy, Michigan
Winston C.V. Parris, MD, CMG, FACPM, DABPM Professor Department of Anesthesiology; Chief Division of Pain Medicine Duke University Medical Center Durham, North Carolina
Divya J. Patel, MD Director Carolina Regional Orthopedics Rocky Mount, North Carolina †
Deceased.
ix
David R. Patterson, PhD, ABPP, ABPH Professor Department of Rehabilitation Medicine University of Washington School of Medicine Seattle, Washington
Marco R. Perez-Toro, MD David Petersen, MD Department of Orthopaedic Surgery Minsurg Corporation Clearwater, Florida
Brett T. Quave, MD Medical Director Water's Edge Memorial's Pain Relief Institute Yakima, Washington
Gabor B. Racz, MD, ABA, FIPP, ABIPP Grover Murray Professor Professor and Chair Emeritus Department of Anesthesiology and Pain Medicine Texas Tech University Health Sciences Center Lubbock, Texas
P. Prithvi Raj, MD Professor Emeritus Department of Anesthesiology and Pain Medicine Texas Tech University Health Sciences Center Lubbock, Texas
Somayaji Ramamurthy, MD Professor Department of Anesthesiology; Director Pain Medicine Fellowship Program Department of Anesthesiology The University of Texas Health Science Center at San Antonio San Antonio, Texas
Matthew T. Ranson, MD Attending Physician The Center for Pain Relief Charleston, West Virginia
K. Dean Reeves, MD Clinical Associate Professor Department of Physical Medicine and Rehabilitation University of Kansas Medical Center Kansas City, Kansas
Lowell W. Reynolds, MD Professor Department of Anesthesiology Loma Linda University School of Medicine; Director of Acute Pain Department of Anesthesiology; Program Director Regional Anesthesia Fellowship Loma Linda University Medical Center Loma Linda, California
x
Contributors
Carla Rime, MA
Sam R. Sharar, MD
C.R. Sridhara, MD
Counselor and Biofeedback Technician Intermountain Children's Home Helena, Montana
Professor Department of Anesthesiology and Pain Medicine University of Washington School of Medicine; Head, Pediatric Anesthesia Section Harborview Medical Center Seattle, Washington
Director MossRehab Electrodiagnostic Center Department of Pain Management and Rehabilitation Albert Einstein Medical Center Elkins Park, Pennsylvania; Clinical Professor Department of Rehabilitation Medicine Thomas Jefferson University; Associate Chair Department of Pain Management and Rehabilitation Albert Einstein Medical Center; Adjunct Clinical Professor Department of Pain Management and Rehabilitation Temple University School of Medicine Philadelphia, Pennsylvania
Richard M. Rosenthal, MD, DABPM, FIPP Medical Director Nexus Pain Care Fellowship Director; Utah Center for Pain Management and Research Provo, Utah
Matthew P. Rupert, MD, MS, FIPP, DABIPP
Khuram A. Sial, MD Medical Director PainMedGroup, Inc. Murrieta, California
Shawn M. Sills, MD
Director Integrative Pain Solutions Franklin, Tennessee
Medical Director Interventional Pain Consultants, LLC Medford, Oregon
Lloyd R. Saberski, MD
Steven Simon, MD, RPh
Medical Director Advanced Diagnostic Pain Treatment Center Yale-New Haven at Long Wharf Yale-New Haven Hospital New Haven, Connecticut
Assistant Clinical Professor Department of Physical Medicine and Rehabilitation University of Kansas; Clinical Associate Professor Department of Family Medicine Kansas City University of Medicine and Biosciences Kansas City, Missouri; Medical Director Department of Pain Management Pain Management Institute Leawood, Kansas
Jörn Schattschneider, MD Consultant Division of Neurological Pain Research and Therapy Department of Neurology University Hospital of Schleswig-Holstein, Campus Kiel Kiel, Germany
Thomas Schrattenholzer, MD Medical Director Legacy Pain Management Center Portland, Oregon
Curtis P. Schreiber, MD Neurologist Headache Care Center Primary Care Network Springfield, Missouri
David M. Schultz, MD Medical Director Medical Advanced Pain Specialists Minneapolis, Minnesota
Jared Scott, MD Physician Advanced Pain Medicine Associates Wichita, Kansas; Pain Fellowship at Texas Tech University of Health Sciences Lubbock, Texas
Mehul Sekhadia, DO Assistant Professor Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, Illinois
Thomas T. Simopoulos, MD, MA Assistant Professor Department of Anesthesia Harvard Medical School; Director Interventional Pain Management Arnold Pain Management Center Department of Anesthesia, Critical Care, and Pain Medicine Beth Israel Deaconess Medical Center Boston, Massachusetts
Vijay Singh, MD Medical Director Pain Diagnostics Associates Niagara, Wisconsin
Daneshvari Solanki, FRCA (Eng) Laura B. McDaniel Distinguished Professor Department of Anesthesiology University of Texas Medical Branch Galveston, Texas
David A. Soto-Quijano, MD Staff Physician Department of Physical Medicine and Rehabilitation Veterans Affairs Caribbean Healthcare System; Assistant Professor Department of Physical Medicine, Rehabilitation and Sports Medicine University of Puerto Rico School of Medicine San Juan, Puerto Rico
Michael Stanton-Hicks, MB, BS, DrMed, FRCA, ABPM, FIPP Staff Member Department of Pain Management Cleveland Clinic; Consulting Staff Member Pediatric Pain Rehabilitation Program Cleveland Clinic Children's Hospital Shaker Campus; Joint Appointment to Outcomes and Research Department Anesthesiology Institute; Joint Appointment to Center for Neurological Restoration Imaging Institute Cleveland Clinic; Professor of Anesthesiology Lerner College of Medicine Case Medical School Case Western Reserve University Cleveland, Ohio
M. Alan Stiles, DMD Clinical Professor Facial Pain Management Department of Oral Maxillofacial Surgery Thomas Jefferson University Philadelphia, Pennsylvania
Robert B. Supernaw, PharmD Professor and Dean School of Pharmacy Wingate University Wingate, North Carolina
Rand S. Swenson, MD, PhD, DC Professor and Chair Department of Anatomy; Professor Department of Anatomy and Neurology Dartmouth Medical School Hanover, New Hampshire
Victor M. Taylor, MD President and Medical Director Amarillo Interventional Pain Management; Pain Management Fellowship Department of Anesthesiology Texas Tech University School of Medicine Lubbock, Texas
Contributors
Kevin D. Treffer, DO
Howard J. Waldman, MD
Shelley A. Wiechman, PhD
Associate Professor Departments of Family Medicine and Osteopathic Manipulative Medicine College of Osteopathic Medicine Kansas City University of Medicine and Biosciences Kansas City, Missouri
Consultant in Physical Medicine and Rehabilitation The Headache and Pain Center; Director of Neurophysiology Laboratory Doctors Hospital Leawood, Kansas
Associate Professor Rehabilitation Medicine University of Washington School of Medicine; Attending Psychologist Harborview Medical Center Seattle, Washington
Robert Trout, MD
Jennifer E. Waldman
Alon P. Winnie, MD
Consultant in Physical Medicine and Rehabilitation Headache and Pain Center Leawood, Kansas
Neuroscience Brain Tissue Bank and Research Laboratory University of Missouri–Kansas City School of Medicine Kansas City, Missouri
Clinical Professor Department of Anesthesiology Northwestern University Feinberg School of Medicine Chicago, Illinois
George J. Urban, MD
Steven D. Waldman, MD, JD
Cynthia A. Wong, MD
Co-Director Diamond Headache Clinic Chicago, Illinois; Clinical Instructor of Medicine Chicago Medical School Rosalind Franklin University of Medicine and Science North Chicago, Illinois; Lecturer Department of Medicine (Neurology) Stritch School of Medicine Loyola University of Chicago Maywood, Illinois
Clinical Professor of Anesthesiology Professor of Medical Humanities and Bioethics University of Missouri–Kansas City School of Medicine Kansas City, Missouri
Professor Department of Anesthesiology Northwestern University Feinberg School of Medicine; Section Chief, Obstetric Anesthesiology Northwestern Memorial Hospital Chicago, Illinois
Sobhan Vinjamuri, MD, MSc, FRCP Professor Department of Nuclear Medicine Royal Liverpool University Hospitals Trust Liverpool, United Kingdom
Corey W. Waldman Red 2 Docent Unit University of Missouri–Kansas City School of Medicine Kansas City, Missouri
Mark S. Wallace, MD Professor Department of Clinical Anesthesiology; Chair Division of Pain Medicine Department of Anesthesiology University of California, San Diego La Jolla, California
Carol A. Warfield, MD Lowenstein Professor Department of Anesthesia Harvard Medical School Boston, Massachusetts
Michael L. Whitworth, MD Pain Management Specialist Pain Center Columbus Regional Hospital Columbus, Indiana
xi
Tony L. Yaksh, PhD Professor Department of Anesthesiology and Pharmacology; Vice Chair for Research Department of Anesthesiology University of California, San Diego La Jolla, California
Manuel Ybarra, MD Assistant Professor Department of Anesthesiology The University of Texas Health Science Center at San Antonio San Antonio, Texas
Preface It is hard to believe that 5 years have passed since the publication of the first edition of Pain Management. Even at that time, when we had no knowledge of where electronic publishing would be in 2011, the conventional wisdom was that large, comprehensive textbooks were dinosaurs and that the future of medical books would be in smaller, more manageable, more specialized texts. Fortunately, this bit of conventional wisdom was off the mark. The first edition of Pain Management was published and has established itself as a popular reference among pain management practitioners across a variety of specialties. Electronic publishing has changed the face of the publishing business and has revolutionized the way in which we, as practitioners, consume content and learn new things. The
xii
explosion in the use of smart phones, e-readers and, more recently, tablets have made some of us hard-core readers wonder whether the printed book would go the way of the handwritten illuminated scroll. Actually, the challenge for publishers now is to deliver valuable content more quickly and in many different formats. In response to the changing times, this edition will also be published online at www. expertconsult.com, where you will find fully searchable text and images, as well as all the references hyperlinked to PubMed. It is with great pride, and a sigh of relief, that I give you Pain Management, Second Edition! Steven D. Waldman, MD, JD
Acknowledgments Many thanks to the dedicated clinicians and scientists who took time from their already busy schedules to contribute chapters to the second edition of Pain Management. I'd like to extend a special note of thanks to Milton H. Landers, DO, PhD; Mark A. Greenfield, MD; Mauricio Garcia, MD; Robert Campbell, MD; and Frank Judilla, MD, for their generosity in sharing their
knowledge, experience, and images for this edition. I'd also like to thank the staff at Elsevier for their advice and expertise— Pamela Hetherington, acquisitions editor; Lucia Gunzel, developmental editor; and Doug Turner, project manager. Steven D. Waldman, MD, JD
xiii
I
Chapter
1
A Conceptual Framework for Understanding Pain in the Human Joel Katz and Ronald Melzack
CHAPTER OUTLINE A Brief History of Pain in the 20th Century 2 The Gate Control Theory of Pain 3 Beyond the Gate 3 Phantom Limbs and the Concept of a Neuromatrix 4 Outline of the Theory 4 The Body-Self Neuromatrix 5
Theories of pain, like all scientific theories, evolve as result of the accumulation of new facts as well as leaps of the imagination.1 The gate control theory's most revolutionary contribution to understanding pain was its emphasis on central neural mechanisms.2 The theory forced the medical and biologic sciences to accept the brain as an active system that filters, selects, and modulates inputs. The dorsal horns, too, are not merely passive transmission stations but sites at which dynamic activities—inhibition, excitation, and modulation— occur. The great challenge ahead of us is to understand how the brain functions.
A Brief History of Pain in the 20th Century The theory of pain we inherited in the 20th century was proposed by Descartes 3 centuries earlier. The impact of Descartes' specificity theory was enormous. It influenced experiments on the anatomy and physiology of pain up to the first half of the 20th century (reviewed in Melzack and Wall3). This body of research is marked by a search for specific pain fibers and pathways and a pain center in the brain. The result was a concept of pain as a specific, straightthrough sensory projection system. This rigid anatomy of pain in the 1950s led to attempts to treat severe chronic pain by a variety of neurosurgical lesions. Descartes' specificity theory, then, determined the “facts” as they were known up to the middle of the 20th century and even determined therapy. 2
Conceptual Reasons for a Neuromatrix 5 Action Patterns: The Action-Neuromatrix 6
Pain and Neuroplasticity 7 Denervation Hypersensitivity and Neuronal Hyperactivity 7
Pain and Psychopathology 8 Conclusion: The Multiple Determinants of Pain 8
Specificity theory proposed that injury activates specific pain receptors and fibers that, in turn, project pain impulses through a spinal pain pathway to a pain center in the brain. The psychological experience of pain, therefore, was virtually equated with peripheral injury. In the 1950s, there was no room for psychological contributions to pain, such as attention, past experience, anxiety, depression, and the meaning of the situation. Instead, pain experience was held to be proportional to peripheral injury or disease. Patients who suffered back pain without presenting signs of organic disease were often labeled as psychologically disturbed and were sent to psychiatrists. The concept, in short, was simple and, not surprisingly, often failed to help patients who suffered severe chronic pain. To thoughtful clinical observers, specificity theory was clearly wrong. Several attempts were made to find a new theory. The major opponent to specificity was labeled “pattern theory,” but several different pattern theories were put forth, and they were generally vague and inadequate (see Melzack and Wall3). However, seen in retrospect, pattern theories gradually evolved (Fig. 1.1) and set the stage for the gate control theory. Goldscheider4 proposed that central summation in the dorsal horns is one of the critical determinants of pain. Livingston's5 theory postulated a reverberatory circuit in the dorsal horns to explain summation, referred pain, and pain that persisted long after healing was completed. Noordenbos'6 theory proposed that large-diameter fibers inhibited small-diameter fibers, and he even suggested that the substantia gelatinosa in the dorsal horns plays a major role in the summation and other dynamic processes described by Livingston. However, none of these theories had an explicit
© 2011 Elsevier Inc. All rights reserved.
Chapter 1—A Conceptual Framework for Understanding Pain in the Human
3
L S
S
L
A
C
CENTRAL CONTROL
L
GATE CONTROL SYSTEM
S
L SG
S
S
B
D
T
ACTION SYSTEM
Fig. 1.1 Schematic representation of conceptual models of pain mechanisms. A, Specificity theory. Large (L) and small (S) fibers are assumed to transmit touch and pain impulses, respectively, in separate, specific, straight-through pathways to touch and pain centers in the brain. B, Goldscheider's4 summation theory, showing convergence of small fibers onto a dorsal horn cell. The central network projecting to the central cell represents Livingston's5 conceptual model of reverberatory circuits underlying pathologic pain states. Touch is assumed to be carried by large fibers. C, Sensory interaction theory, in which large (L) fibers inhibit (−) and small (S) fibers excite (+) central transmission neurons. The output projects to spinal cord neurons, which are conceived by Noordenbos6 to comprise a multisynaptic afferent system. D, Gate control theory. The large (L) and small (S) fibers project to the substantia gelatinosa (SG) and first central transmission (T) cells. The central control trigger is represented by a line running from the large fiber system to central control mechanisms, which in turn project back to the gate control system. The T cells project to the entry cells of the action system. +, excitation; −, inhibition. (From Melzack R: The gate control theory 25 years later: new perspectives on phantom limb pain. In Bond MR, Charlton JE, Woolf CJ, editors: Pain research and therapy: proceedings of the VIth World Congress on Pain, Amsterdam, 1991, Elsevier, pp 9–21.)
role for the brain other than as a passive receiver of messages. Nevertheless, the successive theoretical concepts moved the field in the right direction: into the spinal cord and away from the periphery as the exclusive answer to pain. At least the field of pain was making its way up toward the brain.
The Gate Control Theory of Pain In 1965, Melzack and Wall2 proposed the gate control theory of pain. The final model, depicted in Figure 1.1D in the context of earlier theories of pain, is the first theory of pain that incorporated the central control processes of the brain. The gate control theory of pain2 proposed that the transmission of nerve impulses from afferent fibers to spinal cord transmission (T) cells is modulated by a gating mechanism in the spinal dorsal horn. This gating mechanism is influenced by the relative amount of activity in large- and small-diameter fibers, so that large fibers tend to inhibit transmission (close the gate), whereas small fibers tend to facilitate transmission (open the gate). In addition, the spinal gating mechanism is influenced by nerve impulses that descend from the brain. When the output of the spinal T cells exceeds a critical level, it activates the Action System—those neural areas that underlie the complex, sequential patterns of behavior and experience characteristic of pain. The theory's emphasis on the modulation of inputs in the spinal dorsal horns and the dynamic role of the brain in pain processes had a clinical as well as a scientific impact. Psychological factors, which were previously dismissed as
“reactions to pain,” were now seen to be an integral part of pain processing, and new avenues for pain control by psychological therapies were opened. Similarly, cutting of nerves and pathways was gradually replaced by a host of methods to modulate the input. Physical therapists and other health care professionals who use a multitude of modulation techniques were brought into the picture, and transcutaneous electrical nerve stimulation became an important modality for the treatment of chronic and acute pain. The current status of pain research and therapy indicates that, despite the addition of a massive amount of detail, the conceptual components of the theory remain basically intact up to the present.
Beyond the Gate The great challenge ahead of us is to understand brain function. Melzack and Casey7 made a start by proposing that specialized systems in the brain are involved in the sensory-discriminative, motivational-affective, and cognitiveevaluative dimensions of subjective pain experience (Fig. 1.2). These names for the dimensions of subjective experience seemed strange when they were coined, but they are now used so frequently and seem so “logical” that they have become part of our language. So, too, the McGill Pain Questionnaire, which taps into subjective experience—one of the functions of the brain— is the most widely used instrument to measure pain.8–10 The newest version, the Short-Form McGill Pain Questionnaire-2,10 was designed to measure the qualities of both neuropathic and non-neuropathic pain in research and clinical settings.
4
Section I—The Basic Science of Pain CENTRAL CONTROL PROCESSES
Fig. 1.2 Conceptual model of the sensory, moti vational, and central control determinants of pain. The output of the T (transmission) cells of the gate control system projects to the sensory-discriminative system and the motivational-affective system. The central control trigger is represented by a line running from the large fiber system to central control processes; these, in turn, project back to the gate control system, and to the sensory-discriminative and motivational-affective systems. All three systems interact with one another and project to the motor system. L, large fiber; S, small fiber. (From Melzack R, Casey KL: Sensory, motivational, and central control determinants of pain. In Kenshalo D, editor: The skin senses, Springfield, Ill, 1968, Charles C Thomas, pp 423–443.)
Motivational-affective processing (central intensity monitor)
L Input S
GATE CONTROL T SYSTEM
In 1978, Melzack and Loeser11 described severe pains in the phantom body of paraplegic patients with verified total sections of the spinal cord and proposed a central “pattern generating mechanism” above the level of the section. This concept, generally ignored for more than 2 decades, is now beginning to be accepted. It represents a revolutionary advance: it did not merely extend the gate; it said that pain could be generated by brain mechanisms in paraplegic patients in the absence of a spinal gate because the brain is completely disconnected from the spinal cord. Psychophysical specificity, in such a concept, makes no sense; instead we must explore how patterns of nerve impulses generated in the brain can give rise to somesthetic experience.
Phantom Limbs and the Concept of a Neuromatrix It is evident that the gate control theory has taken us a long way. Yet, as historians of science have pointed out, good theories are instrumental in producing facts that eventually require a new theory to incorporate them, and this is what has happened. It is possible to make adjustments to the gate theory so that, for example, it includes long-lasting activity of the sort Wall has described (see Melzack and Wall3). However, one set of observations on pain in paraplegic patients just does not fit the theory. This does not negate the gate theory, of course. Peripheral and spinal processes are obviously an important part of pain, and we need to know more about the mechanisms of peripheral inflammation, spinal modulation, midbrain descending control, and so forth. However, the data on painful phantoms below the level of total spinal section12,13 indicate that we need to go above the spinal cord and into the brain. Note that more than the spinal projection areas in the thalamus and cortex are meant. These areas are important, of course, but they are only part of the neural processes that underlie perception. The cortex, Gybels and Tasker14 made amply clear, is not the pain center, and neither is the thalamus. The areas of the brain involved in pain experience and behavior must include somatosensory projections as well as the limbic system. Furthermore, cognitive processes are known to involve widespread areas of the brain. Despite this increased knowledge, we do not yet have an adequate theory of how the brain works.
MOTOR MECHANISMS
Sensory-discriminative processing (spatio-temporal analysis)
Melzack's13 analysis of phantom limb phenomena, particularly the astonishing reports of a phantom body and severe phantom limb pain in people with a total thoracic spinal cord section,11 has led to four conclusions that point to a newer conceptual model of the nervous system. First, because the phantom limb (or other body part) feels so real, it is reasonable to conclude that the body we normally feel is subserved by the same neural processes in the brain as the phantom; these brain processes are normally activated and modulated by inputs from the body, but they can act in the absence of any inputs. Second, all the qualities we normally feel from the body, including pain, are also felt in the absence of inputs from the body; from this we may conclude that the origins of the patterns that underlie the qualities of experience lie in neural networks in the brain; stimuli may trigger the patterns but do not produce them. Third, the body is perceived as a unity and is identified as the “self,” distinct from other people and the surrounding world. The experience of a unity of such diverse feelings, including the self as the point of orientation in the surrounding environment, is produced by central neural processes and cannot derive from the peripheral nervous system or the spinal cord. Fourth, the brain processes that underlie the body-self are “built in” by genetic specification, although this built-in substrate must, of course, be modified by experience. These conclusions provide the basis of the newer conceptual model12,13,15 depicted in Figure 1.3.
Outline of the Theory Melzack12,13,15 proposed that the anatomic substrate of the body-self is a large, widespread network of neurons that consists of loops between the thalamus and cortex as well as between the cortex and limbic system. He labeled the entire network, whose spatial distribution and synaptic links are initially determined genetically and are later sculpted by sensory inputs, a neuromatrix. The loops diverge to permit parallel processing in different components of the neuromatrix and converge repeatedly to permit interactions among the output products of processing. The repeated cyclical processing and synthesis of nerve impulses through the neuromatrix imparts a characteristic pattern: the neurosignature. The neurosignature of the neuromatrix is imparted on all nerve impulse patterns that flow through it; the neurosignature is produced by the patterns of synaptic connections in the entire neuromatrix. All inputs from the body undergo cyclical
Chapter 1—A Conceptual Framework for Understanding Pain in the Human INPUTS TO BODY-SELF NEUROMATRIX FROM: COGNITIVE-RELATED BRAIN AREAS Memories of past experience, attention, meaning, and anxiety
BODY-SELF NEUROMATRIX
C SENSORY SIGNALLING SYSTEMS Cutaneous, visceral, and musculoskeletal inputs
S
5
OUTPUTS TO BRAIN AREAS THAT PRODUCE: PAIN PERCEPTION Sensory, affective, and cognitive dimensions
ACTION PROGRAMS Involuntary and voluntary action patterns
A EMOTION-RELATED BRAIN AREAS Limbic system and associated homeostatic/stress mechanisms
TIME
STRESS-REGULATION PROGRAMS Cortisol, noradrenalin, and endorphin levels Immune system activity
TIME
Fig. 1.3 Factors that contribute to the patterns of activity generated by the body-self neuromatrix, which is composed of sensory, affective, and cognitive neuromodules. The output patterns from the neuromatrix produce the multiple dimensions of pain experience, as well as concurrent homeostatic and behavioral responses. (From Melzack R: Pain and the neuromatrix in the brain, J Dent Educ 65:1378–1382, 2001.)
processing and synthesis so that characteristic patterns are impressed on them in the neuromatrix. Portions of the neuromatrix are specialized to process information related to major sensory events (e.g., injury, temperature change, and stimulation of erogenous tissue) and may be labeled neuromodules that impress subsignatures on the larger neurosignature. The neurosignature, which is a continuous output from the body-self neuromatrix, is projected to areas in the brain— the sentient neural hub—in which the stream of nerve impulses (the neurosignature modulated by ongoing inputs) is converted into a continually changing stream of awareness. Furthermore, the neurosignature patterns may also activate a neuromatrix to produce movement. That is, the signature patterns bifurcate so that a pattern proceeds to the sentient neural hub (where the pattern is transformed into the experience of movement), and a similar pattern proceeds through a neuromatrix that eventually activates spinal cord neurons to produce muscle patterns for complex actions.
The Body-Self Neuromatrix The body is felt as a unity, with different qualities at different times. Melzack12,13,15 proposed that the brain mechanism that underlies the experience also comprises a unified system that acts as a whole and produces a neurosignature pattern of a whole body. The conceptualization of this unified brain mechanism lies at the heart of this theory, and the word “neuromatrix” best characterizes it. The neuromatrix (not the stimulus, peripheral nerves, or “brain center”) is the origin of the neurosignature; the neurosignature originates and takes form in the neuromatrix. Although the neurosignature may be triggered or modulated by input, the input is only a “trigger” and does not produce the neurosignature itself. The neuromatrix “casts” its distinctive signature on all inputs (nerve impulse patterns) that flow through it. Finally, the array of neurons in a neuromatrix is genetically programmed to perform the specific function of producing the signature pattern. The final,
integrated neurosignature pattern for the body-self ultimately produces awareness and action. The neuromatrix, distributed throughout many areas of the brain, comprises a widespread network of neurons that generates patterns, processes information that flows through it, and ultimately produces the pattern that is felt as a whole body. The stream of neurosignature output with constantly varying patterns riding on the main signature pattern produces the feelings of the whole body with constantly changing qualities.
Conceptual Reasons for a Neuromatrix It is difficult to comprehend how individual bits of information from skin, joints, or muscles can all come together to produce the experience of a coherent, articulated body. At any instant in time, millions of nerve impulses arrive at the brain from all the body's sensory systems, including the proprioceptive and vestibular systems. How can all this be integrated in a constantly changing unity of experience? Where does it all come together? Melzack12,13,15 conceptualized a genetically built-in neuromatrix for the whole body. This neuromatrix produces a characteristic neurosignature for the body that carries with it patterns for the myriad qualities we feel. The neuromatrix, as Melzack conceived of it, produces a continuous message that represents the whole body in which details are differentiated within the whole as inputs come into it. We start from the top, with the experience of a unity of the body, and look for differentiation of detail within the whole. The neuromatrix, then, is a template of the whole, which provides the characteristic neural pattern for the whole body (the body's neurosignature), as well as subsets of signature patterns (from neuromodules) that relate to events at (or in) different parts of the body. These views are in sharp contrast to the classical specificity theory in which the qualities of experience are presumed to be inherent in peripheral nerve fibers. Pain is not injury; the quality of pain experiences must not be confused with the
6
Section I—The Basic Science of Pain
hysical event of breaking skin or bone. Warmth and cold p are not “out there”; temperature changes occur “out there,” but the qualities of experience must be generated by structures in the brain. Stinging, smarting, tickling, and itch have no external equivalents; the qualities are produced by builtin neuromodules whose neurosignatures innately produce the qualities. We do not learn to feel qualities of experience: our brains are built to produce them. The inadequacy of the traditional peripheralist view becomes especially evident when we consider paraplegic patients with high-level complete spinal breaks. In spite of the absence of inputs from the body, virtually every quality of sensation and affect is experienced. It is known that the absence of input produces hyperactivity and abnormal firing patterns in spinal cells above the level of the break,11 but how, from this jumble of activity, do we get the meaningful experience of movement, the coordination of limbs with other limbs, cramping pain in specific (nonexistent) muscle groups, and so on? This must occur in the brain, in which neurosignatures are produced by neuromatrixes that are triggered by the output of hyperactive cells. When all sensory systems are intact, inputs modulate the continuous neuromatrix output to produce the wide variety of experiences we feel. We may feel position, warmth, and several kinds of pain and pressure all at once. It is a single unitary feeling, just as an orchestra produces a single unitary sound at any moment even though the sound comprises violins, cellos, horns, and so forth. Similarly, at a particular moment in time we feel complex qualities from all of the body. In addition, our experience of the body includes visual images, affect, and “knowledge” of the self (versus not-self), as well as the meaning of body parts in terms of social norms and values. It is hard to conceive of all of these bits and pieces coming together to produce a unitary body-self, but we can visualize a neuromatrix that impresses a characteristic signature on all the inputs that converge on it and thereby produces the never-ending stream of feeling from the body. The experience of the body-self involves multiple dimensions—sensory, affective, evaluative, postural, and many others. The sensory dimensions are subserved, in part at least, by portions of the neuromatrix that lie in the sensory projection areas of the brain; the affective dimensions, Melzack assumed, are subserved by areas in the brainstem and limbic system. Each major psychological dimension (or quality) of experience, Melzack12,13,15 proposed, is subserved by a particular portion of the neuromatrix that contributes a distinct portion of the total neurosignature. To use a musical analogy once again, it is like the strings, tympani, woodwinds, and brasses of a symphony orchestra that each make up a part of the whole; each instrument makes its unique contribution yet is an integral part of a single symphony that varies continually from beginning to end. The neuromatrix resembles Hebb's “cell assembly” by being a widespread network of cells that subserves a particular psychological function. However, Hebb16 conceived of the cell assembly as a network developed by gradual sensory learning, whereas Melzack proposed that the structure of the neuromatrix is predominantly determined by genetic factors, although its eventual synaptic architecture is influenced by sensory inputs. This emphasis on the genetic contribution to the brain does not diminish the importance of sensory inputs. The
euromatrix is a psychologically meaningful unit, developed n by both heredity and learning, that represents an entire unified entity.12,13,15
Action Patterns: The Action-Neuromatrix The output of the body neuromatrix, Melzack12,13,15 proposed, is directed at two systems: (1) the neuromatrix that produces awareness of the output and (2) a neuromatrix involved in overt action patterns. In this discussion, it is important to keep in mind that just as there is a steady stream of awareness, there is also a steady output of behavior (including movements during sleep). Behavior occurs only after the input has been at least partially synthesized and recognized. For example, when we respond to the experience of pain or itch, it is evident that the experience has been synthesized by the body-self neuromatrix (or relevant neuromodules) sufficiently for the neuromatrix to have imparted the neurosignature patterns that underlie the quality of experience, affect, and meaning. Apart from a few reflexes (e.g., withdrawal of a limb and eye blink), behavior occurs only after inputs have been analyzed and synthesized sufficiently to produce meaningful experience. When we reach for an apple, the visual input has clearly been synthesized by a neuromatrix so that it has three-dimensional shape, color, and meaning as an edible, desirable object, all of which are produced by the brain and are not in the object “out there.” When we respond to pain (by withdrawal or even by telephoning for an ambulance), we respond to an experience that has sensory qualities, affect, and meaning as a dangerous (or potentially dangerous) event to the body. Melzack12,13,15 proposed that after inputs from the body undergo transformation in the body-neuromatrix, the appropriate action patterns are activated concurrently (or nearly so) with the neuromatrix for experience. Thus, in the actionneuromatrix, cyclical processing and synthesis produce activation of several possible patterns and their successive elimination until one particular pattern emerges as the most appropriate for the circumstances at the moment. In this way, input and output are synthesized simultaneously, in parallel, not in series. This permits a smooth, continuous stream of action patterns. The command, which originates in the brain, to perform a pattern such as running activates the neuromodule, which then produces firing in sequences of neurons that send precise messages through ventral horn neuron pools to appropriate sets of muscles. At the same time, the output patterns from the body-neuromatrix that engage the neuromodules for particular actions are also projected to the sentient neural hub and produce experience. In this way, the brain commands may produce the experience of movement of phantom limbs even though the patient has no limbs to move and no proprioceptive feedback. Indeed, reports by paraplegic patients of terrible fatigue resulting from persistent bicycling movements17 and the painful fatigue in a tightly clenched phantom fist in arm amputees18 indicate that feelings of effort and fatigue are produced by the signature of a neuromodule rather than by particular input patterns from muscles and joints. The phenomenon of phantom limbs has allowed researchers to examine some fundamental assumptions in psychology. Among these assumptions are that sensations are produced only by stimuli and perceptions in the absence of stimuli
Chapter 1—A Conceptual Framework for Understanding Pain in the Human
are psychologically abnormal. Yet phantom limbs, as well as phantom seeing,19 indicate that this notion is wrong. The brain does more than detect and analyze inputs; it generates perceptual experience even when no external inputs occur. Another entrenched assumption is that perception of one's body results from sensory inputs that leave a memory in the brain; the total of these signals becomes the body image. However, the existence of phantoms in people born without a limb or who lost a limb at an early age suggests that the neural networks for perceiving the body and its parts are built into the brain.12,13,20,21 The absence of inputs does not stop the networks from generating messages about missing body parts; the networks continue to produce such messages throughout life. In short, phantom limbs are a mystery only if we assume that the body sends sensory messages to a passively receiving brain. Phantoms become comprehensible once we recognize that the brain generates the experience of the body. Sensory inputs merely modulate that experience; they do not directly cause it.
Pain and Neuroplasticity The specificity concept of the nervous system for had no place for “plasticity,” in which neuronal and synaptic functions are capable of being molded or shaped so that they influence subsequent perceptual experiences. Plasticity related to pain represents persistent functional changes, or “somatic memories,”22,23 produced in the nervous system by injuries or other pathologic events. The recognition that such changes can occur is essential to understanding the chronic pain syndromes, such as low back pain and phantom limb pain, that persist and often destroy the lives of the people who suffer them.
Denervation Hypersensitivity and Neuronal Hyperactivity Sensory disturbances associated with nerve injury have been closely linked to alterations in central nervous system (CNS) function. Markus, Pomerantz and Krushelnyky24 demonstrated that the development of hypersensitivity in a rat's hind paw following sciatic nerve section occurs concurrently with the expansion of the saphenous nerve's somatotopic projection in the spinal cord. Nerve injury may also lead to the development of increased neuronal activity at various levels of the somatosensory system (see review by Coderre et al25). In addition to spontaneous activity generated from the neuroma, peripheral neurectomy also leads to increased spontaneous activity in the dorsal root ganglion and the spinal cord. Furthermore, after dorsal rhizotomy, increases in spontaneous neural activity occur in the dorsal horn, the spinal trigeminal nucleus, and the thalamus. Clinical neurosurgery studies reveal a similar relationship between denervation and CNS hyperactivity. Neurons in the somatosensory thalamus of patients with neuropathic pain display high spontaneous firing rates, abnormal bursting activity, and evoked responses to stimulation of body areas that normally do not activate these neurons.26,27 The site of abnormality in thalamic function appears to be somatotopically related to the painful region. In patients with complete spinal cord transection and dysesthesias referred below the level of the break, neuronal hyperactivity was observed in thalamic regions that had lost their normal sensory input, but not in
7
regions with apparently normal afferent input.26 Furthermore, in patients with neuropathic pain, electrical stimulation of subthalamic, thalamic, and capsular regions may evoke pain,28 and in some instances it may even reproduce the patient's pain.29–31 Direct electrical stimulation of spontaneously hyperactive cells evokes pain in some but not all patients with pain; this finding raises the possibility that in certain patients the observed changes in neuronal activity may contribute to the perception of pain.26 Studies of patients undergoing electrical brain stimulation during brain surgery reveal that pain is rarely elicited by test stimuli unless the patient suffers from a chronic pain problem. However, brain stimulation can elicit pain responses in patients with chronic pain that does not involve extensive nerve injury or deafferentation. Lenz et al30 described the case of a woman with unstable angina who, during electrical stimulation of the thalamus, reported “heart pain like what I took nitroglycerin for” except that “it starts and stops suddenly”. The possibility that the patient's angina was the result of myocardial strain, and not the activation of a somatosensory pain memory, was ruled out by demonstrating that electrocardiograms, blood pressure, and cardiac enzymes remained unchanged over the course of stimulation. It is possible that receptive field expansions and spontaneous activity generated in the CNS following peripheral nerve injury are, in part, mediated by alterations in normal inhibitory processes in the dorsal horn. Within 4 days of a peripheral nerve section, one notes a reduction in the dorsal root potential and, therefore, in the presynaptic inhibition it represents.32 Nerve section also induces a reduction in the inhibitory effect of A-fiber stimulation on activity in dorsal horn neurons.33 Furthermore, nerve injury affects descending inhibitory controls from brainstem nuclei. In the intact nervous system, stimulation of the locus ceruleus34 or the nucleus raphe magnus35 produces inhibition of dorsal horn neurons. Following dorsal rhizotomy, however, stimulation of these areas produces excitation, rather than inhibition, in half the cells studied.36 Advances in our understanding of the mechanisms that underlie pathologic pain have important implications for the treatment of both acute and chronic pain. Because it has been established that intense noxious stimulation produces sensitization of CNS neurons, it is possible to direct treatments not only at the site of peripheral tissue damage, but also at the site of central changes (see review by Coderre and Katz37). Furthermore, it may be possible in some instances to prevent the development of central sensitization, which contributes to pathologic pain states. The evidence that acute postoperative pain intensity and the amount of pain medication patients require after surgery are reduced by preoperative administration of variety of agents administered by the epidural38–40 or systemic route41–43 suggests that the surgically induced afferent injury barrage arriving within the CNS, and the central sensitization it induces, can be prevented or at least obtunded significantly (see review by Katz44). The reduction in acute pain intensity associated with preoperative epidural anesthesia may even translate into reduced pain45 and pain disability46 weeks after patients have left the hospital and returned home. The finding that amputees are more likely to develop phantom limb pain if they had pain in the limb before amputation23 raises the possibility that the development of longer-term neuropathic pain also can be prevented by reducing the potential for central sensitization at the time of amputation
8
Section I—The Basic Science of Pain
(see Katz and Melzack47). Whether chronic postoperative problems such as painful scars, postthoracotomy chest wall pain, and phantom limb and stump pain can be reduced by blocking perioperative nociceptive inputs awaits additional wellcontrolled clinical trials (see Katz and Seltzer48). Furthermore, research is required to determine whether multiple-treatment approaches (involving local and epidural anesthesia, as well as pretreatment with opiates and anti-inflammatory drugs) that produce effective blockade of afferent input may also prevent or relieve other forms of severe chronic pain such as postherpetic neuralgia49 and complete regional pain syndrome. It is hoped that a combination of new pharmacologic developments, careful clinical trials, and an increased understanding of the contribution and mechanisms of noxious stimulus– induced neuroplasticity will lead to improved clinical treatment and prevention of pathologic pain.
Pain and Psychopathology Pains that do not conform to present day anatomic and neurophysiologic knowledge are often attributed to psychological dysfunction. There are many pains whose cause is not known. If a d iligent search has been made in the periphery and no cause is found, we have seen that clinicians act as though there was only one alternative. They blame faulty thinking, which for many classically thinking doctors is the same thing as saying that there is no cause and even no disease. They ignore a century's work on disorders of the spinal cord and brainstem and target the mind. . . . These are the doctors who repeat again and again to a Second World War amputee in pain that there is nothing wrong with him and that it is all in his head.50, p. 107 This view of the role of psychological generation in pain persists to this day notwithstanding evidence to the contrary. Psychopathology has been proposed to underlie phantom limb pain,18 dyspareunia,51 orofacial pain,52 and a host of others including pelvic pain, abdominal pain, chest pain, and headache.53 However, the complexity of the pain transmission circuitry described in the previous sections means that many pains that defy our current understanding will ultimately be explained without having to resort to a psychopathologic etiology. Pain that is “nonanatomic” in distribution, spread of pain to noninjured territory, pain that is said to be out of proportion to the degree of injury, and pain in the absence of injury have all, at one time or another, been used as evidence to support the idea that psychological disturbance underlies the pain. Yet each of these features of supposed psychopathology can now be explained by neurophysiologic mechanisms that involve an interplay between peripheral and central neural activity.3,52 Data linking the immune system and the CNS have provided an explanation for another heretofore medically unexplained pain problem. Mirror-image pain, or allochiria, has puzzled clinicians and basic scientists ever since it was first documented in the late 1800s.54 Injury to one side of the body is experienced as pain at the site of injury as well as at the contralateral, mirror-image point.55,56 Animal studies show that induction of sciatic inflammatory neuritis by perisciatic microinjection of immune system activators results in both ipsilateral hyperalgesia and hyperalgesia at the mirror-image
point on the opposite side in the territory of the contralateral healthy sciatic nerve.57 Moreover, both ipsilateral hyperalgesia and contralateral hyperalgesia are prevented or reversed by intrathecal injection of a variety of proinflammatory cytokine antagonists.58 Mirror-image pain is likely not a unitary phenomenon, and other nonimmune mechanisms may also be involved.59 For example, human60 and animal61 evidence points to a potential combination of central and peripheral contributions to mirror-image pain because nerve injury to one side of the body has been shown to result in a 50% reduction in the innervation of the territory of the same nerve on the opposite side of the body in uninjured skin.61 Although documented contralateral neurite loss can occur in the absence of contralateral pain or hyperalgesia, pain intensity at the site of the injury correlates significantly with the extent of contralateral neurite loss.60 This finding raises the intriguing possibility that the intensity of pain at the site of an injury may be facilitated by contralateral neurite loss induced by the ipsilateral injury,61 a situation that most clinicians would never have imagined possible. Taken together, these novel mechanisms that explain some of the most puzzling pain symptoms must keep us mindful that emotional distress and psychological disturbance in our patients are not at the root of the pain. Attributing pain to a psychological disturbance is damaging to the patient and provider alike; it poisons the patient-provider relationship by introducing an element of mutual distrust and implicit (and at times, explicit) blame. It is devastating to the patient, who feels at fault, disbelieved, and alone.
Conclusion: The Multiple Determinants of Pain The neuromatrix theory of pain proposes that the neurosignature for pain experience is determined by the synaptic architecture of the neuromatrix, which is produced by genetic and sensory influences. The neurosignature pattern is also modulated by sensory inputs and by cognitive events, such as psychological stress.62 Furthermore, stressors, physical as well as psychological, act on stress regulation systems, which may produce lesions of muscle, bone, and nerve tissue and thereby contribute to the neurosignature patterns that give rise to chronic pain. In short, the neuromatrix, as a result of homeostasis regulation patterns that have failed, may produce the destructive conditions that give rise to many of the chronic pains that so far have been resistant to treatments developed primarily to manage pains that are triggered by sensory inputs. The stress regulation system, with its complex, delicately balanced interactions, is an integral part of the multiple contributions that give rise to chronic pain. The neuromatrix theory guides us away from the Cartesian concept of pain as a sensation produced by injury or other tissue disease and toward the concept of pain as a multidimensional experience produced by multiple influences. These influences range from the existing synaptic architecture of the neuromatrix to influences from within the body and from other areas in the brain. Genetic influences on synaptic architecture may determine—or predispose to—the development of chronic pain syndromes. Figure 1.3 summarizes the factors that contribute to the output pattern from the neuromatrix that produce the sensory, affective, and cognitive dimensions of pain experience and the resultant behavior.
Chapter 1—A Conceptual Framework for Understanding Pain in the Human
Multiple inputs act on the neuromatrix programs and c ontribute to the output neurosignature. They include the following: (1) sensory inputs (cutaneous, visceral, and other somatic receptors); (2) visual and other sensory inputs that influence the cognitive interpretation of the situation; (3) phasic and tonic cognitive and emotional inputs from other areas of the brain; (4) intrinsic neural inhibitory modulation inherent in all brain function; and (5) the activity of the body's stress regulation systems, including cytokines as well as the endocrine, autonomic, immune, and opioid systems. We have
9
traveled a long way from the psychophysical concept that seeks a simple one-to-one relationship between injury and pain. We now have a theoretical framework in which a genetically determined template for the body-self is modulated by the powerful stress system and the cognitive functions of the brain, in addition to the traditional sensory inputs.
References Full references for this chapter can be found on www.expertconsult.com.
I
Chapter
2
Anatomy of the Pain Processing System Tony L. Yaksh and Z. David Luo
CHAPTER OUTLINE Anatomic Systems Associated with Pain Processing 10 Primary Afferents 10
Ascending Spinal Tracts 14 Ventral Funicular Projection Systems 14 Dorsal Funicular Projection Systems 14 Intersegmental Systems 14
Fiber Classes 10 Properties of Primary Afferent Function 10 Afferents with High Thresholds and Pain Behavior 12
Supraspinal Projections 15 Spinoreticulothalamic Projections 15 Spinomesencephalic Projections 15 Spinoparabrachial Projections 15 Spinothalamic Projections 16
Spinal Dorsal Horn 12 Afferent Projections 12 Anatomy of the Dorsal Horn 12
Functional Overview of Pain Processing Systems 16
Dorsal Horn Neurons 12
Frequency Encoding 17 Afferent Line Labeling 17 Functionally Distinct Pathways 17 Plasticity of Ascending Projections 17
Anatomic Localization 12 Marginal Zone (Lamina I) 12 Substantia Gelatinosa (Lamina II) 13 Nucleus Proprius (Laminae III, IV, and V) 13 Central Canal (Lamina X) 13 Functional Properties 14 Nociceptive Specific 14 Wide Dynamic Range Neurons 14
Pharmacology of Afferent Transmitter Systems in Nociception 17 Primary Afferent Transmitters 17 Ascending Projection System Transmitters 18
Anatomic Systems Associated with Pain Processing*
Primary Afferents†
Extreme mechanical distortion, thermal stimuli (>42°C [108°F]), or changes in the chemical milieu (plasma products, pH, potassium) at the peripheral sensory terminal will evoke the verbal report of pain in humans and efforts to escape in animals, as well as the elicitation of activity in the adrenalpituitary axis. This chapter provides a broad overview of the circuitry that serves in the transduction and encoding of this information. First, the stimuli already mentioned evoke activity in specific groups of small myelinated or unmyelinated primary afferents of ganglionic sensory neurons, which make their synaptic contact with several distinct populations of dorsal horn neurons. By long spinal tracts and through a variety of intersegmental systems, the information gains access to supraspinal centers that lie in the brainstem and in the thalamus. These rostrally projecting systems represent the substrate by which unconditioned, high-intensity somatic and visceral stimuli give rise to escape behavior and verbal report of pain. This circuitry constitutes the afferent limb of the pain pathway.
Sensory neurons in dorsal root ganglia have a single process (glomerulus) that bifurcates into a peripheral (nerve) and central (root) axon. The peripheral axon collects sensory input originating from the environment of the innervated tissue. The central axon relays sensory input to the spinal cord or brainstem. Sensory axons are classified according to their diameter, state of myelination, and conduction velocity, as outlined in Table 2.1. In general, conduction velocity varies directly with axon diameter and the presence of myelination. Thus, Aß axons are large and myelinated, and they conduct rapidly; A∂ axons are smaller in diameter and myelinated, and they conduct more slowly; and C fibers are small and unmyelinated, and they conduct very slowly.
*For a more detailed discussion of the material in this section, see Reference 1.
†
10
Fiber Classes
Properties of Primary Afferent Function Recording from single peripheral afferent fibers reveals three important characteristics. First, in the absence of stimulation, minimal, if any, “spontaneous” afferent traffic occurs. Accordingly, For more detailed discussions of the material in this section, see References 2 to 4.
Chapter 2—Anatomy of the Pain Processing System
the system operates on a very high signal-to-noise ratio. Second, regardless of the fiber type examined, with increasing intensities of the appropriate stimulus, a monotonic increase in the discharge frequency for that axon is observed (Fig. 2.1). This finding reflects the fact that the more intense the stimulus, the greater is the depolarization of the terminal and the more frequently will the axon discharge. Third, different axons may respond most efficiently to a particular stimulus modality. This modality specificity reflects the nature of the terminal properties of the particular afferent axon that transduces the physical or chemical stimulus into a depolarization of the axon. These nerve endings may be morphologically specialized, as with the pacinian corpuscle that is found on the terminals of large afferents. The specialized structure translates the mechanical distortion of the structure
Table 2.1 Classification of Primary Afferents by Physical Characteristics, Conduction Velocity, and Effective Stimuli Fiber Class*
Velocity Group*
Effective Stimuli
A-beta
Group II (>40–50 m/sec)
Low-threshold Specialized nerve endings (pacinian corpuscles)
A-delta
Group III (>10 and 52C
TRPV3
>34–38C
TRPV4
>27–35C
TRPM8 Somatosensory cortex
Fig. 2.12 Schematic of an overview of the characteristics of the projections of wide dynamic range (WDR) lamina V (Lam V) neurons in to the somatotopically mapped ventrobasal (VBL) thalamus and from there to the somatosensory (SS) cortex. As described in the text, this organization suggests the properties that would mediate the sensory-discriminative aspects of pain. VLT, ventrolateral tract.
Ascending thalamic projections Lam V-> Ventrobasal (VBL) Precise anatomical mapping
Diencephalon Ventrobasal thalamus
Spinothalamic tract
Ascending axons in VLT Spinothalamic Spinofugal projections Lam V: WDR-intensity encoded High degree of localization
Spinothalamic Projections This predominantly crossed system displays the following three principal targets of termination (Fig. 2.11): 1. The ventrobasal thalamus represents the classic somatosensory thalamic nucleus. Input is distributed in a strict somatotopic pattern. This region projects in a strict somatotopic organization to the somatosensory cortex (see Fig. 2.8). 2. The VMpo then projects into the insula. 3. The media thalamus receives primary input from lamina I (high-threshold nociceptive specific cells). Cells in this region then project to the anterior cingulate cortex (Fig. 2.12).
Spinal Cord Ventrolateral tracts
Functional Overview of Pain Processing Systems* The preceding discussion considers various elements that constitute linkages whereby information generated by a highintensity stimulus activates small high-threshold afferents and activates brainstem and cortical systems. With a broad perspective, several salient features of this system activated by high-threshold input can be emphasized.
*For more detailed discussions of the material in this section, see References 10 to 12.
Chapter 2—Anatomy of the Pain Processing System
17
Frequency Encoding
Plasticity of Ascending Projections
It appears evident that stimulus intensity in a given system is encoded in terms of frequency of discharge. This holds true for any given link at the level of the primary afferent for both highand low-threshold axons, in the spinal dorsal horn for WDR, marginal neurons, and at brainstem and cortical loci. The relationship between stimulus intensity and the neuronal response is in the form of a monotonic increase in discharge frequency.
Whereas the pathways outlined are clearly pertinent to the nature of the message generated by a high-intensity stimulus, the encoding of a pain message depends not only on the physical characteristics of the otherwise effective stimulus but also on the properties of associated systems that can modulate (either up or down) the excitability of each of these synaptic linkages. Thus, local interneurons releasing γ-aminobutyric acid and glycine at the level of the spinal dorsal horn commonly regulate the frequency of discharge of second-order neurons excited by large afferent input. Pharmacologically blocking that local spinal inhibition can profoundly change the nature of the sensory experience to become highly aversive. This afferent plasticity is further considered in Chapter 3. In another dimension, such plasticity may also be seen at supraspinal levels. Thus, the potential role of this plasticity is reflected by the finding, in work by Pierre Rainville et al, hypnotic suggestions leading to an enhanced pain report in response to a given experimental stimulus resulted in greater activity in the anterior cingulate. Numerous lesions in humans and animals have been shown to dissociate the reported stimulus intensity psychophysically from its affective component. Such disconnection syndromes are produced by prefrontal lobectomies, cingulotomies, and temporal lobe–amygdala lesions.
Afferent Line Labeling Although frequency of discharge covaries with intensity, it is evident that the nature of the connectivity also defines the content of the afferent activity. As indicated, the biologic significance of a high-frequency burst of an Aß versus a highthreshold A-delta or C fiber for pain is evident.
Functionally Distinct Pathways At the spinal level, it is possible to characterize two functionally distinct families of response. In one spinofugal projection system (see Fig. 2.11), WDR neurons encode information over a wide range of non-noxious to severely aversive intensities consistent with the convergence of low- and high-threshold afferent neurons (either directly or through interneurons) onto their dendrites and soma. These cells project heavily into a variety of brainstem and diencephalic sites to the somatosensory cortex. At every level, the map of the body surface is precisely preserved, as is the broad range of intensity-frequency encoding. In the second spinofugal projection system (see Fig. 2.12), populations of superficial marginal cells display a strong nociceptive-specific encoding property, as defined by the highthreshold afferent input that they receive. These marginal cells project heavily to the parabrachial nuclei, to the amygdala, to the VMpo, the insula, medial thalamic nuclei, and then to the anterior cingulate cortex. The WDR system is uniquely able to preserve spatial localization information and information regarding the stimulus over a range of intensities from modest to extreme, as initially provided by the frequency response characteristics of the WDR neurons. This type of system is able to provide the information needed for mapping the “sensory-discriminative” dimension of pain. The nociceptive-specific pathway arising from the marginal cells appears less well organized in terms of its ability to encode precise place and response intensity until it is, by definition, potentially tissue injuring. These systems project heavily through the medial thalamic region and VMpo to the anterior cingulate and the insula/amygdala, respectively. These regions are classically appreciated to be associated with emotionality and affect. Accordingly, this type of circuitry would provide an important substrate for systems underlying the affective-motivational components of the pain experience. Functional magnetic resonance imaging and positron emission tomography have demonstrated that although non-noxious stimuli often have little effect, strong somatic and visceral stimuli initiate activation within the anterior cingulate cortex. This substrate involving a precise somatosensory map represents a system capable of mapping a sensory-discriminative dimension of pain. In contrast, the other system involving the limbic forebrain suggests a circuit that can mediate an “affective-motivational” component of the pain pathway. These dimensions were first formally described by Ronald Melzack and Ken Casey.
Pharmacology of Afferent Transmitter Systems in Nociception* An important question relates to the nature of the neurotransmitters and receptors that link the afferent projection systems. Such transmitter-receptor systems have several defining characteristics. First, the linkages between the primary afferent and secondorder spinal neurons, the linkages between the spinofugal axon and the third-order axon, and so on, have as a common property that the interaction leads to the excitation of the proximate neurons. Thus, the neurotransmitters mediating that synaptic transmission are excitatory. For example, at the spinal level, no “monosynaptic inhibition driven by primary afferents” occurs. Although powerful inhibitory events occur in the dorsal horn (and at every synaptic link), such inhibition must take place because of the excitation of a second neuron that releases an inhibitory transmitter. Second, it is increasingly evident that neurotransmission at any given synaptic link may consist not of one transmitter but of several cocontained and coreleased transmitters. At the small primary afferent, an excitatory amino acid (glutamate) and a peptide (e.g., substance P [sP]) are typically released. Third, although not discussed further here, each synaptic link is subject to modifications because of a dynamic regulation of the presynaptic transmitter content and the postsynaptic receptor and its linkages (e.g., with repetitive stimulation, the glutamate receptor undergoes phosphorylation, which serves to accentuate its excitatory response to a given amount of glutamate).
Primary Afferent Transmitters Considerable effort has been directed at establishing the identity of the excitatory transmitters in the primary afferent transmitters. Currently, excitatory amino acids, such as glutamate and certain peptides, including sP, vasoactive intestinal peptide (VIP), *For more detailed discussions of the material in this section, see References 3 and 13 to 17.
18
Section I—The Basic Science of Pain Anterior Cigulate Cortical Anterior Cingulate: Limbic-emotion Thalamocortical projections Submedius -> Anterior Cingulate Ascending thalamic projections Lam I -> mediodorsalis (?)
Fig. 2.13 Schematic of an overview of the characteristics of the projections of nociceptivespecific lamina I (Lam I) neurons into the mediodorsalis and from there to the anterior cingulate (Ant cingulate) cortex. As described in the text, this organization suggests the properties that would mediate the affectivemotivational aspects of pain. VLT, ventrolateral tract.
Primary afferent C terminal
Membrane A
B
Ascending axons in VLT Spinothalamic Spinofugal projections Lam I: Marginal-nociceptive specific Poor spatial encoding
Excitation Recording Dorsal horn neuron
mV Intracellular recording
C
Time (msec)
Fig. 2.14 Schematic displays the general characteristics of the primary afferent transmitters released from small, capsaicin-sensitive, primary afferents: C fibers. A, Small afferents terminate in laminae I and II of the dorsal horn and make synaptic contact with second-order spinal neurons. B, Peptides and excitatory amino acids are cocontained in small primary afferent ganglion cells (type B) and in dorsal horn terminals in dense core and clear core vesicles, respectively. C, On release, the excitatory amino acids are able to produce a rapid, early depolarization, whereas the peptides tend to evoke a long and prolonged depolarization of the second-order membrane. mV: transmembrane potential.
somatostatin, calcitonin gene–related peptide (CGRP), bombesin, and related peptides have been observed. C fibers possess the following characteristics (Figs. 2.13 and 2.14): Peptides have been shown to exist within subpopulations of small type B dorsal root ganglion cells. n Peptides are in the dorsal horn of the spinal cord (where most primary afferent terminals are found), and these levels in the dorsal horn are reduced by rhizotomy or ganglionectomy or by treatment with the small afferent neurotoxin capsaicin (acting on the TRPV1 receptor). n Many peptides are cocontained (e.g., sP and CGRP in the same C-fiber terminal) as well as contained with excitatory amino acids (e.g., sP and glutamate). n Release of peptides is reduced by the spinal action of agents known to be analgesic, such as opiates (see later). n Iontophoretic application onto the dorsal horn of the several amino acids and peptides found in primary afferents has been shown to produce excitatory effects. Amino acids produce very rapid, short-lasting depolarization. The peptides tend to produce delayed and long-lasting discharge. n
Ventrobasal Thalamus Mediodorsalis
Spinothalamic Tract
Spinal Cord Ventrolateral Tracts
Sensory afferent Receptor
Dorsal horn neuron
Diencephalon
Local spinal administration of several agents such as sP and glutamate does yield pain behavior, a finding suggesting the possible role of these agents as transmitters in the pain process.
n
Receptor antagonists exist for the receptors acted on by many of these agents (sP, VIP, glutamate). By using such agents, it has been possible to demonstrate that the primary charge carrier for depolarization of the second-order neurons is the α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) subtype of the glutamate receptor. Block of other glutamate receptors (e.g., the N-methyl-D-aspartate [NMDA] receptor) or the peptidergic transmitter receptors such as for sP (neurokinin-1) typically have a modest effect on the acute excitability of the second-order neuron and appear to reflect their role in augmenting the excitability of the neuron. Given the plethora of excitatory transmitter receptors that decorate the second-order neuron, nociceptive-evoked excitation of the second-order neuron may be poorly modified by the block of a single receptor type.
Ascending Projection System Transmitters Dorsal horn neurons projecting to brainstem sites have been shown to contain numerous peptides (including cholecystokinin, dynorphin, somatostatin, bombesin, VIPs, and sP). Glutamate has also been identified in spinothalamic projections, a finding suggesting the probable role of that excitatory amino acid. sP-containing fibers arising from brainstem sites have been shown to project to the parafascicular and central medial nuclei of the thalamus. In unanesthetized animals, the microinjection of glutamate in the vicinity of the terminals of ascending pathways, notably within the mesencephalic central gray area, evokes spontaneous painlike behavior with vocalization and vigorous efforts to escape, a finding emphasizing the presence of at least an NMDA site mediating the behavioral effects produced by NMDA in this region. Other systems will no doubt be identified as these supraspinal systems are studied in detail.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
3
I
Dynamics of the Pain Processing System Tony L. Yaksh and Z. David Luo
CHAPTER OUTLINE Acute Activation of Afferent Pain Processing 19 Tissue Injury–Induced Hyperalgesia 20 Psychophysics of Tissue Injury 20 Peripheral Afferent Terminal and Tissue Injury 20 Afferent Response Properties 20 Pharmacology of Peripheral Sensitization 20 Central Sensitization and Tissue Injury 21 Dorsal Horn Response Properties 21 Pharmacology of Central Facilitation 22 Glutamate Receptors and Spinal Facilitation 22 Lipid Mediators 22 Nitric Oxide 22 Phosphorylating Enzymes 23 Bulbospinal Systems 23 Nonneuronal Cells 24
Nerve Injury–Induced Hyperalgesia 24 Psychophysics of Nerve Injury Pain 24 Morphologic Correlates of Nerve Injury Pain 24 Spontaneous Pain State 24 Peripheral and Central Activity Generation 24 Changes in Afferent Terminal Sensitivity 26 Evoked Hyperpathia 26
Primary afferent input results in the activation of numerous circuits at the spinal and supraspinal levels. As reviewed in Chapter 2, there are multiple linkages in these systems. An important consequence of research since the 1990s has been the appreciation that afferent input at each synaptic link is subject to modulation by a variety of specific inputs. The net result is that the response evoked by a given stimulus is subject to welldefined influences that can serve to attenuate or enhance the excitation produced by a given physical stimulus. Specifically, these interactive systems alter the encoding of the afferent message and thereby change the perceived characteristics of the stimulus. For the sake of discussion, the processing of nociceptive information may be considered in terms of the pain behavior that arises from the following three conditions: (1) the behavior evoked by an acute activation of a high-threshold, slowly conducting afferent, (2) the exaggerated pain behavior (hyperalgesia/hyperesthesia) generated following local tissue injury or inflammation, and (3) the hyperalgesia that results secondary to a local peripheral nerve injury. Current work © 2011 Elsevier Inc. All rights reserved.
Dorsal Root Ganglion Cell Cross-Talk 26 Afferent Sprouting 26 Dorsal Horn Reorganization 26
Convergence Between Inflammatory and Nerve Injury Pain States 27 Overview of Mechanisms of Action of Several Common Pharmacologic Agents That Modify Pain Processing 27 Opioids 27 Sites of Action 27 Mechanisms of Opioid Analgesia 28 Supraspinal Action of Opioids 28 Spinal Action of Opiates 28 Peripheral Action of Opioids 29 Interactions Between Supraspinal and Spinal Systems 29 Nonsteroidal Anti-Inflammatory Drugs 29 Peripheral Action of Nonsteroidal Anti-Inflammatory Drugs 29 Spinal Action of Nonsteroidal Anti-Inflammatory Drugs 29 N-Methyl-d-Aspartate Receptor Antagonists 30 Alpha2-Adrenergic Agonists 30 Gabapentinoid Agents 30 Intravenous Local Anesthetics 30
Conclusion 30
suggests some convergence of these underlying mechanisms in the presence of certain persistent inflammatory states. An overview of the pharmacology and physiology of these dynamic states is provided subsequently.
Acute Activation of Afferent Pain Processing* Acute activation of small afferents by a transient, noninjurious stimulus results in clearly defined pain behavior in humans and animals. This event is mediated by the local stimulus-evoked activation of small, high-threshold afferents leading to the release of excitatory afferent transmitters outlined previously (see Chapter 2) and, consequently, the depolarization of spinal projection neurons. The organization of this acutely driven system is typically modeled in terms *For a more detailed discussion of the material in this section, see Reference 1.
19
20
Section I—The Basic Science of Pain
of linear relationships among stimulus intensity, activity in the peripheral afferent, the magnitude of spinal transmitter release, and the activity of neurons that project out of the spinal cord to the brain. In its most straightforward rendition, this organization resembles the classic “pain pathway” that appears in most texts (Fig. 3.1).
injury site where a moderate stimulus applied to uninjured tissue generates an aversive sensation (secondary hyperalgesia). It is important to understand what initiates these pain components. As discussed later, it is evident that these events reflect both peripheral and central consequences of the injury and the stimulus presented.
Tissue Injury–Induced Hyperalgesia
Peripheral Afferent Terminal and Tissue Injury† Afferent Response Properties
Psychophysics of Tissue Injury* With tissue injury, a triad of events is noted shortly after the initiation of the injury: (1) a dull throbbing, aching sensation; (2) an exaggerated response to a moderate intense stimulus (primary hyperalgesia); and (3) an enlarged area around the
Injury and inflammation in the vicinity of the sensory terminals increase the excitability of C-polymodal nociceptors innervating the injured site. This enhanced excitability is reflected by the appearance of spontaneous afferent activity and a left shift in the stimulus-response curve of the afferent (Fig. 3.2). These events underlie the “triple response”: a red flush around the site of the stimulus (local arterial dilation), local edema (capillary permeability), and a regional reduction in the magnitude of the stimulus required to elicit a pain response (i.e., hyperalgesia). This local response is in part neurogenic in that it results from local antidromic activity in the peripheral collaterals of the sensory terminal. Here activity initiated in the branch proceeds orthodromically. At a local branch point, the action potential proceeds centrally and antidromically, back toward the periphery. At the peripheral terminal, the action potential results in the local release of the content of the afferent terminal for C fibers, such as substance P (SP) and calcitonin gene–related peptide (CGRP), which lead, respectively, to vasodilation (reddening) and plasma extravasation (swelling).
*For more detailed discussions of the material in this section, see References 2 and 3.
Transient High-Intensity Stimuli Treatment Acute Thermal Mechanical
Afferent Traffic
Spinal Activity
Behavioral Indices
A∂/C
DHN
Escape, verbal report
Pharmacology of Peripheral Sensitization‡
Fig. 3.1 Schematic depicting the principal components of the afferent spinal cord response to an acute high-intensity afferent stimulus. A stimulus intensity–dependent increase in discharge frequency in specific populations of high-threshold primary afferents initiates a stimulus intensity–dependent increase in the firing of dorsal horn neurons (DHN) that projects to higher centers (a wide dynamic range [WDR] neuron is shown here). The outflow of the spinal cord projects to higher centers, as described in Chapter 2.
After local tissue injury and inflammation, the milieu of the peripheral terminal is altered secondary to tissue damage and the accompanying extravasation of plasma. These effects result
For more detailed discussions of the material in this section, see References 3 and 4. For more detailed discussions of the material in this section, see References 5 and 6.
†
‡
Stimulus
Injury
Hz
Fig. 3.2 Left top panel, Primary afferent terminal. Local tissue-damaging stimulus leads to firing of the fine afferents and local activation of inflammatory cells. Right top panel, This injury causes the response profile of a high-threshold afferent to shift up and to the left, thus indicating the appearance of spontaneous activity at non-noxious stimulus intensities and an inflection of the stimulus response curve at a lower stimulus intensity. Lower panel, In response to the stimulus, afferent fibers display antidromic release of neuropeptides (substance P/calcitonin gene–related peptide [SP/CGRP]). Hormones, such as bradykinin (Bk), prostaglandins (PGs), and cytokines, or potassium and hydrogen ions (K+/H+) released from inflammatory cells and plasma extravasation products result in stimulation and sensitization of free nerve endings. 5-HT, 5-hydroxytryptamine (serotonin).
Normal Local Injury
30
38
46
54
60
Thermal Stimulus (°C) Blood Products
5-HT
Inflammatory cells
Proteinases Cytokines
Tissue injury products
Bk / PGs K / H
Afferent terminal release
SP/CGRP
Spontaneous Activity Sensitization of Terminal
Chapter 3—Dynamics of the Pain Processing System
in the concurrent release of a variety of algogenic agents from damaged tissue and from the peripheral terminals of sensory afferents activated by local C-fiber axon reflexes (Table 3.1). These chemical intermediaries have two distinct effects: (1) direct excitation of afferent C fibers; and (2) facilitation of C-fiber activation, resulting in a left shift and increasing slope of the frequency response curve of the C-fiber axon. These
Table 3.1 Representative Classes of Agents Released by Tissue Injury: Activity and Sensitivity of Primary Afferent Fibers 1. Amines: Histamine (mast cells) and serotonin (platelets) are released by a variety of stimuli, including trauma, and many are released by chemical products of tissue damage. 2. Kinin: Bradykinin is synthesized by a cascade that is triggered by the activation of the clotting cascade. Bradykinin acts by specific bradykinin receptors (B1/B2) to activate free nerve endings. 3. Lipidic acids: Lipids such as prostanoids and leukotrienes are synthesized by cyclooxygenases and lipoxygenases. Many prostanoids, such as prostaglandin E2 can directly activate C fibers and facilitate the excitability of C fibers through specific membrane receptors. 4. Cytokines: Cytokines, such as the interleukins or tumor necrosis factor, are formed as part of the inflammatory reaction involving macrophages and powerfully sensitize C-fiber terminals. 5. Primary afferent peptides: Calcitonin gene–related peptide and substance P are found in and released from the peripheral terminals of C fibers and produce local cutaneous vasodilation, plasma extravasation, and sensitization in the region of skin innervated by the stimulated sensory nerve. 6. Hydrogen ion/potassium ion ([H+]/[K+]): Elevated H+ (low pH) and high K+ are found in injured tissue. These ions directly stimulate C fibers and evoke the local release of various vasodilatory peptides. Various receptors of triglyceride-rich lipoprotein particles are activated by increased H+. 7. Proteinases: Proteinases, such as thrombin or trypsin, are released from inflammatory cells and can cleave tethered peptide ligands that exist on the surface of small primary afferents. These tethered peptides act on adjacent receptors, proteinase-activated receptors, that can depolarize the terminal.
21
peripheral events likely contribute to the ongoing pain and the increase in the reported magnitude of the pain response evoked by a given stimulus (hyperalgesia).
Central Sensitization and Tissue Injury* Dorsal Horn Response Properties As reviewed in Chapter 2, a close linkage exists between stimulus intensity and frequency of dorsal horn discharge and pain magnitude. In the presence of tissue injury, there is the onset of a persistent discharge of small afferents. It is now appreciated that this persistent discharge can lead to a facilitation of dorsal horn reactivity. In animal studies, dorsal horn wide dynamic range (WDR) in the deep dorsal horn displays a stimulusdependent response to low-frequency (0.1-Hz) activation of afferent C fibers. Repetitive stimulation of C (but not A) fibers at a moderately faster rate (>0.5 Hz) results in a progressively facilitated discharge. This exaggerated discharge was named wind-up by Lorne Mendell and Pat Wall in 1966 (Fig. 3.3). Intracellular recording has indicated that the facilitated state is represented by a progressive, long-sustained, partial depolarization of the cell that renders the membrane increasingly susceptible to afferent input. Given the likelihood that WDR discharge frequency is part of the encoding of the intensity of a high-threshold stimulus, and that many of these WDR neurons project in the ventrolateral quadrant of the spinal cord (i.e., spinobulbar projections), this augmented response is believed to be an important component of the pain message. Protracted pain states such as those that occur with inflamed or injured tissue would routinely result in such an augmented afferent drive of the WDR neuron and then to the ongoing facilitation. Thus, there would be an enhanced response to a given stimulus (leading to a left shift in the stimulus response curve for the dorsal horn WDR neuron). This sensitization also provides a probable mechanism for the otherwise puzzling change in the size of the receptive field where a stimulus applied to a dermatome adjacent to the injury may yield a pain sensation. As reviewed in Chapter 2, primary afferents entering through a given root make synaptic contact in the spinal level of entry, but they also send collaterals rostrally and caudally to more distant segments, where they can activate these distant neurons (although with less *For more detailed discussions of the material in this section, see References 7 to 12.
S
Number
80
WDR Wind-up
40
Normal
0 A and C 0.5 Hz
A 0.5 Hz Afferent Stimulation Parameters
A and C 0.1 Hz
— 10 s
Fig. 3.3 Right, Single-unit recording from a wide dynamic range (WDR) neuron in response to an electrical stimulus delivered at 0.1 Hz. A very reliable, stimulus-linked response is evoked at this frequency. Left, In contrast, when the stimulation rate is increased to 0.5 Hz, there is a progressive increase in the magnitude of the response generated by the stimulation. Middle, This facilitation, which results from the C-fiber input and not from A-fiber input, is called wind-up.
22
Section I—The Basic Science of Pain Horizontal
Injury in RF 1
• Sensitization of neuron 1 • Minor input from RF 2 • now leads neuron 1 to be • activated • RF-neuron 1 = RF (12)
1
2
Fig. 3.4 Receptive field (RF) of a dorsal horn neuron depends on its segmental input and the input from other segments that can activate it. After injury in RF 1, neuron 1 becomes “sensitized.” Collateral input from RF 2 normally is unable to initiate sufficient excitatory activity to activate neuron 1, but after sensitization, RF 2 input is sufficient. Now the RF of neuron 1 is effectively RF1 + RF2. Thus, local injury by spinal mechanisms can lead acutely to increased receptive fields such that stimuli applied to a noninjured RF can contribute to the post–tissue injury sensation.
security than at the segment of entry). However, as schematically defined in Figure 3.4, current thinking suggests that, in the presence of a conditioning injury stimulus, the distant second-order neuron may become sensitized by the high-frequency activity such that input from that proximal dermatome will lead to an intense activation of the distant neuron that provides a “pain signal” referred to the proximal dermatome. The preceding observations regarding this dorsal horn system have been shown to have behavioral consequences. Psychophysical studies have shown that a discrete injury to the skin of the volar surface of the arm or the direct activation of small afferents by the focal injection of a C-fiber stimulant (capsaicin) results in a small area of primary hyperesthesia surrounded by a much larger area of secondary hyperesthesia. If a local anesthetic block is placed proximal to the injection site before the insult, the onset of the secondary hyperesthesia is prevented. Moreover, WDR wind-up studies are typically carried out in animals under 1 MAC (i.e., minimum alveolar concentration) anesthesia. One would speculate that in patients, the processes considered in the following discussion that lead to spinal facilitation would occur even with such MAC anesthesia. The implication of the afferent-evoked facilitation is that it is better to prevent small afferent input than to deal with its sequelae. This observation is believed to represent the basis for the consideration of the use of preemptive analgesics (e.g., agents and modalities that block small afferent input).
Pharmacology of Central Facilitation* Based on the foregoing commentary and the discussion in Chapter 2, a reduction in C-fiber–evoked excitation in the dorsal horn by blocking axon transmission (sodium channel blockers), by blocking release of small afferent transmitter (as with opiates), or by blocking the postsynaptic receptor (e.g., NK1 for SP or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA] for glutamate) will diminish the magnitude of the afferent drive and, accordingly, the facilitated processing evoked by protracted small afferent input. However, the windup state reflects more than the repetitive activation of a simple excitatory system. The following is a review of systems that are part of the afferent pathway and other systems that particularly contribute to facilitated p rocessing at the spinal level. *For a more detailed discussion of the material in this section, see Reference 13.
Glutamate Receptors and Spinal Facilitation The first real demonstration that spinal facilitation represented unique pharmacology was presented by showing that the phenomenon was prevented by the spinal delivery of antagonists for the N-methyl-d-aspartate (NMDA) receptor. Importantly, these antagonists had no effect on acute evoked activity in dorsal horn neurons, but they reduced wind-up. Behavioral work demonstrated that such drugs had no effect on acute pain thresholds but reduced the facilitated states induced after tissue injury and inflammation. As noted, the NMDA receptor does not appear to mediate acute excitation. This finding reflects an important property of this receptor. Under normal resting membrane potentials, the NMDA receptor is in a state referred to as a magnesium block. In this condition, occupancy by glutamate will not activate the ionophore. If a modest depolarization of the membrane (as produced during repetitive stimulation secondary to the activation of AMPA and SP receptors) occurs, the magnesium block is removed, permitting glutamate to activate the NMDA receptor. When this happens, the NMDA channel permits the passage of calcium (Fig. 3.5). This increase in intracellular calcium then serves to initiate the downstream components of the excitatory and facilitatory cascade. The excitation generated by small primary afferent input has been found to lead to many distinct biochemical events that can serve to enhance the response of dorsal horn neurons and lead to phenomena such as wind-up. Although the activation of the NMDA receptor is an important element of that facilitatory process, it is only one of many. Several representative examples of cascades leading to spinal sensitization are considered here.
Lipid Mediators In the presence of repetitive afferent stimulation, increased intracellular calcium in spinal neurons leads to the activation of a cascade that releases prostaglandins. These prostanoids act on specific receptors that are presynaptic and postsynaptic to the primary afferent and serve to enhance primary afferent transmitter release and to facilitate the discharge of the postsynaptic dorsal horn neuron (Fig. 3.6). The presynaptic effect is believed to be through a facilitation of the opening of the voltage-sensitive calcium channel that is necessary for transmitter release. The postsynaptic action is mediated by the inactivation of a glycine receptor, which is otherwise acted on by glycine released from an inhibitory interneuron. This glycinergic inhibitor interneuron reflexively regulates the magnitude of the firing of the second-order neuron. Loss of the glycinergic inhibition is believed to result in an enhanced response to the afferent input. Cyclooxygenase (COX) inhibitors inhibiting the COX-2 enzyme have been shown to act spinally to block spinal prostanoid release and to diminish injury-evoked hyperalgesia. These results are consistent with the demonstration of the constitutive expression of the several synthetic enzymes, including several phospholipases (PLA2) and the two COX isoforms.
Nitric Oxide Nitric oxide (NO) is released following spinal afferent activation through several constitutively expressed NO synthases. NO has been shown to play a role in central facilitation phenomena by increasing transmitter release (see Fig. 3.6). Similarly, in the spinal cord, NO synthase inhibitors have been shown to prevent hyperalgesia.
Chapter 3—Dynamics of the Pain Processing System
23
C Terminal Glutamate
Receptors Channels
Mg
AMPA NK1
SP Ca
GLU
NMDA
Glycine GLU
Ca
Ca
Dorsal Horn Neuron
C Terminal
Glycine-r NMDA-r
SP
NO
Ca
EP-r
GLU NOS
PGE2
Ca COX2
Polyamine
Dorsal Horn Neuron
P38 MAPK PLA 2
Glycine
Fig. 3.6 Schematic of primary afferent synapse with second-order neuron in the superficial dorsal horn. On depolarization, multiple transmitters are released. In the presence of persistent depolarization, the glutamate (GLU) receptor is activated, and this leads to increased intracellular calcium (Ca++). This process initiates a variety of cascades, including the activation of nitric oxide synthase (NOS) and the release of nitric oxide. Through P38 mitogen–activated kinase (P38 MAPK), phospholipase A2 (PLA2) and cyclooxygenase (COX) lead to the formation and release of prostaglandins (PGE2). Prostaglandins can act presynaptically to increase the opening of voltage-sensitive calcium channels and postsynaptically to inhibit the activation of a glycinergic inhibitory interneuron. These combined effects are believed to facilitate the activation of the secondorder neuron by an afferent input. EP-r, prostaglandin receptor; NMDA-r, N-methyl-D-aspartate receptor; SP, substance P.
Phosphorylating Enzymes Many enzymes found in neurons can phosphorylate specific sites on various enzyme channels, receptors, and channels. Several of these protein kinases in spinal neurons have been shown to be activated by high-frequency small afferent input.
Na
Fig. 3.5 Left, Schematic showing the synapse between a C fiber and a secondorder dendrite I in the superficial dorsal horn. The synaptic linkage is composed of multiple excitatory transmitters acting on several receptors on the second-order neuron. Right, Schematic of an N-methyld-aspartate (NMDA) ionophore. As indicated in the text, the NMDA receptor is a calcium (Ca++) ionophore that, when activated, results in an influx of Ca. To be activated, the receptor requires the occupancy by glutamate (GLU), the removal of the magnesium (Mg) block by a mild membrane depolarization, the occupancy of the “glycine site,” and several allosterically coupled elements, including the “polyamine site.” Together, these events permit the ionophore to be activated. AMPA, α-amino-3-hydroxy5-methyl-4-isoxazolepropionic acid; Na, sodium; NK1, neurokinin 1 receptor; SP, substance P.
Two examples of this effect are provided by the role of protein kinase C (PKC) and P38 mitogen–activated protein kinase (P38 MAPK). PKC is activated in the presence of increased intracellular calcium and has been shown to phosphorylate certain proteins, including the NMDA receptor. This NMDA receptor phosphorylation has been demonstrated to enhance the functionality of that channel and to lead to increased calcium passage when the channel is activated. This process enhances the postsynaptic effect of any given amount of glutamate release. P38 MAPK is known to be one of the kinases that serve to activate PLA2. Thus, the formation of prostaglandins dependent on the freeing of arachidonic acid by this enzyme is activated by that kinase. Importantly, activation of P38 MAPK is also known to increase the transcription of specific proteins. In the case of P38 MAPK, one such protein whose expression is increased by P38 MAPK activation is COX-2. Therefore, in the presence of persistent afferent stimulation, activation of this isoform initiates downstream events that change the expression of several proteins relevant to pain processing. This recitation is meant to provide an insight into the types of events that can be mediated by these kinases and is not exhaustive.
Bulbospinal Systems It is known that afferent input particularly arising from the lamina I marginal cells (see Chapter 2) will activate ascending pathways and lead to excitatory input into the brainstem. At the medullary level, norepinephrine- and serotonin-containing cells have been identified that project into the spinal dorsal horn (e.g., bulbospinal projections). Although these descending pathways have long been considered to be inhibitory, this inhibitory effect is likely the result of the noradrenergic systems. Of particular interest, the serotonergic systems have been shown to play an important facilitatory role in the wind-up observed in WDR neurons evoked by small afferent input. Thus, small afferent input activates lamina I projections into the medulla. These activate descending 5-hydroxytryptamine (serotonin; 5-HT) projections, which are excitatory, facilitate the discharge of WDR n eurons (Fig. 3.7).
24
Section I—The Basic Science of Pain injury and tissue injury rapidly and significantly. In addition to their ability to be influenced by local neuronal circuitry, circulating cytokines (interleukin-1ß [IL-1ß]/tumor necrosis factor-α [TNFα]) released by injury and inflammation can activate perivascular astrocytes and microglia. Accordingly, these cells provide an avenue whereby circulating products can influence neuraxial e xcitability (Fig. 3.8).
Medulla Raphe magnus (5-HT)
Nerve Injury–Induced Hyperalgesia
Bulbospinal projection
Psychophysics of Nerve Injury Pain* Spinomedullary projection
Marginal neuron
WDR neuron
Over time, after a variety of injuries to the peripheral nerve, a constellation of pain events will appear. Frequent components of this evolving syndrome are as follows: (1) incidences of sharp, shooting sensations referred to the peripheral distribution of the injured nerve; and (2) pain secondary to light tactile stimulation of the peripheral body surface (tactile allodynia). This composite of sensory events was formally recognized by Silas Weir Mitchell in the 1860s. This pain state emphasizes the anomalous role of low-threshold mechanoreceptors (Aß afferents). The ability of light touch to evoke this anomalous pain state indicates that the injury has led to a reorganization of central processing (i.e., it is not necessarily the result of a peripheral sensitization of high-threshold afferents). In addition to these behavioral changes, the neuropathic pain condition may display other contrasting anomalies, including, on occasion, an ameliorating effect of sympathectomy of the afflicted limb and an attenuated responsiveness to analgesics, such as opiates. As an overview, the spontaneous pain and the miscoding of low-threshold afferent nerves are believed to reflect (1) an increase in spontaneous activity in axons in the injured afferent nerve and/or the dorsal horn neurons and (2) an exaggerated response of dorsal horn neurons to normally innocuous afferent input.
Morphologic Correlates of Nerve Injury Pain Fig. 3.7 Schematic showing the linkage whereby small afferent input activates a lamina I cell that projects to the medulla. This projection has been shown to activate a raphe spinal serotonergic projection into the dorsal horn. This input, although an excitatory serotonin receptor, will augment the discharge of the wide dynamic range (WDR) neuron. 5-HT, 5-hydroxytryptamine (serotonin).
Nonneuronal Cells At the spinal level, large populations of astrocytes and microglia are present. Although these cell systems play an important trophic role, it is increasingly evident that they are also able to regulate the excitability of local neuronal circuits effectively. Thus, astrocytes can regulate extracellular glutamate levels by active reuptake and secretion. These cells also are potent releasers of a variety of active factors such as adenosine triphosphate, lipid mediators, and cytokines. By gap junctions, activation of one astrocyte can lead to a spread of activation that can influence cells over a spatially extended volume. Microglia are similarly interactive by their ability to be activated by a variety of products released from primary afferents and from other neuronal and non-neuronal cells. Spinal agents known to block the activation of astrocytes (fluorocitrate) and microglia (minocycline) have been shown to diminish excitatory states initiated by peripheral
Following peripheral nerve ligation or section, several events occur that signal long-term changes in peripheral and central processing. Thus, in the periphery after an acute mechanical injury of the peripheral afferent axon, an initial dying back (retrograde chromatolysis) proceeds for some interval, at which time the axon begins to sprout and to send growth cones forward. The growth cone frequently fails to make contact with the original target and displays significant proliferation. Collections of these proliferated growth cones form structures called neuromas. As reviewed in the following sections, the peripheral injury leads not only to changes at the injury site but also to a very prominent reorganization of the nature of the proteins that are expressed in the dorsal root ganglion (DRG) and spinal cord, as well as the activation of a variety of circuits and cascades involving neuronal and non-neuronal cells.
Spontaneous Pain State† Peripheral and Central Activity Generation Under normal conditions, primary afferents show little if any spontaneous activity. After peripheral nerve ligation or section, several events are noted to occur: (1) persistent small afferent *For more detailed discussions of the material in this section, see References 14 and 15. † For more detailed discussions of the material in this section, see References 16 to 18.
Chapter 3—Dynamics of the Pain Processing System
25
Neurovasculature Circulating products of inflammation Microglial Activation p38 Astrocyte Fractalkine ATP Glutamate
IL-1, TNF, BDNF Proteases, glutamate PG, NO
Cytokines Afferent Terminal
BDNF other peptides SP Glu Etc
Nerve Injury
AMPA/-r receptor NMDA-r receptor 20 Neuron mGlu-r Peptide-r
Spontaneous Afferent Activity
Mechanism: Na Channel Receptors Transmitter (amines) Cytokines (TNF) Enzymes (trypsin) Locally activates membrane of neuroma/DRG
Fig. 3.9 Following nerve injury over an interval of days to weeks, the neuroma of the injured afferent and its dorsal root ganglion (DRG) cell begin to display ectopic activity. Na, sodium; TNFα, tumor necrosis factor-α.
fiber activity originating after a period from the lesioned nerve in both myelinated and unmyelinated axons and (2) spontaneous activity developing from the DRG of the injured nerve. Accordingly, the spontaneous pain sensation may be related to this ongoing afferent traffic. An important question is the source of this afferent traffic. One cannot exclude the likelihood of a spinal generator. Early work indeed demonstrated that after rhizotomy, an increase in activity over time was observed in WDR neurons. With regard to the peripheral generator, several mechanisms have become likely (Fig. 3.9). Increased Expression of Channels The events occurring following nerve injury have shown major changes in the proteomics of the DRGs and associated injured axon. Several families of protein that are of particular interest are those associated with the several classes of voltage-gated channels.
Fig. 3.8 Schematic displays the linkage between the primary afferent and the second-order neuron. The illustration also emphasizes the presence of astrocytes and microglia, which are activated by various products released from activated neurons and from the nonneuronal cells. In addition, the microglia are able to sample the content of the vasculature and these products, such as interleukin-1ß (IL-1ß), can activate these cells. The net effect is that these nonneuronal cells can alter the excitability of local neuronal circuits. AMPA-r, α-amino3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; ATP, adenosine triphosphate; BDNF, brain-derived neurotrophic factor; Glu, glutamate; NMDA-r, N-methyl-Daspartate receptor; NO, nitric oxide; PG, prostaglandin; SP, substance P; TNF, tumor necrosis factor.
Sodium Channels Multiple sodium channels have been identified, based on structure (NaV 1.1 to NaV 1.9), tetrodotoxin sensitivity (TTX), and their activation kinetics. Based on these designations, some of the subtypes are limited in their expression to small primary afferents (NaV 1.8 and 1.9), and some are limited to large myelinated afferents as well as to the central nervous system (NaV 1.3). After nerve injury, there is significant up-regulation of a variety of sodium channels in the neuroma and in the DRG of the injured large and small axons (e.g., NaV 1.3, 1.8, and 1.9). Consistent with the role of sodium channels is that the spontaneous activity originating from the neuromas and from the DRG is blocked by intravenous lidocaine at plasma concentrations lower than those that block conduction in the nerve. Potassium Channels Potassium channels regulate the terminal and soma polarization state. In the action potential, increased potassium channel activity leads to repolarization of the membrane and thus reduces the probability of repetitive discharge. Decreasing membrane expression on a variety of potassium channels has been observed. This down-regulation of potassium channels leads to enhanced axonal activity. Calcium Channels Calcium channels serve as charge carriers and as vehicles by which depolarization may lead to increased influx of calcium. For transmitter release, this influx serves to mobilize synaptic vesicles for transmitter release. Various calcium channels (CaV) are expressed in the DRG, and their up-regulation has been reported. Of particular interest is that a component of the N-type calcium channel expressed on the extracellular lumen, which is prominently up-regulated after nerve injury, is the alpha2 delta subunit. As noted later, this is the probable binding site for a family of agents that have efficacy in nerve injury pain states. Many of these changes represent a reversion of the DRG to a neonatal phenotype that is associated with increased excitability.
26
Section I—The Basic Science of Pain
Changes in Afferent Terminal Sensitivity The sprouted terminals of the injured afferent axon display a characteristic growth cone that has transduction properties that were not possessed by the original axon. These properties include significant mechanical and chemical sensitivity. Thus, these spouted endings may have sensitivity to numerous humoral factors, such as prostanoids, catecholamines, and cytokines such as TNFα. This evolving sensitivity is of particular importance given that current data suggest that after local nerve injury there is the release of a variety of cytokines, particularly TNFα, that can directly activate the nerve and neuroma. In addition, after nerve injury, an important sprouting of postganglionic sympathetic efferents can lead to the local release of catecholamines. This situation is consistent with the observation that after nerve injury, the postganglionic axons can initiate excitation in the injured axon (see later). These events are believed to contribute to the development of spontaneous afferent traffic after peripheral nerve injury.
Evoked Hyperpathia* The observation that low-threshold tactile stimulation yields a pain state has been the subject of considerable interest. As noted, most investigators agree that these effects are often mediated by low-threshold afferent stimulation. Several underlying mechanisms have been proposed to account for this seemingly anomalous linkage.
Dorsal Root Ganglion Cell Cross-Talk Following nerve injury, evidence suggests that “cross-talk” develops between afferents in the DRG and those in the neuroma. Depolarizing currents in one axon would generate a depolarizing voltage in an adjacent quiescent axon. This depolarization would permit activity arising in one axon to drive activity in a second. In this manner, it is hypothesized that a large low-threshold afferent would drive activity in an adjacent high-threshold afferent.
Afferent Sprouting Under normal circumstances, large myelinated (Aß) afferents project into the spinal Rexed laminae III and deeper. Small afferents (C fibers) tend to project into spinal laminae II and I, a region consisting mostly of nociceptor-responsive neurons. Following peripheral nerve injury, it has been argued that the central terminals of these myelinated afferents (A fibers) sprout into lamina II of the spinal cord. With this synaptic reorganization, stimulation of low-threshold mechanoreceptors (Aß fibers) could produce excitation of these neurons and could be perceived as painful. The degree to which this sprouting occurs is a point of current discussion, and although it appears to occur, it is considerably less prominent than originally proposed.
Dorsal Horn Reorganization Following peripheral nerve injury, numerous events occur in the dorsal horn. This finding suggests altered processing wherein the response to low-threshold afferent traffic can be exaggerated. SPINAL GLUTAMATE RELEASE The post–nerve injury pain state is dependent on spinal glutamate release. After nerve injury, a significant enhancement in resting spinal glutamate secretion occurs. This release is in accord with (1) an increased spontaneous activity in the *For more detailed discussions of the material in this section, see References 13 and 19 to 21.
primary afferent and (2) the loss of intrinsic inhibition that may serve to modulate resting glutamate secretion (see later). The physiologic significance of this release is emphasized by the following convergent observations: (1) intrathecally delivered glutamate evokes powerful tactile allodynia and thermal hyperalgesia through the activation of spinal NMDA and non-NMDA receptors and (2) the spinal delivery of NMDA antagonists attenuates the hyperpathic states arising in animal models of nerve injury. As reviewed earlier in this chapter, NMDA receptor activation mediates neuronal excitability. In addition, the NMDA receptor is a calcium ionophore that, when activated, leads to prominent increases in intracellular calcium. This increased calcium initiates a cascade of events that includes the activation of a variety of enzymes (kinases), some of which phosphorylate membrane proteins (e.g., calcium channels and the NMDA receptors), whereas others (e.g., the mitogenactivated kinases [MAP kinases]) mediate intracellular signaling that leads to the altered expression of a variety of proteins and peptides (e.g., COXe and dynorphin). This downstream nuclear action is believed to herald long-term and persistent changes in function. Various factors have been shown to enhance glutamate release. Two examples are discussed further here. NONNEURONAL CELLS Following nerve injury, investigators have shown a significant increase in activation of spinal microglia and astrocytes in the spinal segments receiving input from the injured nerves. Of particular interest is that, in the presence of diseases such as bone cancer, such up-regulation has also been clearly shown. As reviewed earlier, microglia and astrocytes are activated by a variety of neurotransmitters and growth factors. Although the origin of this activation is not clear, when it occurs, it leads to increased spinal expression of COX, NO synthase, glutamate transporters, and proteinases. Such biochemical components have been shown to play important roles in the facilitated state. LOSS OF INTRINSIC GABAERGIC/GLYCINERGIC CONTROL In the spinal dorsal horn, large numbers of small interneurons contain and release γ-aminobutyric acid (GABA) and glycine. GABA/glycinergic terminals are frequently presynaptic to the large central afferent terminal complexes and form reciprocal synapses, whereas GABAergic axosomatic connections on spinothalamic cells have also been identified. Accordingly, these amino acids normally exert an important tonic or evoked inhibitory control over the activity of Aß primary afferent terminals and second-order neurons in the spinal dorsal horn. The relevance of this intrinsic inhibition to pain processing is provided by the observation that simple intrathecal delivery of GABA-A receptor or glycine receptor antagonists will lead to powerful, behaviorally defined tactile allodynia. Similarly, animals genetically lacking glycine-binding sites often display a high level of spinal hyperexcitability. These observations lead to consideration that following nerve injury, loss of GABAergic neurons may occur. Although data do support a loss of such GABAergic neurons, the loss appears to be minimal. A second alternative is that after nerve injury, spinal neurons regress to a neonatal phenotype in which GABA-A activation becomes excitatory. This excitatory effect is secondary to reduced activity of the membrane chloride (Cl−) transporter, which changes the reversal current for the Cl− conductance. Increasing membrane Cl− conductance, as occurs with GABA-A receptor activation, results in membrane depolarization.
Chapter 3—Dynamics of the Pain Processing System
DYNORPHIN The peptide dynorphin has been identified within the spinal cord. Following peripheral nerve injury, spinal dorsal horn expression of dynorphin is increased. Intrathecal delivery of dynorphin can initiate the concurrent release of spinal glutamate and potent tactile allodynia. This allodynia is reversed by NMDA antagonists. SYMPATHETIC INPUT Following peripheral tissue injury, spontaneous discharge appears in otherwise silent small axons. This spontaneous activity is blocked by lidocaine, the sodium channel blocker, at concentrations that do not block the conducted potential. After peripheral nerve injury, innervation of the peripheral neuroma by postganglionic sympathetic terminals is increased. Investigators have shown that an ingrowth of postganglionic sympathetic terminals occurs in the DRGs of the injured axons. These postganglionic fibers form baskets of terminals around the ganglion cells. Several properties of this innervation are interesting: (1) they invest all sizes of ganglion cells, but particularly type A (large ganglion cells); (2) the innervation occurs principally in the DRG ipsilateral to the lesion, but in addition, there is innervation of the contralateral ganglion cell; and (3) stimulation of the ventral roots of the segments containing the preganglionic efferents will produce activity in the sensory axon by an interaction either at the peripheral terminal at the site of injury or by an interaction at the level of the DRG. This excitation is blocked by intravenous phentolamine, a finding emphasizing an adrenergic effect (Fig. 3.10). The observations that sympathetic innervation increases in the ganglion after nerve injury and that afferent activity can be driven by sympathetic stimulation provide some linkage between these efferent and afferent systems and suggest that an overall increase in sympathetic activity per se is not necessary to evoke the activity. These observations also provide a mechanism for the action of alpha antagonists (phentolamine) and alpha2 agonists (clonidine), agents that have been reported to be effective after topical or intrathecal delivery. Thus, alpha2 receptors may act presynaptically to reduce sympathetic terminal release. Spinally, alpha2 agonists are known to depress preganglionic sympathetic outflow. In either case, to the extent that pain states are driven by sympathetic input, these states would be diminished accordingly. This consideration provides some explanation of why opiates do not exert a potent effect on the allodynia observed after nerve injury. As summarized earlier,
27
neither microagonists nor alpha2 agonists alter large afferent input, yet alpha2 agonists may reduce allodynia. This differential action may result from the fact that opiates, unlike the alpha2 agonist agents, do not alter sympathetic outflow (as indicated by the lack of effect of spinal opiates on resting blood pressure).
Convergence Between Inflammatory and Nerve Injury Pain States In the preceding section, the discussion emphasized that several sets of mechanisms underlie the altered processing that arises after tissue and nerve injury. In the presence of persistent injury and inflammation, signs suggesting of a systems response engendered by nerve injury may appear. Thus, with nerve injury, activation of satellite cells and the appearance of cyclic adenosine monophosphate–dependent transcription factor (ATF-3) are commonly observed in the DRG. Investigations have suggested that such changes may also be observed in the presence of persistent inflammatory states. This property suggests that a component of the effects (e.g., observed in rheumatoid disease in which the pain state persists in spite of a significant resolution of the inflammatory signs) may reflect a transition from acute inflammatory mechanisms to a condition representing nerve injury.
Overview of Mechanisms of Action of Several Common Pharmacologic Agents That Modify Pain Processing Earlier, the discussion considered the various aspects of the pharmacology of the systems that underlie the dynamic aspects of pain processing. The following text briefly considers mechanisms whereby certain pharmacologic modalities exert their action to produce a change in pain processing.
Opioids* Systemic opioids have been shown to produce a powerful and selective reduction in the human and animal response to a strong and otherwise noxious stimulus. Current data emphasize that these agents may interact with one or a combination of three receptors: mu, delta, and kappa. Given the widespread use of this class of drugs, the site through which these effects are mediated and the mechanisms of those actions are points of interest. Direct assessment of the locus of action can be addressed initially by the focal application of the agent to the various purported sites of action, and the effects of such injections on behavior and the pharmacology of those local effects (to ensure a receptor-mediated effect) can be examined.
Sites of Action
Fig. 3.10 After injury to the peripheral nerve, postganglionic sympathetic afferents sprout into the neuroma. Similar sprouting occurs to the dorsal root ganglion (DRG) of the injured axon. Importantly, electrophysiologic studies have shown that the activation of preganglionic sympathetic outflow to the neuroma or the DRG initiates ectopic activity.
SUPRASPINAL SITES Microinjection mapping in animals prepared with stereotactically placed guide cannulae revealed that opioid receptors are functionally coupled to the regulation of the animal's response to strong and otherwise noxious mechanical, thermal, and chemical stimuli, which excite small primary afferents. Of the sites that have been principally identified, the most potent is the mesencephalic periaqueductal gray matter (PAG). Here, the local action of morphine blocks nociceptive responses in *For more detailed discussions of the material in this section, see References 22 and 23.
28
Section I—The Basic Science of Pain
a variety of species. Other sites identified to modulate pain behavior in the presence of an opiate are the mesencephalic reticular formation (MRF), medial medulla, substantia nigra, nucleus accumbens and ventral forebrain, and amygdala.
These effects are in accord with a variety of studies in which (1) activation of bulbospinal pathways known to contain norepinephrine or 5-HT inhibit spinal nociceptive activity; (2) pharmacologic enhancement of spinal monoamine activity (by the delivery of alpha agonists) leads to an inhibition of spinal activity; (3) microinjection of morphine into the brainstem increases the spinal release of norepinephrine; and (4) the spinal delivery of alpha2 antagonists reverses the effects of brainstem opiates on spinal reflexes and analgesia. These observations are in accord with the effects produced when the bulbospinal pathways are directly stimulated and emphasize that the actions of opiates in the PAG are, in fact, associated with an increase in spinifugal outflow.
SPINAL CORD Intrathecal opiates produce a powerful effect on nociceptive thresholds in all species. PERIPHERAL SITES Early studies suggested a possible action of morphine at the site of peripheral injury. Investigators emphasized that the peripheral injection of opiates following the initiation of an inflammation would reduce the hyperalgesic component at doses that did not redistribute centrally.
FOREBRAIN MECHANISMS MODULATING AFFERENT INPUT Although ample evidence suggests that opiates interact with the mesencephalon to alter input by a variety of direct and indirect systems, the behavioral sequelae of opioids possess a significant component that reflects the affective component of the organism's response to the pain state. Significant rostral projections from the dorsal raphe nucleus (5-HT) and the locus ceruleus (norepinephrine) connect the PAG with forebrain systems and are known to influence motivational and affective components of behavior.
Mechanisms of Opioid Analgesia Given the diversity of sites, it is unlikely that all the mechanisms whereby opiates act within the brain to alter nociceptive transmission are identical. Several mechanisms through which opiates may act to alter nociceptive transmission have been identified.
Supraspinal Action of Opioids Several specific mechanisms are recognized. Two are discussed here (Fig. 3.11).
Spinal Action of Opiates
BULBOSPINAL PROJECTIONS Morphine in the brainstem inhibits spinal nociceptive reflexes. Microinjection of morphine into various brainstem sites reduces the spinal neuronal activity evoked by noxious stimuli.
At the spinal level, opioid receptors are present presynaptically on the terminals of small primary afferents and postsynaptically on the second-order neurons. The presynaptic action of morphine 5
4 3
Fig. 3.11 Schematic of organization of opiate action within the periaqueductal gray matter (PAG). In this schema, mu (μ) opiate actions block the release of γ-aminobutyric acid (GABA) from tonically active systems that otherwise regulate the projections to the medulla, thus leading to an activation of PAG outflow. The overall organization of the mechanisms whereby a PAG mu opiate agonist can alter nociceptive processing is presented in the adjacent schematic. The following mechanisms are hypothesized: (1) PAG projection to the medulla, which serves to activate bulbospinal projections releasing serotonin and/or norepinephrine at the spinal level; (2) PAG outflow to the medulla, where local inhibitory interaction results in an inhibition of ascending medullary projections to higher centers; (3) opiate binding within the PAG may be preterminal on the ascending spinofugal projection; this preterminal action would inhibit input into the medullary care and mesencephalic core; outflow from the PAG can modulate excitability of dorsal raphe (4) and locus ceruleus (5), from which ascending serotonergic and noradrenergic projections originate to project to the limbic system and forebrain.
2
GABAergic neuron (tonically active) µ agonist (inhibits GABA release) Medullopetal neuron (GABA-r) Medulla
1
Chapter 3—Dynamics of the Pain Processing System
through the G-protein–coupled receptor reduces the opening of voltage-sensitive calcium channels and thereby reduces the release of small afferent transmitters. The postsynaptic action reflects a facilitating linkage to voltage-sensitive potassium channels, which then hyperpolarize the second-order neuron and render it resistant to depolarization. These joint effects are believed to underlie the primary regulatory effects of spinal opiates on spinal n ociceptive input (Fig. 3.12).
Peripheral Action of Opioids Opioid binding sites are transported in the peripheral sensory axon, but there is no evidence that these sites are coupled to mechanisms governing the excitability of the membrane. High doses of agents, such as sufentanil, can block the compound action potential, but this effect is not naloxone reversible and is thought to reflect a local anesthetic action of the lipid-soluble agent. It is certain that opiate receptors exist on the distant peripheral terminals. Opioid receptors have been shown to be present on the distal terminals of C fibers, and agonist occupancy of these sites can block antidromic release of C-fiber transmitters (e.g., SP/CGRP, “axon reflex”; see the discussion of pharmacology of peripheral sensitization). Importantly, the models in which peripheral opiates appear to work are those that possess a significant degree of inflammation and are characterized by a hyperalgesic component. This finding raises the possibility that these peripheral actions normalize a process leading to an increased sensitivity to the local stimulus environment but do not alter normal transduction. The mechanisms of the antihyperalgesic effects of opiates applied to the inflamed regions (e.g., in the knee joint) are, at present, unexplained. It is possible, for example, that opiates may act on inflammatory cells that are releasing cytokines and products that activate or sensitize the nerve terminal.
Interactions Between Supraspinal and Spinal Systems As discussed earlier, opioids with an action limited to the spinal cord and to the brainstem are able to produce a powerful alteration in nociceptive processing. Ample evidence indicates that the effects of opiate receptor occupancy in the brain synergize with the effects produced by the concurrent occupancy of spinal receptors. Various studies have shown that the concurrent administration of morphine spinally and supraspinally leads to prominent synergy (i.e., maximal effect with a minimal combination dose).
29
Nonsteroidal Anti-Inflammatory Drugs* Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely prescribed agents that have been shown to have significant utility in a variety of acute (postoperative) as well as chronic (cancer, arthritis) pain states. Although NSAIDs may differ in potency, all are believed to have the same efficacy. Importantly, human and animal studies have emphasized that these agents serve not to alter pain thresholds under normal conditions but to reduce a hyperalgesic component of the underlying pain state. NSAIDs are structurally diverse but have a common feature in their ability to function as inhibitors of the enzyme COX, the essential enzyme in the synthesis of prostaglandins. Current thinking emphasizes both peripheral and central mechanisms of action.
Peripheral Action of Nonsteroidal Anti-Inflammatory Drugs Prostanoids are synthesized at the site of injury and can act on the peripheral afferent terminal to facilitate afferent transduction and augment the inflammatory state. To that degree, inhibition of prostaglandin synthesis by blocking COX can diminish that hyperalgesic state and can reduce the magnitude of inflammation. The analgesic potency of the NSAIDs, however, does not co-vary uniquely with the potency of these agents as inhibitors of inflammation.
Spinal Action of Nonsteroidal Anti-Inflammatory Drugs Intrathecal injection of NSAIDs, at doses that are inactive with systemic administration, attenuates the behavioral response to certain types of noxious stimuli, a finding that indicates a central action of the agent. As reviewed earlier, the repetitive activation of spinal neurons or the direct excitation of dorsal horn glutamate or SP receptors evokes a facilitated state of processing and the release of prostaglandins. The direct application of several prostanoids to the spinal cord leads to a facilitated state of processing (hyperalgesia). Accordingly, it is currently considered that COX inhibitors can, by their effect on COX-2, exert an acute action that prevents the initiation of the hyperalgesic state otherwise produced by the local spinal action of prostaglandins (see Fig. 3.6).
*For more detailed discussions of the material in this section, see References 24 and 25.
Wide Dynamic Range Neuron R S
Control Hz
Morphine H zZ Z
Fig. 3.12 Poststimulus histogram showing the effects of intravenous morphine on the firing of a single dorsal horn wide dynamic range neuron after single activation of A- and C-fiber input. As indicated, early (A-mediated) and late (A/C) activation of the cell occurs. The laterphase activation is preferentially sensitive to morphine (5 mg/kg intravenously) compared with the early component. These effects are readily reversed by naloxone. R, reording; S, stimulating.
30
Section I—The Basic Science of Pain O
CH2NH2 NH2
HO
Neuroma
3
= 2
Gabapentin
Peripheral Terminal
Fig. 3.13 Gabapentinoid agents. GABA, γ-aminobutyric acid.
Site 1. 2. 3. 4. 5.
N-Methyl-d-Aspartate Receptor Antagonists* Ketamine is classified as a dissociative anesthetic, but there is a clinical appreciation that ketamine can provide a significant degree of “analgesia.” The current thinking is that ketamine acts as an antagonist at the glutamate receptor of the NMDA subtype. As reviewed earlier, the NMDA site is thought to be essential in evoking a hyperalgesic state following repetitive small afferent (C-fiber) input (see Fig. 3.5). In addition, some investigators believe that certain states of allodynia may be mediated by a separate spinal NMDA receptor system, and NMDA antagonists have been shown to diminish the dysesthetic component of the causalgic pain states.
Alpha2-Adrenergic Agonists
†
Systemic alpha2 -adrenoceptor agonists have been shown to produce significant sedation and mild analgesia. As reviewed earlier, bulbospinal noradrenergic pathways can regulate dorsal horn nociceptive processing by the release of norepinephrine and the subsequent activation of alpha2-adrenergic receptors. Consequently, the spinal delivery of alpha2 agonists can produce powerful analgesia in humans and animal models. This spinal action of alpha2 is mediated by a distinct receptor but with a mechanism similar to that employed by spinal opiates: (1) alpha2 binding is presynaptic on C fibers and postsynaptic on dorsal horn neurons, (2) alpha2 receptors can depress the release of C-fiber transmitters, and (3) alpha2 agonists can hyperpolarize dorsal horn neurons through a Gi-coupled potassium channel. There is growing appreciation that clonidine may be useful in neuropathic pain states. The mechanism is not clear, but the ability of alpha2 agonists to diminish sympathetic outflow, either by a direct preterminal action on the postganglionic fiber, thereby directly blocking catecholamine release, or by action spinally on preganglionic sympathetic outflow, has been suggested.
Gabapentinoid Agents (Fig. 3.13)‡ Several molecules with a similar structural motif were synthesized to be GABA mimetics with anticonvulsant activity. Their activity in a variety of neuropathic conditions was defined, and subsequent work emphasized that these agents had no affinity for GABA sites. Mechanistically, these molecules show high affinity for a neuronal membrane site that corresponds to the alpha2delta subunit. This subunit is associated with the extracellular component of the voltage-sensitive calcium channel family. At the spinal level, this binding site is densely present in the superficial dorsal horn in the substantia gelatinosa The importance of the alpha2delta binding is strongly supported by the observation that point mutations of the alpha2delta sequence leads to a loss of binding of gabapentin and a parallel loss of anti-hyperalgesic activity. At present, it can be stated that although the mechanism
4
1
CH2CO2H GABA
DRG
Central terminal WDR Neuron
Blockade Axon conduction Spontaneous activity in injured fiber Neuroma firing DRG firing Glutamate evoked excitation
mg/mL 5-10 5 3-5 1-3 1-3
Fig. 3.14 Schematic showing sites of generation of spontaneous activity (1-5, top); the table (below) indicates the sites at which systemically administered lidocaine has been hypothesized to reduce spontaneous or evoked activity. Note that axonal and peripheral nerve terminal blockade has not been demonstrated in whole animal preparations at sublethal systemic lidocaine concentrations, whereas abnormal activity in neuromas, dorsal root ganglia (DRG), and dorsal horn is suppressed by nontoxic lidocaine plasma concentrations. WDR, wide dynamic range.
of action of this family of agents is not fully understood, this family of agents exerts a potent action on facilitated processing, as evoked in the postinjury pain state in the changes in spinal function that occur after peripheral nerve injury.
Intravenous Local Anesthetics§ The systemic delivery of sodium channel blockers has been shown to have analgesic efficacy in a variety of neuropathies (diabetic), nerve injury pain states (causalgia), and late-stage cancer, as well as in lowering intraoperative anesthetic requirements. Importantly, these effects occur at plasma concentrations lower than those required to produce frank block of nerve conduction; for lidocaine, effective concentrations may be on the order of 1 to 3 µg/mL. As reviewed earlier, the mechanism of this action is believed to reflect the importance of the up-regulation of the sodium channel that occurs in the injured axon and DRG. This increase is believed to underlie, in part, the ectopic activity arising from the injured nerve. Figure 3.14 indicates the potential sites where local anesthetics may interfere with impulse generation that leads to a pain state.
Conclusion The discussions of the mechanism of nociceptive processing in Chapter 2 and in this chapter only touch on a complex organized substrate. The common threads connecting these comments are that the complexity emphasizes that pain is not a monolithic entity and that, as with other organ systems (e.g., cardiovascular regulation and hypertension), multiple causes lead to the pain report. Because many approaches to regulating elevated blood pressure are available, and the selection of the appropriate therapy depends on the mechanism in the disorder, so too is it likely that a single approach will not be appropriate for all pain states. Improving insight into the pharmacology and physiology of these multiple components should continue to provide new tools for the management of nociception.
References Full references for this chapter can be found on www.expertconsult.com.
*For a more detailed discussion of the material in this section, see Reference 26. † For a more detailed discussion of the material in this section, see Reference 27. ‡ For more detailed discussions of the material in this section, see References 28 and 29.
5
§
For a more detailed discussion of the material in this section, see Reference 30.
Chapter
4
I
Central Pain Modulation Anthony Dickenson
Chapter Outline Spinal Excitatory Systems 31 Spinal Modulatory Systems 33
Pain provides a model for the study of how the central nervous system (CNS) deals with inputs from the outside world in the context of a system with enormous functional implications for human health and suffering. Plasticity is inherent in the sensory pathways in that the peripheral and central neuronal systems alter in different pain states. The aim of this overview is to summarize the potential targets at central levels in terms of both pain modulation and analgesic therapy. Pain can be acute, but persistent pains can be caused by inflammation and tissue damage, operative procedures, trauma, and diseases such as osteoarthritis and cancer. In addition, pain from nerve damage, neuropathic pain, can be produced by trauma, viral factors, diabetes, and tumors invading nervous tissue. The mechanisms of inflammatory and neuropathic pain are very different from those of acute pain in terms of peripheral origins, and marked changes occur in both the transmission and modulating systems in these prolonged pain states. Finally, some diffuse pains, such as those experienced in irritable bowel syndrome and fibromyalgia, have no clear peripheral pathologic process. In these conditions, central mechanisms may drive the pain state.
Spinal Excitatory Systems The arrival of sensory information from nociceptors in the dorsal horn of the spinal cord adds considerable complexity to the study of pain and analgesia because most of the receptors found in the CNS are also present in the areas where the C fibers terminate. The density of neurons in these areas is equal to or exceeds that seen elsewhere in the CNS so complex pain syndromes are not unexpected. As peripheral fibers enter the spinal cord, interactions between peptides and excitatory amino acids become critical for setting the level of pain transmission from the spinal cord to the brain and through local connections to motoneurons (Fig. 4.1). L-, N- and P-type calcium channels responsible for the release of these transmitters are differentially and temporally changed by neuropathic and inflammatory nociception (Fig. 4.2). In terms of therapy, the N-type channel blocker ziconotide is effective but has secondary effects even with spinal delivery because of the ubiquitous role of this channel. The calcium channels have associated subunits, and © 2011 Elsevier Inc. All rights reserved.
Supraspinal Modulatory Systems 33
the alpha2delta subunit is the site of action of gabapentin and pregabalin. The subunit is up-regulated after nerve injury. These drugs appear to prevent the trafficking of the subunit so the channels are not in the membrane and are unable to release transmitter. In addition, the actions of the drugs are regulated by descending monoamine systems perhaps linking pain with mood disorders and sleep disturbances.1,2 The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor for the excitatory amino acids sets the baseline response of the spinal neurons and is active during both noxious and innocuous responses. Kainate receptors on terminal and neurons may also be important in the generation of neuronal activity. Release of substance P and its actions on the neurokinin-1 receptor removes the magnesium (Mg++) block of the N-methyl-D-aspartate (NMDA) receptor and allows this receptor to operate. Other peptides may also contribute. Activation of the NMDA receptor underlies wind-up and long term potentiation, whereby the baseline response is amplified and prolonged even though the peripheral input remains the same. This increased responsivity of dorsal horn neurons is probably a major basis for central hypersensitivity whereby neurons show enhanced responses and expanded receptive fields. The NMDA receptor does not participate in responses to acute stimuli but is involved in persistent inflammatory and neuropathic pains in which peripheral sensitization in the former and altered ion channel activity in the latter favor enhanced activity. Here the NMDA receptor is critical for both the induction and subsequent maintenance of the enhanced pain state.1,2 Both volunteer and clinical studies support the ideas that have come from basic research in that the NMDA receptor appears to underlie the hyperalgesia and allodynia seen in inflammatory, postoperative, and neuropathic pains. Ketamine effectively blocks the NMDA receptor but with cognitive and other side effects, so novel antagonists are eagerly awaited. Induction of certain early genes in spinal neurons may result in prolongation of the excitable state or contribute to its maintenance. Numerous intracellular events downstream of the receptor are subsequently changed, and the gas nitric oxide contributes to wind-up. Spinal generation of prostanoids also occurs after noxious stimuli, and this may be the target for the central actions of nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase-2 (COX-2) inhibitors. 31
C-fiber synapse
Postsynaptic potential
AMPA rec.
Large (dashed) and small afferent innervation of deep and superficial dorsal horn, respectively. PRIMARY AFFERENT TRANSMITTER Peptides Substance P CGRP Growth factors BDNF Purine Adenosine triphosphate (ATP)
EAA
Peptide
RECEPTOR
POSTSYNAPTIC ACTION
Neurokinin 1 (NK-1) CGRP1
G protein–coupled; slow, long-lasting depolarization
TRK B
Depolarizes, activates tyrosine kinase (TRK) cascade
P2X receptor (P2X1-7)
Ligand-gated ion channels that differ in ion selectivity, gating properties Metabotropic G protein–coupled receptors
P2Y receptor (P2Y1-14)
Excitatory amino acids Aspartate, glutamate
NMDA rec. NK-1 rec. VSCC
AMPA receptor NMDA receptor
Sodium ionophore; rapid, short-lasting depolarization; gates sodium A subtype of the AMPA receptor; can also gate calcium Calcium ionophore; slow onset, long-lasting; gates calcium
AMPA, DL-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid; BDNF, brain-derived nerve growth factor; CGRP, calcitonin gene-related peptide; EAA, excitatory amino acids; NMDA, N-methyl-D-aspartate; VSCC, voltage-sensitive calcium channel. Fig. 4.1 Summary of primary afferent transmitter organization. (From Benzon H: Raj's practical management of pain, ed 4, St Louis, 2008, Mosby.) REPETITIVE C-FIBER INPUT
↑ Ca2+ P38 MAPK PLA2 AA
↑ Arginine NOS (neuron inducible) ↑ NO extracellular Activates terminal cGMP
COX 1, 2 PG
NO
C fiber
Ca2+ P38 MAPK NOS PG
COX2
PLA2
↑ Presynaptic transmitter release NMDA rec.
PG-r
Gly rec. PG rec.
↑ Afferent terminal release (↑VSCC) and inhibition of postsynaptic glycinereceptor–mediated inhibition
Second-order neuron
VSCC
↑ Spinofugal output for a given stimulus
Fig. 4.2 Small-afferent input actives second-order neurons and leads to increased intracellular calcium (Ca2+) concentration, which initiates several intracellular cascades. In the left column, activation of phospholipase A2 (PLA2) increases free arachidonic acid (AA). This serves as a substrate for cyclooxygenase (COX1 and COX2), which leads to prostaglandin (PG) release. These substances act on eponymous prostanoid receptors located presynaptically on the primary afferent terminal and postsynaptically on the higher-order neurons. In the right column, activation of nitric oxide synthase (NOS) in the presence of arginine leads to nitric oxide (NO), which diffuses to enhance transmitter release (e.g., glutamate). These events can serve to increase terminal release and increase postsynaptic excitability. cGMP, cyclic guanine monophosphate; Gly, glycine; NMDA, N-methyl-D-aspartate; P38 MAPK, P38 mitogen-activated protein kinase; rec., receptor; VSCC, voltage-sensitive calcium channel. (From Benzon H: Raj's practical management of pain, ed 4, St Louis, 2008, Mosby.)
Spinal Modulatory Systems The roles of the mu, delta, and kappa opioid receptors have been established with actions at spinal and supraspinal sites.3 Most clinically used drugs act on the mu receptor, whereas the delta receptor may provide a target for opioids with fewer side effects than morphine that have not yet reached the clinic. The more recently discovered ORL-1 receptor appears to produce spinal analgesia but may well function as an antiopioid at supraspinal sites. The endogenous opioid peptides, the enkephalins, have clear controlling influences on the spinal transmission of pain, whereas the dynorphins have complex actions. Inhibitors of the degradation of the enkephalins have been produced in an attempt to enhance endogenous opioid controls. Because the mu receptor is remarkably similar in structure and function in all species studied, basic research studies will be good predictors for human applications. The detailed structure of these receptors has been described, and some polymorphisms in the receptor appear to relate to opioid efficacy. The best described central sites of action of morphine are at spinal, brainstem, and midbrain loci. Other actions certainly occur at the highest centers of the brain, but these are poorly understood in terms of their contribution to analgesia. The spinal actions of opioids and their mechanisms of analgesia involve the following: (1) reduced transmitter release from nociceptive C–fibers, so that spinal neurons are less excited by incoming painful messages; and (2) postsynaptic inhibitions of neurons conveying information from the spinal cord to the brain. This dual action of opioids can result in total block of sensory inputs as the drugs arrive in the spinal cord, but obviously this effect may not be achievable at therapeutic systemic doses. Because spinal neurons project to both cortical (sensory-discriminative aspects of pain) and limbic areas (affective components of pain), block of their spinal inputs has a powerful effect on the pain experience. Some opioids, such as methadone, may have additional NMDA blocking actions and so may be valuable in cases where morphine effectiveness is reduced, such as in neuropathic pain. However, it not clear that this extra action contributes to clinical effects. Certain pathologic factors can influence the degree of opioid analgesia and are relevant to pain after nerve injury. Nerve damage can cause a loss of the presynaptic opioid receptors that would be expected to contribute to a reduction in opioid sensitivity. In addition, levels of the peptide cholecystokinin in the spinal cord can also determine the potency of morphine. Changes after nerve damage can result in overexcitability of spinal neurons so that a hypersensitive state is induced, against which opioid controls are insufficiently efficacious. The transmission of painful messages through the normally innocuous A-fiber population can occur after neuropathy as a result of pathologic changes in peripheral or central processes. No opioid receptors are present on the central terminals of these fibers.3 Tonic γ-aminobutyric acid (GABAA) and GABAB receptor controls are important endogenous inhibitory systems in terms of controlling acute, inflammatory, and neuropathic pain states. The GABAA receptor appears to prevent lowthreshold inputs from triggering nociception. GABA levels are reduced after nerve damage yet are increased in the presence of inflammation. Clinically, the widespread roles of this major
Chapter 4—Central Pain Modulation
33
inhibitory receptor obviate therapy with present drugs acting on this transmitter system.
Supraspinal Modulatory Systems As pain messages ascend to the brain, inputs into the midbrain can trigger reciprocal projections back to the spinal cord through descending controls. Thus, monoamine systems, originating in the midbrain and brainstem, can modulate the spinal transmission of pain. Early ideas suggested that the descending controls were inhibitory and formed the basis for deep brain stimulation for pain control. However, it is now clear that the balance between descending controls, both excitatory and inhibitory, can be altered in various pain states. Good evidence indicates a prominent noradrenergic alpha2-adrenoceptor–mediated inhibitory system originating from the locus ceruleus in the brain and mimicked by drugs such as clonidine and dexmedetomidine that directly activate the spinal receptors. However, the multiple 5-hydroxytryptamine (5-HT) receptors lead to both inhibitory and excitatory effects of this transmitter. 5-HT3-receptor and likely also 5-HT2-receptor–mediated excitatory controls have been described, as well as 5-HT1 inhibitions, exemplified by the use of the triptans, agonists at this receptor, in headaches. 5-HT in the descending pathways originates from complex networks within the rostroventral medial medulla (RVM) where both on and off cells exist and dually control spinal functions.1,2 The ability of cortical function, through these descending controls, to influence spinal function allows for “top-down” processing by these monoamines and so may be one the links between pain and the comorbidities of sleep problems, anxiety, and depression. Evidence from patient studies indicates that diffuse noxious inhibitory controls have reduced inhibitory modulation in several pain states. By contrast, in the case of peripheral neuropathy, spinal injury, and cancer-induced bone pain, the excitatory descending controls appear to be enhanced and further enhance states of increased spinal neuronal hypersensitivity. At least in animals, descending drives can be observed to occur without any alteration in peripheral processes. Possibly, in pain states in which fatigue, mood changes, and diffuse pain occur, such as fibromyalgia and irritable bowel syndrome, there could be altered balances between descending facilitations and inhibitions caused by shifts in central monoamine function. Drugs that are most effective in neuropathy are the older tricyclic antidepressants and the newer serotoninnorepinephrine reuptake inhibitors. The lesser efficacy of selective serotonin reuptake inhibitors leads credence to the idea that norepinephrine inhibition is a key part of the analgesic effects of these drugs.4 The antidepressant drugs in clinical use block the uptake of both norepinephrine and 5-HT. Therefore, these drugs alter function within these descending monoamine pathways and so have efficacy in both neuropathic patients and those with fibromyalgia. Opioids have long been known to have both spinal actions and supraspinal effects. With regard to supraspinal effects, opioids activate the off cells and switch off on cells and thus move RVM output toward descending inhibition. Finally, other drugs may also interact with these systems. Tramadol, a weak opioid with both norepinephrine and 5-HT uptake block, has some efficacy in pain, but the newer
34
Section I—The Basic Science of Pain
molecule, tapentadol, is a mu opioid with norepinephrine reuptake inhibition only. The actions of gabapentin and pregabalin can be governed by supraspinal processes. The spinal actions of these drugs on calcium channel function by their binding to the alpha2delta subunit depends on descending facilitatory 5-HT3 mediated influences from the RVM. Other studies have implicated increases in descending alpha2-adrenoceptor–mediated inhibitions through supraspinal actions of these drugs. These studies illustrate the interplay between spinal and supraspinal processes and
how these relate not only to the pain condition but also to the efficacy of drugs. Thus, the central modulation of pain involves multiple sites and mechanisms. If a single agent or approach is not sufficiently effective in controlling pain, then combination therapy is a logical option.
References Full references for this chapter can be found on www.expertconsult.com.
II
Chapter
5
History and Physical Examination of the Pain Patient Charles D. Donohoe
CHAPTER OUTLINE The Targeted Pain History 36 The Pain Litany 37 Mode of Onset and Location 37 Chronicity 37 Tempo (Duration and Frequency) 38 Character and Severity 38 Associated Factors 38 General Aspects of the Targeted Pain History 38 Medication History 39 General Aspects of the Patient Interview 40 Summary of the Targeted History 42
The cornerstone of clinical success in the practice of pain management is a correct diagnosis. Unfortunately, in this era of increasing reliance on technology and constant pressure on the physician to become more efficient, the core elements in achieving the correct diagnosis—namely, a targeted history and physical examination—are sadly regarded as less critical in the care of the patient. Proceeding without a concise history often leads to clinical errors that not only squander our limited health care resources but also compromise the patient's o pportunity to obtain pain relief. Indeed, shortcuts taken in obtaining old records, personally reviewing imaging studies, contacting prior treating physicians, calling family members of a confused patient, and most importantly just sitting and listening to what the patient believes to be important frequently lead to misdiagnosis and an unsatisfactory outcome for the patient and pain specialist alike. Frequently, the most cost-effective use of technology is a telephone call to a family member or prior treating physician. Often the discipline to engage in several minutes of conversation with a knowledgeable party can yield countless benefits both in cost saving and in added medical and psychological insight into the patient's predicament. The bond of trust that is so integral to the relationship between patient and pain specialist is often determined by the care and thoroughness with which the initial historical material is obtained. Experience has shown that when physicians are rushed for time, the intake interview becomes abbreviated, thereby setting the stage for medical errors and interpersonal dissatisfaction. 36
The Targeted Physical Examination 42 General Aspects 43 Assessment of Mental Status 43 Cranial Nerves 43 Motor Examination 46 Sensory Examination 47 Deep Tendon Reflexes 48 Examination of Gait 49
Conclusion 49
Many of the chapters that follow highlight the utility of highly sophisticated technology, invasive testing modalities, and diagnostic and therapeutic nerve blocks. Although these clinical interventions may be extremely important in the evaluation of a given patient, they do not replace the preeminent role of the history and physical examination in the diagnosis of the patient in pain. Most, if not all, of what a pain specialist needs to know can be gleaned from simply taking the time to take a concise history and perform a targeted physical examination. By far, the most cost-effective endeavor in the evaluation of the patient in pain is to be thorough in the initial targeted history taking and physical examination. If this initial consultation ends without a clear direction regarding the underlying pathologic process, the likelihood that technology will “save the day” is very remote. It has been said, with varying degrees of conviction, that “one magnetic resonance scanner (MRI) scanner is worth 100 neurologists (or pain specialists).” In this 21st century with an MRI on every other street, this adage can be restated as follows: “One physician (of any specialty) willing to sit and actually listen to patients can be of more practical benefit than 100 magnets (of any Tesla strength).”
The Targeted Pain History Obtaining a history is a skill. Practice and repetition improve our skills, reduce the tendency to omit important material, and ultimately enable us to focus our questions to conserve © 2011 Elsevier Inc. All rights reserved.
Chapter 5—History and Physical Examination of the Pain Patient
37
time without sacrificing accuracy. As a starting point, the search should be directed to answer two questions1: “Where is the disease causing the pain—in the brain, spinal cord, plexus, muscle, tendon, or bone?” and “What is the nature of the disease?” It is the trademark of an experienced clinician to formulate an efficient line of questioning that deals with both these issues simultaneously. Highlights of the critical elements in that process follow. The goal is to keep the process brief, simple, and workable. The secret of becoming skilled at taking a history is being a good listener. The physician should put the patient at ease. The patient should never be given the impression that the physician is rushed or overworked and that only limited time is available to get the story across. The physician must remember that the patient in pain is usually anxious, if not overtly frightened, and may be inadequate in presenting the situation and having his or her plight properly perceived. Experience teaches us that the physician cannot force the pace of the interview without losing vital information and valuable mutual trust and insight. The following discussion describes the elements of the targeted history that not only define pain in a context useful for proper identification, localization, and source but also enable the physician to determine priorities about the urgency of care.
of a subarachnoid hemorrhage secondary to a ruptured intracranial aneurysm, manifested by severe headache, neck pain, and a sense of impending doom, contrasts sharply with the chronic diffuse headache and vague neck tightness of tension-type cephalalgia. The location of pain provides additional diagnostic information. The pain in trigeminal neuralgia, for instance, is usually limited to one or more branches of cranial nerve (CN) V and does not spread beyond the distribution of the nerve.4 The V2 and V3 divisions of this nerve are much more frequently involved than is V1 (Fig. 5.1). The pain is rarely bilateral except in certain cases of multiple sclerosis, brainstem neoplasms and skull base tumors, and infections.5 Another example of the importance of pain location is the burning, prickling dysesthesias of meralgia paresthetica. The unilateral involvement of the lateral femoral cutaneous nerve produces painful dysesthesias in the anterior thigh, more commonly in men, who notice the disturbance when they put a hand in a trouser pocket. The physician must find out how and where the pain started. The patient should be asked to identify the site of maximum pain.
The Pain Litany
The duration of awareness of a painful illness targets the initial history and heavily influences the sick from well distinction. For this reason, it often serves as a starting point. “How long have you had this pain?” is an essential question. The patient should be asked to try to date the pain in relation to other medical events, such as trauma, surgery, and other illnesses. In general, back pain that has been present for 30 years and is not associated with any progression is strong evidence of a self-limited pain syndrome, hence the “well” determination.
The pain litany—a formulaic exploration of the patient's pain history—enables the physician to identify the signature of the specific pain syndrome from its usual manifesting characteristics.2,3 The pain litany takes the following form3: 1. 2. 3. 4. 5. 6.
Mode of onset Location Chronicity Tempo (duration and frequency) Character and severity Associated factors: n Premonitory symptoms and aura n Precipitating factors n Environmental factors (occupation) n Family history n Age at onset n Pregnancy and menstruation n Gender n Past medical and surgical history n Socioeconomic considerations n Psychiatric history n Medications and drug and alcohol use
Chronicity
V1
V2
The targeted history also allows physicians to distinguish sick patients from well ones. If it is determined that in all probability the patient is well (i.e., has no life-threatening illness), the workup and treatment plan may proceed at a more conservative pace. From the outset, the interviewer proceeds in an orderly fashion but remains vigilant for signals of an urgent situation. Pain of uncertain origin should always be regarded as a potential emergency.
Mode of Onset and Location The mode of onset of the pain sets the direction of the initial history and carries much weight in distinguishing sick from well patients. For example, the sudden, explosive presentation
V3
V1, Ophthalmic nerve
V2, Maxillary nerve
V3, Mandibular nerve
Fig. 5.1 Sensory distribution of the trigeminal nerve. (From Waldman SD: Atlas of interventional pain management, ed 2, Philadelphia, 2004, Saunders, 34.)
38
Section II—The Evaluation of the Patient in Pain
Conversely, a patient with severe low back pain of sudden onset or pain that suddenly changes in character must be assigned to the category of “sick until proved otherwise.” This type of accentuated pain presentation has often been called the first or worst syndrome. It applies to both spinal pain and headache. Patients in this category deserve serious concern, and their pain should be viewed with medical urgency. Equating the concept of chronicity with benign disease has its pitfalls; the physician must beware of failing to Identify ominous changes in a long-standing, stable pain syndrome (e.g., when a patient with chronic low back pain suddenly becomes incontinent). n Attribute the onset of symptoms to a benign cause without adequate evaluation (e.g., dismissing a sudden increase in low back pain in the postoperative patient as muscle spasm without considering diskitis and bacterial epidural abscess). n Recognize new symptoms superimposed on chronic complaints (e.g., attributing an increase in headache with cough to chronic cervical spondylitis disease rather than considering that because the patient has a known breast malignancy, silent metastasis may be causing increased intracranial pressure). n
Indeed, the characteristics of thoroughness, experience, insight into the patient's personality, and constant resistance to being lulled into false security prevent such diagnostic disasters. As Mark Twain observed, “Good decisions come from experience and experience comes from making bad decisions.”6
Tempo (Duration and Frequency) The tempo of a disorder may provide one of the best clues to the diagnosis of the pain. In facial pain, trigeminal neuralgia (tic douloureux) is described as brief electric shocks or stabbing pain. Onset and termination of attacks are abrupt, and affected patients are usually pain free between episodes. Attacks last only a few seconds. It is not unusual for a series of attacks to occur in rapid succession over several hours. In contrast, the pain of temporal (giant cell) arteritis is usually described as a dull, persistent, gnawing pain that is exacerbated by chewing.3 In migraine, the pain is frequently throbbing and may last for hours to days. Cluster headaches, by contrast, are named for their periodicity: they occur once or more often each day, last about 30 minutes, and often appear shortly after the onset of sleep. They may occur in clusters for weeks to months with headache-free intervals. In short, the concept of pain tempo is another feature of the targeted history that is helpful in differentiating pain syndromes.
Character and Severity Although considerable overlap exists between character and severity of pain, some generalization can be made when taking a targeted history. Vascular headaches tend to be throbbing and pulsatile, and the pain intensity is often described as severe.3 Cluster headaches may have a deeper, boring, burning, wrenching quality. This pain is reputed to be among the worst known to humans. Trigeminal neuralgia is typically described as paroxysmal, jabbing, or shocklike, in contrast to non-neuralgic pain such as experienced in temporomandibular joint (TMJ) dysfunction, which is often described as a unilateral, dull, aching pain in
the periauricular region. TMJ pain is exacerbated by bruxism, eating, and yawning but may be patternless. The characteristic pain of postherpetic neuralgia usually includes both burning and aching superimposed on paroxysms of shocks and jabs. It usually occurs in association with dysesthesias, resulting in an unpleasant sensation even with the slightest touch over the skin (allodynia). Many of the more common pain syndromes have a distinctive character and level of severity that is helpful in properly identifying them. Clinical insight into these characteristics comes with time and through listening to many patients describe their pain. Certain patients with cluster headaches or trigeminal neuralgia have a frantic, almost desperate demeanor that is proportionate to the severity of their pain. The patient with acute lumbar disk herniation often writhes before the physician and is essentially unable to sit in a chair. The body language and facial expressions associated with true excruciating pain are difficult to feign, and exaggerated behaviors often immediately become suspect almost on a visceral level.
Associated Factors Multiple associated factors round out the targeted pain history. The subtle differences among painful conditions allow clinicians to use these factors to complete the various parts of the puzzle. For example, intermittent throbbing pain behind the eye is consistent with cluster headache. If the patient is a young woman, however, the diagnosis of cluster headache is improbable because of the known male preponderance of this condition.3 Accordingly, the combination of associated factors such as age and sex aid in the diagnosis. A dull, persistent pain over one temple in a young African American male patient probably is not giant cell or temporal arteritis, a disease most often seen in white women older than 50 years. Table 5.1 describes various pain syndromes according to patient age, sex, family history, precipitating factors, and occupational issues. As Osler said, “Medicine is a science of uncertainty and an art of probability.”2 Matching our knowledge about the natural history and characteristics of the various diseases that cause pain with information derived from the patient's history is the physician's most powerful diagnostic tool. It is through this process that the physician develops confidence in the diagnosis that often exceeds that based on information from ancillary tests. An autoworker who uses an impact wrench 10 hours a day, complains of numbness in the first three digits of his right hand, and wakes up four times a night “shaking his hand out” has carpal tunnel syndrome, regardless of the results of nerve conduction studies and electromyography.
General Aspects of the Targeted Pain History An old clinical maxim states, “Healing begins with the history!”2 The clinician should be able to put the patient at ease and should then ask open-ended questions that will give the patient an opportunity to describe the pain in his or her own words. “Now, tell me about your pain” is an excellent prompt. This approach allows the patient to describe what he or she believes is most important. It is therapeutic in itself. Physicians are often wary of the open-ended question,
Chapter 5—History and Physical Examination of the Pain Patient
39
Table 5.1 Demographics of Some Common Pain Syndromes Pain Syndrome
Sex Preponderance (Ratio)
Family History
Age of Onset (yr)
Migraine Childhood ( 10 yr)
M (1.5:1) F (3:1)
Positive Positive
3 15–20
Abdominal pain, episodic vertigo, mood changes Decrease by third month of pregnancy, increase with menstruation and oral contraceptives
Cluster headache
M (8:1)
Not positive
25–40
Common at night, precipitated by alcohol and nitrates
Multiple sclerosis
F (2:1)
Positive
20–40
Trigeminal neuralgia, tonic spasms, dysesthesia, extremity pain
Temporal arteritis
F (3:1)
Not positive
>60
Increased erythrocyte sedimentation rate, anemia, low-grade fever, jaw claudication
Trigeminal neuralgia
F (2:1)
Not positive
>55
V2 (45%) > V3 (35%) > V1 (20%); triggered by jaw movement, heat, and cold
Ankylosing spondylitis
M (5:1)
Positive
20–30
Pain forces patient out of bed at night, is not relieved by lying flat
Rheumatoid arthritis
F (3:1)
Positive
35–50
Higher rate in nulliparous women not exposed to oral contraceptives
Thromboangiitis obliterans
M (8:1)
Not positive
20–40
Smoking
Carpal tunnel syndrome
F (2:1)
Not positive
30–60
Certain occupations, pregnancy, diabetes, hypothyroidism
Associated Features and Comments
Data from references 1, 3, 4, 9, and 10.
because they are afraid that the patient will ramble. Although this can occur, a far more common problem is that the physician narrows the line of questioning after jumping to a premature conclusion. The patient's past medical history and family history are often as important as the current complaints. Medications, surgical procedures, and prior imaging studies are not explored in adequate detail. Many patients have been subjected to thousands of dollars of imaging, blood work and neurodiagnostic studies but often remain in the dark not only about their test results but also about the modality or even the actual body part interrogated. When a patient without records who complains of chronic headaches states that all the “scans” were normal, the physician must be careful. These “scans” may be an MRI image of the brain but could also refer to a computed tomography (CT) scan of the paranasal sinuses or even plain radiographs of the skull. The best policy is to review all pertinent imaging studies and not just the reports. Radiologists truly do a remarkable job of interpreting studies, often with very limited clinical information. In difficult cases, however, review of prior imaging studies in light of a newly derived specific historical or physical finding can be particularly helpful and may even “save the day.” When the pain is chronic, other doctors may already have been consulted. They probably have ordered diagnostic tests and tried therapies; indeed, it is always wise to obtain previous records or, preferably, to contact the other physicians directly. If a diagnosis seems obvious but previous doctors missed it, the physician should be cautious. When nothing has worked before, there is usually a good reason for the treatment failures. Under these circumstances, it is prudent and wise to assume that the other physicians were competent. Physicians are frequent violators of the maxim, “Do unto others as you would have them do unto you.” Frank or subtle criticism of a colleague's efforts is pointless, upsets the patient, and may even initiate litigation.
One other impulse that should be resisted is the tendency to ascribe pain to psychogenic causes. Learning to believe patients who have pain averts many awkward and potentially costly errors. Once the physician projects the belief that a patient's pain is based mainly on psychogenic mechanisms, it is an extremely difficult position to recant. At all costs, the pain specialist should remain nonjudgmental, should believe in the patient's pain, and should gain the patient's confidence. The only proven “cure” for having dismissed a patients' pain as psychogenic is to learn that serious organic disease was uncovered by another physician who saw the patient later in the course of the disease. Like everyone in medicine, pain specialists should be humble and careful with their words.
Medication History The importance of a thorough drug history cannot be overstated, particularly in the setting of chronic benign pain. It is not unusual for a patient to relate a very involved history of pain and multiple operations, diagnostic studies, and consultations. At the end of the interview, not uncommonly as the patient is preparing to leave, he or she will casually mention needing to have a prescription renewed and will add that it is “just a pain pill.” It is at this very point that an otherwise pleasant consultation can become confrontational. Confusion among physicians about the differences among narcotics and opioids is widespread. Many physicians also fail to recognize that the relative analgesic, euphoric, and anxiolytic properties of a given compound are not equivalent. For example, the analgesic strength of propoxyphene (Darvon) may be equivalent to one or two aspirins, but the magnitude of its anxiolytic effects in a given patient can be considerable. Not only opioids pose a problem. Carisoprodol (Soma, Rela) is a noncontrolled skeletal muscle relaxant that is also available through veterinary supply catalogs.7 Its active metabolite is
40
Section II—The Evaluation of the Patient in Pain
meprobamate (Equanil, Miltown), an anxiolytic-sedative agent popular in the late 1950s. Patients using carisoprodol may be at risk (frequently unrecognized) for meprobamate dependency. Triptans, ergots, aspirin, acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), minor tranquilizers, and barbiturate-containing compounds (Fiorinal, Esgic, and Phrenilin) taken in varying doses can contribute to reboundtype headache. In this setting, the daily use of headache-abortive drugs enhances and increases the frequency of daily headaches. The scope of this problem is difficult to assess, but in certain headache clinics, the use of such drugs is the single most common reason for chronic refractory daily headaches.8 Although every pharmacologic agent has some inherent risk, two practical considerations may be crucial in the targeted pain history. The first involves many individuals, particularly older persons, who are taking anticoagulants (warfarin, heparin) or antiplatelet agents (aspirin, clopidogrel [Plavix], and ticlopidine [Ticlid]) for any of a variety of reasons. Many disasters can occur in this setting. Inadvertent overdosing of an older, confused patient can cause intracerebral bleeding (headache) or back and radicular pain (secondary to retroperitoneal hemorrhage). Second, the physician evaluating headache symptoms should keep in mind that estrogen, progesterone, and nitrates can play major roles as headache-provocative agents and that simply discontinuing these drugs can provide almost immediate improvement. Both the scope and the frequency of problems related to chemical dependency have been underrecognized in many clinical settings. Some patients are willing to subject themselves to expensive diagnostic studies, multiple nerve blocks, and even surgery to ensure an uninterrupted supply of specific medications (frequently opioids). The specialist in pain management is uniquely positioned to recognize these problems and to offer suggestions in a compassionate, nonjudgmental fashion that may ultimately extricate patients from both their chemical dependency and their convoluted relationship with the medical system. Until drug dependency issues are addressed, effective inroads into the management of chronic pain will be thwarted. Certain clinicians have described a satisfactory experience administering opioids for chronic benign pain.9,10 Their positive experience (along with aggressive pharmaceutical company marketing) has promoted liberal prescribing policies among primary care physicians and specialists treating common conditions such as back pain, arthritis, and fibromyalgia. The long-term use of opioids in these diseases is not supported by strong scientific evidence and remains controversial.11 Such an ambiguous situation only accentuates the importance of obtaining a thorough drug history and assessing the true impact of drug use on the individual patient's pain problems. Table 5.2 lists the “red flag” agents that, when used by a patient in pain, should alert the physician to consider possible drug abuse or exacerbation of pain by medication. Information on dosage and duration of use is important. Pain specialists should make it policy to insist that patients bring all their medications at the time of the consultation. If you as a physician believe that a patient has a drug dependency problem, face the problem openly and with kindness. Resist the all too common practice of writing a prescription for that magical minimal amount of the drug being abused, an amount that can end the consultation without a dreaded angry confrontation. For those of us in clinical practice, this is an all too familiar “end of consult” strategy of providing what we
know to be part of the problem. Prepare to assume your share of the guilt, Dr. Feelgood, in this major public health disaster.
General Aspects of the Patient Interview The following general but significant points enhance the patient interview process: The surroundings are professional, comfortable, and private. n The patient is appropriately gowned, is chaperoned if appropriate, and is sitting upright and at eye level with the interviewer, if possible. n Old records, scans, radiographs, and consultations have been obtained and reviewed before the consultation. n The physician listens to and does not interrupt the patient or allow outside interruptions. n The physician remains nonjudgmental; moral, religious, and political beliefs of the physician are irrelevant to this process. n The physician is honest and open with the patient; keeping information from the patient at the family's request is usually a bad decision. n Both the patient and the physician can trust in the confidentiality of both the consultation and the medical records. n
The specialty of pain management is practiced by physicians from numerous disciplines. In particular, physicians trained in operating room anesthesia may not be as sensitive to some certain issues. From the standpoint of neurologists, for whom interviewing patients is a major component of practice, these basic rules of common etiquette are frequently ignored. First, the office should be both professional and comfortable. For reasons of economy, pain clinics are frequently placed in noisy and crowded additions to either the operating room suite or the emergency department. This atmosphere may not be conducive to dealing with patients with acute and chronic pain, who are often extremely apprehensive and easily frustrated. It is important that patients have a private place where they undress and are examined. Although this may appear to be a small point, a chaotic examining site can inspire a patient's resentment, even if the medical care is of high quality. One other point that needs reinforcing is that physician and patient should always be properly chaperoned. It is not unusual, because of the hectic schedules of both physicians and ancillary personnel, for a patient and physician to be left alone in situations in which this arrangement is at best uncomfortable and at worst compromising and dangerous. Strict adherence to standardized protocol for chaperoning is really the best way of averting serious problems in this area. The keys to obtaining a complete and effective targeted pain history are listed here The examiner should use the following protocol: 1. Build rapport with the patient by introducing self properly, taking an initial social history, and simultaneously assessing the patient's mood, anxiety level, and capability of giving a history on his or her own. 2. Most importantly: Establish the chief complaint at the outset of the history. Why is the patient here? Openended questions allow the patient to tell his or her own story.
Chapter 5—History and Physical Examination of the Pain Patient
41
Table 5.2 “Red Flag” Drugs in the Targeted Pain History Drug Class
Drug
CONTROLLED ABUSED SUBSTANCES*
Schedule II narcotics
Morphine (Roxanol, MS Contin) Codeine, fentanyl (Sublimaze) Sufentanil (Sufenta) Hydromorphone (Dilaudid) Meperidine (Demerol) Methadone (Dolophine) Oxycodone (Percodan, Tylox, OxyContin, Roxicodone) Opium Cocaine
Non-narcotic agents
Dextroamphetamine (Dexedrine, Adderall) Methamphetamine (Desoxyn) Methylphenidate (Ritalin) Phenmetrazine (Preludin) Amobarbital (Amytal) Pentobarbital (Nembutal) Secobarbital (Seconal) Glutethimide (Doriden) Secobarbital-amobarbital (Tuinal)
Schedule III narcotics
Codeine (Tylenol with codeine, Fiorinal with codeine) Dihydrocodeine (Synalgos-DC) Hydrocodone (Tussionex, Hycodan, Vicodin, Lortab, Lorcet) Butalbital (Fiorinal, Esgic, Phrenilin, Medigesic)
Schedule IV narcotics
Propoxyphene (Darvon, Darvocet, Wygesic) Butorphanol (Stadol) Pentazocine (Talwin) Alprazolam (Xanax) Chlordiazepoxide (Librium) Clonazepam (Klonopin) Clorazepate (Tranxene) Diazepam (Valium) Eszopiclone (Lunesta) Flurazepam (Dalmane) Lorazepam (Ativan) Midazolam (Versed) Oxazepam (Serax) Quazepam (Doral) Temazepam (Restoril) Triazolam (Halcion) Zaleplon (Sonata) Zolpidem (Ambien)
Non-narcotic agents
Phenobarbital Mephobarbital (Mebaral) Chloral hydrate Ethchlorvynol (Placidyl) Meprobamate (Equanil, Equagesic) Carisoprodol (Soma, Rela)
Schedule V
Buprenorphine (Buprenex) Diphenoxylate (Lomotil) Pregabalin (Lyrica)
NONCONTROLLED ABUSED SUBSTANCES
Triptans (Imitrex, Zomig, Relpax, Amerge, Frova, Treximet, Maxalt, Axert) Ergotamine (Cafergot, Wigraine, Ergostat) Dihydoergotamine (Migranal nasal spray, D.H.E.45) Chlordiazepoxide (Librax) Tramadol (Ultram, Ultracet) (nonscheduled opioid) Nalbuphine (Nubain) (nonscheduled opioid) Caffeine (Excedrin, Anacin)
NONABUSED DRUGS IMPORTANT IN A TARGETED PAIN HISTORY
Oral contraceptives Anticoagulants (heparin, warfarin, clopidogrel [Plavix]) Antiplatelet agents (aspirin, ticlopidine) Antianginals (nitrates)
*Narcotic is a nonspecific term still used by state boards to describe a drug that induces sleep or dependence. It is not interchangeable with opioid. This table lists many (but not all) drugs that may be abused by patients with pain. Data from Brust JC: Neurological aspects of substance abuse, Boston, 1993, Butterworth-Heinemann, and Missouri Taskforce on the Misuse, Abuse, and Diversion of Prescription Drugs, 1994.
42
Section II—The Evaluation of the Patient in Pain
3. Use the framework of the pain litany (discussed earlier) to investigate the pain further. Where is the pain? What is its nature? 4. Do not jump to conclusions. This is the most common cause of error because the interview too soon becomes narrowly focused, and important associations are not pursued or are ignored. The examiner should ask about other doctors whom the patient has seen and their treatments. 5. Determine the impact of the pain on the patient's life— psychological fears, family issues (marriage), compensation, and work record. 6. Explore past medical and family history. Using a timeline approach to establish continuity, the current pain should be placed in context with other major medical events: previous surgery, hospitalizations, cancer, and medical and paramedical relationships. 7. Obtain a thorough drug history (see Table 5.2). Information on duration, frequency, amount, and source of medication should be sought. The importance of this information cannot be overemphasized. The examination should begin with the physician's introducing himself or herself to the patient and putting the patient at ease. A routine social history, such as occupation, place of employment, marital status, and number of children, should be obtained. During this interchange, the physician should be assessing the verbal and nonverbal cues that ultimately determine the caliber of the historical information. This social introduction affords the physician insight into what type of person the patient is. Over time and with the refinements of experience, this portion of the interview assumes diagnostic importance equal to that of the data-gathering portion of the consultation. It seems obvious that the patient's chief complaint would be the logical starting point of any history. Unfortunately, too much time can be spent taking a history without ever addressing the chief complaint. Coming to grips with the patient's primary reason for seeking medical attention is really the crucial piece of data. Is it the pain? Is it questions about disability or worker's compensation? Is it a morbid fear of cancer? Is it that the physician who prescribed the patient's pain medications has retired and the patient is concerned about prescription renewal? Until the physician has a strong sense of the principal reason for the consultation, the history is often both misguided and aimless. Sitting in front of the patient, the physician should always ask himself or herself, “Why has this patient come to see me?” Sometimes, the patient's motives are not what they first appear to be.
Summary of the Targeted History The value of the targeted history cannot be overstated. It affords the physician the greatest chance of understanding the nature of the pain and, more important, its effects on the patient. Diagnostic tests, laboratory reports, and other consultants' opinions often introduce error when they are interpreted from a perspective detached from the patient. The physician should remember that, no matter how many physicians have seen the patient earlier, historical facts critical to the diagnosis may have been overlooked or not properly sought. Taking the targeted history is a social interaction. Courtesy, professionalism, and kindness consistently result in patient satisfaction. Issues related to compensation, returning to work,
and concurrent drug use should be dealt with openly and directly, without imposing the physician's personal, political, or religious value judgments.
The Targeted Physical Examination If, after obtaining the targeted historical information, the pain specialist is lost, the chance that the situation may be suddenly illuminated by the physical examination findings is extremely remote. As a basic point, the physical examination should follow the history and, indeed, be specifically directed by clues obtained during the patient interview. For example, it makes little sense to concentrate on a detailed examination of sensory function and individual muscle testing in the lower extremities of a patient who has diplopia, facial pain, and a family history of multiple sclerosis.12 The physical examination is an extension of the history. The examination provides objective support and is performed efficiently and systematically so that important findings are not overlooked. The problem with the neurologic examination has been selecting those elements that are truly critical. In 2009, Canadian neurologists and medical students reached a helpful consensus (Table 5.3). It is c ompact, yet an excellent screening tool.13 The examination should not consume a great deal of time. Basic aspects, such as taking blood pressure, performing a screening mental status examination, and checking visual acuity, strength, and deep tendon reflexes, however, pay multiple dividends. On occasion, certain important diseases, such as unrecognized hypertension, diabetic retinopathy, and skin cancer, can be uncovered. The very physical aspect of examining the patient imparts a reassuring sense of personal caring to the entire consultation. The benefits of this experience are considerable. Pain patients want to be examined, expect to be examined, and ultimately derive benefit from the process. As Goethe said, “We see only what we know.”14 The facility with which we examine patients is ultimately a function of our knowledge, experience, and willingness to learn. The neurologic examination is not difficult and should not intimidate physicians in training or non-neurologists. It can be performed effectively in most cases in less than 10 minutes. The physician should develop a routine and keep it simple.
Table 5.3 Neurologic Examination Key Elements of the Neurologic Examination
Time to Complete
1. Mental status
90 seconds
2. Cranial nerves/funduscopic examination
90 seconds
3. Power arms/legs
60 seconds
4. Pinprick, vibratory sensation
60 seconds
5. Reflexes, gait, Romberg’s sign, tandem walking
90 seconds Total time: 6–7 minutes
Data from Heyman CH, Rossman HS: A multimodal approach to managing the symptoms of multiple sclerosis, Neurology 14:63:S12, 2004.
Chapter 5—History and Physical Examination of the Pain Patient
General Aspects The patient's temperature, pulse, and blood pressure should always be recorded, as should height and weight. The patient should be undressed and properly gowned. It is a constant source of amazement how frequently examinations are performed to evaluate painful conditions, even disorders involving the neck and low back, while patients are fully clothed. The pain specialist should do the following: examine the patient's entire body for skin lesions such as hemangiomas, areas of hyperpigmentation, and café au lait spots (neurofibromatosis); document scars from previous operations; and inquire into other scars not mentioned in the initial history. Needle marks, skin ulcerations, and tattoos (which sometimes betray drug culture orientation) may be surprising findings. The spine should be examined for kyphosis, lordosis, scoliosis, and focal areas of tenderness. Dimpling of the skin or excessive hair growth may suggest spina bifida or meningocele. The motility of the spine should also be evaluated in flexion, extension, and lateral rotation. During this period of the examination, an overall assessment of multiple joints can be done for deformities, arthritic change, trauma, and prior surgical procedures. Clearly, much can be learned just by having the patient stand before the physician and asking the patient about abnormalities that become noticeable. No matter how inconvenient or uncomfortable it is, the physician should try not to omit this portion of the examination. Particularly in patients with chronic pain, this part of the examination may yield crucial and unexpected revelations.
Assessment of Mental Status Most major intellectual and psychiatric problems become apparent during the history taking. The frequency with which serious intellectual deficits are missed is surprising, however. For example, subtle aspects of memory, comprehension, and language may not be caught unless they are specifically sought. In my experience, aphasia (a general term for all disturbances of language not the result of faulty articulation) is frequently mistaken for an organic mental syndrome or dementia. Recognition of this point not only is critical in diagnostic evaluation but also has important implications for obtaining informed consent for testing, nerve blocks, and surgical procedures. Table 5.4 summarizes an approach to rapid assessment of the patient's mental status. Each practitioner should develop a personal set of standard questions to gain a sense of the normal versus the abnormal. Attention to these details in assessing mental status helps to avoid the embarrassment of overlooking receptive aphasia, Alzheimer's disease, or Korsakoff 's syndrome. Table 5.5 is the classic Folstein Mini-Mental State Examination with age-adjusted normative data. A score of 24 or higher is considered normal. Although this examination is effective in detecting clinically significant defects in speech and cognitive function, the average practitioner will find it overly tedious for use in routine pain management evaluation. In many of these situations, patients exhibit an unusual capacity to disguise underlying deficits by reverting to evasions or generalities or by filling in gaps with stereotypical responses that they have used before to escape the embarrassment of the discovery of major problems in language, memory, and other spheres of cognitive function.15 One final point relates to the patient's emotional state. The examiner must remain vigilant about the patient's mood and
43
displays of emotion. An unusually silly, euphoric, or grandiose presentation may be seen in manic states. Similarly, a discouraged, hopeless, or self-deprecating presentation may signal serious depression. As highlighted in the discussion on the targeted history, the physician must remain alert for clinical manifestations of drug use, such as slurred speech, motor hyperactivity, sweating, flushing, and distractibility. In short, the physician should get to know the patient but, in the end, should vigorously resist any early impulse to suggest that stress or anxiety alone is the principal cause of the patient's pain.
Cranial Nerves To return to the theme of keeping the targeted physical examination simple so that important points are not missed, the evaluation of CN function often overwhelms practitioners not trained in clinical neurology. It remains an important area, particularly in the evaluation of headache and facial pain. Rapid recognition of CN dysfunction may have profound significance for localizing a cerebral lesion or identifying increased intracranial pressure. In combination with the history, CN dysfunction may also be a strong indicator of a specific disease (e.g., the combined presence of explosive headache and CN III palsy implies a ruptured aneurysm until that diagnosis is excluded). Table 5.6 highlights an efficient approach to the clinical evaluation of the CNs. Certainly, when headache and facial
Table 5.4 The “Quick and Dirty” Mental Status Examination* Orientation
Ask the following questions: What is your full name? What is today’s date? What is the year? Who is the president? Who is the vice president?
Calculations
Ask the following questions: How many nickels are in a dollar? How many dollars do 60 nickels make?
Memory
Ask the following questions: What was your mother’s maiden name? Who was President before George W. Bush? Give the patient three items to remember (examples: a red ball, a blue telephone, and address 66 Hill Street). After several minutes of conversation, ask the patient to repeat the list.
Speech
Have the patient repeat two simple sentences, such as the following: Today is a lovely day. The weather this weekend is expected to be excellent. Have the patient name several objects in the room. Ask the patient to rhyme simple words, such as ball, pat, and can.
Comprehension
Ask the patient to do the following: Put the right hand on the left hand. Point to the ceiling with the left index finger.
*This simple screening mental status examination uncovers many (but not all) cognitive deficits. It can be performed in less than 3 minutes and is useful in evaluating basic aspects of memory, language, and general intellectual capacity.
44
Section II—The Evaluation of the Patient in Pain
Table 5.5 Folstein Mini-Mental State Examination Task
Instructions
Scoring
Date orientation
“Tell me the date.” Ask for omitted items.
One point each for year, season, date, day of week, and month
5
Place orientation
“Where are you?” Ask for omitted items.
One point each for state, county, town, building, and floor or room
5
Register three objects
Name three objects slowly and clearly. Ask the patient to repeat them.
One point for each item correctly repeated
3
Serial 7s
Ask the patient to count backward from 100 by 7. Stop after 5 answers. (Or ask the patient to spell “world” backward.)
One point for each correct answer (or letter)
5
Recall three objects
Ask the patient to recall the objects mentioned earlier.
One point for each item correctly remembered
3
Naming
Point to your watch and ask the patient, “What is this?” Repeat with a pencil.
One point for each correct answer
2
Repeating a phrase
Ask the patient to say, “No ifs, ands, or buts.”
One point if successful on first try
1
Verbal commands
Give the patient a plain piece of paper and say, “Take this paper in your right hand, fold it in half, and put it on the floor.”
One point for each correct action
3
Written commands
Show the patient a piece of paper with “CLOSE YOUR EYES” printed on it.
One point if the patient’s eyes close
1
Writing
Ask the patient to write a sentence.
One point if sentence has a subject, a verb, and makes sense
1
One point if the figure has 10 corners and 2 intersecting lines
1
Drawing
Ask the patient to copy a pair of intersecting pentagons onto a piece of paper.
Scoring
A score of 24 or above is considered normal.
30
Adapted from Folstein et al: Mini Mental State, J Psych Res 12:196–198, 1975.
Table 5.6 Clinical Evaluations of Cranial Nerve Function Cranial Nerves Number
Name
Evaluation Procedures
I
Olfactory
Test ability to identify familiar aromatic odors, one naris at a time with eyes closed (not routinely tested)
II
Optic
Test vision with Snellen chart or Rosenbaum near-vision chart Perform ophthalmoscopic examination of fundi Be able to recognize papilledema Test fields of vision using confrontation and double simultaneous stimulation
III, IV, VI
Oculomotor, trochlear, abducens
Inspect eyelids for drooping (ptosis) Inspect pupil size for equality (direct and consensual response) Check for nystagmus Assess basic fields of gaze Note asymmetrical extraocular movements
V
Trigeminal
Palpate jaw muscles for tone and strength while patient clenches teeth Test superficial pain and touch sensation in each branch: V1, V2, V3
VII
Facial
Test corneal reflex Inspect symmetry of facial features Have patient smile, frown, puff cheeks, wrinkle forehead Watch for spasmodic, jerking movements of face
VIII
Acoustic
Test sense of hearing with watch or tuning fork Compare bone and air conduction of sound
IX
Glossopharyngeal
Test gag reflex and ability to swallow
X
Vagus
Inspect palate and uvula for symmetry with gag reflex Observe for swallowing difficulty Have patient take small sip of water Watch for nasal or hoarse quality of speech
XI
Spinal accessory
Test trapezius strength (have patient shrug shoulders against resistance) Test sternocleidomastoid muscle strength (have patient turn head to each side against resistance)
XII
Hypoglossal
Inspect tongue in mouth and while protruded for symmetry, fasciculations, and atrophy Test tongue strength with index fingers when tongue is pressed against cheek
Chapter 5—History and Physical Examination of the Pain Patient
45
Fig. 5.2 Normal optic disc. Fig. 5.4 Advanced papilledema.
Fig. 5.3 Early papilledema.
pain are the basic issues, particular attention should be given to this portion of the examination. The key, once again, is developing a routine that, with practice, becomes thorough. It is far beyond the scope of this chapter to describe all the nuances of CN function.16 Anyone evaluating patients for headache or facial pain must be able to recognize papilledema and abnormalities of ocular motor nerve function, must be familiar with the sensory division of the trigeminal nerve, and must be able to recognize isolated CN palsies. More complex problems, such as diplopia, cavernous sinus disease, and complex brainstem lesions, are best left to specialists in neuroophthalmology and neurology. The importance of developing the ability to recognize papilledema cannot be overstated. Physicians who evaluate patients with headache who do not examine the patients' fundi are doing substandard work. Using an ophthalmoscope, the physician should turn down the lights and, if the fundus is still not visualized clearly, not hesitate to dilate the patient's eyes. The use of 0.5% tropicamide (Mydriacyl) is helpful for this purpose. Plate 1 demonstrates a few commonly encountered funduscopic findings. It is but a start as the physician begins to gain confidence in this aspect of physical diagnosis. The normal optic disc (Fig. 5.2) can be compared with discs seen in early (Fig. 5.3) and advanced papilledema (Fig. 5.4). Pseudopapilledema can be encountered both with optic nerve drusen (Fig. 5.5), which are globules of calcified mucoproteins that accumulate at the optic disc, and with myopic degeneration of the disc (Fig. 5.6). Central retinal vein occlusion (Fig. 5.7) frequently manifests with loss of central visual acuity with retinal hemorrhages, disc edema, and tortuous dilated veins. Finally, the color of the disc and the configuration and size of the optic cup should be
Fig. 5.5 Optic nerve drusen. These globules of calcified mucoproteins accumulate at the optic disc.
Fig. 5.6 Myopic degeneration of the disc.
assessed. Figure 5.8 demonstrates the pallor of optic atrophy as a result of inadequately treated papilledema. Figure 5.9 is an example of an enlarged deep optic cup seen in glaucoma. Getting started is always the hard part, but learning to examine an optic fundus is well worth the effort. This point is emphasized because Donohoe has four young women in his practice who are blind because their papilledema and increased intracranial pressure resulting from pseudotumor cerebri (idiopathic intracranial hypertension) were discovered far too late. Their stories were
46
Section II—The Evaluation of the Patient in Pain
asically the same. They were all overweight, all had headb aches, all were seen by multiple physicians, all had normal MRI brain imaging, and all had lost most of their vision before the correct diagnosis was made and proper therapy was instituted. This diagnosis rests on the ability to maintain a high index of suspicion and properly perform a funduscopic examination.
In general, the pain specialist, even one whose basic training has been in anesthesia or psychiatry, can, with proper effort, become familiar with the basics of common disorders. Ultimately, the physician who does make the effort to learn this material and incorporate it into clinical pain management practice will not have to deal constantly with feeling uneasy about a weakness in clinical aptitude. Such a physician will also avoid losing precious time in developing experience with these key physical findings associated with a variety of headache and facial pain problems.
Motor Examination
Fig. 5.7 Central retinal vein occlusion.
Fig. 5.8 The pallor of optic atrophy as a result of inadequately treated papilledema.
Motor examination should begin with inspection of muscle volume and contour. The physician should pay particular attention to atrophy and hypertrophy. The patient should be properly gowned so that these observations can be made without invading the patient's privacy. During this examination, fasciculations, contractures, alterations in posture, and adventitious movements may be identified. Strength is measured both proximally and distally in the upper and lower extremities and is graded according to the scale shown in Table 5.7. Detailed individual muscle testing is not carried out unless a specific nerve root or plexopathy is under investigation. Tone is best tested by passive manipulation, with note made of the resistance of muscle when voluntary control is absent. Changes in tone are more readily detected in muscles of the arms and legs than in muscles of the trunk. Relaxation is critical to proper evaluation. Hypertonicity is usually seen with lesions rostral to the anterior horn cells, including brain, brainstem, and spinal cord. Hypotonicity is associated with diseases affecting the neuraxis below this level, involving nerve root, peripheral nerve, neuromuscular junction, and muscle. Study of the motor system should be integrated with evaluation of the sensory examination and deep tendon reflexes, to provide cumulative information critical to identifying the site of the lesion—brain, brainstem, spinal cord, root, plexus, nerve, or muscle.
Table 5.7 Grading of Muscle Strength Clinical Finding
Fig. 5.9 An enlarged deep optic cup seen in glaucoma.
Grade
Percentage of Normal Response
No evidence of contractility
0
0
Slight contractility, no movement
1
10
Full range of motion, gravity eliminated
2
25
Full range of motion with gravity
3
50
Full range of motion against gravity, some resistance
4
75
Full range of motion against gravity, full resistance
5
100
From Chipps EM, Clanin NJ, Campbell VG: Neurologic disorder, St Louis, 1992, Mosby-Year Book.
Chapter 5—History and Physical Examination of the Pain Patient
Sensory Examination The sensory examination should be kept simple and should be targeted by clues obtained through the history. Certainly, time spent in defining sensory loss in the lower extremities would be justified in a patient who complains of pain, weakness, and numbness in the foot but not in a patient who has double vision and facial pain. Note in Figure 5.10 the difference between the skin areas innervated by dermatomes—specific segments of the cord, roots, or dorsal root ganglia—and the corresponding peripheral nerve cutaneous sensory distribution. These specific differences and changes in motor function and reflexes clinically define a nerve root from a peripheral nerve abnormality. Tables 5.8 and 5.9 highlight comparisons between specific spinal root and peripheral nerve lesions of the upper and lower
47
extremities. With time, experience, and persistence, the pain specialist can become confident in the evaluation of peripheral nerve root lesions. So many of the common pain syndromes (cervical radiculopathies, lumbar radiculopathies, carpal tunnel syndrome, femoral neuropathy, peroneal neuropathy) may be rapidly and accurately diagnosed without expensive and uncomfortable neurodiagnostic testing. Being persistent and resisting the fear that the task is overwhelming result in the ability to evaluate patients in pain efficiently. For pain syndromes of the upper extremity, the examiner should be able to differentiate sensory involvement of the radial, median, and ulnar nerves from that of specific roots (C5-T1) (see Table 5.8). For pain syndromes of the lower extremities, the examiner should be able to differentiate the C2
Trigeminal I Great auricular n Trigeminal II Trigeminal III Cut cervical n (C2, 3) Supraclavicular n (C3, 4) Axillary n (C5-6) Intercostobrachial n (Th2)
C3 C4 C5 T1 T2 T3 T4 T5 T6
Med brachial cut n (C8, Th1)
T7
Radial n (C5-Th1)
T8 T9
Genitofemoral n (L1, 2) Lat antebrachial cut n (C5-7) Med antebrachial cut n (C8, Th1)
T10
Illiohypogastric n (L1)
T12
Radial n (C5-Th1) Median n (C5-Th1)
T1 C5
T11 C6
L1 C8
L2
Ulnar n (C8, Th1)
L3
Ilioinguinal n (L1) Lat femoral n (L2-3)
L4
C7
Obturator n (L2-4) Femoral n (L2-4) Saphenous n (femoral; L3-4)
Common peroneal n (L4-S2)
L5
S1
Sural n (S1-2) Superficial peroneal n (L4-S1) Deep peroneal n (L4, 5) Fig. 5.10 Comparison of spinal segmental (dermatomal) and peripheral nerve cutaneous sensory supply. (Adapted from Haerer AF, editor: DeJong’s the neurologic examination, ed 5, Philadelphia, 1992, Lippincott.)
48
Section II—The Evaluation of the Patient in Pain
Table 5.8 Clinical Manifestations of Root Versus Nerve Lesions in the Arm Roots
C5
C6
C7
C8
T1
Sensory supply
Lateral border upper arm
Lateral forearm, including finger I
Over triceps, midforearm, and finger III
Medial forearm to finger V
Axilla to elbow
Reflex affected
Biceps reflex
None
Triceps reflex
None
None
Motor loss
Deltoid Infraspinatus Rhomboids Supraspinatus
Biceps Brachialis Brachioradialis
Latissimus dorsi Pectoralis major Triceps Wrist extensors Wrist flexors
Finger extensors Finger flexors Flexor carpi ulnaris
Intrinsic hand muscles (in some thenar muscles through C8)
Nerves
Axillary (C5, C6)
Median (C6–C8, T1)
Ulnar (C8, T1)
Sensory supply
Over deltoid
Lateral forearm to wrist
Lateral dorsal forearm and back of thumb and finger II
Lateral palm and lateral finger I, II, III, and half of IV
Medial palm and finger V and medial half of finger IV
Reflex affected
None
Biceps reflex
Triceps reflex
None
None
Motor loss
Deltoid
Biceps Brachialis
Brachioradialis Finger extensors Forearm supinator Triceps wrist extensors
Abductor pollicis brevis Long flexors of fingers I, II, III Pronators of forearm Wrist flexors
Intrinsic hand muscles Flexor carpi ulnaris Flexors of fingers IV, V
Musculotaneous (C5, C6)
Radial (C5–C8)
From Patten J: Neurological differential diagnosis, New York, 1977, Springer-Verlag.
Table 5.9 Clinical Manifestations of Root Versus Nerve Lesions in the Leg Roots
L2
L3
L4
L5
S1
Sensory supply
Across upper thigh
Across lower thigh
Across knee to medial malleolus
Side of leg to dorsum and sole of foot
Behind lateral malleolus to lateral foot
Reflex affected
None
None
Patellar reflex
None
Achilles reflex
Motor loss
Hip flexion
Knee extension
Inversion of foot
Dorsiflexion of toes and foot
Plantar flexion and eversion of foot
Nerves
Obturator (L2–L4)
Femoral (L2–L4)
Peroneal Division of Sciatic (L4, L5, S1–S3)
Tibial Division of Sciatic (L4, L5, S1–S3)
Sensory supply
Medial thigh
Anterior thigh to medial malleolus
Anterior leg to dorsum of foot
Posterior leg to sole and lateral aspect of foot
Reflex affected
None
Patellar reflex
None
Achilles reflex
Motor loss
Adduction of thigh
Extension of knee
Dorsiflexion, inversion, and eversion of foot
Plantar flexion and inversion of foot
From Patten J: Neurological differential diagnosis, New York, 1977, Springer-Verlag.
peroneal and tibial nerve sensory distribution from that of the L4, L5, and S1 roots (see Table 5.9). Such distinctions elucidate most of the common problems. Over time, the pain specialist can increase confidence in the examination and may develop a stronger foundation in peripheral neurology than many neurologists, neurosurgeons, and orthopedists possess.
Deep Tendon Reflexes Deep tendon reflexes are actually muscle stretch reflexes mediated through neuromuscular spindles. This are the one facet of the clinical examination that is objective (Table 5.10). Responses to mental status testing and motor examination, performance
Table 5.10 Deep Tendon Reflex Scale Grade
Deep Tendon Reflex Response
0+
No response
1+
Sluggish
2+
Active or normal
3+
More brisk than expected, slightly hyperactive
4+
Abnormally hyperactive, with intermittent clonus
From Seidel HM, Ball J, Daines J, et al: Mosby’s guide to physical examination, ed 7. St Louis, 2010, Mosby.
Chapter 5—History and Physical Examination of the Pain Patient
49
peripheral nerve, a specific nerve root, a diffuse peripheral nerve, or the spinal cord. It should take less than 30 seconds to complete this part of the examination. 2+
Triceps C7, C8
2+
Biceps C5, C6
Patellar L2, L3, L4 2+ 2+
Achilles S1
Fig. 5.11 Diagram of a deep tendon reflex examination. (From Waldman SD, editor: Interventional pain management, ed 2, Philadelphia, 2001, Saunders, 95.)
on sensory testing, and even gait can be consciously altered by the patient for any of a variety of reasons. Guillain-Barré syndrome (acute inflammatory polyneuropathy), however, a condition that in its initial stages may be misdiagnosed as anxiety related, characteristically shows absence of all the deep tendon reflexes, an important early clue to the organic nature of the disorder. A deep tendon reflex examination can be graded using the numerals 1 through 4 (Fig. 5.11). Testing of the superficial reflexes, such as the abdominal or cremasteric reflexes, is not particularly valuable in clinical assessment. The only superficial reflex worth evaluating is the plantar reflex (a superficial reflex innervated by the tibial nerve, L4-S2). The response to stroking the plantar surface of the foot is usually flexion of both the foot and the toes. In diseases of the cortical spinal system, dorsiflexion of the toes occurs, especially the great toe, with separation or fanning of the others; this finding, Babinski's sign of upper motoneuron involvement (brain, brainstem, and spinal cord), is often paired with increased deep tendon reflexes and clonus (i.e., sustained muscular contractions following a stretch stimulus noted frequently in the ankle). Unilateral absence of a deep tendon reflex implies disease at the peripheral nerve or root level. Diffuse reduction or absence of deep tendon reflexes suggests a more generalized process affecting the peripheral nerve, seen frequently in peripheral neuropathies secondary to diabetes, alcohol abuse, or inflammation. The objective data obtained quite rapidly from testing deep tendon reflexes are correlated with motor and sensory findings to determine whether a problem lies in a specific
Examination of Gait Walking is an intricate process influenced by mechanical factors such as muscles, bones, tendons, and joints and, more importantly, dependent on nervous system integration. Just watching the patient walk during the examination is an extremely valuable exercise. The patient should be asked to walk with eyes open and closed and to stand with eyes open and closed (Romberg's sign). Gaits associated with parkinsonism (small, short steps with a stooped posture), normal-pressure hydrocephalus (magnetic gait, as if the patient were walking in magnetic shoes across a metal floor), muscular dystrophy, stroke, peripheral nerve injury, cerebellar ataxia, Huntington's chorea, and hysteria (astasia-abasia) are but a few characteristic patterns of disturbed locomotion. In short, a strong measure of neuro-orthopedic well-being is implied by the patient who walks well with eyes open and closed.
Conclusion The basic point of this chapter is simple. A targeted and well-organized pain history is the foundation of proper diagnosis. Advances in diagnostic technology, no matter how sophisticated, cannot replace listening to the patient's own story of the illness. It is through this process that physicians most effectively gain insight, not only into the nature of the illness but also, and more importantly, into the personality of the patient who is in pain. The professionalism and sensitivity with which physicians obtain this information do much to establish the relationship with the patient and the ultimate success of therapies. If any room exists for shortcuts, it is not in this portion of the evaluation. The targeted physical examination should be viewed as an extension of the insights derived from the history. It should be performed in a professional, thorough, but not laborious fashion. As the calling of pain management becomes more popular, physicians of various disciplines should avoid faddish technologic advances and opportunism made possible by inequities in reimbursement and should commit themselves to the very basics: obtaining historical data and eliciting physical findings. Energy expended to this end will reduce costs, enhance patient satisfaction, and foster lasting credibility in the evolving field of pain management.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
8
II
Radiography Hifz Aniq and Robert Campbell
CHAPTER OUTLINE Cervical Spine 75 Thoracic Spine 77 Lumbar Spine 77 Shoulder 78 Elbow 79
X-rays are produced when highly energetic electrons interact with matter and convert their kinetic energy into electromagnetic radiation. The x-ray tube contains the electron source in the form of a cathode tube filament, as well as a tungsten target in a copper anode. Collimators are used to define the x-ray field. With varying voltage, current, and exposure time, x-ray beams of varying penetrability and spatial distribution can be created. Radiography depends on differences in radiographic density. A radiograph is a two-dimensional image of a threedimensional object. This is known as a projection imaging technique, in contradistinction to cross-sectional modalities. The difficulty of interpreting these images results from this superimposition of structures, and thus pathologic processes may appear less clearly defined. Traditional radiography systems use a film-screen combination consisting of a cassette, one or two intensifying screens, and a sheet of film. The film is simply thin plastic with a photosensitive emulsion coated onto one or both sides. The cassette is designed to protect the film from ambient light before the film is exposed with x-rays. For routine radiography, double-screen, double-emulsion film-screen combinations are often used to improve sensitivity and to reduce radiation exposure. Radiographic views are named by the direction of the x-ray beam from the source to the imaging recording device. Several different systems are currently available for the acquisition of digital radiographs: the ones most commonly seen in clinical use are computed radiography (CR), chargedcoupled devices (CCDs), direct detection flat panel systems, and indirect detection flat panel systems. The workflow of CR systems is similar to that of conventional screen-film radiography. The CR imaging plate is made of barium fluorobromide or barium fluoride (barium fluorohalide). The CR imaging plate traps the x-ray beam (the electron) within the phosphor layer, and this electromagnetic energy is stored until processing. The CR plate is inserted into a reader that contains a laser that scans across the imaging plate, releases the stored energy, and causes the emission of © 2011 Elsevier Inc. All rights reserved.
Wrist and Hand 80 Pelvis and Hip 81 Knee 82 Ankle and Foot 84
light. These light emissions are read by a photodiode scanning the imaging plate. The imaging plate is then “cleaned” with a flood of light. The prime advantage of CR over film-screen radiography is the increase in dynamic range. The system can tolerate a wider exposure range, and the result is a smaller number of diagnostically inadequate films. However, the raw data require processing algorithms to produce clinically useful images. CCD detectors form images from visible light. The surface of a CCD chip is photosensitive, and when a pixel is exposed to light, electrons are produced and are built up within the pixel. This technology is used in modern video and digital cameras.
Cervical Spine Neck pain is a common human experience, although less common than that of low back pain. Neck pain may be a result of local noxious stimulation, or it may be referred from distant structures supplied by the cervical spinal nerves. Although somatic pain is typically referred distally, the acromioclavicular joint and sternoclavicular joints are two sites that may have neck pain by proximal referral. Most cases of neck pain are self-limiting, resulting from mechanical problems; however, in a small percentage of cases, the pain becomes chronic. The standard cervical spinal radiographic series consists of anteroposterior, lateral, and odontoid views. If the cervicothoracic junction is not demonstrated on the lateral view, one may obtain a swimmer's view, taken while the patient's arm is extended over the head. Plain radiographs are appropriate when the patient has a history of trauma likely to have produced a fracture or severe subluxation or when concern exists regarding instability. To assess for subluxation, four lines are traced along the lateral radiograph. Lines joining the anterior aspect of the vertebral body, the posterior aspect of the vertebral body, the laminae, and the spinous processes should appear as smooth arcs (Fig. 8.1). Oblique views of the cervical spine demonstrate the neural foramina, pedicles, articular masses, and apophyseal joints. In the setting of trauma, oblique views have been used in identifying fractures 75
76
Section II—The Evaluation of the Patient in Pain
and subluxations of the articular process. Currently, oblique views are rarely performed because computed tomography (CT) is easily available. Atlantoaxial instability should be specifically assessed. This is performed by evaluating the distance between the posterior aspect of the anterior arch of the atlas and the anterior aspect of the odontoid as seen on a lateral view (Fig. 8.2). This measurement normally is less than 3 mm. Atlantoaxial instability can be seen in disease processes that may result in destruction of the transverse ligament complex, such as inflammatory arthropathies (most commonly, rheumatoid arthritis). Radiography for the evaluation of mechanical neck pain is limited and can be used to document the degree of cervical spondylosis. The term spondylosis is often used synonymously with degeneration, which includes both the nucleus pulposus and anulus fibrosus processes. Freidenburg and Miller,1 however, demonstrated no correlation between the presence of degenerative or spondylitic changes in the cervical spine and symptoms of neck pain. Oblique views of the cervical spine have been replaced by magnetic resonance imaging (MRI) scan, which can show the neural foramen much more clearly and does not involve any radiation. The ligament between the vertebrae and the spinal dura is called the posterior longitudinal ligament. Ossification of the posterior longitudinal ligament (OPLL) is more common in the cervical spine (70%), followed by the thoracic (15%) and lumbar (15%) regions. This entity was originally reported in a large number of Japanese patients with a genetic linkage. Although OPLL is typically asymptomatic, patients may present with symptoms of cervical myelopathy.2 The typical radiographic appearance is
that of a linear band of ossification along the posterior margin of the vertebral body with a separating sharp, thin radiolucent line. OPLL may be apparent in as many as 50% of cases of diffuse idiopathic skeletal hyperostosis (DISH); conversely, DISH has been observed in more than 20% of cases of OPLL (Fig. 8.3).3
Fig. 8.2 Lateral cervical spine: two images of a known case of rheumatoid arthritis 8 years apart. A, Normal atlantoaxial joint. B, Atlantoaxial subluxation. The gap between the arch of the atlas and the odontoid process is wider than 3 mm (arrow).
Fig. 8.1 Lateral radiograph of a normal cervical spine. From anterior to posterior, these four parallel lines should be observed in every lateral cervical spine examination (anterior spinal line, posterior spinal line, spinolaminar line, spinous process line).
Fig. 8.3 Ossification of the posterior longitudinal ligament (OPLL) and diffuse idiopathic skeletal hyperostosis (DISH). The lateral view of the cervical spine shows prominent flowing ossification along the anterior margin of four continuous vertebrae compatible with DISH. A dense vertical band of ossification is seen posterior to the vertebral margin (arrow) with a separating radiolucent line consistent with OPLL.
A
B
Chapter 8—Radiography
77
Thoracic Spine
Lumbar Spine
The standard thoracic spinal radiographic series consists of anteroposterior and lateral views. Symptomatic degenerative disk disease is much less common in the thoracic spine than in the cervical and lumbar regions. Thoracic disk herniations are relatively uncommon when compared with cervical and lumbar disk disease. Commonly, thoracic disk herniations manifest as pain, numbness, tingling, and occasionally lower extremity weakness. If the herniation is large enough, bowel or bladder function may be affected. Scheuermann's disease is a type of thoracic kyphosis defined by anterior wedging of at least 5 degrees of three adjacent thoracic vertebral bodies. Secondary changes of Scheuermann's kyphosis are characterized by irregularities of the vertebral end plates, disk space narrowing, and the presence of intervertebral disk herniations known as Schmorl's nodes. The thoracic spine is most commonly affected, although the lumbar spine may also be involved. This disorder of the spine is often discovered initially in adolescents and was formerly thought to be secondary to osteonecrosis but is now believed to be the result of a congenital weakness in the end plates. For diagnosis, three adjacent vertebral bodies must be involved with 5 degrees or more of anterior wedging. DISH is a common cause of regional pain syndromes in patients more than 40 years old. The peak incidence is in the sixth and seventh decades of life, and the disorder is more common in men than in women. Although common in the lower thoracic spine, DISH also can be seen in the lumbar and cervical spine. Patients typically present with localized pain and stiffness with decreased range of motion of the affected area. Radiographs of the spine demonstrate the presence of flowing, nonmarginal syndesmophytes along the anterolateral margins of at least four contiguous vertebrae (Fig. 8.4). Some patients with DISH also have OPLL (see earlier).
Low back pain is the most common musculoskeletal impairment reported and the second most common complaint to primary physicians after the common cold. Most instances of back pain are benign and self-limiting. More than 50% of all patients improve after 1 week, whereas more than 90% are better at 8 weeks. Careful clinical evaluation is necessary to separate patients with mechanical (no primary inflammatory or neoplastic cause) back pain from those with nonmechanical back pain. Radiography is stated to have limited use in the evaluation of low back pain. Patients with mechanical back pain often have normal radiographs. Conversely and more commonly, many individuals with radiographic abnormalities are asymptomatic.4 Evaluation of the lumbar spine includes the anteroposterior and lateral views. The anteroposterior and lateral views demonstrate alignment, disk and vertebral body height, and gross assessment of bone mineral density. The use of lumbar radiography should be limited because it exposes the gonads to significant ionizing radiation. The radiation exposure of oblique views is double the exposure of standard views, which alone are equivalent to the radiation exposure of more than 30 routine chest x-rays.5 Radiography is often used as an initial screening tool for patients with unrelenting back pain. Congenital abnormalities or developmental defects such as scoliosis, spina bifida, or anomalous lumbosacral transitional vertebral bodies may be visualized. Spondylolysis, a break in the pars interarticularis, is a common radiographic abnormality associated with low back pain. Spondylolysis may or may not result in spondylolisthesis. However, the combination of spondylolysis and spondylolisthesis frequently distorts the associated neural foramina and leads to compromise of the exiting nerve. Spondylolysis does not necessarily produce back pain. Oblique views of the lumbar spine are particularly useful for the evaluation of spondylolysis because they demonstrate the pars interarticularis in profile (Fig. 8.5).
A
B
Fig. 8.4 Diffuse idiopathic skeletal hyperostosis (DISH). Antero posterior (A) and lateral (B) views of the thoracic spine show large flowing bony excrescences along at least four vertebral bodies.
Fig. 8.5 Spondylolysis. The lateral radiograph demonstrates disconti nuity of the “Scottie dog” neck compatible with a pars defect.
78
Section II—The Evaluation of the Patient in Pain
Disorders of the intervertebral disks and zygapophyseal joints may also result in low back pain. Lumbar radiographs may not directly demonstrate findings of disk herniation or spinal stenosis. However, it is unusual for lumbar radiographs to be absolutely normal in these conditions. Acute disk herniation may result in loss of intervertebral disk height. Normal lumbar intervertebral disk height demonstrates an interval increase up to the lumbosacral junction. Plain film findings that may be associated with stenosis include narrowing of the intervertebral disk spaces with diskogenic vertebral sclerosis, zygapophyseal joint osteoarthritis, and spondylolisthesis.6 Because these findings are nonspecific and are common in asymptomatic older individuals, they have limited predictive value. Congenital stenosis may result from developmentally narrow spinal canal dimensions (developmentally short pedicles) or bone dysplasias such as achondroplasia (dwarfism). Signs of disk degeneration include loss of disk height, sclerosis of the end plates, and osteophytic ridging. In addition, spondylolisthesis can be diagnosed and the degree of forward slip visualized easily on lateral images. Spondylolisthesis as a result of degenerative changes should never be greater than 25%. Meyerding proposed a grading system for spondylolisthesis that is still used today. The degree of slippage is measured as the percentage of distance the anteriorly translated vertebral body has moved forward relative to the superior end plate of the vertebra below. Grade 1 denotes up to 25% forward slip; grade 2, up to 50%; grade 3, up to 75%; grade 4, up to 100%; and grade 5, greater than 100% slippage (Fig. 8.6). In older individuals with low back pain, more ominous causes need to be considered. Patients with fever or weight loss may have an infection or tumor as the cause of their pain. Radiographs may be normal at the initial onset of disk space infection but will demonstrate increasing destruction with prolonged duration. Infections are generally hematogenous in adults and begin at the vertebral end plate. Radiographic evidence of disk infection includes loss of disk height, erosions or destruction of adjacent vertebral end plates, and reactive new bone formation with sclerosis in chronic cases. If clinical suspicion persists despite normal radiographs, crosssectional imaging with CT or MRI may be performed. Both modalities demonstrate increased sensitivity for the detection of vertebral osteomyelitis. Numerous neoplastic lesions, both benign and malignant, may be associated with the lumbar spine. Neoplastic lesions may be lytic (radiolucent), blastic (radiodense), or mixed. From 30% to 50% of trabecular bone must be lost before the loss can be visualized on a radiograph. Osteoporotic patients are at increased risk for developing compression fractures. New or incompletely healed fractures are commonly associated with pain. Although radiographs may be able to distinguish between acute and chronic compression deformities through comparison with prior radiographs, it may be impossible to assess the degree of healing. Scintigraphy and MRI are more useful in this context because they demonstrate increased bone activity and bone marrow edema, respectively, of incompletely healed fractures. Inflammatory arthropathies that affect the axial skeleton may manifest as low back pain. Radiographs of the sacroiliac joints are often obtained in patients suspected of having inflammatory arthropathy of the axial skeleton. Sacroiliitis can be detected early with radiography. Angled views of the sacroiliac joints by 30 degrees (Ferguson's view) provide greater sensitivity than do routine anteroposterior views.7 In patients with ankylosing spondylitis, sacroiliitis begins as erosions, followed by sclerosis
A
B
C
D
Fig. 8.6 Grading of spondylolisthesis. Lateral views of the lumbar spine demonstrate varying degrees of spondylolisthesis in the lower lumbar spine. A, Grade 1: 1% to 25% slippage. B, Grade 2: 26% to 50% slippage. C, Grade 3: 51% to 75% slippage. D, Grade 4: 76% to 100% slippage.
and eventual ankylosis. Sacroiliitis may be unilateral (i.e., infectious), bilaterally symmetrical (i.e., ankylosing spondylitis, enteropathic arthropathy), or bilateral and asymmetrical (i.e., seronegative spondyloarthropathies) (Fig. 8.7). CT or MRI is more sensitive and may show early involvement of the sacroiliac joint when the findings of plain radiographs are equivocal. Kummel's disease, aseptic vertebral osteonecrosis, is an entity that may manifest with localized pain. Although patients may be asymptomatic, local pain and progressive angular kyphotic deformity are clinical hallmarks. Radiographic diagnosis is based on vertebral body collapse or flattening with an associated intranuclear vacuum cleft. Kummel's disease is often associated with a history of trauma, severe osteoporosis, or long-term use of corticosteroids, and it manifests most commonly at the thoracolumbar junction (Fig. 8.8).
Shoulder The shoulder is a complex joint with numerous bony articulations as well as multiple ligamentous and musculotendinous attachments. Shoulder pain may be a result of local trauma or referred pain or may be seen in association with other medical conditions.
Chapter 8—Radiography
A
B
Fig. 8.7 Normal sacroiliac joint and sacroiliitis. Magnified views of the sacroiliac (SI) joints of three different patients. A, Normal ante roposterior view of the left SI joint demonstrates sharply defined sacral and iliac sides of the joint without evidence of sclerosis or erosion. B, Sacroiliitis: Posteroanterior view demonstrates erosions and sclerosis predominantly on the iliac side. C, Fusion of the left SI joint (arrows) that was also evident on the right in this patient with late-stage ankylosing spondylitis.
C
Radiographs may demonstrate chronic rotator cuff arthropathy that may be evidenced by calcific tendinitis (Fig. 8.9). In these long-standing cases, cystic and sclerotic changes may be seen at the greater tuberosity insertion. Superior migration of the humeral head against the undersurface of the acromion with narrowing of the subacromial space (6on a 10-point visual analog, numerical rating, or other pain scale) to be considered a positive provocation. Acceptance of minimal to moderate pain, or “pressure,” as positive would increase the false-positive rate significantly. A recent meta-analysis of the diskography literature by Wolfer et al209 has shown that when the criteria for diskogenic pain, as detailed in the ISIS Practice Guidelines2 are used, there is an acceptably low falsepositive probability. IASP,170 ISIS,1 and PASSOR185 stipulate that to be a valid study and make a diagnosis of diskogenic pain, an anatomic, internal control must be present. Therefore provocation diskography cannot be considered valid if all disks stimulated are shown to be concordantly painful, be it one or several. Valid diskography cannot be performed by stimulation of a single level. If all levels are found to be positive to stimulation, the study is described as “indeterminate.” By the aforementioned criteria, the diagnosis of diskogenic pain is most ensured when a painful disk on stimulation is shown to have two adjacent asymptomatic levels. The gross morphology of the internal disk architecture can be studied by examination of the nucleogram in lateral and AP fluoroscopic spot images. Pattern variations indicating abnormalities with regard to nuclear filling, degeneration of the disk substance, and radial fissures have been described.11,88,210 Pain is often not associated with disk pathology. Full-thickness anular disruption, with contrast flow into the epidural space, is often encountered without a positive pain response. Because pain on injection is thought to be partially due to the mechanical load placed on the disk during pressurization, nonpainful disks with large rents may not be capable of this pressurization, and therefore no painful response is forthcoming. Even disks with large protrusions or extrusions may evidence no pain with high-pressure stimulation. Pathology does not equal pain. Evaluation by axial CT imaging is integral to the diagnostic diskography study. At a minimum, CT axial images of each disk that shows evidence of concordant pain with stimulation is appropriate. Axial images validate the procedure in that contrast is seen to fill the nucleus and reveals anular fissures.211–214 Historically, postdiskography CT scans have been performed to make the diagnosis of disk herniation,215–218 although today MRI is the “gold standard” for this diagnosis. Because CT imaging is an inherent part of diskography and not a separate imaging study per se, correlation between the two components of the test is mandatory, and separate interpretation of the CT scan by a physician radiologist not involved in the actual diskography is not appropriate. Injectionists, no matter what the primary specialty, who are not “comfortable” interpreting the preprocedure MRI, or the postprocedure CT images, should forgo undertaking this, or any other interventional pain/nonsurgical spine procedure, until competence as a spinal diagnostician is ensured. As noted earlier, the outer third of the anulus, in contrast to the inner third, is known to have a high concentration of nerve endings.58,59,219 One would expect a correlation between anular disruptions radiating into this area and pain. Because anular tears radiating into the outer third of the disk have been shown to be the primary indicator
Fig. 14.9 Grades of internal disk disruption. Grade “0,” contrast confined to the nucleus pulposus, no anular disruption; grade I, disruption involving the medial third of the anulus fibrosus; grade II, disruption extending to the outer third of the anulus fibrosus; grade III, disruption extending into the outer third of the anulus fibrosus with circumferential spread of contrast of less than 30 degrees; grade IV, disruption extending into the outer third of the anulus fibrosus with circumferential spread of contrast of greater than 30 degrees; grade V, disruption through the outer third of the anulus fibrosus with contrast outside the bounds of the intervertebral disk.
of diskogenic pain,18,160,220 a grading scale of anular disruption has been developed221 and modified.160 The Modified Dallas Diskogram Scale is widely used in reporting findings on the axial post-diskogram CT scan images, and it describes five grades of anular fissures (Fig. 14.9).222 Grade “0” indicates no anular disruption (Fig. 14.10A). Grade I describes radial disruption into the inner third of the annulus (Fig. 14.10B), whereas in grade II, contrast has spread into the middle third of the annulus (Fig. 14.10C). Grade III and grade IV lesions both denote an anular fissure that involves the outer third of the anulus; they are differentiated by a grade IV lesion extending into a circumferential tear involving more than 30 degrees of the disk perimeter (Fig. 14.10D, E). A Grade V anular disruption describes a fullthickness tear through the anulus with spread of contrast outside the confines of the disk (Fig. 14.10F, G), although some think that this should not be designated as a separate grade of disruption. Once the procedure has been completed and all images examined, a diagnosis of diskogenic pain may be made if the following requirements are met: (1) stimulation of the disk in question produces concordant pain; (2) the concordant pain is greater than 6 on a visual analog or equivalent scale; (3) the pain is produced at less than 50 psi above opening pressure when a manometer is used; and (4) a negative control disk produces no pain when stimulated.2 Though not widely used at present, a numeric scoring system in which points are awarded for the various criteria just presented has been devised2 and, if used, should markedly decrease the frequency of false-positive studies.
Chapter 14—Intervertebral Disk Stimulation Provocation Diskography
A
B
C
D
E
F
G
129
Fig. 14.10 Axial CT images parallel to the end plates through lumbar intervertebral disks, after contrast injection. A, Grade 0. B, Grade I. L4-5 from Figure 14.8. Epidural contrast secondary to a grade V disruption at the infrasegmental level. C, Grade II. D, Grade III. Note needle track, open arrow. E, Grade IV. F, Grade V. L5-S1 from Figure 14.8. G, Grade V with grade III degenerative pattern (>50% anular disruption). Black arrows indicate epidural spread. White arrows indicate anular disruption.
Thoracic Diskography Technique In the past, surgical procedures for the treatment of painful thoracic intervertebral disks were limited and diskography of the dorsal spine rarely indicated or requested. With newer, less invasive percutaneous disk procedures now at least an option (intradiskal anular thermal lesioning, percutaneous thoracic diskectomy, and chemical modulation), thoracic disk stimulation is gaining in indications. Because of the close proximity of the lung, which creates the real possibility of iatrogenic pneumothorax, and the relatively small target, thoracic disk stimulation is technically demanding and, as with cervical diskography, should be attempted only by expert spinal injectionists whose skills have been well honed by significant experience in
erforming fluoroscopically guided procedures. The prop cedural technique as first described by Schellhas et al150 and recently codified223 provides safe access to the thoracic intervertebral disk when the pertinent anatomy is mastered and due diligence afforded. On a radiolucent procedure table, the patient is placed in the prone position. A thin pillow may be used under the chest or upper part of the abdomen to accentuate the normal kyphotic curve. The posterior thoracic and upper lumbar region is prepared and draped in a sterile manner. At each level to be studied the target disk is identified, and with a cephalocaudad tilt of the C-arm fluoroscope, the end plates are aligned so that they are parallel to the x-ray beam. The end plates will be seen as linear rather than ovoid structures.
130
Section II—The Evaluation of the Patient in Pain
RH P
T10
T10
T10
MPL
MRH
IEP
ID
RH
SEP
P
T12
A
T11
T11
T11
T12
T12
C
B
Fig. 14.11 Left oblique view of the thoracic spine at T10-11. A, Scout image. B, Anatomic landmarks labeled. C, Needle at target in anulus of T10-11 disk. Note needle at disk margin, T11-12. ID, T10-11 intervertebral disk; IEP, inferior end plate T10; SEP, superior end plate T11; MPL, projected midpedicular line (superior articular process and lamina); MRH, projected medial rib head line; P, pedicles; RH, rib head; open circle, target.
In most instances, needle placement will be from the side opposite the usual pain. If pain is in the midline, there is no preference with respect to the side of needle insertion. The C-arm is then rotated obliquely to the side where needle insertion will take place. The spinous processes will appear to move laterally toward the contralateral side, followed by the pedicle and rib head. When the pedicle is positioned approximately 40% of the distance across the vertebral body, rotation of the C-arm should cease. A rectangle or square hyperlucent area, or “box,” will be evident and be bounded in the sagittal plane medially by the mid-interpedicular line (lateral superior articular process and lamina) and laterally by a line connecting the medial aspect of the rib heads and costovertebral joints. In the axial plane, the rectangular hyperlucent area is delineated by the superior end plate of the vertebral body caudal to the targeted disk and the inferior end plate of the vertebral body cephalad to the targeted disk (Fig. 14.11A, B). The skin is marked over the hyperlucent box (Fig. 14.11B), local anesthetic is injected, and a 25- or 22-gauge, 3.5-inch needle with a slightly bent tip is inserted. Depending on target level and body habitus, a longer, 5-inch needle might be required. The needle is advanced toward the target in small increments with the frequent use of spot fluoroscopy. It is important to stay medial to the medial aspect of the rib heads or the pleura may be penetrated (Fig. 14.12). Often, as the needle is advanced, os will be contacted. By withdrawing the needle 1 to 2 mm to disengage the needle tip from the boney contact, and rotating the needle, the bent needle tip will alter direction, and continued advancement of the needle between the rib head and superior articular process should be accomplished without significant difficulty. The unique feel of resistance will be met as the needle tip contacts the disk anulus (Fig. 14.11C). After contacting the anulus, the disk is entered under active lateral fluoroscopic guidance and the needle positioned in the center of the disk.
Lung
Lung RH SAP IAP
Fig. 14.12 Thoracic axial CT image at T6-7 with the needle path indicated. IAP, Inferior articular process; RH, rib head; SAP, superior articular process.
Once needle position in the center of each disk is verified and documented by AP and lateral imaging (Fig. 14.13), contrast is injected under active lateral fluoroscopy. The capacity of injectate in a thoracic intervertebral disk with a competent anulus will range from 0.5 to 2.5 mL, depending on the level, with capacity decreasing as one proceeds cephalad from the lumbothoracic junction. The author prefers to use a manometer for thoracic disk stimulation in that additional objective data can be obtained. During injection of contrast, the volume injected, the patient's pain response, the concordance of pain, the pressure generated or characteristic of the end point (none, soft, or firm), and the pattern of contrast within
Chapter 14—Intervertebral Disk Stimulation Provocation Diskography
131
T10 T10
T11 T11
T12
T12
Fig. 14.13 Anteroposterior (A) and lateral (B) images of the thoracic spine with needles in position within the intervertebral disks.
B
A
(–)
(–) T10
T11
(–)
(+)
T11 (+)
T12 (–)
T12 (–) L1
A
B
the disk, including anular competence, should be recorded. Spot AP and lateral images are saved after disk injection (Fig. 14.14). If desired, following the procedure a CT scan will provide information on pathology involving the internal architecture of each injected intervertebral disk (Fig. 14.15) but provides little new information if an anular tear was noted on the fluoroscopic images.
Cervical Diskography Technique The cervical region is a compact area with a high concentration of vulnerable structures; if these structures are violated, significant morbidity or mortality can occur. Cervical diskography is a technically demanding and unforgiving procedure that requires a precision gained only after much experience with fluoroscopically guided procedures. Although some welltrained diskographers recommend diskography only if positive results will be acted on (i.e., a surgical or a percutaneous
Fig. 14.14 Anteroposterior (A) and lateral (B) images of the thoracic spine after disk stimulation. Contrast is seen within the intervertebral disks at T9-10 through T12L1. (−), No provocation of concordant pain with injection; (+), positive provocation of concordant pain with injection; arrows indicate anular disruption with contrast seen extending into the outer annulus.
disk procedure is contemplated), this author is adamant that the obtaining of a diagnosis is of paramount importance. Cervical diskography traces its history back to techniques described by Smith and Nichols142 and Cloward.224 Both reports discussed indications for the procedure144,145 and surgical approaches to treatment.224,225 Cord compression or symptoms of myelopathy are absolute contraindications to the performance of cervical diskography. Iatrogenic disk herniation226 during disk stimulation, and the severe untoward consequences, can result from spinal cord compression.227 Therefore, before initiation of cervical diskography, high-quality CT or MRI scans, or both, must be examined by the physician performing the procedure to ensure that adequate reserve space within the spinal canal is present at the target level, or levels, to accommodate disk material possibly being forced into the canal during the procedure, with the resulting possible cord compression and morbidity. Axial views must be examined to ensure a sagittal (i.e., AP) diameter of 10 mm or greater.228 Patients with congenitally narrow
132
A
Section II—The Evaluation of the Patient in Pain
B
Fig. 14.15 Axial CT images of the thoracic spine through adjacent intervertebral disks after diskography. A, Contrast is confined to the nucleus pulposus without anular disruption. B, Marked disruption of the internal intervertebral disk architecture. Epidural spread, dark arrow, is noted in association with a significant disk protrusion, open arrow.
spinal canals may not be candidates for this procedure. If a physician does not possess the competence to interpret the preprocedure CT or MRI scans, he or she is not competent to perform any disk procedure. Review of a report by a radiologist, or assurances by a surgeon, who may or may not be a competent diskographer, are not an adequate substitute for personal interpretation of the imaging studies by the physician actually performing the procedure, and who is solely responsible to ensure that the patient is a safe candidate for the procedure. Physicians who do not “feel comfortable” interpreting MRI and CT images should not be performing cervical diskography under any circumstance. A high-quality C-arm fluoroscopy unit is required. The patient is placed on a radiolucent procedure table in a supine position. A pillow or triangular sponge is positioned under the upper part of the thorax and shoulders to extend the neck. Before preparation and draping of the skin, verification by preprocedure fluoroscopic screening guarantees adequate visualization in the AP, lateral, and oblique views. Disk puncture should not be attempted at any level if accurate evaluation of needle tip position within the disk cannot be obtained. Depending on the procedural technique used (see later discussion), the body of the C-arm will be either perpendicular to the patient on the left or at the head of the table. The neck, mandible, clavicular regions, and shoulders are prepared and draped in sterile fashion. Inclusion of the shoulders is necessary so that they may be depressed by the physician to improve lateral visualization of the C6-7 and C7-T1 disks as needed. Beards prevent adequate preparation of the skin and must be removed before the procedure. Prophylactic antibiotic and light sedative medications are administered as previously discussed. Because the esophagus lies toward the left at the lower cervical levels, a right-sided approach is used for cervical disk access. The skin entry point will be along the medial margin of the sternocleidomastoid muscle with the needle track running lateral to the trachea and esophagus and medial to the carotid artery. Depending on the targeted disk level, other structures may come into play. The hypopharynx can be distended at C2-3, and therefore a slightly more lateral approach is
indicated. Thyroid cartilage is present at C5-6. A more medial approach is necessitated at C7-T1 to avoid the apex of the lung and the common carotid and thyroid arteries. Although a double-needle technique has been described and advocated,229 most experienced cervical diskographers today use 25-gauge, 3.5-inch needles with stylet.228,230 As noted in the lumbar technique, a slight bend in the needle tip facilitates directional control. Local anesthetic, if used, should be limited to the skin because deeper infiltration may track along the cervical sympathetic chain and cause an alteration in the pain response. Two alternative techniques are used by practitioners to gain access to the cervical disk. The traditional approach involves the use of the fluoroscope in an AP or slightly oblique view, whereas the alternative calls for a foraminal (i.e., anterior oblique) image. The actual needle insertion site and needle tract to the disk are virtually identical with both techniques, as demonstrated in cadaver studies by Dr. Charles Aprill231 and this author. With the traditional, less precise, more experience intensive, approach to the cervical intervertebral disk, the C-arm in an AP or slight right oblique view is used to identify the target disk. Cephalocaudad tilt of the image intensifier is used to align the vertebral body end plates. Two hands are used, with the nondominant middle and index fingers advanced toward the anterior aspect of the spine at the skin entry point. This significant digital pressure displaces the laryngeal structures medially, whereas the carotid artery is distracted laterally and can be palpated under the fingers. The spine is felt under the finger tips. With the dominant hand, the needle is then inserted between, directly over, or under the fingers and, with active fluoroscopic guidance, advanced swiftly toward the right anteriorlateral aspect of the spine. Aprill228 advocates directing the needle so that it touches the superior aspect of the vertebral body caudad to the disk in order to ascertain the depth of the disk. Slight manipulation of the needle, including rotation to make use of bevel control, is then performed to direct the needle into the disk anulus just medial to the uncinate process. With the use of a lateral view and active fluoroscopy, the needle is then advanced into the center of the disk core. AP and lateral images are saved to document needle placement. The alternative technique for cervical disk access has advantages that include ease of use, excellent visualization of the target disk, ability to use a down-the-beam (i.e., tunnel vision) approach, and somewhat less x-ray exposure to the hands. This approach is adapted for the use of a C-arm and is favored by the author. The fluoroscope is positioned at the head of the table to provide ease of imaging in all planes. A right anterior oblique projection, or foraminal view, is used to visualize the intervertebral foramina at their greatest diameter (Fig. 14.16A). The target disk is identified by counting down from C2-3, and the end plates of the chosen disk are aligned by using cephalocaudad tilt of the image intensifier. A target on the disk is chosen that is approximately one third to one half the distance between the uncinate process and the anterior aspect of the disk (Fig. 14.16B). The skin entry site is marked with a sterile skin marker and should lie just medial to the sternocleidomastoid muscle and carotid artery (Fig. 14.17). If desired, a local anesthetic skin wheal can be made, although if 25-gauge needles are used, this is not necessary. A blunt sterile metal instrument is then pressed firmly against the skin, over the skin entry point, until resistance by the underlying tissues and spine is felt. This decreases the distance between the skin and
Chapter 14—Intervertebral Disk Stimulation Provocation Diskography
133
SEP IEP CP
C5 C6
ID C7 U
F
T1
IP
A
Fig. 14.17 Cervical axial CT view at C5-6 with the needle path. CA, Carotid artery; E, esophagus; JV, internal jugular vein; T, trachea; TH, thyroid; VA, vertebral artery.
C6 C7
VA
B
C6 C7
C Fig. 14.16 Oblique-anterior, “foraminal,” views of the cervical spine. A, Anatomic landmarks labeled. B, Target for safe disk access. C, Needle in outer anulus. ID, Intervertebral disk; F, C6-7 foramen; IP, ipsilateral pedicle; CP, contralateral pedicle; IEP, inferior end plate of C6; SEP, superior end plate of C7; U, uncinate process.
disk and distracts any vulnerable soft tissue structures away from the needle track. The position over the disk target is verified, and a 25-gauge needle is inserted at the tip of the instrument. With the assistance of active fluoroscopy the needle is quickly maneuvered toward the disk in one movement using rotation to control the needle direction. The patient is asked to refrain from vocalization, coughing, or swallowing during this portion of the procedure in that movement of the soft tissue
and larynx makes needle control difficult. Resistance to needle insertion is felt as the anulus is contacted and entered (Fig. 14.16C). Further insertion is halted until depth can be ascertained using a lateral view. Active lateral and AP fluoroscopy is then used to advance the needle to the approximate center of the disk core. Care must be taken to ensure that the needle will not be unintentionally advanced through the posterior aspect of the disk and into the spinal canal and cord. Once all needles are in place, AP, oblique, and lateral images are saved to document needle placement (Fig. 14.18). Whether the traditional or alternative technique is used, once needle position at all disks to be studied is verified, the stylets are removed. The needle hubs are filled with contrast, and a contrast-filled, 3 mL Luer-Lok syringe with small-bore, minimal-volume, Luer-Lok extension tubing attached and connected to each needle. Care must be taken to ensure that the needles are not advanced or withdrawn during connection of the extension tubing. At the present time, manometry is used by few cervical diskographers in that the literature on its benefit has not yet been advanced. Active, lateral fluoroscopy is used during contrast injection (i.e., disk stimulation). The patient is blinded with respect to initiation of stimulation and the disk level. Injection into the disk proceeds by slowly increasing the pressure on the syringe until the intrinsic, opening, pressure of the disk is overcome and contrast is seen to flow into the disk core. If injection of contrast into the disk is not forthcoming, slight rotation, advancement, or withdrawal of the needle frequently allows flow of contrast to be seen within the disk. Firm resistance is often noted with injection of as little as 0.2 mL, and separation of the disk end plates during injection is expected. Injection into a normal cervical intervertebral disk will be limited to less than 0.5 mL of solution232 at a sustained high pressure.233 Intervertebral disks that accept more than 0.5 mL of injectate will be seen to have evidence of abnormalities on imaging studies. During disk stimulation, parameters of the injection are recorded on a standardized form by procedure room personnel. At a minimum, volume of injectate, the presence
134
Section II—The Evaluation of the Patient in Pain
C3
C4
C5
C6 C7
(–)
(–)
(–)
C5
C4
C3
(+) C6 C7
A
A
(–)
(–) C5
C4
C3
C3
C6
C4
(+) C5
(–) C6
C7
C7
B
B Fig. 14.19 Lateral (A) and AP (B) images of the cervical spine after disk stimulation. (−), No provocation of concordant pain with injection; (+), positive provocation of concordant pain with injection; closed arrow, filling of the uncovertebral recess (joints of Luschka); open arrow, anterior anular disruption. C3
C4
C5
C6
C7
C Fig. 14.18 A, Oblique; B, lateral; and C, AP images of the cervical spine with needles in position within the core of the intervertebral disks C3-4 through C6-7. Arrows indicated needle tips in the approximate center of each disk.
or absence of pain, the severity of pain, pain location and description, and concordance must be assessed at each level stimulated.230 In addition, the pressure generated (soft versus a firm end point) and vocal or physical pain responses are often recorded. Because even at nonpathologic levels cervical disk stimulation is uncomfortable, evaluation of the patient's response requires experience beyond that demanded by the technical aspects of the procedure. Individuals vary in their
pain tolerance, and thus some degree of subjectivity is required by the diskographer. As per the ISIS Practice Guidelines,230 the injection end points include any of the following: concordant pain greater than 6/10, neurologic symptoms reported by the patient, contrast solution escaping from the disk, displacement of the vertebral body end plates, firm resistance to injection, and the disk accepting no further volume at a reasonable pressure. To be considered a valid study, a negative control level, without pain on stimulation, must be present. Analgesic diskography,148 or the injection of local anesthetic and corticosteroid into a painful, pathologic disk, has been advocated by some authors.228,234 Although there is little consensus among diskographers concerning this practice, and no convincing data validating its use, anecdotal experience has led some to promote this practice. AP and lateral images of all disks injected, both before and after injection of contrast, must be saved for a permanent record of the study (Fig. 14.19). These images confirm injection of contrast into the disk core. However, because changes in the internal architecture of the disk are widespread in mature asymptomatic individuals, little in the way of diagnostic credibility is gained by images alone. Contrast seen to fill one or both of the uncovertebral recesses, or the joints of
Chapter 14—Intervertebral Disk Stimulation Provocation Diskography
135
Patients are observed for a minimum of 1 hour after the procedure and discharged home with a responsible adult. Discharge instructions include no driving the day of the procedure. The patient is told to expect some increase in discomfort for a few days after the procedure, and a limited prescription of oral analgesics can be provided. Patients are encouraged to call if they feel any unusual or severe pain not relieved by the oral analgesics. Pneumothorax is discussed with all patients who have undergone diskography of the lower cervical and thoracic regions.
Documentation A
A detailed record of the procedure must be completed. It is mandatory that this medical-legal document be a true and exact record of the specific procedure. If a template is used, it must be significantly modified to reflect the procedure it purports to detail. This procedure note must included the following information: name of patient; name of injectionist; date of procedure; indication for procedure, history; preinjection diagnosis; postinjection diagnosis; procedures performed; consent; and a detailed narrative of the procedure. See Appendix A.
Complications
B Fig. 14.20 Axial CT image through the C4-5 (A) and C5-6 (B) disks from Figure 14.19. Although significant disruption of the internal disk anatomy is present in both disks, only C5-6 was painful with stimulation. Closed black arrow, filling of the uncovertebral recess (joint of Luschka); open arrow, anterior anular disruption.
Luschka, is not a sign of abnormal degenerative changes but rather reflects the normal maturation of the cervical intervertebral disk.228,235 A postprocedure CT scan provides little additional information and should not be considered routine (Fig. 14.20). Because of the high frequency of internal disk disruption in nonsymptomatic individuals, the criteria for a diagnosis of diskogenic pain in the cervical region is based solely on the provocation of concordant pain rather than a combination of pain provocation and pathology by imaging studies as in the lumbar and thoracic spine.
Postprocedure Considerations After completion of the diskogram, independent of the level, sterile self-adhesive dressings are applied to the puncture wounds and the patient is taken to a recovery room with nurses trained to care for patients recovering from spinal injections. Periodic evaluation of the patient, including vital signs, level of comfort, level of consciousness, and visualization of the injection sites, is recommended. Analgesic medications, oral, intramuscular, or intravenous, are provided as needed. Following the recovery period, once stable, the patient can be taken for a postdiskogram CT to provide axial images of the injected disks if deemed appropriate.
A myriad of complications after diskography have been well documented.195,227,236,237 Complications can be inherent to disk penetration, the medications used, or unintentional misadventures involving needle placement. They range in severity from minor inconveniences, such as nausea and headache, to death. Historically, diskitis is the most common complication of diskography, with a rate of less than 0.08% per disk injected.184 Fraser et al238 provided evidence that all cases of diskitis are due to an infectious process, with the most common organisms being S. aureus, S. epidermidis, and E. coli from the skin, hypopharynx, esophagus, or bowel. In that the intervertebral disk is an essentially avascular structure, it provides an excellent growth medium for bacteria. However, with the use of preprocedure screening for chronic or acute infections, strict aseptic preparation of the skin, styletted needles, meticulous sterile technique, and intravenous and intradiskal antibiotics, diskitis should be an exceedingly rare occurrence today.196,228 Whether occurring after diskography or a surgical procedure, diskitis is manifested in similar fashion.201,239 A patient with diskitis usually has severe, intractable, debilitating pain of the cervical, thoracic, or lumbar spine days to weeks after the procedure; however, mild self-limited cases have been described.219 Diskitis needs to be ruled out in any postdiskogram patient who notes a marked change in the severity or quality of the pain after the procedure. The workup consists of obtaining laboratory and imaging studies. C-reactive protein levels will increase within days of the onset, whereas the sedimentation rate may remain in the normal range for over a month. Blood cultures will be negative and a complete blood count normal until the end plates are breached. MRI is the imaging study of choice,240–242 with hyperemia of the end plates and marrow space changes noted on T2-weighted images 3 to 4 days after the onset of symptoms. Radionuclide bone scanning has been shown to be inferior to MRI in specificity and sensitivity.243 If an adequate sample of tissue can be obtained, disk aspiration or biopsy, or both, will be positive in the acute phase of diskitis, but once the end plates are violated, a sterile environment within the disk is soon noted in response to the patient's immune system.228
136
Section II—The Evaluation of the Patient in Pain
Once diskitis is suspected, consultations with a spine surgeon and infectious disease specialist are appropriate. Treatment of infections within the disk and sepsis often requires antibiotic therapy. Though rare, abscess or empyema244–246 may necessitate surgical intervention. The cervical region has many vulnerable structures packed in a small area. Although vascular structures are plentiful, penetration of a vein or artery will rarely cause any significant problems. Poor technique can result in penetration of the cord either during insertion of the needle or when connecting the syringe to the needle. Good visualization and verification of needle position are mandatory during all parts of the procedure. Pneumothorax must be considered if marked shortness of breath occurs in a patient who has undergone diskography at levels between C5-6 and T12-L1. Boswell and Wolfe247 described a case in which intractable seizures, coma, and death developed in a woman after diskography. Their conclusion was that unintentional intrathecal administration of cefazolin (12.5 mg/mL), which had been included in the contrast agent for prophylaxis of infection, precipitated this catastrophic event. However, misadventure into the spinal canal is nearly impossible if proper technique is used; the operator understands the anatomy and has received appropriate fluoroscopic training; and AP, lateral, and oblique images are obtained and interpreted before injection of contrast as is standard of care.
Conclusion As with any diagnostic spinal injection procedure, diskography, be it cervical, thoracic, or lumbar, can be performed in a safe manner with the appropriate knowledge, training, and vigilance. However, diskography is more than a technique. Analysis of data obtained from the procedure, along with knowledge of the patient's history, clinical features, and psychologic condition, must be considered before a final diagnosis
is determined. A highly invasive procedure, anterior-posterior spinal fusion at multiple levels, may be performed on the basis of your findings. Therefore meticulous technique and awareness of the procedure's limitations are of utmost importance. Mark Twain once said, “The reports of my death are greatly exaggerated”; this statement could apply to diskography as well. Throughout its history, provocation diskography has been controversial and more than once pronounced “dead.” But, like the Phoenix of legend rising from the ashes, or the zombie rising from the grave, diskography is reborn after each notice of its demise. Today diskography lives, and is well recognized as the only diagnostic modality that can be used to determine whether an intervertebral disk is painful to mechanical forces. Provocation disk stimulation is, without a doubt, the “gold standard” for diagnosing diskogenic pain secondary to internal disk disruption.2,248,249 The technique has been endorsed by the majority of professional organizations whose objectives lie in advancing knowledge of the spine and its myriad pathologies. In the future, although refinements in our use and interpretation of diskography are certain to occur, the procedure will continue to provide information about our patients' afflictions and guide the treatment those modalities offer.
Dedication This chapter is dedicated to my mentor, friend, and diskographer extraordinaire, Professor Charles N. Aprill.
Acknowledgment I wish to acknowledge the contribution of John D. Fisk, MD, to the Historical Considerations section.
References Full references for this chapter can be found on www.expertconsult.com.
Appendix A Lumbar Diskogram: Sample Procedure Note Patient name: John Pain Injectionist: Dr. Needle History: See previously dictated consultation. Mr. Pain suffers from low back pain with radiation into the left buttock for 2 years. Preoperative diagnosis: (1) Low back pain etiology unknown. (2) L4-5 disk degeneration with a high-intensity zone. (3) Probable diskogenic pain. Postoperative diagnosis: (1) L4-5 internal disk disruption, with intermediate pressure diskogenic pain. Procedures: (1) Injection into lumbar intervertebral disks ×3 levels. (2) Lumbar diskography supervision and interpretation ×3 levels. (3) Sedation ×45 minutes. (4) Interpretation of lumbar CT scan after diskography.
Procedure Informed consent was obtained from the patient with regard to risks and complications were discussed. Diskitis and the provocative nature of the study were discussed at length. Mr. Pain elected to proceed. He was taken to an operating room with an intravenous drip in place. He was placed in prone position with a pillow under the abdomen to decrease the lordotic curve. Physiologic monitors were attached. Prophylactic cefazolin was give. Sedation with midazolam only was afforded for the duration of the procedure. The patient was conversant throughout the procedure. The lower thoracic, lumbar, and sacral regions were “prepped” and draped in a sterile manner. A C-arm was used to examine the lumbar spine. Five lumbar, non–rib bearing vertebral bodies were noted. The intervertebral disks at L3-4, L4-5, and L5-S1 were identified sequentially. At each level the superior endplate of the level below the targeted disk was aligned parallel to the beam. A right oblique view was then obtained so that the superior articular process of the level below appeared to lie as closely as possible under the approximate midpoint of the endplate above. At each level sequentially, a skin weal was made with local anesthetic and carried down to the level of the superior articular process. A puncture was made with a 15-gauge needle, through which an 18-gauge introducer needle was passed using “tunnel vision” toward the lateral aspect of the superior articular process at each level. Once all three introducer needles were in place, a lateral view evidenced all introducer needles as lying ventral to the posterior elements and dorsal to the intervertebral disk. Using active lateral fluoroscopy, the 22-gauge disk puncture needles were advanced through the introducer needles and seen and felt to enter the intervertebral disks. The needles were advanced into the center of each disk. No dysesthetic radicular type pain was noted during insertion of any needle. An anteroposterior (AP) view indicated excellent needle position at all levels.
Injection was then made into each disk using an injectate of iopamidol containing gentamycin 2 mg/mL. A manometer was used. During injection, volume injected, opening pressure, final pressure, pain response, and contrast pattern were recorded. L3-4: Volume: 1.5 mL Opening pressure: 22 psi Final pressure: 90 psi Pain: None Remarks: Contrast is noted within the nucleus pulposis in both AP and lateral views. No anular disruption is present. L4-5: Volume: 1.25 mL Opening pressure: 8 psi Final pressure: 31 psi Pain: Concordant, 9/10 with vocal and physical pain response. Patient stated, “Oh shucky darn.” Remarks: Contrast is noted within the nucleus pulposus. In lateral view, a posterior anular tear is noted. L5-S1: Volume: 2.75 mL Opening pressure: 14 psi Final pressure: 90 psi Pain: Nonconcordant, dissimilar pain, to right, 4/10 Remarks: Contrast is noted within the intervertebral disk. An anular tear to the left is noted. Mr. Pain tolerated the procedure well, was taken to recovery, and then taken for a postprocedure CT scan. He will follow up with Dr. Surgeon in the near future. He knows to follow up with his physician if any problems were to develop.
Interpretation of Lumbar CT after Diskography This interpretation should be considered the functional report for the record. It should take precedence over all other reports, past and future, in that correlation with the provocation diskography is an essential part of the interpretation and can only be afforded by the physician actually injecting the intervertebral disks. Scout sagittal and 3 mm axial views through the lumbar cistern were examined this date. Axial views included bone and soft tissue windows and included contiguous slices, parallel to the end plates, through the intervertebral disks at L3-4, L4-5, and L5-S1. Contrast is noted within the intervertebral disks at all levels noted above. L3-4: Contrast is noted within the nucleus pulposus. No anular disruption is present. A grade 0 nuclear pattern is evident. L4-5: Contrast is noted within the nucleus pulposus. A grade III posterior left anular disruption is noted.
137
138
Section II—The Evaluation of the Patient in Pain
L5-S1: Contrast is noted within the intervertebral disk. A wide, left lateral grade IV anular disruption is present with circumferential spread of contrast ∼180 degrees.
Interpretation L3-4 This is a negative level for diskogenic pain. No pain was noted with disk stimulation up to 90 psi. No disruption of the normal internal disk architecture is evident. This is a negative level for diskogenic pain without internal disk disruption, and provides a negative control level.
L4-5 This is a positive level for diskogenic pain. Marked concordant pain was noted at 23 psi above an opening pressure of 8 psi This is a positive level for diskogenic pain at intermediate pressure stimulation, with internal disk disruption.
L5-S1 This is a negative level for diskogenic pain. Although some discomfort was noted at 90 psi, that is, 76 psi above an opening pressure of 14 psi, this pain was nonconcordant, at high pressure, and only at an intensity of 4/10. This is a negative level for diskogenic pain, with disruption of the normal internal disk architecture.
Chapter
15
II
Myelography Hifz Aniq and Robert Campbell The correct diagnosis of spinal stenosis and nerve root impingement depends on the precise correlation between a neurologic finding and radiologic imaging studies. Several imaging diagnostic tests exist for spinal disorders. For many years, myelography, computed tomography (CT), and a combination of CT and myelography have been the modalities of choice for evaluation of spinal diseases. The introduction of magnetic resonance imaging (MRI) has revolutionized the way we diagnose and treat these conditions. It is superior to CT because it has better soft tissue contrast, spinal structures can be seen in multiple planes, it allows direct visualization of subligamentous disk prolapse, and it provides the ability to evaluate the spinal cord directly. Like any other diagnostic modality, MRI has its own strengths and weaknesses. Myelography is a simple and economical modality, but it is an invasive procedure, as contrast is injected into the thecal sac, and it involves radiation. In most cases, lumbar puncture is usually performed at the L3-4 or L4-5 level and non-ionic contrast (iopamidol-300) is injected into the subarachnoid space under fluoroscopic guidance. During injection the foot end of the table is kept slightly down. Erect anteroposterior (AP), lateral, and oblique radiographs are taken. The thecal sac is assessed on AP and lateral views whereas nerve roots are best seen on oblique views. With the use of non-ionic contrast after myelography, morbidity has been significantly reduced. However, patients should be informed of the possibility of nausea, vomiting, headache, and meningitis. Approximately 10% to 15% of patients have postmyelography headache, which usually starts 24 hours after the procedure, attributed to low cerebrospinal fluid (CSF) pressure syndrome. A remote possibility of nerve damage exists during the procedure. For cervical spine myelograms, the lumbar approach for contrast injection can be used in which the patient lies in prone or in decubitus position after the injection for contrast to flow toward the cervical region. Direct cervical puncture can also be performed at the C1-2 level through a lateral approach under fluoroscopy. This approach should be reserved for patients with complete spinal block, severe degenerative change, scoliosis, or infection preventing lumbar puncture. Cervical cord and vertebral artery puncture are potential complications. This approach should be used with caution in cases of suspected Chiari malformation. A standard volume of 10 mL is injected for lumbar regions, 20 mL for ascending lumbo-cervical myelograms, and 10 mL for cervical myelograms after C1-2 lateral puncture.1 CT examination of the cervical spine is usually performed immediately after the injection, and the lumbar spine CT is performed after an interval of 2 to 3 hours to reduce high contrast between the thecal sac and soft tissues. Multislice CT is performed with coronal and sagittal reformats. Spinal stenosis is assessed by © 2011 Elsevier Inc. All rights reserved.
encroachment of the spinal canal secondary to osteophyte formation and vertebral degeneration along with a degree of displacement of the contrast-filled thecal sac (Fig. 15.1). Asymmetries of displacement of nerve roots can also be easily accessed using CT myelogram. However, asymmetries caused by disk herniation should be differentiated from normal physiologic variances such as conjoined nerve root spinal ganglia and perineural cysts. Magnetic resonance myelogram is performed by choosing a particular set of sequences in which the main signal contribution comes from CSF in the thecal sac. In these heavily T2-weighted sequences, signal from tissue other than fluid is almost completely canceled. Magnetic resonance myelography demonstrates the thecal sac and nerve root sleeves similar to conventional myelography and postmyelographic CT. The major advantages of this modality include its noninvasive nature, its lack of ionizing radiation, and no requirement for intrathecal contrast injection. Many studies have been performed that compared the efficiency of MRI and postmyelography CT scan.2 Bartlett et al3 demonstrated that MRI could be quite insensitive for small lateral disk herniation in the cervical exiting foramen. It is difficult to differentiate between soft disk herniation and osteophyte in the neural exiting foramen on MRI. Reul et al4 proved in their study that MRI overestimates the degree of canal stenosis in the cervical spine compared with postmyelogram CT. However, MRI produced correct measurements in a normal-sized spinal canal. Several reasons for this overestimation were given, including truncation, chemical shift, and CSF pulsation artifacts. The artifacts can alter the shape, anatomic details, and structure of the spine. Truncation and chemical shift artifacts can be avoided by selecting a large data acquisition matrix and by changing the frequency and phase encoding directions, respectively. However, CSF motion artifacts appear to be the most important factor in incorrect measurements. Pulsation of CSF is strongest in the cervical spinal canal. In degenerative spinal narrowing, CSF motions become turbulent and accelerated leading to a reduction in the signal strength, which can look like advanced spinal stenosis, but this will not change the therapeutic management. Overestimation in mild to moderate spinal stenosis could be misleading and dangerous, leading to unnecessary intervention. CT myelogram was found to be highly sensitive and accurate in the diagnosis of spinal stenosis and lateral lumbar recess syndrome.5 Osteophytes with subperiosteal new bone formation in the vertebral body and its articulations are directed toward the center of the spinal canal and produce spinal stenosis. The extent of this bony involvement is best assessed on CT myelogram (Fig. 15.2). CT myelography has a 139
140
Section II—The Evaluation of the Patient in Pain
B
A
B
Fig. 15.1 A, Myelogram, lateral view, anterior indentation of contrastfilled thecal scan at the L3-4 level. B, Postmyelogram CT, sagittal multiplanar reformation (MPR), anterior indentation at the L3-4 level is due to posterior slip of L3 over L4.
A
B
Fig. 15.2 Cervical fusion: osseous ridge. With the use of cervical spine multi-detector computed tomography (MDCT) myelography in a patient after anterior cervical fusion, coronal (A) and sagittal (B) Multiplanar reformations show an osseous ridge compressing the nerve roots (arrows).
significant role in postoperative spine imaging. On MRI, distortion of images may be caused by screws, plates, and pieces of metal. On CT, the contrast-filled thecal sac is less affected by the postoperative metalwork and is also able to demonstrate arachnoid adhesions and CSF leaks. MR myelography can be used in cases of multisegmental or severe spinal stenosis in which the intrathecal contrast injection may not pass distal to the area of stenosis. On the other hand, this technique overestimates the degree of spinal stenosis compared to conventional MRI. Magnetic resonance and CT myelography are routinely used in brachial plexus injuries. The most common cause of brachial plexus injury is motorcycle accidents involving young adults. In this injury, nerve root avulsion takes place at the preganglionic or postganglionic
A
F
C
Fig. 15.3 Brachial plexus injury. A, Magnetic resonance myelogram, bilateral traumatic meningocele caused by avulsion of the right C6 and left C7-8 nerve roots. B, Axial T2 three-dimensional drive sequence shows left C7 root avulsion and traumatic meningocele. C, Axial CT myelogram (different patient) shows avulsion of ventral and dorsal roots of left C5 with traumatic meningocele.
s egment or a combination of both. The C5 and C6 nerve roots are most commonly involved. Treatment varies in these different types of nerve root avulsions. Conventional MRI may show cord edema and enhancement around the affected nerve root. CT myelography is superior to magnetic resonance myelography as it allows separate evaluation of both the ventral and dorsal nerve roots and detection of intradural nerve defects (Fig. 15.3). Magnetic resonance myelogram can show traumatic meningocele and nerve root avulsion but there may be degradation of images because of respiration and swallowing movements. There may be further loss of information on images because of pulsation artifacts from the cervical vessels.6 As compared to magnetic resonance scanning, CT myelogram is an invasive procedure and involves significant radiation. New high-resolution magnetic resonance scanning is the investigation of choice for all spinal conditions. It is noninvasive, has better soft tissue contrast, is able to visualize the spinal cord directly, and is free of radiation hazards.7 However, small percentages of the population have contraindications for MRI scan or are claustrophobic. In these cases CT myelogram can be the alternative modality for diagnosing spine-related problems. Many studies have proved that MRI is the most cost-effective modality for spinal imaging.8 CT myelogram should be reserved for elective presurgical patients when MRI fails to answer the clinical question or symptoms are not explained by the MRI findings.9
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
16
II
Epidurography Jeffrey P. Meyer, Miles R. Day, and Gabor B. Racz
CHAPTER OUTLINE Historical Considerations 141 Indications 141 Clinically Relevant Anatomy 141 Materials 142
Historical Considerations Epidurography is one of the most commonly performed interventional pain procedures, yet is likely taken for granted by most pain practitioners. The accurate interpretation of epidural contrast patterns is key to the success of many interventional pain procedures, and remains a vital skill in the interventional pain arena. First described in 1921 by the accidental injection of lipiodol into the epidural space by Sicard and Forestier,1 epidurography has been performed with many different agents including air,2 perobrodil,3 and metrizamide.4 The use of ionic contrast agents such as diatrizoate (Renografin, Hypaque) led to complications related to both anaphylactic and contrastinduced seizures, and the use of non-ionic contrast agent has now become widely accepted. The use of radiopaque contrast agents to identify correct needle positioning in epidural steroid injections was described by White et al in 1980,5 and has since become widespread practice.6–8 Epidural contrast patterns and their interpretation are central to caudal neuroplasty,7 and have been described in the management of indwelling epidural catheters.9 The current practice of epidurography has evolved with necessity. It is currently performed whenever confirmation of epidural localization of needle placement is desired. When performed via the caudal approach, it is useful in delineating the presence of epidural fibrosis, with concomitant nerve root entrapment. In the cervical, thoracic, and lumbar transforaminal approaches, correct needle positioning is confirmed, as well as delineating the extent of spread. Interlaminar epidurography not only confirms correct positioning but defines “safe” runoff patterns that ensure that loculation (and subsequent intrathecal space compression) is not occurring.
Indications Epidurography is indicated in any instance in which correct needle positioning within the epidural space is desired. Previous reports have identified false-positive rates as high as © 2011 Elsevier Inc. All rights reserved.
Technique 142 Side Effects and Complications 143 Conclusion 143
25% in the identification of the caudal epidural space,10 and confirmation of correct needle positioning is necessary for both therapeutic effect and safety. In the presence of failed back/neck surgery syndrome, the pattern of contrast distribution and runoff ensure that loculation is not occurring, and that further volumes may be instilled safely. This is especially important in cervical epidural injections as there is little room within the epidural space for loculation. In the presence of epidural fibrosis, epidurography is useful in delineating the extent and pattern of fibrosis, along with identifying the affected nerve roots. It provides a baseline from which to gauge the extent of adhesiolysis during cervical, thoracic, and caudal epidural neuroplasty, and guides therapeutic decisions as to the necessity for further interventions. Epidurography is essential in the performance of cervical interlaminar and transforaminal epidural steroid injections. The possibility of loculation with concomitant cord compression is ever present, and only epidurography is able to adequately identify runoff. In the case of cervical transforaminal injections, the presence of radicular feeder vessels to the spinal cord necessitates that epidurography be performed to ensure that intravascular injection is not occurring.11 Several reports in the literature detail spinal cord damage following the transforaminal delivery of epidural steroids to the cervical space, and a proposed mechanism for this complication is the delivery of local anesthetic and particulate steroid into these radicular feeder vessels.12,13
Clinically Relevant Anatomy The dorsal epidural space is bounded superiorly by the foramen magnum, inferiorly by the sacral notch, ventrally by the dura mater, and dorsally by the laminar periosteum and ligamentum flavum. It extends to envelop the exiting nerve roots in the foraminal sheath. The space is largest in the sacral canal, and most limited in the midcervical spine. Plica mediana dorsalis are dorsal-median bands that may separate the epidural space into left and right compartments. They are usually incomplete, but may be continuous, limiting contrast spread to the ipsilateral epidural space.14 The ventral epidural space is 141
142
Section II—The Evaluation of the Patient in Pain
bounded superiorly by the foramen magnum, inferiorly by the sacral notch, ventrally by the posterior longitudinal ligament, and dorsally by the dura mater. The epidural space contains fat, loose connective tissue, and veins. It may also contain radicular arterial feeder vessels for the spinal cord,14 which are of particular concern when performing cervical transforaminal epidural steroid injections.13,15
Materials Epidurography may safely be performed in non–iodine-allergic patients by the injection of non-ionic, water-soluble contrast material into the epidural space. Because the possibility of intrathecal administration is always present, the choice of contrast agent is based on the intrathecal application of contrast. The only agent currently approved for use is iohexol (Omnipaque). Although available in concentrations of 140 to 360 mg of organic iodine per milliliter, only the 180, 240, and 300 mL of iodine per milliliter are indicated for intrathecal administration. In children, only the 180 mL of iodine per milliliter concentration is indicated. Iopamidol (Isovue) is another water-soluble, non-ionic contrast agent that is available; however, it is not currently approved for intrathecal injection. Gadolinium has been described as an alternative in iodine-allergic patients.16 The use of ionic or non–water-soluble contrast agents in epidurography is contraindicated. The possibility of inadvertent intrathecal injection is ever present, and the application of these agents to the intrathecal space may lead to life-threatening seizures. Confirmation of the agent to be injected into the epidural space is mandatory before injection because the consequences of inadvertent injection of agents not approved for epidural use may be life threatening.
Fig. 16.1 Normal caudal epidurogram.
Fig. 16.2 Normal epidurogram—note filling of S1-S3 nerve roots.
Technique Epidurography may be performed from any of the commonly used approaches to the epidural space. Following confirmation of epidural needle tip positioning by loss-of-resistance, hanging drop technique, or fluoroscopy, a syringe containing 5 mL of contrast agent is attached to the needle. Careful aspiration to assess possible intrathecal or intravascular needle positioning is carried out. The initial injection of contrast is carried out under continuous fluoroscopy to assess the flow of contrast in an epidural pattern. It is advisable to limit the volume of initial contrast injection to the smallest amount possible to ascertain distal spread of contrast in the epidural space. In the presence of suspected epidural fibrosis, loculation surrounding the access point is an ever-present possibility, and injection of even small (1 to 2 mL) volumes of contrast may compress surrounding structures. This is especially important in the cervical and thoracic epidural space. After confirming that loculation is not occurring, additional volumes of contrast may be injected as necessary to assess the pattern of contrast spread. Contrast injection should always be carried out under continuous fluoroscopy to identify possible vascular runoff patterns, and to assess the continued runoff of contrast material. Contrast will flow to the areas of least resistance, and filling defects may be identified, indicating areas of epidural scarring. Fluoroscopy should be carried out in both the anteroposterior (AP) and lateral projections to confirm spread in an epidural pattern.
Three general patterns of contrast filling may be identified: epidural, subdural, and intrathecal. The epidural pattern is characterized by a reticular pattern limited to the midline epidural space, and flowing in a “Christmas-tree” pattern to fill the exiting nerve roots (Fig. 16.1). When obtained, this contrast pattern responds by further filling of ever higher nerve root levels with the administration of additional contrast. In the presence of plica mediana dorsalis, it is not uncommon for this pattern to fill only one half of the epidural space and exiting nerve roots. Contrast should spread both superiorly and inferiorly in a free-flowing pattern (Fig. 16.2). Subdural injection of contrast results in a patchy, fine pattern in the AP projection (Fig. 16.3). Lateral fluoroscopy will reveal a solid “line” of contrast extending several levels higher than expected given the volume of contrast injected (Fig. 16.4). Subdural therapeutic injections are not recommended, and repositioning of the access needle should be carried out. It is important to note that subdural contrast patterns are very difficult to identify in the AP fluoroscopic projection, emphasizing the necessity for both AP and lateral views to confirm proper needle positioning. Intrathecal contrast injection reveals a myelographic spread, with outlining of the nerve roots/cauda equina when carried out in the lumbar spine. The injected contrast will not spread to outline the exiting nerve roots, and will be limited to the midline spinal space. In the cervical and thoracic regions, intrathecal
Chapter 16—Epidurography
Fig. 16.3 Subdural injection of contrast—note reticular filling pattern.
Fig. 16.4 Subdural contrast (2 mL in sacral space)—note extension to L1 level with 2 mL injection.
injection of contrast will flow laterally, and appear as a “double bar” outlining the spinal cord laterally within the spinal canal. When performed in the sacral space, epidurography is very effective in identifying areas of epidural scarring that may be targeted via caudal neuroplasty. These areas appear as “filling” defects within the dye spread. It is uncommon for these filling defects to appear below the S2 level, but they are common above S1 (Figs. 16.5 and 16.6). Areas of filling defect may be accessed via caudal catheter and the degree of neuroplasty may be assessed by repeat epidurography following injection of hyaluronidase. When performed properly, these filling defects resolve with neuroplasty.
Side Effects and Complications Epidurography can be safely performed in the cervical, thoracic, lumbar, and sacral spinal canals. Loculation with concomitant spinal cord compression and myelopathy is a real concern in the cervical and thoracic epidural spaces, and the need for visualization of distal runoff cannot be overemphasized. Injection into radicular feeder vessels of the spinal cord is a concern at all levels of the spinal cord, and careful observation for vascular patterns must be maintained. Injection into the intrathecal space is occasionally observed. Iohexol (Omnipaque) is the only contrast agent approved for intrathecal use, and is therefore the only agent used at our institution. Tonic-clonic seizures with the intrathecal
143
Fig. 16.5 Epidurogram—note filling defect of left S2 level.
Fig. 16.6 Epidurogram—note filling defect of left S1 level.
administration of iohexol have been reported,17 but are a rare complication. Anaphylactic reactions to injected contrast material may occur. Patients who are allergic to iodine or radiographic contrast material should not be subjected to epidurography until sensitivity testing by appropriate specialists has been performed. Currently, no iodine-free contrast agents are approved for epidural use. Contrast-induced nephropathy is possible with large volumes of contrast injected, but is rare in epidurography because of the slow reabsorption of contrast and limited concentrations delivered to the kidneys. Total doses of contrast should be limited to the least effective dose in patients with preexisting renal insufficiency.
Conclusion Epidurography is a commonly performed procedure in interventional pain management. The correct interpretation of epidurograms is essential to the safe practice of epidural access procedures, and helps guide appropriate interventions in the future. All interventional pain management physicians should become proficient at the performance and interpretation of epidurograms to enhance the safety of their practice.
References Full references for this chapter can be found on www.expertconsult.com.
II
Chapter
17
Neural Blockade for the Diagnosis of Pain Steven D. Waldman
CHAPTER OUTLINE The Historical Imperative and Clinical Rationale for Use of Diagnostic Nerve Blocks 144 A Road Map for the Appropriate Use of Diagnostic Nerve Block 146 Specific Diagnostic Nerve Blocks 147 Neuroaxial Diagnostic Nerve Blocks 147
As emphasized in previous chapters, the cornerstone of successful treatment of the patient suffering from pain is a correct diagnosis. As straightforward as this statement is in theory, it may become difficult to achieve in the individual patient. The reason for this difficulty is due to four disparate but interrelated issues: (1) pain is a subjective response that is difficult, if not impossible, to quantify; (2) pain response in humans is made up of a variety of obvious and not so obvious factors that may modulate the patient's clinical expression of pain either upward or downward (Table 17.1); (3) our current understanding of neurophysiologic, neuroanatomic, and behavioral components of pain is incomplete and imprecise; and (4) there is ongoing debate by the specialty of pain management of whether pain is best treated as a symptom or as a disease. The uncertainly introduced by these factors can often make accurate diagnosis problematic. Given the difficulty in establishing a correct diagnosis of a patient's pain, the clinician often is forced to look for external means to quantify or confirm a dubious clinical impression. Laboratory and radiologic testing are often the next procedures the clinician seeks for reassurance. If such testing is inconclusive or the results are discordant with the clinical impression, diagnostic nerve block may be the next logical step. Done properly, diagnostic nerve block can provide the clinician with useful information to aid in increasing the comfort level with a tentative diagnosis. It cannot be emphasized enough, however, that overreliance on the results of even a properly performed diagnostic nerve block can set in motion a series of events that will, at the very least, provide the patient little or no pain relief and, at the very worst, result in permanent complications from invasive surgeries or neurodestructive procedures that were justified solely on the basis of diagnostic nerve block. 144
Greater, Lesser, and Third Occipital Nerve Block 148 Stellate Ganglion Block 148 Cervical Facet Block 148 Intercostal Nerve Block 148 Celiac Plexus Block 149 Selective Nerve Root Block 149
Conclusion 149
The Historical Imperative and Clinical Rationale for Use of Diagnostic Nerve Blocks Our view of pain has changed over the centuries as our understanding of this universal condition has improved. Early humans viewed pain as a punishment from the deities for a variety of sins as exemplified by the legend of Prometheus. Prometheus was sentenced by Zeus to eternal torture for giving the fire reserved for the gods to mortals (Fig. 17.1). The seventeenth-century scientist and philosopher, Descartes (Fig. 17.2), changed this view in a single instant by his drawing of a fire burning the foot of a man. Descartes postulated a rational basis for pain premised on the then radical notion that pain was sensed in the periphery and then carried via the nerves and spinal cord to the brain (Fig. 17.3). It is not surprising that concurrent advances in the understanding of the anatomy of the peripheral and central nervous system led scientists and clinicians to seek new ways to stop pain. In 1774 English surgeon James Moore described the use of a “C” clamp to compress the peripheral nerves of the upper and lower extremity to induce anesthesia to decrease the pain of amputation and other surgeries of the extremities.1 The development and refinement of the syringe and hollow needle led to the idea of injecting substances such as morphine in proximity to the peripheral nerves to relieve pain. Rynd, in 1845, postulated the utility of delivering morphine directly onto a nerve via a hollow trocar.2 This was a radical departure from the then current practice of surgically exposing the nerve and then topically applying pain relieving agents. It is not surprising that many patients thought that the “cure was worse than the disease.” However, it was the landmark clinical discovery of the utility of cocaine as a surgical anesthetic by Carl Koller in 1884 © 2011 Elsevier Inc. All rights reserved.
Chapter 17—Neural Blockade for the Diagnosis of Pain
145
Table 17.1 Factors That Influence Pain Age Gender Socioeconomic status Ethnicity Pregnancy Stress Chronicity
Fig. 17.3 Drawing by Descartes demonstrating the concept that pain is carried via nerves from the periphery to the brain.
Fig. 17.1 Artist's depiction of Prometheus.
Fig. 17.4 Diagram of chemical structures of procaine and procaine hydrochloride.
Fig. 17.2 A portrait of Descartes.
that ushered in the era of regional anesthesia.3 Corning's first spinal anesthetic in 1885 further solidified the concept that blocking nerves could alleviate human suffering, albeit not without complications—as it was Corning himself who
may have suffered the first spinal headache following induction of an anesthetic. As the specialty of regional anesthesia matured, the technical ability to easily and consistently render nerves incapable of transmitting pain increased. The early work of Halstead and Hall, Corning, and others helped refine the “how-to-do-it” aspects of blocking a nerve. However, the relative toxicity of cocaine, which was the only local anesthetic readily available at the time, significantly limited the clinical utility of otherwise technically satisfactory nerve block techniques. It was not until the synthesis in 1909 by Einhorn of the local anesthetic ester procaine that regional anesthesia was truly safe enough for widespread use (Fig. 17.4). Unfortunately, procaine's short duration of action made its use impractical for longer operations; this limitation led to the development of the longer-acting ester class of local anesthetics, such as tetracaine and dibucaine, albeit with increased systemic toxicity. It was the development of the safer amide class of local
146
Section II—The Evaluation of the Patient in Pain
Table 17.2 The Do’s and Dont’s of Diagnostic Nerve Blocks Do analyze the information obtained from diagnostic nerve blocks in the context of the patient’s history, physical, laboratory, neurophysiologic, and radiographic testing. Don’t overrely on information obtained from diagnostic nerve blocks. Do view with skepticism discordant or contradictory information obtained from diagnostic nerve blocks. Fig. 17.5 Diagram of chemical structure of lidocaine.
a nesthetics, such as lidocaine by Löfgren and Lundquist in 1943, that began the most recent chapter in the quest for the ability to block human pain (Fig. 17.5). Just as it seemed that science had finally given doctors the ability to block pain, other scientific advances began to question the construct that Descartes has given us—that pain is a simple function of a stimulus being carried over an anatomically distinct neural pathway. As clinicians were puzzled that patients who had otherwise seemingly perfect nerve blocks continued to have pain during surgical procedures, research scientists were beginning to unravel the mystery of peripheral and central modulation of pain—as well as the role that the sympathetic nervous system plays in the pain response. The quest for answers as to how these disparate neuroanatomic structures affect, modulate, and subserve a patient's pain continues today. It is this quest for answers that brings us to an evaluation of the role that diagnostic nerve blocks play in contemporary pain management.
A Road Map for the Appropriate Use of Diagnostic Nerve Block It must be said at the outset of this discussion that even the perfectly performed diagnostic nerve block is not without limitations. Table 17.2 provides the reader with a list of do's and dont's when performing and interpreting diagnostic nerve blocks. First and foremost, the clinician should use with caution the information gleaned from diagnostic nerve blocks and use it only as one piece of the overall diagnostic workup of the patient in pain. Results of a diagnostic nerve block that contradicts the clini cal impression that the pain management specialist has formed as a result of the performance of a targeted history and physical examination and consideration of confirmatory laboratory, neurophysiologic, and radiographic testing should be viewed with great skepticism. Such disparate results should never serve as the sole basis for moving ahead with neurodestructive or invasive surgical procedures that, in this setting, have little or no hope of actually helping alleviate a patient's pain. In addition to the admonitions just mentioned, it must be recognized that the clinical utility of the diagnostic nerve block can be affected by technical limitations. In general, the reliability of data gleaned from a diagnostic nerve block is in direct proportion to the clinician's familiarity with the functional anatomy of the area in which the nerve resides and the clinician's experience in performing the block being attempted. Even in the best of hands, some nerve blocks are technically more demanding than others, which increases the likelihood of a less than perfect result. Proximity of other neural structures
Don’t rely on information obtained from diagnostic nerve block as the sole justification to proceed with invasive treatments. Do consider the possibility of technical limitations that limit the ability to perform an accurate diagnostic nerve block. Do consider the possibility of patient anatomic variations that may influence the results of diagnostic nerve blocks. Do consider the presence of incidents pain when analyzing the results of diagnostic nerve blocks. Don’t perform diagnostic nerve blocks when patients are not currently having the pain you are trying to diagnose. Do consider behavioral factors that may influence the results of diagnostic nerve blocks. Do consider that the patient may premedicate before undergoing diagnostic nerve blocks.
to the nerve, ganglion, or plexus being blocked may lead to the inadvertent and often unrecognized block of adjacent nerves, thereby invalidating the results that the clinician sees (e.g., the proximity of the lower cervical nerve roots, phrenic nerve, and brachial plexus to the stellate ganglion). Some of these technical obstacles can be decreased, although by no means completely eliminated, by the use of fluoroscopic or computerized tomographic guidance during needle placement. The addition of small amounts of radiopaque contrast medium to the local anesthetic may also increase the accuracy of the block. However, the clinician must be aware that the overreliance on either of these aids may lead to erroneous conclusions. It should also be remembered that the possibility of undetected anatomic abnormality always exists, which may further confuse the results of the diagnostic nerve block (e.g., conjoined nerve roots, the Martin Gruber anastomosis [a median to ulnar nerve connection]).4 Because each pain experience is unique to the individual patient and the clinician really has no way to quantify it, special care must be taken to ensure that everybody is in agreement insofar as what pain the diagnostic block is intended to diagnose. Many patients have more than one type of pain. A patient may have both radicular pain and the pain of alcoholic neuropathy. A given diagnostic block may relieve one source of the patient's pain while leaving the other untouched. If the patient is having incident pain (e.g., pain when walking or sitting), the performance of a diagnostic block in a setting other than one that will provoke the incident pain is of little or no value. This often means that the clinician must tailor the type of nerve block that is to be performed to allow the patient to be able to safely perform the activity that incites the pain. A diagnostic nerve block should never be performed if the patient is not having or is unable to provoke the pain that the pain management specialist is trying to diagnose because there is nothing to quantify.
Chapter 17—Neural Blockade for the Diagnosis of Pain
The accuracy of diagnostic nerve block can be enhanced by assessing the duration of nerve relief relative to the expected pharmacologic duration of the agent being used to block the pain. If there is discordance between the duration of pain relief relative to duration of the local anesthetic or opioid being used, extreme caution should be exercised before relying solely on the results of that diagnostic nerve block. Such discordance can be due to technical shortcomings in the performance of the block, anatomic variations, and, most commonly, behavioral components of the patient's pain. It must be remembered that the pain and anxiety caused by the diagnostic nerve block itself may confuse the results of an otherwise technically perfect block. The clinician should be alert to the fact that many pain patients may premedicate themselves because of the fear of procedural pain. This also has the potential to confuse the observed results. Obviously, the use of sedation or anxiolytic agents before the performance of diagnostic nerve block will further cloud the very issues the nerve block is, in fact, supposed to clarify.
147
Table 17.3 Common Diagnostic Nerve Blocks Neuroaxial Blocks
Epidural block Subarachnoid block Peripheral Nerve Blocks
Greater and lesser occipital nerve blocks Third occipital nerve blocks Trigeminal nerve block Brachial plexus block Median, radial, and ulnar nerve blocks Intercostal nerve block Selective nerve root block Sciatic nerve block Intra-articular Nerve Blocks
Facet block Sympathetic Nerve Blocks
Stellate ganglion block
Specific Diagnostic Nerve Blocks Early proponents of regional anesthesia, such as Labat and Pitkin, believed it was possible to block just about any nerve in the body.5 Despite the many technical limitations these pioneers faced, these clinicians persevered. They did so not only because they believed in the clinical utility and safety of regional nerve block but because the currently available alternatives to render a patient insensible to surgical pain were much less attractive. The introduction of the muscle relaxant, curare, in 1942 by Dr. Harold Griffith changed this construct, and in a relatively short time, regional anesthesia was relegated to the history of medicine with its remaining proponents viewed as eccentric at best.6 Just as the Egyptian embalming techniques were lost to modern man, many regional anesthesia techniques that were in common use were lost to today's pain management specialists. What we are left with today are those procedures that stood the test of time for surgical anesthesia. For the most part, these were the nerve blocks that were not overly demanding from a technical viewpoint and were reasonably safe to perform. Many of these techniques also have clinical utility as diagnostic nerve blocks. These techniques are summarized in Table 17.3. A discussion of the more commonly used diagnostic nerve blocks follows.
Celiac plexus block Lumbar sympathetic block Hypogastric plexus and ganglion impar blocks
Discussed in detail in Chapter 14, differential spinal and epidural blocks have gained popularity as an aid in the diagnosis of pain. Popularized by Winnie, differential spinal and epidural blocks have as their basis the varying sensitivity of sympathetic and somatic sensory and motor fibers to blockade by local anesthetics.7 Although sound in principle, these techniques are subject to serious technical difficulties that limit the reliability of the information obtained. These difficulties include the following:
3. The impossibility of “blinding” the patient to the sensation of warmth associated with sympathetic blockade, as well as the numbness and weakness that accompany blockade of the somatic sensory and motor fibers. 4. The breakdown of the construct of temporal linearity, which holds that the more “sensitive” sympathetic fibers will become blocked first, followed by the less sensitive somatic sensory fibers, and last by the more resistant motor fibers. As a practical matter, it is not uncommon for the patient to experience some sensory block before noticing the warmth associated with block of the sympathetic fibers, rendering the test results suspect. 5. Afferent nociceptive input can still be demonstrated in the brain, even in the presence of a neuroaxial block that is dense enough to allow a major surgical p rocedure. 6. Neurophysiologic changes associated with pain may increase or decrease the firing threshold of the nerve, suggesting that even in the present of sub-blocking concentrations, there is the possibility that the sensitized afferent nerves will stop firing. 7. Modulation of pain transmission at the spinal cord, brainstem, and higher levels is known to exist and may alter the results of even the most carefully performed differential neural blockade. 8. Significant behavioral components to a patient's pain may influence the subjective response the patient reports to the clinician who is performing differential neuroaxial blockade.
1. The inability to precisely measure the extent to which each type of nerve fiber is blocked. 2. The possibility that more than one nerve fiber type is simultaneously blocked, leading the clinician to attribute the patient's pain to the wrong neuroanatomic structure.
In spite of these shortcomings, neuroaxial differential block remains a clinically useful tool to aid in the diagnosis of unexplained pain. The clinician can increase the sensitivity of this technique by (1) use of reverse differential spinal or epidural block, in which the patient is given a high concentration of local anesthetic that results in a dense motor, sensory, and
Neuroaxial Diagnostic Nerve Blocks
148
Section II—The Evaluation of the Patient in Pain
sympathetic block and then observing the patient as the block regresses; (2) use of opioids instead of local anesthetics that remove the sensory clues that may influence patient responses; and (3) repeating the block on more than one occasion using local anesthetics or opioids of varying durations (e.g., lidocaine versus bupivacaine or morphine versus fentanyl) and comparing the results for consistency. Whether or not this technique stands the test of time, Winnie's admonition to clinicians that sympathetically mediated pain is often underdiagnosed most certainly will.
Greater, Lesser, and Third Occipital Nerve Block The greater occipital nerve arises from fibers of the dorsal primary ramus of the second cervical nerve and to a lesser extent from fibers of the third cervical nerve.8 The greater occipital nerve pierces the fascia just below the superior nuchal ridge along with the occipital artery. It supplies the medial portion of the posterior scalp as far anterior as the vertex. The lesser occipital nerve arises from the ventral primary rami of the second and third cervical nerves. The lesser occipital nerve passes superiorly along the posterior border of the sternocleidomastoid muscle, dividing into cutaneous branches that innervate the lateral portion of the posterior scalp and the cranial surface of the pinna of the ear. The C2-3 facet joint is exclusively innervated by the third occipital nerve, which is the superficial medial branch of the C3 dorsal ramus.9 The third occipital nerve also supplies a small patch of skin immediately below the occipital region. Selective blockade of the greater, lesser, and third occipital nerves can provide the pain management specialist with useful information when trying to determine the cause of cervicogenic headache. By blocking the atlantoaxial, atlanto-occipital, cervical epidural, cervical facet, and greater, lesser, and third occipital nerves on successive visits, the pain management specialist may be able to differentiate the nerves subserving the patient's headache.
Stellate Ganglion Block The stellate ganglion is located on the anterior surface of the longus colli muscle. This muscle lies just anterior to the transverse processes of the seventh cervical and first thoracic vertebrae.10 The stellate ganglion is made up of the fused portion of the seventh cervical and first thoracic sympathetic ganglia. The stellate ganglion lies anteromedial to the vertebral artery and is medial to the common carotid artery and jugular vein. It is lateral to the trachea and esophagus.11 The proximity of the exiting cervical nerve roots and brachial plexus to the stellate ganglion make it easy to inadvertently block these structures when performing stellate ganglion block, making interpretation of the results of the block difficult. Selective blockade of stellate ganglion can provide the pain management specialist with useful information when trying to determine the cause of upper extremity or facial pain without clear diagnosis. By blocking the brachial plexus (preferably by the axillary approach) and stellate ganglion on successive visits, the pain management specialist may be able to differentiate the nerves subserving the patient's upper extremity pain. Selective differential blockade of the stellate ganglion, trigeminal nerve, and sphenopalatine ganglion on
successive visits may elucidate the nerves subserving facial pain that is often difficult to diagnose.
Cervical Facet Block The cervical facet joints are formed by the articulations of the superior and inferior articular facets of adjacent vertebrae.12 Except for the atlanto-occipital and atlantoaxial joints, the remaining cervical facet joints are true joints in that they are lined with synovium and possess a true joint capsule. This c apsule is richly innervated and supports the notion of the facet joint as a pain generator. The cervical facet joint is susceptible to arthritic changes and trauma caused by acceleration-deceleration injuries. Such damage to the joint results in pain s econdary to synovial joint inflammation and adhesions. Each facet joint receives innervation from two spinal levels.13 Each joint receives fibers from the dorsal ramus at the same level as the vertebra, as well as fibers from the dorsal ramus of the vertebra above. This fact explains the ill-defined nature of facet-mediated pain and explains why the branch of the dorsal ramus arising above the offending level must often also be blocked to provide complete pain relief. At each level, the dorsal ramus provides a medial branch that wraps around the convexity of the articular pillar of its respective vertebra and provides innervation to the facet joint. Selective blockade of cervical facet joints can provide the pain management specialist with useful information when trying to determine the cause of cervicogenic headache and/ or neck pain. By blocking the atlantoaxial, atlanto-occipital, cervical epidural, and greater and lesser occipital nerves on successive visits, the clinician may be able to differentiate the nerves subserving the patient's headache and/or neck pain.
Intercostal Nerve Block The intercostal nerves arise from the anterior division of the thoracic paravertebral nerve.14 A typical intercostal nerve has four major branches. The first branch is the unmyelinated postganglionic fibers of the gray rami communicantes, which interface with the sympathetic chain. The second branch is the posterior cutaneous branch, which innervates the muscles and skin of the paraspinal area. The third branch is the lateral cutaneous division, which arises in the anterior axillary line. The lateral cutaneous division provides the majority of the cutaneous innervation of the chest and abdominal wall. The fourth branch is the anterior cutaneous branch supplying innervation to the midline of the chest and abdominal wall. Occasionally, the terminal branches of a given intercostal nerve may actually cross the midline to provide sensory innervation to the contralateral chest and abdominal wall.15 This fact has specific import when utilizing intercostal block as part of a diagnostic workup for the patient with chest wall and/or abdominal pain. The twelfth thoracic nerve is called the subcostal nerve and is unique in that it gives off a branch to the first lumbar nerve, thus contributing to the lumbar plexus. Selective blockade of intercostal and/or subcostal nerves thought to be subserving a patient's pain can provide the pain management specialist with useful information when trying to determine the cause of chest wall and/or abdominal pain. By blocking the intercostal nerves and celiac plexus on successive visits, the pain management specialist may be able to differentiate which nerves are subserving the patient's chest wall and/or abdominal pain.
Chapter 17—Neural Blockade for the Diagnosis of Pain
Celiac Plexus Block The sympathetic innervation of the abdominal viscera originates in the anterolateral horn of the spinal cord. Preganglionic fibers from T5-12 exit the spinal cord in conjunction with the ventral roots to join the white communicating rami on their way to the sympathetic chain. Rather than synapsing with the sympathetic chain, these preganglionic fibers pass through it to ultimately synapse on the celiac ganglia.16 The greater, lesser, and least splanchnic nerves provide the major preganglionic contribution to the celiac plexus. The greater splanchnic nerve has its origin from the T5-10 spinal roots. The nerve travels along the thoracic paravertebral border through the crus of the diaphragm into the abdominal cavity, ending on the celiac ganglion of its respective side. The lesser splanchnic nerve arises from the T10-11 roots and passes with the greater nerve to end at the celiac ganglion. The least splanchnic nerve arises from the T11-12 spinal roots and passes through the diaphragm to the celiac ganglion. Interpatient anatomic variability of the celiac ganglia is significant, but the following generalizations can be drawn from anatomic studies of the celiac ganglia. The number of ganglia varies from one to five, and ganglia range in diameter from 0.5 to 4.5 cm. The ganglia lie anterior and anterolateral to the aorta. The ganglia located on the left are uniformly more inferior than their right-sided counterparts by as much as a vertebral level, but both groups of ganglia lie below the level of the celiac artery. The ganglia usually lie approximately at the level of the first lumbar vertebra. Postganglionic fibers radiate from the celiac ganglia to follow the course of the blood vessels to innervate the abdominal viscera. These organs include much of the distal esophagus, stomach, duodenum, small intestine, ascending and proximal transverse colon, adrenal glands, pancreas, spleen, liver, and biliary system. It is these postganglionic fibers, the fibers arising from the preganglionic splanchnic nerves, and the celiac ganglion that make up the celiac plexus. The diaphragm separates the thorax from the abdominal cavity while still permitting the passage of the thoracoabdominal structures, including the aorta, vena cava, and splanchnic nerves. The diaphragmatic crura are bilateral structures that arise from the anterolateral surfaces of the upper two or three lumbar vertebrae and disks. The crura of the diaphragm serve as a barrier to effectively separate the splanchnic nerves from the celiac ganglia and plexus below. The celiac plexus is anterior to the crus of the diaphragm. The plexus extends in front of and around the aorta, with the
149
greatest concentration of fibers anterior to the aorta.17 With the single-needle transaortic approach to celiac plexus block, the needle is placed close to this concentration of plexus fibers. The relationship of the celiac plexus to the surrounding structures is as follows: The aorta lies anterior and slightly to the left of the anterior margin of the vertebral body. The inferior vena cava lies to the right, with the kidneys posterolateral to the great vessels. The pancreas lies anterior to the celiac plexus. All of these structures lie within the retroperitoneal space. Selective blockade of the celiac plexus can provide the pain management specialist with useful information when trying to determine the cause of chest wall, flank, and/or abdominal pain. By blocking the intercostal nerves and celiac plexus on successive visits, the pain management specialist may be able to differentiate which nerves are subserving the patient's pain.
Selective Nerve Root Block Improvements in fluoroscopy and needle technology have led to increased interest in selective nerve root block in the diagnosis of cervical and lumbar radicular pain. Although technically demanding and not without complications, selective nerve root block is often used in conjunction with provocative diskography to help identify the nidus of the patient's pain complaint. The use of selective nerve root block as a diagnostic maneuver must be approached with caution. Because of the proximity of the epidural, subdural, and subarachnoid spaces, it is easy to inadvertently place local anesthetic into these spaces when intending to block a single cervical or lumbar nerve root. This error is not always readily apparent on fluoroscopy, given the small amounts of local anesthetic and contrast medium used.
Conclusion The use of nerve blocks as part of the evaluation of the patient in pain represents a reasonable next step if a careful targeted history and physical examination and rational radiographic, neurophysiologic, and laboratory testing fail to provide a clear diagnosis. The overreliance on diagnostic nerve block as the sole justification to perform an invasive or neurodestructive procedure can lead to significant patient morbidity and dissatisfaction.
References Full references for this chapter can be found on www.expertconsult.com.
II
Chapter
18
Differential Neural Blockade for the Diagnosis of Pain Alon P. Winnie and Kenneth D. Candido
CHAPTER OUTLINE The Pharmacologic Approach 150 Conventional Sequential Differential Spinal Block 151 Procedure 151 Interpretation 152 Disadvantages 153 The “Modified Differential Spinal” 153 Procedure 153 Interpretation 154 Fundamental Differences Between the Conventional Technique and the Modified Technique of Differential Spinal 154 Advantages over the Conventional Technique 154 Differential Epidural Block 154
Clinically, differential neural blockade is the selective blockade of one type of nerve fiber without blocking other types of nerve fibers. It is an extremely useful diagnostic tool that allows the clinician to observe the effect of a sympathetic block, a sensory block, and, for that matter, a block of all nerve fibers by local anesthetic agents on a patient's pain, and to compare that effect with the effect of an injection of an inactive agent (placebo). Two clinical approaches to the production of differential neural blockade exist: an anatomic approach and a pharmacologic approach. The anatomic approach is based on sufficient anatomic separation of sympathetic and somatic fibers to allow injection of local anesthetic to block one type only (see discussion later in this chapter). The pharmacologic approach is based on the presumed difference in the sensitivity of the various types of nerve fibers to local anesthetics, so that the injection of local anesthetics in different concentrations selectively blocks different types of fibers. Because pain is a totally subjective phenomenon, what is needed to identify the neural pathway that subserves it is some sort of objective diagnostic test, and differential neural blockade is just such a test. Although differential neural blockade is not intended to replace a detailed history, a complete physical examination, and appropriate laboratory, radiographic, and psychologic studies, in our practice it has been a rewarding diagnostic maneuver that has been effective in delineating the neural mechanisms subserving many puzzling pain problems, 150
Differential Brachial Plexus Block 155 Summary 155
The Anatomic Approach 156 Procedure 156 Interpretation 156
Discussion 157 o the Factors Recently Found to Determine Nerve Conduction D and Blockade Invalidate the Concept of Differential Neural Blockade? 157 Do the Complexities of Chronic Pain and the Physiologic, Anatomic, and Psychosocial Factors Involved Limit the Diagnostic Utility of Differential Neural Blockade? 159
Role of Differential Neural Blockade 160
and it has been particularly useful in patients who have intractable pain with no apparent cause.
The Pharmacologic Approach A differential spinal is the simplest pharmacologic approach with the most discrete end points. The first clinical application of this technique1 was based on the seminal work of Gasser and Erlanger, 2,3 and, although these investigators were wrong about the site of conduction (they believed it took place within the axoplasm), they established forever the relationship between fiber size, conduction velocity, and fiber function. Their classification of nerve fibers based on size is still used today (Table 18.1). In a simple but elegant experiment, these researchers showed that when a nerve is stimulated and the response is recorded only a few millimeters away, the record shows a single action potential. Then they demonstrated that, as the recording electrode is moved progressively farther away from the stimulating electrode, the action potential can be shown to consist of several smaller spikes, each representing an impulse traveling at a different rate along a nerve fiber of a different size. The action potentials might be compared to runners in a race who become separated along the course as the faster contestants outstrip the slower. Thus, in a record obtained by a recording electrode 82 mm from the point of stimulation, three waves can be seen; whereas at 12 mm, the potentials are fused, and only one large wave appears (Fig. 18.1). It may be seen in Table 18.1 that the © 2011 Elsevier Inc. All rights reserved.
Chapter 18—Differential Neural Blockade for the Diagnosis of Pain
151
Table 18.1 Classification of Nerve Fibers by Fiber Size and the Relation of Fiber Size to Function and Sensitivity to Local Anesthetics* Group/Subgroup
Diameter (mm)
Conduction Velocity (m/sec)
Modalities Subserved
Sensitivity to Local Anesthetics (%)†
A (myelinated) _A-alpha
15–20
8–120
Large motor, proprioception
1.0
_A-beta
8–15
30–70
Small motor, touch, pressure
↓
_A-gamma
4–8
30–70
Muscle spindle, reflex
↓
_A-delta
3–4
10–30
Temperature, sharp pain, nociception
0.5
B (myelinated)
3–4
10–15
Preganglionic autonomic
0.25
C (unmyelinated)
1–2
1–2
↓
_
Dull pain, temperature, nociception
0.5
*Subarachnoid procaine. † Vertical arrows indicate intermediate values, in descending order.
α β
γ
82
62
46
31
12
0
1
2 Time, σ
3
4
5
Fig. 18.1 Cathode ray oscillographs of the action current in a sciatic nerve of a bullfrog after conduction from the point of stimulation through the distances (mm) shown at the left. The delta wave is not shown. (Modified from Gasser HS, Erlanger J: Role of fiber size in establishment of nerve block by pressure or cocaine, Am J Physiol 88:587, 1929.)
diameter of a nerve fiber is its most important physical dimension, so it is on that basis that they have been subdivided into three classes, A, B, and C fibers, with A fibers being subdivided into four subclasses, alpha, beta, gamma, and delta. It may also be seen that the fiber diameter is an important determinant of conduction velocity—the conduction velocity of A fibers (in meters per second) being approximately 6 times the fiber diameter (in micrometers).4 In addition, the diameter and myelination of a nerve fiber also determine to some degree the modality or modalities subserved by that fiber5: A-alpha
fibers subserve motor function and proprioception; A-beta fibers subserve the transmission of touch and pressure; and A-gamma fibers subserve muscle tone. The thinnest A fibers, the A-delta group, convey sharp pain and temperature sensation and signal nociception (tissue damage). The myelinated B fibers are thin, preganglionic, autonomic fibers, and the nonmyelinated C fibers, like the myelinated A-delta fibers, subserve dull pain, temperature transmission, and nociception. C fibers are thinner than the myelinated fibers and have a much slower conduction velocity than even A-delta fibers. Although the relationship between fiber size and sensitivity to local anesthetics originally proposed by Gasser and Erlanger was challenged recently, the “bathed length principle” proposed by Fink6,7 has restored the functional relationship between fiber size and sensitivity to local anesthetics because the larger the nerve fiber, the greater the internodal distance. It has been postulated that the density of the distribution of sodium channels at the nodes of Ranvier increases with fiber size, so that the “denser channel packing at the nodes” may also result in increased minimum blocking concentration (Cm), so this may be another reason larger fibers require a higher concentration of local anesthetic for blockade than do smaller fibers.8
Conventional Sequential Differential Spinal Block The conventional sequential technique of differential subarachnoid block9,10 is a refinement of the techniques first used by Arrowood and Sarnoff1 and later by McCollum and Stephen.11 The technique has certain inherent shortcomings (see later discussion), which have caused it to be replaced in our practice by the modified technique, but, because this is the prototype of differential neural blockade, understanding the technique and the problems it presents provides insight into the usefulness and the limitations of diagnostic differential spinal blockade using the pharmacologic approach.
Procedure After detailed informed consent is obtained from the patient, an intravenous infusion is started and prehydration with
152
Section II—The Evaluation of the Patient in Pain
Table 18.2 Preparation of Solutions for Conventional Sequential Differential Spinal Blockade Solution D
C
B
A
Preparation of Solution
Yield
Blockade
To 2 mL of 10% procaine add 2 mL of normal saline
4 mL of 5% procaine
Motor
To 1 mL of 5% procaine add 9 mL of normal saline
10 mL of 0.5% procaine
Sensory
To 5 mL of 0.5% procaine add 5 mL of normal saline
10 mL of 0.25% procaine
Sympathetic
Draw up 10 mL of normal saline
10 mL of normal saline
Placebo
Table 18.3 Observations After Each Injection Sequence
Observation
1
Blood pressure and pulse rate
2
Patient's subjective evaluation of the pain at rest
3
Reproduction of patient's pain by movement
4
Signs of sympathetic block (temperature change, psychogalvanic reflex)
5
Signs of sensory block (no response to pinprick)
6
Signs of motor block (inability to move toes, feet, legs)
would clearly reveal the expectation that each sequential injection will produce progressively increasing effects. This would clearly compromise the validity of the information obtained from the procedure.
Interpretation crystalloid is begun, as for any spinal anesthetic. Similarly, all of the monitors routinely used for spinal anesthesia are applied, including blood pressure, electrocardiography (ECG), and pulse oximetry, and baseline values are recorded. Four solutions are prepared (Table 18.2), and the patient is placed into the lateral decubitus position with the painful side down, if possible. After the usual sterile preparation and draping of the back, a 25- to 27-gauge pencil-point spinal needle is introduced into the lumbar subarachnoid space at the L2-3 or L3-4 interspace. The patient is shown the four prepared syringes, all of which appear identical, and is told that each of the solutions will be injected sequentially at 10- to 15-minute intervals. The patient is instructed to tell the physician which, if any, of the solutions relieves the pain. The solutions are referred to as A through D, so that the physicians can discuss the solutions freely in front of the patient without using the word placebo. Solution A, which contains no local anesthetic, is the placebo. Solution B contains 0.25% procaine, which is the mean sympatholytic concentration of procaine in the subarachnoid space.1 That is, it is the concentration that is sufficient to block B fibers but is usually insufficient to block A-delta and C fibers. Solution C contains 0.5% procaine, the mean sensory blocking concentration of procaine. That is, it is the concentration usually sufficient to block, in addition to B fibers, A-delta and C fibers but is insufficient to block A-alpha, A-beta, and A-gamma fibers. Solution D contains 5.0% procaine, which provides complete blockade of all fibers, including sympathetic, sensory, and motor fibers. To prevent bias, it is extremely important that all of the injections be carried out in exactly the same manner, so that to the patient they are identical to and indistinguishable from one another. It is equally important that the physician make exactly the same observations after each injection (Table 18.3). The observations must be carried out in an identical manner after each injection so that the observations themselves do not influence the patient's response. Obviously, an inexperienced clinician who checks only the blood pressure after the sympatholytic injection, or who checks only the response to pinprick after the sensory-blocking injection, and who checks only the motor function after the motor-blocking injection
The conventional sequential differential spinal is interpreted as follows: If the patient's pain is relieved after subarachnoid injection of solution A (the placebo), the patient's pain is classified as “psychogenic.” It is well known that some 30% to 35% of all patients with true, organic pain obtain relief from an inactive agent.12 Therefore relief in response to the normal saline may represent a placebo reaction, but it may also indicate that an entirely psychogenic mechanism is subserving the patient's pain. Clinically, these two can usually be differentiated, because a placebo reaction is usually short-lived and selflimiting, whereas pain relief provided by a placebo to a patient suffering from true, psychogenic pain is usually long-lasting, if not permanent. If the difference between the two is not clinically evident, evaluation by a clinical psychologist or psychiatrist may be deemed to be necessary. If the patient does not obtain relief from the placebo but does obtain relief from the subarachnoid injection of 0.25% procaine, the mechanism subserving the patient's pain is tentatively classified as sympathetic, provided that concurrent with the onset of pain relief, signs of sympathetic blockade are observed without signs of sensory block. Obviously, although 0.25% procaine is the usual sympatholytic concentration in most patients, in some patients (who may have a reduced Cm for A-delta and C fibers) relief may be due to the production of analgesia and/or anesthesia. The finding that a sympathetic mechanism is subserving a patient's pain is extremely fortuitous for the patient, because if the pain is truly sympathetically mediated, if treated early enough, it may be completely and permanently relieved by a series of sympathetic nerve blocks. If 0.25% procaine does not provide pain relief but the subarachnoid injection of the 0.5% concentration does, this usually indicates that the patient's pain is subserved by A-delta and/or C fibers and is classified as somatic pain, provided that the patient did exhibit signs of sympathetic blockade after the previous injection of 0.25% procaine and that the onset of pain relief is accompanied by the onset of analgesia and/or anesthesia. This is important because if a patient has an elevated Cm for B fibers, the pain relief from 0.5% procaine could be due to sympathetic block rather than to sensory block.
Chapter 18—Differential Neural Blockade for the Diagnosis of Pain
153
Table 18.4 Diagnostic Possibilities of “Central Mechanism” Diagnosis
Explanation/Basis of Diagnosis
Central lesion
The patient may have a lesion in the central nervous system that is above the level of the subarachnoid sensory block. For example, we have seen two patients who had a metastatic lesion in the precentral gyrus, which was the origin of the patient's peripheral pain and was clearly above the level of the block.
Psychogenic pain
The patient may have true “psychogenic pain,” which obviously is not going to respond to a block at any level. This is an even more uncommon response in patients with psychogenic pain than a positive response to placebo.
Encephalization
The patient's pain may have undergone “encephalization”—that poorly understood phenomenon whereby persistent, severe, agonizing pain, originally of peripheral origin, becomes self-sustaining at a central level. This usually does not occur until severe pain has been endured for a long time, but once it has occurred, removal or blockade of the original peripheral mechanism fails to provide relief.
Malingering
The patient may be malingering. One cannot prove or disprove this with differential blocks, but if a patient is involved in litigation concerning the cause of his pain and anticipates financial benefit, it is unlikely that any therapeutic modality will relieve the pain. However, empirically, it is our belief that a previous placebo reaction from solution A followed by no relief from solution D strongly suggests that the patient whose pain ultimately appears to have a “central mechanism” is not malingering, since the placebo reaction, depending as it does on a positive motivation to obtain relief, is unlikely in a malingerer. Clearly, there is no way to document the validity of this theory, but it certainly suggests greater motivation to obtain pain relief than to obtain financial gain.
If pain relief is not obtained by any of the first three spinal injections, 5% procaine is injected into the subarachnoid space to block all modalities. If the 5% concentration does relieve the patient's pain, the mechanism is still considered somatic, the presumption being that the patient has an elevated Cm for A-delta and C fibers. If, however, the patient obtains no relief in spite of complete sympathetic, sensory, and motor blockade, the pain is classified as “central” in origin, although this is not a specific diagnosis and may indicate any one of the four possibilities in Table 18.4.
Table 18.5 Preparation of Solutions for Modified Differential Spinal Blockade Preparation and Solution
Yield
D
To 1 mL of 10% procaine add 1 mL of saline
2 mL of 5% procaine (hyperbaric)
A
Draw up 2 mL of normal saline
2 mL of normal saline
Solution
Disadvantages The conventional sequential differential spinal technique just described was used by the authors for many years and was effective in pinpointing the neural mechanisms subserving pain syndromes in a multitude of patients. It was particularly effective in establishing a diagnosis in patients with pain syndromes of questionable or unknown etiology. However, the technique has several obvious drawbacks. First of all, it is quite time consuming, because the physician must wait long enough after each injection for the response to become evident, and then to wane, allowing a subsequent solution to be injected. Second, occasionally a patient is encountered whose Cm for sympathetic blockade is greater than 0.25, so when relief is produced by 0.5% procaine, one might erroneously conclude that this is somatic pain rather than sympathetic pain. Similarly, a patient may occasionally be encountered who has a lower Cm for sensory blockade than 0.5%, and when 0.25% procaine produces relief, one might erroneously conclude that the mechanism is sympathetic rather than somatic. Third, each successive injection with this technique deposits more procaine into the subarachnoid space, so that after the final injection, when all modalities are blocked, it takes quite a while for full function to return. Full recovery is absolutely essential, at least in our pain center, because the vast majority of the patients are outpatients and must be fully able to ambulate before being discharged. This technique demands that the needle remain in place throughout the entire procedure, so the patient must remain in the lateral position throughout the test. Occasionally this is a serious problem, especially when the
patient's pain is associated with a particular position that cannot be assumed with the needle in situ.
The “Modified Differential Spinal” In an effort to overcome the disadvantages just described, the conventional technique has been modified in a way that simplifies it and increases its utility.13–16 For the modified technique, only two solutions need to be prepared, as summarized in Table 18.5, namely, normal saline (solution A) and 5% procaine (solution D).
Procedure As in the conventional technique, after informed consent has been obtained, an infusion started, and the monitors applied, the back is prepared and draped, and a small-bore blunttipped spinal needle is used to enter the subarachnoid space. At this point 2 mL of normal saline is injected, and observations are made as in the conventional technique described previously (see Table 18.3). If the patient obtains no relief or only partial relief from the placebo injection, 2 mL of 5% procaine is injected, the needle is removed, and the patient is returned to the supine position. Because the injected 5% procaine is hyperbaric, the position of the table may have to be adjusted to obtain the desired level of anesthesia. Once this is accomplished, the same observations are made as after the previous injection (see Table 18.3).
154
Section II—The Evaluation of the Patient in Pain
Interpretation If the patient's pain is relieved after the injection of normal saline, the interpretation is the same as if it were relieved by placebo in the conventional differential spinal—that is, the pain is considered to be of psychogenic origin. Again, when the pain relief is prolonged or permanent, the pain is probably truly psychogenic, whereas if relief is transient and self-limited, the response probably represents a placebo reaction. When the patient does not obtain pain relief after the subarachnoid injection of 5% procaine, the diagnosis is considered to be the same as that when the patient obtains no relief after injection of all of the solutions with the conventional technique—that is, the mechanism is considered to be “central.” As in the conventional technique, this diagnosis is not specific; rather, it indicates one of four possibilities (see Table 18.4). Alternatively, when the patient does obtain complete pain relief after the injection of 5% procaine, the cause of the pain is considered to be organic. The mechanism is considered to be somatic (to be subserved by A-delta and/or C fibers) if the pain returns when the patient again perceives pinprick as sharp (recovery from analgesia); whereas it is considered sympathetic if the pain relief persists long after recovery from analgesia.
Fundamental Differences Between the Conventional Technique and the Modified Technique of Differential Spinal The conventional sequential differential spinal sought to block specific types of nerve fibers with specific concentrations of local anesthetics. At the time when we modified the conventional technique, evidence was accumulating that the exact concentrations of local anesthetics required to block different fiber types are unpredictable, to say the least. Thus we abandoned the practice of injecting predetermined concentrations of local anesthetics in an attempt to selectively block one fiber type at a time and adopted a technique not unlike that used to produce surgical spinal anesthesia—a technique that was much better understood. With that technique, after a placebo injection, a concentration of a short-acting local anesthetic sufficient to produce surgical anesthesia is injected into the subarachnoid space to block all types of fibers, and the patient is observed as the concentration of local anesthetic in the cerebrospinal fluid decreases and the fibers recover sequentially, motor fibers first, followed by sensory fibers, and then sympathetic fibers. Whereas the conventional sequential technique attempted to correlate the onset of pain relief with the onset of blockade of the various fiber types, the modified technique attempts to correlate the return of pain with the recovery of the various blocked fibers. It readily becomes apparent that this modified technique of differential spinal block simplifies the differentiation of sympathetic from somatic mechanisms considerably. With the conventional technique, occasionally the concentration required to produce sympathetic blockade is somewhat greater or somewhat less than the usual mean of 0.25%, and the concentration of procaine required to produce a sensory block is greater or less than the usual mean of 0.5%. Significant diagnostic confusion can result. With the modified technique,
when a patient recovers sensation, the only fibers that remain blocked are the sympathetic fibers; thus pain relief that persists beyond the recovery of sensation clearly indicates a sympathetic mechanism.
Advantages over the Conventional Technique The major advantage of the modified differential spinal block over the conventional technique is that it takes less time. The modified technique has consistently provided diagnostic information identical to that provided by the conventional technique, but in approximately one third of the time. The conventional differential technique requires a series of injections into the subarachnoid space of progressively increasing concentrations of local anesthetic, so that when the study is complete, the patient has a high level of anesthesia that takes a long time to dissipate. The modified technique requires only a single injection of active drug; so in addition to the test's taking less time, the time for recovery is likewise reduced—a fact of great importance in a busy pain center. The modified technique also minimizes the extent and duration of discomfort for the patient, who does not have to lie so long in the lateral position with the needle in place. In addition, the modified technique allows a better evaluation of the subjective nature of a patient's pain. Because there is no need to keep the needle in the back throughout the procedure, the patient can lie supine, and positional changes or passive movement of the legs that may be necessary to reproduce the pain are much easier. The advantage of the modified approach over the traditional one in differentiating sympathetic from somatic pain has already been described.
Differential Epidural Block More than 30 years ago, Raj17 suggested using sequential differential epidural block instead of the conventional sequential differential spinal to avoid spinal headaches after the procedure. With his proposed technique, solution A was still to be the placebo, but solution B was 0.5% lidocaine, which was presumed to be the mean sympatholytic concentration of lidocaine in the epidural space; solution C was 1% lidocaine, the presumed mean sensory blocking concentration in the epidural space; and solution D was 2% lidocaine, a concentration sufficient to block all modalities, sympathetic as well as sensory and motor. In short, the technique Raj proposed for differential epidural block was virtually identical to that used for the conventional differential spinal block, except that the local anesthetic doses were injected sequentially into the epidural space and the concentrations were modified as described earlier. There were two problems with the technique proposed by Raj. First, because of the slower onset of blockade after each injection of local anesthetic into the epidural space, more time would be required between injections before the usual observations could be made. So a differential epidural block, as proposed by Raj, would take even longer for complete recovery than the conventional differential spinal technique. An even more serious drawback of this approach, however, relates to the fact that, if local anesthetics occasionally fail to give discrete end points when injected into the subarachnoid space, the end points are even less discrete with injections into the epidural space. For example, 0.5% lidocaine provides
Chapter 18—Differential Neural Blockade for the Diagnosis of Pain
155
sympathetic blockade when injected epidurally, but it commonly causes sensory block as well. Similarly, whereas 1% lidocaine injected epidurally almost always produces sensory block, it frequently also produces paresis, if not paralysis. As a matter of fact, it was the failure of this technique to provide definitive end points that led Raj to decide not to publish it. Nonetheless, conceptually, a differential epidural approach is inherently appealing because it avoids lumbar puncture and the possibility of post–lumbar puncture headache in a predominantly outpatient population. The major problem with the technique Raj proposed, the lack of discrete end points, was due to the attempt to inject a different concentration of local anesthetic to block each type of nerve fiber, something we had attempted with our conventional differential spinal. Because our modified differential spinal eliminated the occasional confusing end points of the conventional technique, we decided to modify Raj's proposed differential epidural as we had modified our differential spinal. This technique as we perform it is as follows14–16: Informed consent is obtained, an infusion is started, and the various monitors are applied. The patient is placed in the lateral (or sitting) position, and the back is prepared and draped in the usual manner. After a 20-gauge Tuohy-type epidural needle has been placed in the epidural space by the modified loss-of-resistance technique, equal volumes of normal saline and 2% chloroprocaine (or lidocaine) are injected sequentially 15 to 20 minutes apart, and the needle is removed. The volume of each is that required to produce the desired level of anesthesia. After each injection, exactly the same observations are made as for a differential spinal (see Table 18.3). The interpretation is virtually identical to that of a modified differential spinal. If the patient experiences pain relief after the injection of saline, the presumptive diagnosis is “psychogenic pain,” a designation that indicates the possibility of either a placebo reaction or true psychogenic pain. If the patient does not experience pain relief after the injection of 2% chloroprocaine (or lidocaine) into the epidural space in spite of complete anesthesia of the painful area, the diagnosis is considered to be “central pain,” that diagnosis again including the four possibilities described earlier (see Table 18.4). When the patient does experience pain relief after the injection of 2% chloroprocaine (or lidocaine), however, the pain is considered organic. It is presumed to be somatic (subserved by A-delta and C fibers) when the pain returns with the return of sensation, and sympathetic when the pain persists long after sensation has been recovered. This approach to differential epidural blockade has been used extensively at our institution and has provided the same valuable information obtained from the modified differential spinal technique without the usual risk of post–dural puncture headache. In addition, differential epidural is a useful alternative to differential spinal when a patient refuses spinal anesthesia or when spinal anesthesia is contraindicated, although both of these situations are rare. A catheter can be placed through a larger epidural needle if it is anticipated that supplemental injections may be necessary to achieve the proper level, but in our experience this has rarely been necessary.
injections are made into the perivascular compartment using an approach appropriate to the site of the patient's pain, one injection consisting of normal saline and the other 2% chloroprocaine. Again, the same observations are made after each injection (see Table 18.3). If the patient is somewhat naive with respect to the injections carried out at a pain center, it may be sufficient for the placebo injection to consist of local infiltration over the anticipated site of injection of the active agent, as long as all of the appropriate observations are made after the injection. If this does not provide relief, the brachial plexus block is carried out with local anesthetic, inserting the needle through the anesthetized skin. If the patient obtains pain relief from the placebo injection, as with a differential spinal or epidural, the pain is considered psychogenic, whereas if the pain disappears after injection of chloroprocaine into the brachial plexus sheath, it is labeled organic. If the pain returns as soon as the sensory block is dissipated, the mechanism is somatic (i.e., it is subserved by A-delta and C fibers); if the relief persists long after recovery from the sensory block, the mechanism is presumed to be sympathetic. Finally, of course, if the pain does not disappear, even when the arm is fully anesthetized, the diagnosis is central pain, and the same four possibilities are again associated with that response (see Table 18.4). It is significant to note that Durrani and Winnie19 reported on 25 patients referred to our pain control center with a clinical diagnosis of “classic” reflex sympathetic dystrophy (Complex Regional Pain Syndrome Type I [CRPS Type I]) of the upper extremity—all of whom obtained no relief from a series of three stellate ganglion blocks, even though each patient developed Horner's syndrome after each block. The significance of this report is that, when these patients were subjected to differential brachial plexus block by one of the perivascular techniques, 16 of the 25 patients (who had not obtained relief from three stellate ganglion blocks) exhibited a typical sympathetic response to the brachial plexus block. Perhaps more important, 12 of the 19 patients so treated obtained complete and permanent relief from a series of therapeutic brachial plexus blocks, even though they had failed to do so after a series of stellate ganglion blocks. Thus it would appear that perivascular brachial plexus blocks provide more complete sympathetic denervation of the upper extremity than do stellate ganglion blocks. The success of brachial plexus block and the failure of stellate ganglion blocks in this report might be explained by the fact that the local anesthetic injected at the stellate ganglion failed to reach the nerve of Kuntz, the nerve by which ascending sympathetic fibers may bypass the stellate ganglion.20,21 Because all of the stellate ganglion blocks at our institution are carried out using a minimum of 8 mL of local anesthetic as well as with fluoroscopic guidance or using ultrasound, however, this is unlikely. A more likely explanation is that stellate ganglion block interrupts only those sympathetic fibers that travel with the peripheral nerves, whereas perivascular brachial plexus block interrupts the sympathetic fibers traveling by both neural and perivascular pathways.22
Differential Brachial Plexus Block
Controversial aspects aside, the pharmacologic approach to differential neural blockade remains a simple but useful technique—whether carried out at a subarachnoid, epidural, or plexus level—because it provides reproducible, objective, and definitive diagnostic information on the neural
Performed in a manner analogous to that of differential epidural block, a differential brachial plexus block can be extremely useful in evaluating upper extremity pain.18 Two successive
Summary
156
Section II—The Evaluation of the Patient in Pain
mechanisms subserving a patient's pain. Obviously, the results of this test must be interpreted in the light of other diagnostic tests (including psychologic tests) and the results must be integrated with the information obtained from the patient's history and the findings on physical examination. Not infrequently, the results of a differential spinal, a differential epidural, or a differential plexus block provide the missing piece in the complex puzzle of pain.
The Anatomic Approach To obviate the problems inherent in high spinal (or epidural) anesthesia, particularly in an outpatient or a patient whose pain is in the upper part of the body, it is occasionally safer and more appropriate to use an anatomic approach to differential neural blockade. In this approach, after the injection of a placebo, the sympathetic and then the sensory and/or motor fibers are blocked sequentially by injecting local anesthetic at points where one modality can be blocked without blocking the other. The procedural sequences by which differential nerve blocks are carried out in this approach for pain in the various parts of the body are presented in Table 18.6.
Procedure For pain in the head, neck, and upper extremity, if a placebo injection fails to provide relief, a stellate ganglion block is carried out with any short-acting, dilute local anesthetic. If the sympathetic block cannot be carried out without spillover onto somatic nerves innervating the painful area, the sequential blocks should be carried out on two separate occasions, allowing the sympathetic block to wear off before proceeding with the somatic block. In any case, if the patient does not obtain relief from the stellate ganglion block, a block of the somatic nerves to the painful area should be carried out. For pain in the thorax, after a placebo injection, the safest procedure (and the one that causes the least discomfort to the patient) is a differential segmental epidural block, as described previously. It must be remembered, however, that, with thoracic pain, relief after an extensive sympathetic block, in addition to suggesting a possible sympathetic mechanism, may indicate visceral rather than somatic pain, because visceral pain is mediated by sympathetic fibers. If it is unwise to carry out a differential thoracic epidural block in a particular
patient because of cachexia, hypovolemia, or dehydration, an alternative is the anatomic approach, using paravertebral or intercostal blocks of the appropriate dermatomes. Failure of these somatic blocks to provide relief implies (but does not prove) a visceral origin for the pain; however, if the blocks provide complete relief and if the pain returns immediately after recovery, a peripheral somatic mechanism is indicated. If the relief provided by the blocks persists long after recovery of sensation, this may indicate a sympathetic mechanism. When a placebo injection fails to provide relief for abdominal pain, before a celiac block is considered, paravertebral or intercostal blocks of the appropriate dermatomes should be done to make certain that the pain is not somatic (body wall). Patients have a great deal of difficulty localizing “abdominal pain,” and therefore they usually cannot differentiate pain that is due to body wall extension of a lesion from pain that is due to true visceral involvement. If the paravertebral or intercostal blocks produce complete anesthesia of the body wall overlying the patient's pain but fail to provide relief, a splanchnic or celiac plexus block should be carried out to confirm that the pain is truly visceral in origin. If a placebo injection fails to provide relief for pelvic pain, before a superior hypogastric plexus block is attempted, paravertebral or appropriate sacral blocks should be carried out to make certain that the pain is not somatic. If these blocks produce appropriate anesthesia but fail to provide relief, a superior hypogastric block is carried out to establish that the pain is visceral. For pain in the lower extremities, the pharmacologic approach (differential spinal or epidural) is preferable because it is more precise and less painful than peripheral nerve blocks. Differential peripheral blocks, however, can be used if the pharmacologic approach is contraindicated or undesirable or if subsequent neurolytic blocks are anticipated. After a placebo block, lumbar paravertebral sympathetic blocks are performed at the levels L2-4, and if these fail to provide relief, lumbosacral plexus block (or any appropriate specific peripheral nerve block) is carried out.
Interpretation Interpretation of the results achieved with differential nerve blocks for head, neck, arm, and leg pain is self-evident. Relief after a placebo injection indicates a psychogenic mechanism,
Table 18.6 Anatomic Approach: Procedural Sequence for Differential Diagnostic Nerve Blocks Site of Pain
Technique
Head
Placebo block
Stellate ganglion block
Block of C2; block of trigeminal I, II, III (or specific nerve block)
Neck
Placebo block
Stellate ganglion block
Cervical plexus block (or specific nerve block)
Arm
Placebo block
Stellate ganglion block
Brachial plexus block (or specific nerve block)
Thorax*
Placebo block
Thoracic paravertebral sympathetic block
Lumbar paravertebral somatic block
Abdomen†
Placebo block
Celiac plexus block
Paravertebral somatic or intercostal block
Pelvis Leg
†
Placebo block
Superior hypogastric plexus block
Paravertebral somatic or intercostal block
Placebo block
Lumbar paravertebral sympathetic block
Lumbosacral plexus block (or specific nerve block)
*In our opinion, thoracic paravertebral sympathetic blocks carry such a high risk of pneumothorax that a pharmacologic approach should be used. † Because of the simplicity of intercostal blocks, as compared with celiac plexus and superior hypogastric plexus blocks, the procedural sequence is altered for abdominal pain (i.e., somatic before sympathetic).
Chapter 18—Differential Neural Blockade for the Diagnosis of Pain
but, as with the pharmacologic approaches, it could indicate either a placebo reaction or true psychogenic pain. Relief after sympathetic blocks indicates a sympathetic mechanism, usually reflex sympathetic dystrophy (CRPS Type I), and relief after blockade of somatic nerves indicates an organic, somatic mechanism. Failure to obtain relief in spite of the establishment of complete anesthesia in the appropriate area would tend to indicate a central mechanism, which could be any of the four possibilities listed in Table 18.4. Interpretation of the results of differential blocks for thoracic and abdominal pain has already been discussed.
Discussion In spite of the clinical success of the various techniques of differential neural blockade in many centers over the last 35 years, the validity of the results has become controversial. There are two reasons for this: (1) the changes in our understanding of the factors that determine the process of nerve conduction and blockade are believed by some to invalidate the concept of differential neural blockade; and (2) the even greater changes in our understanding of the complexities of chronic pain and the physiologic, anatomic, and psychosocial factors involved are believed to limit the diagnostic utility of neural blockade. To establish both the validity and utility of differential neural blockade in the diagnosis of pain mechanisms, it is essential to understand the bases of this controversy by answering two questions: (1) do the factors recently found to determine nerve conduction and blockade invalidate the concept of differential neural blockade, and (2) do the complexities of chronic pain and the physiolgic, anatomic, and psychosocial factors involved limit the diagnostic utility of differential neural blockade?
Do the Factors Recently Found to Determine Nerve Conduction and Blockade Invalidate the Concept of Differential Neural Blockade? The pharmacologic approach to differential neural blockade is based on the assumption that local anesthetic agents can selectively produce conduction block of one type of fiber in a nerve while sparing the other types in that nerve.23 Although the concept of differential block was introduced almost 90 years ago by Gasser and Erlanger,24 in vitro and in vivo studies carried out over the past 35 years have indicated that the basis of Gasser and Erlanger's explanation of this commonly observed clinical phenomenon was totally erroneous, as was their explanation of the process of nerve conduction itself. From the classic studies Gasser and Erlanger carried out on the peripheral nerves of dogs they concluded that, in general, small-diameter fibers were more readily blocked by cocaine than were largerdiameter fibers. At that time, however, it was believed that the site of action of conduction was the axonal protoplasm. Thus the higher ratio of surface to volume in small-diameter fibers was supposed to make them more “sensitive” (easier to enter and render unexcitable) than large ones. Since that theory was articulated in one form or another this “size principle” has influenced the concept of differential block, has led to clinical use of differential spinal block,1 and has provided an explanation for the persistent differential losses of function observed during subarachnoid25 and epidural26 anesthesia.
157
It was over 50 years before the concept of Gasser and Erlanger was challenged. Studies by Franz and Perry in vivo27 and by Fink and Cairns in vitro28 indicated that all mammalian axons require about the same blocking concentration of local anesthetic, regardless of their diameter, and the issue was rendered even more confusing when Gissen et al29 demonstrated that the larger the diameter of an axon, the more susceptible it was to conduction block by local anesthetics, a finding diametrically opposed to Gasser and Erlanger's traditional concept. However, as de Jong30 pointed out, a major flaw in Gissen's study was that the experiments were carried out at room temperature. Because conduction in large fibers is more affected by cold than is conduction in small fibers, relatively little anesthetic may be needed to block large fibers in conditions cooler than body temperature. Subsequently, Palmer et al,31 using a preparation maintained at body temperature, showed that C fibers were, in fact, more susceptible to conduction block by bupivacaine than were A fibers, but they were unable to demonstrate such differential effects with lidocaine. This study introduced a new complexity: different anesthetics may affect various axon types differently. In two sequential in vitro studies, Wildsmith et al32,33 compared the differential nerve-blocking activity of a series of amide-linked local anesthetics with that of a series of ester-linked agents. These studies confirmed Gissen's finding that, in general, A fibers are the most sensitive and C fibers the least sensitive to blockade by local anesthetics but that the absolute and relative rates of development of A fiber blockade were directly related to lipid solubility and inversely related to pKa. On the basis of the findings of these two in vitro studies, Wildsmith postulated that, in vivo, C fibers could be blocked differentially by an agent of low lipid solubility and high pKa, because a compound with these properties (such as procaine) might produce blockade of C fibers relatively quickly, but before it could penetrate the great diffusion barriers around A fibers, it would be removed by the circulation. Ford et al34 tested this hypothesis, studying several local anesthetics in a cat model in vivo and found that, regardless of the local anesthetic, A-alpha fibers were consistently less sensitive to blockade than either A-delta or C fibers, thus reaffirming the original scheme of Gasser and Erlanger. It remained for Fink6 to elucidate the importance of two other factors subserving differential neural blockade. First, he pointed out the importance of the nodes of Ranvier, the internodal distance, and the number of nodes bathed by a local anesthetic to differential neural blockade. It has long been known that to block conduction, an adequate concentration of local anesthetic (Cm) applied to a myelinated axon must bathe at least three consecutive nodes.35 Because the internodal distance increases as the thickness of the axon increases, the probability of three successive nodes of Ranvier being bathed quickly by an injected local anesthetic solution decreases as the internodal distance increases, that is, as the size of the fiber increases (Fig. 18.2). In other words, the chance of a local anesthetic solution blocking a given nerve fiber decreases with increasing fiber size. For example, the internodal distance of small A-delta fibers ranges from 0.3 to 0.7 mm, so that a “puddle” of local anesthetic solution only 2 mm long will fully cover three successive nodes. In contrast, large A-alpha fibers have an internodal distance of 0.8 to 1.4 mm, so their critical blocking length is at least 5 mm.27 Thus, because the internodal distance increases with thickness of the axon, the minimal blocking length ranges from 2 to 5 mm.
158
Section II—The Evaluation of the Patient in Pain Anesthetic
Thin axon
Thick axon
Fig. 18.2 Differential nerve block based on different internodal intervals. Two axons, one thin and one thick, are depicted lying side by side in a puddle of local anesthetic at or above the minimum blocking concentration (Cm). The internodal interval of the thick fiber is twice that of the thin one, so whereas the local anesthetic solution covers three successive nodes of the thin axon, it covers only one node of the thick one. Nerve impulses can skip easily over one node, and even over two, rendered inexcitable by the local anesthetic,35 so conduction along the thick axon will continue uninterrupted. In the thin axon, however, because three nodes are covered by the local anesthetic solution, impulse conduction is halted. Thus conduction appears to proceed normally in the thick (motor) fiber but is blocked in the thin (sensory) fiber. Such a differential block of thin versus thick nerve fibers occurs in spinal roots during spinal anesthesia (see discussion in text). (Modified from de Jong RH: Local anesthetics, St Louis, 1994, Mosby, p 89.)
Anesthetic
Thin axon
Thick axon
Fig. 18.3 Differential decremental nerve block and frequency-dependent block. When both thick and thin axons have more than three nodes covered by a local anesthetic solution, if the solution is at or above the minimum blocking concentration (Cm) all of the sodium channels are occupied and conduction is blocked in both fibers. However, if the concentration of local anesthetic is below Cm, a significant portion (but not all) of the sodium channels are blocked, so that at each node the action potential undergoes a progressive reduction in amplitude, with resultant decremental slowing of impulse conduction. Such decremental conduction will ultimately extinguish the impulse in the nine exposed nodes of the thin fiber (decremental block); but, although the impulse is slowed in its passage along the five incompletely blocked nodes of the thick fiber, it will resume at full speed when normally conducting membrane is reached again. The lower the concentration of the local anesthetic, the longer must be the exposure length (the number of nodes of Ranvier exposed) to yield complete impulse blockade. Conversely, the more concentrated the local anesthetic solution, the shorter is the exposure length required for complete blockade, up to the point of Cm, when the “three-node principle” again applies. In other words, below Cm, the blocking concentration of local anesthetic is inversely proportional to the length of the nerve it bathes. The greater the frequency of nerve stimulation, the shorter is the exposure length (the number of incompletely blocked nodes) required to yield complete impulse blockade. Such a frequency-dependent block superimposed on decremental block is operant clinically in the zone cephalad to the level of somatic block in a spinal anesthesia (see discussion in text). (Modified from de Jong RH: Local anesthetics, St Louis, 1994, Mosby, p 91.)
Next, Fink demonstrated that the differential blockade of the sympathetic nerves observed clinically with spinal anesthesia is probably due, at least in part, to decremental block with a superimposed frequency-dependent effect.36 Decremental block occurs when a nerve is bathed by a weak concentration of local anesthetic (2 weeks) or recreational abuse of opioids (both commonly seen in burn patients), doses needed for burn analgesia may significantly exceed those recommended in standard guidelines. One clinically important consequence of drug tolerance is the potential for opioid withdrawal to occur during inpatient burn treatment. Thus, the period of inpatient burn care is not an appropriate time to institute deliberate opioid withdrawal or detoxification measures in patients who have a premorbid history of opioid abuse because a strategy such as this ignores the very real, acute pain analgesic needs of these patients. Such practices might also lead to illegal drug seeking in hospitalized patients, with associated health risks and hospital system problems. Similarly, when reductions in analgesic therapy are considered as burn wounds heal, reductions should occur via careful taper to prevent acute opioid withdrawal syndrome. Patients with substance abuse histories should be provided with the proper counseling and referral sources and weaned off of opioid medications at discharge or soon after. However, weaning during acute care can potentially be construed as a form of punishment that may serve to exacerbate their addiction problem.
232
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
Table 25-1 Example of Institutional Burn Pain Medication Guidelines ICU (No PO Intake)
ICU (Taking PO)
Ward (Large Open Areas)
Ward (Small Open Areas/Predischage)
Background pain
Continuous morphine sulfate (IV) drip
Scheduled methadone or MS Contin
Scheduled methadone or MS Contin
Scheduled NSAIDs/ acetaminophen or scheduled oxycodone or none
Procedural pain
Morphine sulfate (IV) or fentanyl (IV)
Oxycodone, fentanyl IV, or fentanyl (Actiq)
Oxycodone, fentanyl (IV), Nitrox (IH), or fentanyl (Actiq)
Oxycodone
Breakthrough pain (prn dosing)
Morphine sulfate (IV) or fentanyl (IV)
Oxycodone
Oxycodone
NSAIDs/acetaminophen or oxycodone
Background anxiolysis
Scheduled lorazepam (IV) or continuous lorazepam (IV) drip
Scheduled lorazepam
None or scheduled lorazepam
None
Procedural anxiolysis
Lorazepam or midazolam (IV)
Lorazepam
None or lorazepam
None
Discharge or transfer pain medications
N/A
For transfer to ward: wean drips, establish PO pain medication early; anticipate dose tapering as needs decrease
Oxycodone for procedural pain; methadone taper or MS Contin; taper if applicable
Oxycodone or NSAIDs for procedural pain
ICU, intensive care unit; IH, by inhalation; IV, intravenously; N/A, not applicable; NSAIDs, nonsteroidal anti-inflammatory drugs; PO, by mouth, prn, as needed. Representative pain and sedation management guideline for adult (nonpediatric, nongeriatric) burn patients from the University of Washington Burn Center. General medication recommendations are provided for specific pain and anxiolysis needs encountered in various intensive care units and ward care settings. Medication options are intentionally limited (for simplicity) and do not include specific dose recommendations (to allow for individual patient variability). Complex or refractory cases are managed through special consultation with the burn care team or pain specialists.
Because nociception at the wound site is the predominant mechanism of pain and suffering in patients with acute burn injuries, pharmacologic treatment with potent opioids analgesics, anxiolytics, or other anesthetics is the first line and cornerstone of therapy. In addition, nonpharmacologic methods of treatment of burn pain are also extremely useful but are best applied only after optimal pharmacologic therapy has been established (although abiding by nonpharmacologic principles for pain control in all cases is important, such as minimizing the adversity of wound care and making the environment as patient friendly as possible). Brief descriptions of the analgesic goals and potential general therapeutic options for each of the four clinical settings of burn pain are presented subsequently (see also Fig. 25.3).
Background Pain Management Background pain is relatively constant and is mild to moderate in severity and is consequently best treated pharmacologically with mild-to-moderately potent analgesics administered so that plasma drug concentrations remain relatively constant throughout the day. Examples include continuous IV opioid infusions (with or without patient-controlled analgesia [PCA]), oral administration of long-acting opioids with prolonged elimination (methadone) or prolonged enteral absorption (sustained-release morphine, sustained release oxycodone), or oral administration on a regular schedule of short-acting oral opioid analgesics or nonsteroidal anti-inflammatory agents (NSAIDs). Background pain decreases with time as the burn wound (and associated donor sites) heals, so that analgesics can be slowly tapered. Nonpharmacologic techniques applicable to background pain might include approaches to enhance coping, relaxation, information provision, and participation (see subsequent discussion).
Procedural Pain Management Pain associated with burn wound care presents a unique and significant challenge for the medical staff in that potent sedation or analgesia is often needed on a daily basis, yet general anesthesia is either too dangerous, expensive, or logistically challenging to use on an ongoing basis. Thus, the provision of moderate sedation (formerly conscious sedation) or deep sedation (as defined by the American Society of Anesthesiologists [ASA]19) is frequently needed and should conform to the sedation guidelines set by the ASA19 and adopted by The Joint Commission. For example, the institutional capability to provide adequate monitoring (pulse oximetry, independent patient observer) for moderate sedation by nonanesthesiologists may also dictate which specific agents are used for procedural analgesia, as some of the more potent opioids (e.g., remifentanil) or anesthetics (e.g., ketamine) may result in depths of sedation that far exceed the intended target of moderate sedation. Careful individual and institutional interpretation of sedation levels is necessary to ensure safety and practicality in meeting the appropriate sedation guidelines. The use of potent opioid analgesics and anxiolytics should only occur in settings with adequate monitoring, personnel, and resuscitation equipment appropriate for the degree of sedation anticipated. For most wound debridement procedures, opioid analgesia, with or without the concurrent use of anxiolytic sedatives (e.g., benzodiazepines), typically produces a clinical response consistent with moderate sedation. In contrast to background pain, procedural pain is significantly more intense but shorter in duration; therefore, pharmacologic analgesic regimens for procedural pain are best comprised of moderately-to-highly potent opioids that have a short duration of action, often in combination with
enzodiazepine class anxiolytics. Intravenous access is helpful b in this setting because opioid analgesics with a rapid onset of action and short duration (e.g., fentanyl, remifentanil) may be used, as can other IV anesthetic agents such as ketamine and dexmedetomidine. In the absence of IV access, orally administered opioid analgesics are commonly used, although their relatively long durations of action (2 to 6 hours) may potentially limit postprocedure treatments such as rehabilitative or nutritional therapies. Oral ketamine,20 oral transmucosal fentanyl,21,22 and inhaled nitrous oxide23 are agents of particular use when IV access is not present because of their rapid onsets and short durations of action. Finally, when a particularly painful dressing change or one that requires extreme cooperation in a noncompliant patient (e.g., face debridement in a young child) is anticipated, the provision of brief general anesthesia24,25 or regional anesthesia in the burn unit setting may be indicated. Anticipatory anxiety is an important issue that can develop with the repeated (usually daily) performance of such wound care. When adequate analgesia is not provided for an initial, painful procedure, the effectiveness of analgesia for subsequent procedures is reduced, in large part from anticipatory anxiety and heightened arousal.26,27 Thus, efforts to provide effective procedural burn sedation should begin as early in the hospitalization as possible, preferably with the first (and often most painful) wound care procedure. In addition, nonpharmacologic analgesic techniques are of particular value in the clinical setting of procedural pain and are discussed subsequently in detail.
Breakthrough Pain Management Breakthrough pain occurs when the comfort provided by background pain therapies is exceeded and can be the result of inadequate analgesic support (e.g., undertreatment, development of opioid tolerance) or predictable changes in the burn wound itself that may produce increased pain (e.g., proliferation of epidermal skin buds during the spontaneous burn healing process). Recognition of the correct cause of the breakthrough pain is paramount so that the appropriate change in pharmacologic or nonpharmacologic management can rapidly take place.
Postoperative Pain Management Postoperative pain is an anticipated and temporary (2 to 5 days) increase in background pain that occurs after burn excision or grafting procedures and is most commonly the result of increased pain from newly created wounds at the skin graft harvesting site. Pharmacologic management of postoperative pain includes a temporary increase in background opioid analgesic support but can also include the use of continuous regional block techniques in the immediate postoperative period.28 One of the most useful nonpharmacologic analgesic techniques in this setting is information provision, so that patients also anticipate both the increase and the temporary nature of the postoperative pain.
Pharmacologic Approaches to the Management of Burn Pain Three consistent observations can be made in describing pharmacologic approaches for burn analgesia. First, for patients with injuries extensive enough to need hospitalization, potent opioid analgesics form the cornerstones of pharmacologic pain control, whereas the mild to moderate analgesia provided
Chapter 25—Burn Pain
233
by NSAIDs or acetaminophen may provide some degree of opioid-sparing effect but have limited use until the later rehabilitative or outpatient phases of treatment. Second, because burn pain is largely influenced by the parameters of care (background, procedural, and postoperative pain), pharmacologic choices for analgesia should target each of the four clinical pain settings individually. Finally, because burn pain varies somewhat unpredictably throughout hospitalization, analgesic regimens should be continuously evaluated and reassessed to avoid problems of undermedication or overmedication. Pain assessment is facilitated by the regular use of standardized, selfreport scales for adults and older children and observational scoring systems for the very young, as described elsewhere in this text. Of special note is that the reliance on nurse assessment of patient burn pain can be problematic; it is well documented that nurse and patient assessments of burn pain and analgesic effects are not always comparable.29–31 Unfortunately, nursing staff assessments frequently underestimate the need for analgesic therapy in the burn setting (a problem that is echoed in the evaluations of physicians and other health care professionals). Thus, whenever possible, patient reports of pain should be elicited and should be the basis for analgesic decisions, rather than observations of the staff.
Opioid Analgesics The most commonly used analgesics in the treatment of burn pain are opioid agonists, in part because: (1) they are potent; (2) the benefits and risks of their use are familiar to most care providers; and (3) they provide some dose-dependent degree of sedation that can be advantageous to both burn patients and staff, particularly during burn wound care procedures. The wide spectrum of opioid analgesics available for clinical use provides dosing flexibility (i.e., variable routes of administration, variable durations of action) that is ideal for the targeted treatment of burn pain. The pharmacokinetics of opioid analgesics in burn patients are not consistently different from nonburn patients,32,33 although decreased volume of distribution and clearance and increased elimination half-life have been reported for morphine.34 Similarly, pharmacodynamic potency of opioids has inconsistently been reported as increased35 and decreased34 in burn patients. The route of opioid administration is an important issue in burn patients, with the principal choice between IV or oral administration dictated by the severity of burn (critically ill patients need IV access and may have abnormal gut function) and the high risk of burn patients for development of intravascular catheter-related sepsis (hence, physician reluctance to maintain long-term IV access).36 Intramuscular opioid administration is avoided because of the need for repeated, painful injections and because of variable vascular absorption from unpredictable compartmental fluid shifts and muscle perfusion in burn patients, particularly those undergoing burn shock resuscitation immediately after the burn injury. PCA with IV opioids offers the burn patient a safe and efficient method of achieving more flexible analgesia. PCA also offers patients the nonpharmacologic benefit of control coping by allowing some degree of control over their medical care, which often is a major issue for burn patients whose waking hours are often completely scheduled with care activities ranging from wound care to physical and rehabilitation therapy, all within the foreign confines of the hospital. Studies that compare PCA opioid
234
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
use with other routes of administration in the burn population have shown positive, but limited, benefits of PCA.37 Finally, oral transmucosal administration of opioids is reported in burn patients21,22 and appears to be particularly advantageous in those patients without IV access and in children.
Nonopioid Analgesics The list of nonopioid analgesics in widespread use for the treatment of burn pain is currently limited, although not without potential benefit. Oral NSAIDs and acetaminophen, as outlined previously, are only mild analgesics that exhibit a ceiling effect in their dose-response relationship, rendering them unsuitable for the treatment of typical, severe burn pain, except to the degree that they provide a limited opioid-sparing effect. However, they are of benefit in treatment of minor burns, particularly in the outpatient setting. The opioid agonist-antagonist drugs (e.g., nalbuphine, butorphanol) produce "mixed" actions at the opiate receptor level, theoretically providing analgesia (agonist property) with lesser side effects (antagonist properties), but also exhibit ceiling effects. Although studies have shown this class of drugs to be effective in treatment of burn pain,38 experience with them is both limited and suggestive of efficacy in patients with only relatively mild burn pain. Centrally acting alpha2 agonists have been proposed as potential analgesic agents for burn pain based on their known mechanisms of action in other acute pain states. In case reports, clonidine has shown analgesic efficacy in burned children39,40; the efficacy of dexmedetomidine is limited to anecdotal reports to date.
Anxiolytics Aggressive surgical treatment and debridement of burn wounds, together with the persistent and repetitive qualities of background and procedural burn pain, make burn care an experience that creates significant anxiety in most patients of all ages. The recognition that anxiety can exacerbate acute pain has led to the common practice in US burn centers of use of anxiolytic drugs in combination with opioid analgesics, a practice that has become more widespread in the past two decades.3,12 Intuitively, this practice is particularly useful in premedicating patients for wound care because of the anticipatory anxiety experienced by these patients before and during such procedures. However, benzodiazepine therapy has also been shown to improve postoperative pain scores in nonburn41 and burn42 settings. Specific to burns, patients who appear most likely to benefit from this therapy are not necessarily those with high trait (premorbid) anxiety but rather those with either high state (at the time of the procedure) anxiety or high baseline pain scores.42
Anesthetics Given the brief, but intense pain associated with many burn wound procedures, the provision of a limited duration general anesthetic may at first glance seem a reasonable analgesic approach. However, the repeated (often daily) need for such procedures poses economic and logistic obstacles that makes general anesthesia not feasible. Nonetheless, the provision of deep sedation with carefully titrated inhaled or IV anesthetic agents, brief general anesthetics, and regional analgesic techniques have a large role in procedural burn pain settings. Inhaled nitrous oxide is an analgesic agent safe for administration by nonanesthesia personnel and provides safe and
effective analgesia without loss of consciousness for moderately painful procedures in other health care settings. It is also used for the treatment of burn pain,23,43 typically as a 50% mixture in 50% oxygen and self administered by an awake, cooperative, spontaneously breathing patient via a mouthpiece or mask. Although the level of sedation achieved with such inhalation is typically light (minimal or moderate by ASA definitions), the analgesic effect of the drug can be very good. Furthermore, the technique allows patients some degree of control in their medical care (i.e., deciding when to breathe and when not to breathe the agent during the procedure) and can consequently benefit patients psychologically. On the negative side, nitrous oxide has also been implicated in a small but measurable incidence of toxicity issues (e.g., spontaneous abortion, bone marrow suppression) to patients or staff exposed for prolonged periods,44,45 although not in the setting of burn pain treatment. Certain aggressive wound care procedures are, in terms of invasiveness, on a scale well below that of surgical burn care (and associated general anesthesia) yet are nonetheless difficult to perform on a conscious patient (e.g., the removal of hundreds of skin staples from recently grafted wounds, meticulous wound care of recently grafted and often tenuous skin on the face or neck, or wound care procedures in variably cooperative children). For such cases, deep sedation or general anesthesia with intravenous agents may be indicated, in spite of the logistic or economic challenges they present. Historically, IV or intramuscular ketamine has been used for these procedures46,47; more recently, oral ketamine use is described for pediatric burn patients.20 However, ketamine use is limited by the potential risk of associated emergence delirium reactions (5% to 30% incidence rate), particularly in the elderly. Alternatively, propofol has been reported safe and effective when administered by appropriately trained physicians (anesthesiologists) in the burn setting48 and has even been suggested to be a potential drug for PCA delivery for less aggressive wound care procedures.49 Propofol is particularly advantageous because it can be titrated to effect in terms of both level of consciousness and duration of action with continuous IV infusion techniques and carries the benefit of a rapid awakening with a minimal risk of nausea. The extension of full anesthetic care capabilities outside of the operating room and into the burn ward has been implemented in high-volume, specialized burn centers.24,25 This has been facilitated by the recent introduction into clinical anesthetic practice of a variety of drugs with a rapid onset and short duration of action, a more rapid awakening and recovery, and fewer associated side effects— ideal qualities for agents to be used for procedural burn wound care—that include IV propofol, IV remifentanil, and inhaled sevoflurane. The provision of brief, dense analgesia or anesthesia in a comprehensively monitored setting by individuals specifically trained to provide the service appears safe and efficient, both in terms of allowing wound care to proceed rapidly under ideal conditions for patient and nursing staff and in terms of cost-effective use of the operating room only for true surgical burn care procedures. Regional anesthetic blockades in various forms may also be considered for inpatient burn pain management. Neuraxial administration of local anesthetics (or opioid analgesics) via an epidural catheter seem to be of benefit in patients with lower extremity burns, resulting in both background and procedural analgesia and autonomic sympathectomy and peripheral vasodilation (of theoretical benefit to wound healing). However, such use has only been reported anecdotally.50 A major drawback of this technique is that the accompanying
indwelling catheter can become densely colonized with infectious organisms at the wound site, thus increasing the risk for the serious complication of epidural abscess formation51 Targeted non-neuraxial regional blockade, in contrast, is relatively easy to perform, carries minimal risks, and has been reported primarily for lower extremity analgesia after skin graft harvesting (fascia iliaca block). This technique can be used both for immediate postoperative analgesia (one-shot injection52) and for prolonged postoperative analgesia (continuous local anesthetic infusion via indwelling catheter28). Local anesthetics are of obvious use in regional blockade for wound care procedures but may also be considered for burn pain analgesia in the form of a topical gel. The use of topical local anesthetics on burn wounds is controversial. The commonly available prilocaine (2.5%)–lidocaine (2.5%) cream (eutetic mixture of local anesthestics [EMLA]), when administered at a total dose of 2g, had no effect in a study on burn pain in volunteers.53 Topical 5% lidocaine applied at 1 mg/ cm2 offered analgesic benefit in one study without associated side effects54; however, enthusiasm for its use is significantly tempered by reports of local anesthetic-induced seizures from enhanced systemic absorption at open wound sites.55
Nonpharmacologic Approaches to the Management of Burn Pain Pharmacologic and nonpharmacologic treatments should be complementary in treatment of pain and anxiety in the burn patient. Considerable empirical evidence for the efficacy of nonpharmacologic treatments has been reported with burn pain, particularly when used as an adjunct to opioid analgesics. Beginning nonpharmacologic treatments as early as possible in the patient's hospital course is important to prevent anticipatory anxiety and the subsequent anxiety-pain cycle. Before the various nonpharmacologic techniques are explained in detail, the psychologic factors that come into play during burn care that can exacerbate pain should be understood. Perhaps the most important example of such a process is the potential loss of control that burn patients experience and its relation to coping.
Coping with Decreased Control The experience of sustaining a burn injury, and enduring the many subsequent treatments, taxes a person's coping resources by reducing the sense of control. Most patients describe feelings of having less control in the hospital setting because of a number of factors, including high pain levels, the unfamiliar environment, a forced dependency on caregivers, the lack of input into daily schedules and routines, and the uncertainty about the future (e.g., appearance, wound status, work, or even survival). Such uncertainty about the nature and outcome of treatment often leads to feelings of helplessness in both adults and children. Patients and staff need effective strategies to maximize a patient's sense of control.27 For selection of appropriate strategies, one should understand the types of coping mechanisms that patients might be actively using and also ones of which they are not aware and may be of potential use.27 The two-process model of control is applicable in this respect to both adults and children.56 This model distinguishes between primary, secondary, and relinquished control strategies. Primary control is when persons manipulate the situation or environment to fit their needs; secondary control is when persons modify themselves to better fit the situation. Relinquished control describes the coping style of
Chapter 25—Burn Pain
235
“giving up” and often involves a process of emoting or withdrawal and depression. Research has shown that flexible coping, using both primary and secondary control strategies, is most adaptive.57 Selection of a coping style that suits the particular situation works better than strict adherence to one approach. Patients who assertively request more medication in response to pain are demonstrating adaptive primary coping, and those who mediate or pray while having a particularly bad day are likely illustrating secondary coping strategies; both can be useful under some circumstances. On the other hand, adults and children who rely too much on a relinquished control style show greater psychologic distress.58,59 This type of coping often leads to learned helplessness and is characterized by negative catastrophic thoughts, more pain behaviors, higher pain levels, and slower physical recovery.27,60 The nonpharmacologic pain management techniques listed in the remainder of this chapter ideally help patients regain some control over their environment through primary or secondary control coping techniques. A number of nonpharmacologic treatments are available for use with burn pain. In choosing the most effective approach, the team should be guided by the manner in which patients have typically responded to stressful medical procedures. Such responses lie on a continuum that ranges from giving up control to the health care professional and desiring little information to seeking out as much information as possible and actively participating in care. Those patients who wish to give up control to the health care professional have a tendency toward cognitive avoidance and likely use various types of distraction techniques to avoid the painful stimuli. These patients are said to have more of an avoidant coping style. Those who seek out information about the procedure and like to participate as much as they can often find distraction techniques distressing; for them, trying to ignore a procedure may serve to relinquish too much control. Such patients are thought to have more of an approach coping style.61 One should note that both coping styles can be adaptive and it is best for the care team to support an individual's coping style rather than try to change the natural response. Also important to note is that patients may change their coping style depending on the procedure. For example, patients may find it is easier to use distraction techniques for short procedures such as receiving injections, whereas they are more comfortable attending to details of their long wound care sessions and participating when possible. Patients may also change their coping style as they become more familiar and comfortable with the environment. The approach avoidance coping continuum and the interventions that can be considered along it are illustrated in Table 25.2. Techniques (e.g., imagery or hypnosis) may fall into various places on the continuum, and depending on the outcome goals and script, the continuum can be a useful heuristic to guide clinicians in choosing an appropriate technique for a specific patient. The remainder of this section describes the nature of various nonpharmacologic interventions for burn pain management and how they fall on the continuum.
Avoidance DISTRACTION The types of distraction techniques available to reduce burn pain are limited only by the creativity of patients and health care professionals. Common distraction techniques used with children include bubble blowing, singing songs, reading a story, and counting. Generating strategies for adults may
236
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
Table 25-2 Control Coping Continuum and Nonpharmacologic Techniques Avoidance Coping style | | | | | | | | | | | Approach Coping Style
1. Avoidance Distraction Imagery Hypnotic analgesia Virtual reality 2. Relaxation Deep breathing Progressive relaxation 3. Operant Techniques Regular medication schedule Quota system Positive reinforcement 4. Information Medication effects Procedures Timelines 5. Cognitive Restructuring Thought stopping Cognitive reappraisal 6. Participation Setting schedules Wound care
require a bit more creativity, but adults can do a number of things, including engaging in enjoyable conversation during the procedure, listening to music, playing a video game, or immersing themselves in interactive virtual reality (see subsequent discussion) during the procedure. IMAGERY Patients who use imagery simply create or recreate an image in their mind, presumably one that they find pleasant and engaging. Types of imagery can be infinite and depend on the desired goals. For example, many people use healing imagery to facilitate recovery from overcoming disease or injury. In the case of burn injuries, they might imagine processes such as increased blood flow to the injured area in an effort to carry away damaged tissue and rebuild new tissue or decreased inflammation in the injured area. Although healing imagery can be an effective means of helping the burn patient feel more in control of the situation, it forces a person to focus on their injury and is consequently not a distraction technique when used in this way. In contrast, relaxation imagery tends to work best for pain control and is a better example of use of imagery for distraction. Before a painful procedure, the patient elicits a “safe” or “favorite” place to go. This can be a place where they have been before (e.g., a favorite vacation spot) or simply a place that they imagine to be relaxing and safe. Some common examples include the beach, a spot for camping or hiking or fishing, a grandmother's kitchen, or a childhood bedroom. The clinician then collects as many details as possible about what this place looks like (the colors, the sounds, the smells, objects in this place), and the patient practices the imagery; before the procedure, patients are encouraged to relax through deep breathing, closing their eyes, and imagining this favorite place. The clinician simply cues the patient with the details that they have provided before beginning relaxation. Next, the patient is encouraged to imagine this place during subsequent wound care, and if necessary, the clinician is present during the wound care to facilitate “taking them” to this place. Children often enjoy more active forms of imagery that relate to fantasy, such as taking a magic
carpet ride or jumping on a broomstick with Harry Potter and flying through the woods at Hogwarts.62 Numerous imagery scripts have been published and can be used when a person is unable to think of a safe or favorite place.63 These scripts often entail a person “flying” or “floating on a cloud” through beautiful places. An important note is that a patient should be asked about any fears such as heights, flying, or water so that use of these images does not actually create more anxiety. Imagery is usually most effective when all of the senses are incorporated to make it as realistic and absorbing as possible. Most people need practice to be able to create vivid images, and some people are unable to visualize much at all, particularly when they are in significant pain and are too distracted. Virtual reality may be a better option for these patients (see subsequent discussion). HYPNOTIC ANALGESIA Although hypnosis involves much more than just avoidance or distraction, the end result is often similar in that this technique takes a person's focus off of the painful procedure. Hypnosis is an altered state of consciousness characterized by an increased receptivity to suggestion, ability to alter perceptions and sensations, and an increased capacity for dissociation.64 Several features make it a unique method of pain control that differs markedly from imagery or relaxation. In fact, hypnosis may or may not lead to relaxation depending on the nature of the suggestions. In turn, it is not necessary for a patient to be relaxed or even in a deep hypnotic state for suggestions to be useful.65 The belief is that the dramatic shift in consciousness that occurs with hypnosis is the cornerstone of an individual's ability to change awareness of pain.66 Hypnosis involves several stages, including building clinician-patient rapport, enhancing relaxation through deep breathing, suggestions for deepening the hypnotic state and narrowing attention, providing posthypnotic suggestions, and alerting.67 A full hypnotic induction for burn care is published in Patterson's64 Clinical Hypnosis for Pain, as are inductions for the patient in the intensive care unit (ICU) or a crisis situation. In addition, the rapid induction analgesia format was described by Patterson67 and originally published by Barber.68 Hypnosis should only be used by trained clinicians who can assess the risks and benefits of this powerful technique. As an example, patients with a history of sexual abuse may have a tendency to dissociate too easily and are not served by hypnosis in some instances. Hypnotic analgesia has increased in popularity with recent reports that it can reduce medical costs64,69 or possibly even facilitate wound healing.70,71 Although the mechanism for how hypnosis works is not fully understood, hypnotic analgesia has shown demonstrable brain function changes in neuroimaging studies.72 A metaanalysis by Montgomery, DuHamel, and Redd73 reported analgesic effects in most studies that used hypnosis for clinical and experimental pain. A more recent review by Patterson and Jensen74 indicated that anecdotal reports of hypnotic pain relief have been published for decades on virtually every type of pain imaginable. They found 17 randomized controlled studies on the use of hypnosis for acute pain and concluded that the evidence for hypnotic analgesia was strong and seems to be related to the trait of hypnotizability. Several studies have shown the efficacy of hypnosis for patients with burn injuries.75–77 Patterson, Adcock, and Bombardier78 have
Chapter 25—Burn Pain
237
Fig. 25.4 Virtual reality environment “SnowWorld.“
proposed several reasons why patients with burn injuries may make good candidates for hypnotic analgesia. First, the intense nature of burn pain motivates patients to engage in this technique that they might normally disregard. This is supported by research findings that show that patients with higher baseline pain levels have a greater drop in pain after hypnosis than patients with lower baseline pain levels.75,79 Second, the behavioral regression that often occurs after a traumatic injury makes patients more willing to be taken care of by others. Third, patients with burn injuries often experience a dissociative response as a means of coping that may moderate hypnotizability. Finally, although burn pain associated with procedures is the most intense, it is also the most amenable to hypnotic analgesia; because these procedures are often planned in advance, patients can be adequately prepared for these aversive events with hypnosis. Despite occasional dramatic responses to hypnosis in burn patients, not every patient benefits from this technique, and resources for a trained clinician may not be available on every burn unit. Research into ways of making hypnosis more available to patients and more effective for those with low hypnotizability scores would be valuable.80 These goals could be accomplished by eliminating the need for a live hypnotist with either audiotaped or computer-assisted hypnosis and by making hypnosis less effortful for those with low hypnotizability scores or whose cognitive effort is compromised from pain. Patterson64 discusses every element of this and the following section (virtual reality) in much more detail in a recent book. VIRTUAL REALITY Immersive virtual reality (VR) is a technology that isolates patients from the outside world, including any threatening stimuli associated with health care. Immersive VR uses a helmet or goggles that block the user's view of the real world and gives the patient the illusion of going into the threedimensional computer-generated environment, a condition known as presence.64 This quality makes immersive VR particularly effective in capturing participants' attention.81 In the burn pain setting, a virtual environment called “SnowWorld” is used (Fig. 25.4)82 in which patients float through an icy canyon and are able to direct snowballs at virtual snowmen and igloos as they appear. The image of snow was specifically
Fig. 25.5 Clinical use of virtual reality distraction during burn wound care.
c hosen because its connotation of cooling is in direct contrast to the sensations often associated with burn pain. VR is effective in theory because attention involves the limited selection of relevant information from a variety of inputs or tasks, and each human has a finite amount of it available.83,84 The strength of the illusion, or presence, is thought to reflect the amount of attention drawn into the virtual world.85 Because it is designed to be a highly attention-grabbing experience, VR is thereby thought to reduce the amount of conscious attention available to process pain (Fig. 25.5). Less attention to pain can reduce perceived pain intensity and unpleasantness and can also reduce the amount of time patients spend thinking about pain. VR has been shown to be effective in reducing pain in a number of clinical studies that used it for pain distraction.82,86–88 Virtual reality technology can also be used to administer hypnotic analgesia and is particularly effective with patients who have difficulty imagining a scene.64,81
Relaxation DEEP BREATHING Deep breathing, or diaphragmatic breathing, is one of the least time-consuming techniques to use and is easiest for adults and children to learn. When a person becomes anxious or experiences pain, breathing can become shallow and irregular because of the increased muscle tension in the chest wall. Such shallow breathing, known as thoracic breathing,89 leads to an increase in muscle tension and subsequent heightened pain. Teaching patients to become aware of this cycle, and teaching deep breathing techniques that allow them to break it, usually leads to a relaxation response that can alleviate some pain. Bubble blowing and blowing on a pinwheel are helpful tools to use with children to encourage deep breathing. Adults can be taught to place a hand on their stomach and take a breath deep enough to passes through their chest and fills their stomach (shallow breathing is more in the chest and does not cause
238
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
as much hand movement on the stomach). Their hand should rise and fall with the stomach. The exhalation is the most important part of the deep breath and should not be rushed. Diaphragmatic breathing is central to all forms of relaxation and is simple and time efficient.89 PROGRESSIVE MUSCLE RELAXATION Patients tend to use muscles inefficiently89 when they experience stress such as pain, which results in muscle bracing that can lead to an increase in pain. Progressive muscle relaxation is a technique developed by a physician, Edmund Jacobson, after he observed increased muscle tension in hospitalized patients and discovered that those with more tension took longer to recuperate and had poorer outcomes.90 He taught patients to systematically focus on a muscle group, tense and relax it, and then progress to a different group. This progression usually starts with the distal muscle groups and moves to the proximal ones until total body relaxation is achieved. Most patients are able to learn this technique with practice, facilitated by scripts or audiotapes. If a person is unable to actively tense a muscle group because of pain or injury, he or she can still imagine each muscle becoming progressively “warm, heaving and relaxed,” a process known as autogenic training.64 Patients repeat each statement to themselves as they hear in on a tape (e.g., “My right hand is heavy, my right hand is relaxed, my right hand is becoming warm…”).
Operant Techniques Operant techniques rely on the principles of reinforcement learning and are based on the assumption that patients repeat behaviors that have positive consequences and avoid those that lead to punishment.64 These principles can be applied in various ways to alleviate burn pain. REGULAR MEDICATION SCHEDULING Many inpatient acute care settings administer pain medication on a pro re nata (prn) or “as needed” basis (i.e., waiting for patients to report they are in pain before providing analgesic medications). From a behavioral perspective, waiting to medicate patients until they report pain reinforces them for pain behaviors; this can later become problematic.10 The reinforcing properties of this process come from the euphorigenic properties of short-acting opioid analgesics and the attention received from caregivers and family for displaying pain behaviors. In contrast, providing opioid analgesics on a regular schedule minimizes the potential for these reinforcing properties of drugs and attention to worsen the pain problem. The superiority of regularly scheduled medications over prn dosing has been shown with nonburn pain91 and has also been confirmed in background pain management for burninjured children.92 Simply put, treating pain before it occurs with regularly scheduled medication is a superior approach based on psychologic, and neurophysiologic and pharmacologic, principles. Although research has shown that there is little chance of creating a chronic drug problem when opioid analgesics are given for acute pain in patients with no substance abuse histories, there is a risk of exacerbating a preexisting substance abuse problem.93 Therefore, adherence to a regular opioid schedule is even more important for patients with substance abuse histories. Patients with drug histories often have
frequent pain reports or drug-seeking behaviors and typically have lower tolerance for pain. They may also approach multiple caregivers for medications that create staff splitting and caregiver resentment toward the patient. Adhering to a regular medication schedule and having only one caregiver responsible for discussing or changing medications and doses can help alleviate some of these problems. As noted previously, patients who present with premorbid opioid abuse issues, or who are on methadone maintenance programs, still need to receive adequate levels of opioid analgesics to manage the acute burn pain. The consequences of patients self administering street narcotics for pain control can be extremely disruptive, if not fatal for the patient. QUOTA SYSTEM Patients can become easily overwhelmed through the multiple invasive therapies involved in burn care. They can also lose a sense of control and develop a type of learned helplessness. The quota system is one of the more effective techniques to address this. The quota system is an operant technique often used by burn providers to promote a sense of mastery among patients undergoing painful wound care procedures and difficult physical therapies.94 Caregivers are encouraged to pace their procedural demands in a manner that is consistent with what is within the individual's level of tolerance by taking baseline measurements for each task that needs to be performed and gradually (10% per day) increasing the demands of each task. Rest is used as the reinforcement for successfully reaching a quota or, in other words, meeting a predetermined level of exercise (task). Goals for each task are determined based on what was done the previous day, and patients are expected to work until the goal is accomplished, rather than work until they feel pain or fatigue. This technique puts more control in the hands of the patient and consequently offsets the syndrome of learned helplessness discussed previously. It also avoids reinforcement of pain behaviors. The quota system is based on the notion that although physical therapies after a burn injury are painful, this pain itself is not damaging and does not negatively impact outcome. As discussed subsequently, patients are taught the difference between hurt and harm. POSITIVE REINFORCEMENT Positive reinforcement is another operant principle that is often successful with patients with burn injuries, particularly children. There is no intrinsically rewarding aspect of sustaining a burn injury or going through the care necessary for recovery. In fact, children often see the treatment for a burn injury as a punishment. Explaining to children that they are not undergoing painful procedures because they have done anything wrong, particularly if they see themselves as responsible for their injury, is often important. Children need to be rewarded for participation in the recovery process and for displaying appropriate behavior. For example, a common practice on a burn unit is use of a sticker board and prize box in each child's room. Behavioral expectations are established in advance and define what responsibilities the child has for that day, such as wound care, physical and occupational therapy, eating meals, etc. Children receive a reward (sticker) for each responsibility that they accomplish. Once they have a set amount of stickers, they are able to pick a prize from the prize box. This practice
is known in the behavioral literature as establishing a token economy. Other creative means of positive reinforcement can also be effective, such as reading stories, watching movies or television, or offering adult attention. When children are frequently reinforced for good behavior or for completing a therapeutic goal, it lessens the need for punishment for bad behavior and makes the hospital environment more tolerable. In essence, the positive consequence after the adverse care on the burn unit is designed to be more prominent for the child; when reinforcement is not working, it is often because the magnitude of the reward is not sufficient. With use of positive reinforcement, caregivers should also be careful not to reward (i.e., ignore) inappropriate behaviors such as tantrums or escape or avoidance behavior. For example, children often have a tantrum during wound care to try and get the nurse to cease what he or she is doing. If the nurse complies and stops wound care, the child has just been reinforced for the tantrum and learns to scream and cry to avoid a critical component of care. Once reinforced, this tactic then is likely to be tried in situations outside of wound care and in the next day's wound care. In contrast, once a behavioral expectation has been established (i.e., “we need to do our wound care now”), staff and parents need to commit to following through on the task, regardless of the child's response. Some of these responses can be avoided by allowing children to determine when their wound care will be, or to assist in the wound care, and by giving them positive reinforcement throughout wound care. However, although minimizing attention to acting out in response to pain is often important, it is also important that reinforcement contingencies for children not be based on bravery or stoic pain. It is a subtle form of punishment to withhold rewards in wound care except when the child reacts calmly. Rather, acting out is ignored and the child is rewarded for successfully completing a therapy or wound care session. Ignoring pain behavior during wound care should only be considered after the burn team has done everything possible to minimize pain, in terms of both pharmacology and decreasing adversity of wound care (e.g., less caustic cleaning agents, longer water soaks).
Information Patients differ in how much information they wish to receive about medical care. Most patients, however, find that the unknown is anxiety provoking and that receiving general information is helpful in reducing some anxiety. It is important to ask a patient how much detail they desire to know and follow their individual proclivities in providing information. Patients may benefit from information in several elements of burn care. First, side effects from medication can be worrisome, particularly for those who have no experience with potent opioid analgesics. Letting patients know that weird dreams, itching, and constipation are normal effects of pain medications and that long-term opioid dependency or addiction is unlikely can help alleviate these concerns. Second, some patients may not want to know details of procedures or tests but nevertheless should be warned that they will occur and told why and when they will occur. This information then allows patients to garner their coping skills and appropriately prepare for the situation. Finally, patients often report that not knowing the medical plan or timeline for upcoming surgeries, treatments, etc, is one of the biggest stressors in burn care. The nature of wound healing is such that the medical team
Chapter 25—Burn Pain
239
cannot predict whether the burn will need surgery or will heal on its own. Once this determination is made, however, it is important to sit down with patients and lay out a timeline for upcoming surgeries, dressing removals, therapies, rehabilitation, estimated discharge dates, and long-term care plans.
Cognitive Restructuring Patients' thoughts about burn pain can be can be modified to reduce their perceptions of pain. Such cognitive restructuring is frequently used as a coping technique for patients with chronic pain.95,96 Studies have identified the maladaptive thought pattern of catastrophizing as being particularly influential in how patients perceive pain. Teaching patients to recognize when they are engaging in catastrophic thoughts and to learn how to change that style will likely lead to a positive change in how they experience pain. A few reports in the literature have used this technique for various type of acute pain, including that from dental work and surgical procedures.97 A handful of studies have investigated this approach with burn pain.27,98 These techniques are likely to only be successful with patients who want to use more of an approach coping style because it forces them to be aware and tend to their thoughts of pain. THOUGHT STOPPING The first step in cognitive restructuring is to identify and stop negative catastrophizing thoughts. Thoughts such as “this is really going to hurt” and “I can't handle this pain” only lead to an increase in anxiety and a subsequent increase in pain. Patients can learn to recognize such negative thoughts and stop them, perhaps by picturing a stop sign or red light in their mind. They can also distract themselves by turning their attention to another topic. Children as young as 7 years of age have been taught to use this technique successfully.27,99 REAPPRAISAL Ideally, patients should transform their catastrophic thoughts into positive, or at least neutral, statements. This is known as reappraisal, or reframing. For example, a patient may change the thoughts in the previous example to “I have been through this wound care procedure before, and it did not hurt as much as I thought it would” or “however much this hurts, it will go away.” Patients may also benefit from being taught the difference between hurt and harm when interpreting pain sensations.100 Specifically, an increase in pain is often a good sign with respect to burn wound healing. As discussed previously in the chapter, deep (third-degree) burns often destroy nerve endings and limit the capacity for nociception. In deep burns that begin to heal, or in more shallow burns, skin buds develop that are highly innervated and sensitive to pain and temperature.10 An explanation of this healing process to patients can help them to understand the nature of their pain and to reframe negative thoughts into reassuring, positive ones. The treatment for burn wounds, including daily removal of bandages and the aggressive washing of the open wounds, is counterintuitive to what most adults and children instinctively believe should be the appropriate treatment for open wounds. Most of us are taught to believe that we do not touch open wounds, and we certainly should not rub them aggressively. An explanation that this type of treatment, and the subsequent pain, is necessary to heal the wound can help patients to reframe any negative beliefs they may have toward wound
240
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
care. Given the counterintuitive nature of the information, patients often must be given this information repeatedly; they have to have trust in the staff member (particularly children), and combining the information with relaxation or hypnosis is often useful.
Participation Allowing patients who have more of an approach coping style to participate in their own burn care and recovery is one of the simplest and most effective ways to increase their sense of control and reduce anxiety. We often use the technique of forced choice for children to create more of a sense of control over their environment without overwhelming them with choices. When a child needs to accomplish an unpleasant task, parents and caregivers can often create a situation where the child is given two choices in how to proceed with the task. For example, children who have difficulty in wound care may be given the choice of having the nurse wash their arm or of washing the arm themselves. Or if children need to get out of bed to walk, they can be given the choice of either doing it before lunch or after lunch. They must choose one of the two options, and if they cannot decide within a certain time frame, they are told that the nurse or parent will decide for them. This method is likely to fail if more than two choices are given or if a child is presented with an option that caregivers or parents have no intention of allowing. Although patient participation may not be feasible in all aspects of burn care, several areas lend themselves to giving patients more control (e.g., uncomplicated wound care, physical therapy, nutritional intake). SETTING SCHEDULES Adults and children may benefit from having input into when certain tasks are done, such as wound care or physical therapy. Although open-ended choices in this matter are not feasible, a choice of two or three options may be reasonable. For example, patients can be given the choice of having wound care before lunch or after lunch, or physical therapy immediately after wound care in the morning or in the later afternoon. If a scheduling choice is not possible, sufficient notice of when the event will occur can help patients to adequately prepare themselves. WOUND CARE Patients who use more of an approach coping style can participate in their own wound care in a variety of different ways. One simple way is to allow the patient to choose if and what type of music is played during wound care. Patients are often encouraged to create a repeatable routine for each wound care procedure, in which they mentally prepare and do certain things the same way every day in an effort to help reduce anxiety. Because patients have different nurses from day to day, the patient must let the nurses know what works best and the details of the routine. Patients should be encouraged to take responsibility for communicating these plans to their nurse or therapist. Patients can also regulate the pace of wound care by asking for periodic breaks or by telling a nurse to wash slower or faster. One useful approach is to give children a set number of “timeout cards” (around five) that allow them a short (30-second) break during wound care. They can use them at any time until they are gone. Often, patients progress to the point of wanting to assist the nurses in their own wound care, particularly after they have
been in the hospital for some time. Easy ways to assist are to have them unwrap their bandages or wash areas that are easily reachable or particularly painful. Finally, patients preparing for hospital discharge may even want to perform their entire wound care independently if possible.
Side Effects and Complications Analgesic Management Based on Valid Pain Assessment As with any type of pain management paradigm, therapeutic burn pain decisions are related to what analgesic techniques to use, what drugs to use, and what drug doses to use, all of which hinge dramatically on the valid assessment of the patient's pain. Pain assessment is no less challenging in burn patients and may be further complicated by the multiple premorbid or comorbid psychologic issues that frequently accompany the burn injury.11 As already noted, patient reports of pain are preferred because they differ from (and are typically greater than) those reported by burn caregivers.29–31 However, patient reports are not always possible, as in cases of severely injured, noncommunicative (intubated and mechanically ventilated) adults or young children who cannot provide meaningful pain reports. Pain assessment in burns has been extensively reviewed, with details on appropriate tools for various clinical settings described elsewhere in adults31 and children.18 Although pain assessment in the clinical and research setting has traditionally relied on patient reports (0 to 10 verbal scales, 0 to 10 visual analog scales [VAS], or 0 to 10 graphic rating scales [GRS]), increasing interest is found in assessment of patient satisfaction with pain control as an alternative measure of analgesic success. For example, asking a patient for a “treatment or analgesic goal” with the same measurement scale as for pain intensity can be useful. This concept has been recommended for clinical use by The Joint Commission6 but is not in widespread use. However, in limited studies in the burn population,101 those patients who experience the least amount of pain (by standard pain ratings) appear to have greater analgesic satisfaction than do those who report pain ratings that most closely match their stated analgesic treatment goals. Thus, the ideal choice and interpretation of pain assessment tools in burn pain settings is yet to be defined.
Complications From Excessive Analgesic Medications The wide spectrum of untoward side effects associated with potent benzodiazepines, opioid analgesics, and anesthetics is well known and ranges from the relatively benign (e.g., transient nausea) to life threatening (e.g., respiratory depression). The prevention and treatment of these various analgesic side effects is detailed elsewhere in this text. However, general recommendations should include that all analgesia and sedation procedures be carried out under the guidelines published by the American Society of Anesthesiologists19 and supported by The Joint Commission.6 These guidelines include requirements for appropriate physiologic and consciousness monitoring and for appropriate training of all caregivers who administer pharmacologic sedation. Specifically, because the desired level of sedation (typically a moderate level) cannot be guaranteed in a given patient with a given pharmacologic regimen, providers must be trained and skilled at managing
the next greater depth of sedation (deep sedation), including airway, respiratory, and cardiovascular support, in the event this level of sedation unexpectedly occurs.
Overlooking Anxiety One of the biggest mistakes made in burn pain management is not recognizing anxiety and treating it accordingly. As mentioned previously, anxiety exacerbates, and often precedes, pain. Poorly managed pain, particularly early in the hospitalization, leads to anticipatory anxiety for any future procedures. An effective pain management program needs to target anxiety and pain, with use of both pharmacologic and nonpharmacologic techniques. For assessment of anxiety, one can ask patients to rate both their pain and their anxiety on separate 0 to 10 scales. In both adults and children who are unable to distinguish between pain and anxiety, staff should watch for behavioral signs, such as the display of pain behaviors before a procedure even begins. Taal and Faber102,103 have published the Burn Specific Anxiety Scale, which is a measure validated with burn patients that focuses on anxiety during burn care procedures.
Staff Changeover Patients have many caregivers during their hospitalization. Inconsistencies in the care that patients receive from various staff members can frustrate them and make pain and anxiety harder to manage. The familiarity and training that staff has had in nonpharmacologic pain management techniques also vary significantly. Inpatient units often have a shortage of nurses, and nursing time may be stretched between multiple patients. Thus, even when health care providers are well trained in nonpharmacologic techniques, they may not have adequate time to apply them effectively. Most burn centers recognize the importance of having psychologists and other specialists trained in these techniques as part of the burn team. These individuals may be available to assist in applying the techniques in many cases; however, it is not reasonable to assume that they will be available to meet every patient's daily needs. Therefore, they should continue to train nurses and patients in these techniques to the extent possible. Differences in how nurses perform wound care and lack of training in nonpharmacologic techniques can cause patients to lose confidence in the medical team and make pain even harder to manage. Thus, empowering patients to direct their own care by sharing with caregivers their care needs and preferences is even more necessary.
Mismatch of Techniques and Coping Style As mentioned previously, matching various nonpharmacologic techniques to patient coping style is crucial. For example, one can see the problem in using a distraction technique with patients who have a high need for control and desire to participate in their wound care. Further, providing a patient who is closer to the avoidance end of the control continuum with too much information on a medical procedure may actually increase anxiety. Again, periodic assessment of a person's preference is important because patients often shift where they are on the continuum of control during hospitalization.
Inadequate Planning “Surprises” Even with the most vigilant preparation, unplanned procedures, quick changes in schedules, and other “surprises” are bound to occur. These unplanned procedures can cause
Chapter 25—Burn Pain
241
significant anxiety for patients and may increase pain levels. Teaching patients distress tolerance and to “expect the unexpected” and providing them with quick strategies to use when the unexpected occurs can go a long way toward decreasing anxiety and pain. Patients may even get to the point of being able to anticipate the chaos often associated with acute inpatient hospitalization. Although seemingly counterintuitive to the clinician, this is an example of the patient adopting a secondary coping mechanism as described previously.
Premorbid Psychologic Problems Patients with preexisting problems, including anxiety disorders, substance abuse, and chronic pain, have even more difficulty with the management of acute pain and anxiety. As noted previously, preinjury psychologic problems are common in burn patients and are much higher than in the general population.11 A burn injury and its subsequent treatment can often exacerbate depression in patients with this premorbid diagnosis. Treatment for depression should not only continue on the burn unit but should be pursued even more aggressively. Patients with DSM-IV revised (American Psychiatric Association) Axis II personality disorders often cause great difficulty for the staff. Caregivers need to be educated about such personality disorder and understand that a person with a burn injury will not be “cured” of such while on the burn unit. Psychologists or psychiatrists should be consulted to devise appropriate behavior plans and to train staff in managing such patients. Often patients with substance abuse problems have a strong reliance on the pharmacologic management of pain. Depending on the drug of choice, they may have a lower pain tolerance or display more pain behaviors. Specialists, such as anesthesiologists, may need to be consulted. Patients with substance abuse problems should still be offered nonpharmacologic approaches and should be encouraged to use them. Sufficient medication for acute pain through a regular medication schedule (versus prn) is particularly important for these patients. In the instance of premorbid anxiety and chronic pain problems, patients should be encouraged to use whatever coping techniques they have used in the past to manage these problems. Burn hospitalization and care may be an ideal time for such patients to learn new such techniques.
Wound Care Environment Nurses can help make wound care procedures more relaxing by having the dressings and necessary supplies prepared in advance and laid out before the patient arrives in the tank room, by keeping the room warm, by having relaxing music playing low in the background, by dimming bright lights, by reducing clutter in the tank room, by keeping their voices low, and by speaking in relaxed tones. When a patient comes into a tank room that is not prepared and is cold and uninviting and encounters nurses who are rushed, an atmosphere of tension and anxiety for both the nurses and the patient is created. When a patient expresses significant anxiety and pain, the nurses must remain calm because patients often pick up on the anxiety or discomfort of the staff. Also, any painful procedure, including wound care, should be done in a location outside of the patient's room, particularly with children. A pediatric patient must feel that his or her room is a relaxing
242
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
place that can be viewed as a safe retreat after painful procedures or therapies. Keeping the patient's room as a safe area also leads to more restful sleep.
Conclusion The control of burn pain continues to be a challenge that demands creativity and continued staff training on pain assessment, traditional pharmacologic analgesic approaches, and adjunctive nonpharmacologic techniques. Pharmacologic analgesics need to be administered by appropriately trained and experienced staff, under appropriate monitoring conditions. Likewise, assessment of a patient's coping style and matching of nonpharmacologic techniques accordingly are crucial. Assessment is necessarily ongoing because patient coping styles and preferences may change throughout the hospitalization. Future directions in burn pain management include improvements in the diagnostic and prognostic assessment of burn wounds and prediction of which analgesic techniques are best suited for individual patients. With regard to burn wound diagnosis, improved early and accurate definition of burns that will heal only with surgical excision and grafting helps minimize the number of patients who currently undergo days to weeks of hopeful watching of the burn wound, waiting for the wound to declare itself as self healing or not. There is a subpopulation of these patients who
undergo days and weeks of painful wound care and significant background pain, only to discover that the burn could have been treated initially with excision and grafting, thus avoiding the prolonged period burn pain. With regard to predicting the most effective analgesic techniques in an individual burn patient, advances in both pharmacologic and nonpharmacologic techniques are anticipated. Pharmacologic analgesia potential for specific drugs may be more accurately predicted as genetic screening for opioid metabolic enzymes comes into common clinical practice, thus enabling caregivers to choose the most appropriate drug and dose for a given metabolic genotype.104 Similarly, tools that predict the success of nonpharmacologic analgesic interventions will undoubtedly be developed. One such example is the assessment of hypnotizability (Stanford Hypnotic Clinical Scale105) that predicts the potential success of hypnotic analgesia in individual patients. With numerous such genetic and behavioral screening tools available for clinical use, one can imagine the power and clinical benefit of identifying and implementing, early in the clinical course of the burn patient, the most effective pharmacologic and nonpharmacologic analgesic techniques for a particular patient, thereby maximizing analgesic benefit and minimizing analgesic side effects.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
26
III
Sickle Cell Pain Samir K. Ballas
CHAPTER OUTLINE Acknowledgements 243 Introduction 243 Pathophysiology 243 Types of Sickle Pain 244 Acute Sickle Cell Pain Syndromes 244 Acute Painful Episodes (Painful Crises) 244 Acute Chest Syndrome 245 Right Upper Quadrant Syndrome 246 Left Upper Quadrant Syndrome 246 Acute Splenic Infarction 246 Hand-Foot Syndrome (Dactylitis) 246 Priapism 246 Chronic Sickle Cell Pain Syndromes 246 Leg Ulcers 246
Acknowledgements Supported in part by the Sickle Cell program of the Commonwealth of Pennsylvania for the Philadelphia Region.
Introduction The healthy adult hemoglobin (Hb A) is a tetramer of 2 alpha-globin chains and 2 beta-globin chains (α2β2).1,2 Each chain contains a heme moiety that carries oxygen. Thus, the major function of hemoglobin is to transport oxygen from the lungs to all organs and tissues throughout the body. Hemoglobinopathies are disorders of the structure or function of Hb A. They are broadly divided into two major groups: structural variants and thalassemias. Structural variants are, most commonly, the result of single base mutation in the globin genes. Thalassemias are characterized by decreased synthesis of globin chains. Thus beta-thalassemia major or Cooley's anemia is the result of lack of or decreased synthesis of the beta-globin chains of hemoglobin.1,2 The sickle hemoglobin (Hb S) is the most common structural variant of normal hemoglobin, followed by hemoglobin C (Hb C). Both of these hemoglobins are the result of single base mutation in the 6th codon of exon I of the beta-globin gene responsible for the synthesis of the betaglobin chain hemoglobin. In the case of Hb S, g lutamic acid is replaced by valine; in Hb C, glutamic acid is replaced by lysine. These mutations change the net charge of the © 2011 Elsevier Inc. All rights reserved.
Avascular Necrosis 247 Intractable Chronic Pain Without Obvious Objective Signs 247 Neuropathic Pain 247 Management of Sickle Cell Pain 247 Nonpharmacologic Management of Pain 247 Pharmacologic Management of Pain 247 Pain Management of Outpatients 247 Pain Management in the Day Unit 247 Pain Management in the Emergency Department 248 Management of Sickle Cell Pain in the Hospital 248 Preventative Therapy 248
Conclusion 248
variant hemoglobin, thus allowing their separation via electrophoresis.3,4 Sickle cell syndromes, also collectively referred to as sickle cell disease (SCD), are generic terms for a group of chronic inherited disorders of hemoglobin structure in which the affected individual inherits two mutant globin genes (one from each parent), at least one of which is always the sickle mutation. Sickle cell anemia (SS) is the homozygous state in which the sickle gene is inherited from both parents. Other sickle cell syndromes result from the coinheritance of the sickle gene and a nonsickle gene, such as Hb C, Hb OArab, Hb D, beta+-thalassemia, betao-thalassemia, etc. Table 26.1 lists the common sickle cell syndromes among Africans and African-Americans. Structural variants of hemoglobin are inherited in an autosomal codominant manner according to Mendelian principles. Thus, if one parent is healthy and the other has sickle cell anemia, then all children have sickle cell trait.
Pathophysiology Sickle cell anemia is almost synonymous with pain, and the acute painful crisis is its hallmark. The most important pathophysiologic event in SS that explains most of its clinical manifestations is vasoocclusion.5–8 The primary process that leads to vascular occlusion is the polymerization of Hb S on deoxygenation, which, in turn, results in distortion of the shape of red blood cells (RBCs), cellular dehydration, and decreased deformability and stickiness of RBCs that 243
244
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
Table 26.1 Major Types of Sickle Cell Syndromes and Their Typical Hematologic Parameters Hemoglobin Composition Abbreviation
Genotype
Hb (g/dL)
1. No alpha-gene deletion
SS
βS/βS; αα/αα
7.0-8.0
10-20
85-110
0
2.5-3.5
75-96
1-20
2. Deletion of 2 alpha-genes
SS, α-Thal
βS/βS; -α/-α
9.0-10.0
6-12
70-80
0
3.0-4.5
75-94
1-20
Sickle-betaothalassemia
S-β°-Thal
βS/β° thal
7.0-10.0
6-15
60-70
0
4.0-6.0
70-90
1-20
Sickle-beta+thalassemia
S-β+-Thal
βS/β+ thal
>10.0
5-10
60-70
10-20
4.0-6.0
65-85
1-15
Hb SCD
SC
βS/βC
>10.0
5-10
75-85
0
45-50
50
1-6
Sickle cell trait
AS
β /β
12-16
1.0-2.0
>82
55-57
2.5-3.5
40
8 wk to years
Example: Diabetes
Cancer surgeries
Table 28.5 Common Drugs Associated with Peripheral Neuropathy Antiretrovirals Chloroquine Cisplatin Colchicine Dapsone Disulfiram Gold salts Isoniazid Metronidazole
(e.g., chemotherapeutic agents), and some less so, such as vitamin overuse, which occurs with increasing frequency as patients become more concerned about a healthy diet.6
Nitrous oxide Nitrofurantoins Paclitaxel Phenytoin
Targeted Family History
Pyridoxine overuse
Perhaps nowhere in the specialty of pain medicine is the family history more helpful than in the diagnosis of peripheral neuropathy. Although a comprehensive discussion of the heritable diseases associated with peripheral neuropathies is beyond the scope of this chapter, several generalizations can be made:
Thalidomide
(1) A significant number of heritable peripheral neuropathies exists (the most common being Charcot-Marie-Tooth disease, with an incidence rate of 1:2500 patients).
Vinca alkaloids
(2) Failure to diagnose these disorders early on can lead to significant problems for the patient in the future. (3) The history of both parents, siblings, and children relative to signs and symptoms that suggest a peripheral neuropathy is important.
Chapter 28—Evaluation and Treatment of Peripheral Neuropathies
Table 28.6 Occupations and Behaviors Associated with Peripheral Neuropathies
263
Table 28.7 Components of the Physical Examination in a Patient with Suspected Peripheral Neuropathy
Occupation or Behavior
Offending Agent
Agriculture
Organophosphates
Examination of the feet
Alcohol overuse
Nutritional or vitamin deficiencies
Neurologic examination
Anesthesia delivery (anesthesiologists, nurse anesthetists, dentists)
Nitrous oxide
Pathologic reflexes
Dry cleaning
Trichloroethylene solvent
Sensory examination
Homosexuality
HIV
Autonomic nervous system evaluation
Intravenous drug abuse
HIV
Eye examination
Painters
Hexacarbon solvents
Skin, hair, and nail examination
Plastics manufacturing
Acrylamide residue
Organ system examination
Rayon manufacturing
Carbon disulfide
Plumbers or building demolition crews
Lead
Tobacco abuse
Paraneoplastic syndromes
Tree sprayers, copper smelters, or jewelers
Arsenic
Vegetarian diet
Cobalamin deficiency
Deep tendon reflexes Manual muscle testing
HIV, human immunodeficiency virus.
(4) All family members should be asked whether they have any difficulty walking. (5) All family members should be asked whether they or any other family members need canes, walkers, or wheelchairs. (6) All family members should be asked whether they or any family members have “funny-looking feet” or have foot problems. Many patients with peripheral neuropathy have pain and functional disability that they and their physicians have attributed erroneously to arthritis or aging.7
Social History From a statistical perspective, with the exception of alcohol exposure, the incidence of patients with a toxic neuropathy is extremely small. Because removal or limiting of the patient's ongoing exposure to nerve-damaging substances is possible, however, careful inquiry about high-risk occupations and behaviors is important. As summarized in Table 28.6, certain occupations and behaviors put the patient at greater risk for the development of peripheral neuropathies, some of which are reversible if the cause is identified and removed in a timely manner. As the number of patients with HIV increases and the mean survival time grows, the number of patients presenting to the pain center with HIV as the underlying cause of peripheral neuropathy will increase. Remember that the increasing use of often neurotoxic retroviral drugs in the treatment of HIV can also be responsible for the development of peripheral neuropathy.
Review of Systems A targeted review of systems aids the clinician in identification of systemic diseases that are often a factor in the evolution of a patient's peripheral neuropathy. To maximize the useful information received from the review of systems, the questions asked should be tailored to ferret out underlying diseases. Polyuria and polydipsia might point the clinician toward a diagnosis of diabetes mellitus.8 Temperature intolerance might suggest possible thyroid disease. Arthralgias and musculoskeletal symptoms might suggest a diagnosis of collagen-vascular disorders. Previous lung cancer might point the clinician toward a paraneoplastic syndrome. Although uncommon, conversion disorders may mimic the signs and symptoms of peripheral neuropathy. A carefully performed review of symptoms may be time consuming, but it often helps identify the underlying cause of a previously undiagnosed peripheral neuropathy and allows the clinician to implement treatment.
Physical Examination The targeted physical examination can often provide the clinician with important clues to aid in diagnosis of peripheral neuropathy (Table 28.7). Although the patient may encourage the clinician to focus the examination on a numb hand or numb feet, many of the physical findings associated with peripheral neuropathy are identified in locations far removed from the anatomic region the patient is concerned about.
Foot Examination Perhaps the best single piece of advice that can be given regarding the non-neurologic portion of the physical examination is to have patients take off their shoes. Many heritable peripheral neuropathies are associated with abnormal-looking feet. Often, such physical findings are overlooked because patients are embarrassed about the way their feet appear and go to great lengths to avoid exposing their feet. Embarrassment coupled with the functional disability the peripheral neuropathy imposes can cause patients with peripheral neuropathy to avoid activities such as running or swimming. Many patients with feet affected by peripheral neuropathy relate that the first
264
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
time they realized that their feet “weren't right” was when they saw their footprints in the dirt or sand when playing barefoot as a child. These abnormal footprints are often the result of pes cavus or pes planus deformities, which are easily identified on physical examination. In addition to these structural abnormalities of the foot, patients with peripheral neuropathy often have additional physical findings develop as a result of distal denervation of the joints of the phalanges and tarsal and metatarsal bones, such as claw toes, hammer toes, and the like. If the peripheral neuropathy remains undiagnosed and untreated, the clinician may observe Charcot neuropathic joint destruction, characteristic plantar foot ulcers called mals perforans, and ultimately necrotic acropathy as repeatedly traumatized phalanges become ischemic and autoamputate (Figs. 28.2 and 28.3).
with the polyneuropathies tends to be symmetric, although the length-dependent polyneuropathies tend to affect the distal motor groups preferentially. Asymmetric weakness is seen most commonly in the entrapment neuropathies, such as
Pes planus
Pes cavus
Neurologic Examination The neurologic examination of a patient suspected to have peripheral neuropathy can yield important information to aid the clinician in diagnosis and treatment. Most peripheral neuropathies have in common the following findings on physical examination: (1) reflex changes; (2) weakness; and (3) sensory deficit (Table 28.8). In addition to this classic triad of physical findings, many patients with peripheral neuropathy have significant autonomic dysfunction, especially patients with diabetic polyneuropathy. The next step in the neurologic examination of suspected peripheral neuropathy is careful manual motor testing. Similar to deep tendon reflex evaluation, this provides more objective information than the sensory examination, which largely depends on the patient's subjective response. As in the deep tendon reflex evaluation, when testing the muscle groups, the clinician should assess not only the presence or absence of muscle weakness but also the pattern in which any abnormality occurs. Muscle weakness associated
Fig. 28.3 A and B, Magnetic resonance imaging of Charcot joint. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 2123.)
Claw toe
Hammer toe
Fig. 28.2 Physical findings in the foot associated with peripheral neuropathy.
Chapter 28—Evaluation and Treatment of Peripheral Neuropathies
c arpal tunnel syndrome, although serious systemic diseases, such as amyloidosis, may manifest as an isolated mononeuropathy that may be misdiagnosed as a simple entrapment neuropathy. Plexopathies may manifest with a confusing pattern of muscle weakness and pain that may seem out of proportion to the patient's physical findings. Electromyography (EMG) combined with magnetic resonance imaging (MRI) helps with correct diagnosis. Finally, the sensory examination is performed. As mentioned previously, obtaining clinically useful information from the sensory examination is more difficult than gleaning information from the deep tendon reflex and motor examination because the clinician must rely on the patient's subjective responses. For this reason, the clinician must confirm findings of abnormal pain sensation with side-to-side temperature sensation evaluation in the affected areas. The clinician should not ignore sensory and temperature testing of the thoracoabdominal regions; more subtle neuropathic changes are often missed. Testing of vibration sense and proprioception also helps confirm the pattern of the neural compromise: symmetric versus asymmetric, diffuse versus localized. All of this information can be used to confirm the clinical diagnosis.
Eye Examination Although beyond the scope of expertise of most clinicians who care for patients in pain, eye symptoms in the presence of peripheral neuropathy should raise the index of suspicion that a peripheral neuropathy exists. The report of dry eyes is often associated with Sjögren's syndrome. Uveitis is often associated with the inflammatory systemic diseases associated with peripheral neuropathies, such as Behçet's disease, inflammatory bowel disease, and sarcoidosis. Optic atrophy has long been known to be associated with Charcot-Marie-Tooth disease, and scleritis is commonly seen in patients with vasculitis and connective tissue disease. Any of these symptoms warrants immediate referral to an ophthalmologist.
Skin, Hair, and Nail Examination As in the ophthalmologic examination, the clinician who cares for the patient in pain may not have adequate clinical expertise to diagnosis the myriad abnormalities of the skin, hair, and nails associated with peripheral neuropathies. The presence of such abnormalities should strengthen the clinical impression that peripheral neuropathy is the correct diagnosis, however, and prompt referral to a qualified dermatologist to help sort things out. Obvious findings on the skin, nail, and hair examination are summarized in Table 28.9.
s arcoidosis, AIDS, and collagen-vascular diseases. Chronic alcohol abuse also can lead to hepatosplenomegaly, as can a variety of heritable causes of peripheral neuropathy, such as Tangier disease. An enlarged tongue is thought to be pathognomonic for amyloidosis. Whether or not ultimately associated with peripheral neuropathy, the finding of organomegaly should alert the clinician to search diligently for the systemic disease responsible for this physical finding.
Neurophysiologic Testing Neurophysiologic testing, including the rational use of nerve conduction testing, EMG, and in selected patients quantitative sensory testing, is invaluable in the evaluation of a patient suspected to have peripheral neuropathy.9 Neurophysiologic testing is an extension of the targeted history and physical examination, rather than a replacement for it. In most instances, the results of neurophysiologic testing are used to confirm or fine tune a diagnosis of peripheral neuropathy, rather than make the diagnosis. For the purposes of this chapter, the following generalizations may break down in the individual patient, given the highly complex subject matter, but may serve to improve the basic understanding of the clinician faced with the presumptive diagnosis of peripheral neuropathy. Neurophysiologic testing is discussed in detail in Chapter 20.
Sensory Nerve Conduction Testing Sensory nerve conduction testing is usually the starting point for neurophysiologic testing of suspected peripheral neuropathy for confirming or excluding sensory nerve involvement.10 For the purposes of this discussion, assume that normal sensory nerve action potentials mean that the cells of the dorsal root ganglion and the large myelinated axons are healthy and that if the patient is having numbness, the pathologic process lies proximal to the dorsal root ganglion, or the patient has common small fiber or nociceptive neuropathy. This
Table 28.9 Common Skin, Nail, and Hair Changes Associated with Peripheral Neuropathies Abnormal Physical Finding
Cause
Foot ulcers
Diabetes
Angiokeratomas
Fabry's disease
Pruritus
Renal and liver failure
Hair loss
Hypothyroidism, thallium poisoning
Mees' lines
Heavy metal poisoning, especially arsenic
Clubbing of digits
Table 28.8 Triad of Physical Findings in Peripheral Neuropathy
Pulmonary failure, lung cancer
Livedo reticularis
Cryoglobulinemia
Tight curly hair
Giant axonal neuropathy
Loss of deep tendon reflexes
Hypopigmentation
Leprosy, sarcoid
Weakness
Hyperpigmentation
Cobalamin deficiency
Loss of sensation
Vesicles and bullae
Porphyria
Finding of Organomegaly The finding of organomegaly, although nonspecific, is often associated with peripheral neuropathies. Hepatomegaly and splenomegaly are often seen in patients with amyloidosis,
265
266
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
i nformation can lead the clinician to look to diagnoses other than peripheral neuropathy to explain the patient's symptoms (e.g., myelopathy).
Motor Nerve Conduction Testing Motor nerve conduction studies represent another piece of the neurodiagnostic puzzle in the diagnosis of peripheral neuropathy. The motor nerve conduction test is performed by stimulating a nerve and recording a response for the corresponding muscle. The motor nerve conduction study is useful in the identification and localization of lesions of the motor neuron, root, plexus, and peripheral nerve. As with sensory nerve conduction studies, side-by-side comparisons are useful.
Needle Electromyography Needle EMG is most useful in helping the clinician determine whether loss of motor unit fibers innervating the muscle has occurred.11 EMG needle examination shows the presence of muscle denervation by identifying: (1) the presence of muscle fibrillation and positive sharp waves; (2) the presence of increased amplitude of motor unit potentials; (3) the presence of an increased recruitment pattern; (4) the presence of an increased firing rate to offset the loss of motor nerve fibers; and (5) the presence of reduced recruitment of motor units as the muscle contracts. Although the information obtained from EMG needle examination is extremely useful in helping diagnose the myriad causes of muscle weakness and pain, EMG generally provides less specific information in and of itself regarding the presence of peripheral neuropathy relative to the nerve conduction testing.
Quantitative Sensory Testing Quantitative sensory testing is gaining acceptance as a useful adjunct in the evaluation of peripheral neuropathies.12 Although its widespread use has been limited by the lack of third-party reimbursement, quantitative sensory testing is extremely helpful in diagnosis of a relatively large subset of patients who clinically have peripheral neuropathy but in whom conventional nerve conduction testing and EMG are nondiagnostic. This subset of patients have in common damage to small nociceptive fibers that may not be identified on nerve conduction testing, which focuses primarily on large fiber function. Diseases that have a propensity to cause such damage include idiopathic distal painful neuropathy, HIV-related neuropathy, and some subsets of painful diabetic polyneuropathy. Because quantitative sensory testing still requires patient participation, it cannot be considered a true “objective” neurophysiologic test, and in patients with suspected small fiber neuropathy, a confirmatory skin biopsy for analysis of intraepidermal small nerve fibers and peripheral nerve biopsy (e.g., sural nerve) may be helpful.
Autonomic Reflex Testing As mentioned previously, the autonomic nervous system is often profoundly affected by peripheral neuropathies. Despite the frequency of autonomic dysfunction in patients with peripheral neuropathies, given the lack of easy and readily available testing of autonomic dysfunction, this component of the patient's disease often may go overlooked and be undertreated. If the patient is experiencing significant abnormalities of sweating, orthostatic hypotension, hypertension,
Table 28.10 Treatment Strategies for Most Common Causes of Peripheral Neuropathy Disease
Treatment
Diabetes
Control hyperglycemia
Nutritional and vitamin deficiencies
Add missing nutrients or vitamins or both
Alcohol overuse
Abstain from alcohol
HIV-induced neuropathy
Improve nutrition and symptomatic treatment
Amyloidosis
Liver transplantation
Toxic substances
Removal of toxic substances
Uremia
Vigorous dialysis and renal transplantation
Cryoglobulinemias
Plasmapheresis and immunosuppression
Guillain-Barré syndrome
Plasmapheresis
Porphyria-induced neuropathy
Glucose infusions and hematin
Entrapment neuropathies
Surgery, splinting
HIV, human immunodeficiency virus.
tachycardia or bradycardia, gastrointestinal hypomotility, or urinary retention, referral to a center skilled in diagnosis of autonomic dysfunction is indicated.
Magnetic Resonance Imaging and Computed Tomography Although not specific tests for the diagnosis of peripheral neuropathy per se, MRI and computed tomographic (CT) scan are useful adjuncts in the evaluation of a patient thought to have peripheral neuropathy because of their ability to help diagnose accurately many of the underlying pathologies associated with peripheral neuropathy. MRI and CT scan are of particular clinical use in evaluation of the central nervous system, axial skeleton, brachial and lumbar plexus, and anatomic area of suspected entrapment neuropathy (e.g., the tarsal tunnel). The clinician should use these methods early on in the diagnostic workup of patients who present with pain, numbness, weakness, and functional disability because they often may provide a specific diagnosis without the need for more invasive testing.
Treatment of Common Peripheral Neuropathies The goal of the evaluation of the patient suspected of having peripheral neuropathy is the identification of the specific cause of the patient's pain, numbness, weakness, and functional disability. Such identification allows a treatment plan to be designed specifically to treat the underlying pathologic process and avoid further nerve damage. Tables 28.10 and 28.11 provide the clinician with treatment strategies that have been shown to be useful in the treatment of specific types of peripheral neuropathy. Although use of the diagnostic approach as outlined previously allows the clinician to make such a specific diagnosis in many instances, a relatively large subset of
Chapter 28—Evaluation and Treatment of Peripheral Neuropathies
Table 28.11 Treatment Strategies for Painful Peripheral Neuropathies Treat any underlying disease or diseases thought to contribute to the patient's problem (e.g., better control of hyperglycemia in diabetes). Remove any toxic substance that may cause ongoing damage to the nerve (e.g., removal of thallium or lead exposure). Use simple analgesics, nonsteroidal anti-inflammatory drugs, and opioids to provide acute symptomatic relief. Use adjuvant analgesics, such as tricyclic antidepressants and anticonvulsants (e.g., amitriptyline and gabapentin). Use topical pharmacologic treatments, such as topical lidocaine patches, capsaicin, and analgesic balms. Use somatic and sympathetic nerve blocks and neuroaugmentation techniques, such as spinal cord stimulation, in carefully selected patients. Use occupational and physical therapy to instruct the patient how to protect insensate areas and joints and to restore and maintain function. Use nonpharmacologic pain relief techniques (e.g., hypnosis, guided imagery, coping strategies, acupuncture, contrast baths).
patients remains in whom a specific cause of the neuropathy cannot be identified. Most of these patients seem to have some form of idiopathic small fiber nociceptive neuropathy. Treatment for these patients centers primarily on symptom management and restoration of function. After ensuring that all that can be done to make a specific diagnosis has been done, and any specific treatments have been implemented (e.g., better control of hyperglycemia), the clinician should determine what symptoms cause the patient the most distress. Frequently, the numbness, functional disability, or sleep disturbance associated with the peripheral neuropathy bothers the patient more than pain. By focusing on the most troublesome aspects of the disease first, the clinician can maximize success and avoid making the cure worse than the disease by doing too much too soon. In general, the clinician is strongly recommended to avoid the temptation to treat everything at once with polypharmacy and to begin treatment with monotherapy targeted at the most problematic symptoms. For pain alone, treatment should begin with simple analgesics or nonsteroidal anti-inflammatory drugs with an eye to end-organ side effects (Table 28.12). Topical lidocaine patches or capsaicin also may be considered. If dysesthesia or numbness is present, a good starting point is gabapentin, or pregabalin, which should be started slowly as outlined in Table 28.13. If sleep disturbance is a prominent feature of the patient's pain report, the use of amitriptyline in a starting nighttime dose of 35 to 50 mg is indicated. Given the relative resistance of neuropathic pain to treatment with opioids, and given the increasingly obvious downside to the use of long-term opioid therapy in this setting, the routine use of opioids as a primary treatment of the symptoms of peripheral neuropathy should be discouraged.
Conclusion Peripheral neuropathies are a common problem encountered in clinical practice. The conditions are often misdiagnosed, so a patient with peripheral neuropathy may present to the
267
Table 28.12 Adjuvant Analgesics in Pharmacologic Management of Painful Peripheral Neuropathies Drug
Starting Dose
Maximum Daily Dose
Antidepressants
Amitriptyline
25-50 mg at bedtime
200 mg
Nortriptyline
25 mg at bedtime
200 mg
Desipramine
25 mg at bedtime
200 mg
Trazodone
50 mg at bedtime
300 mg
Gabapentin
100 mg at bedtime
3600 mg in divided doses
Pregabalin
50 mg three times daily
200 mg three times daily
Phenytoin
100 mg at bedtime
400 mg in divided doses
Topiramate
25 mg daily
300 mg twice daily
Carbamazepine
100 mg at bedtime
1200 mg in divided doses
150 mg at bedtime
200 mg three times daily
Anticonvulsants
Antiarrhythmics
Mexiletine
Table 28.13 Use of Gabapentin for Management of Painful Peripheral Neuropathies Start with 100 mg at bedtime for 2 nights. Increase to 100 mg twice daily for 2 days. Increase to 100 mg three times daily for 2 days. Increase to 300 mg four times daily. Increase to 400 mg at bedtime and 300 mg three times daily. Increase to 400 mg four times daily.
pain specialist feeling frustrated, discouraged, sleep deprived, and often iatrogenically addicted to narcotic analgesics. The goal of evaluation of peripheral neuropathies is identification of specific types of peripheral neuropathies with an eye to implementation of specific successful treatment strategies. When this is not possible, the goal is to rule out other treatable causes of the patient's symptoms and to begin a rational course of treatment that maximizes results and minimizes iatrogenic complications.
References Full references for this chapter can be found on www.expertconsult.com.
III
Chapter
29
Acute Herpes Zoster and Postherpetic Neuralgia Steven D. Waldman
CHAPTER OUTLINE Signs and Symptoms 268 Treatment 269 Basic Considerations 269 Treatment Options 269 Nerve Blocks 269
Herpes zoster is an infectious disease that is caused by the varicella-zoster virus (VZV), which also is the causative agent of chickenpox (varicella). Primary infection in the nonimmune host manifests itself clinically as the childhood disease chickenpox. During the course of primary infection with VZV, the virus is postulated to migrate to the dorsal root or cranial ganglia. The virus then remains dormant in the ganglia, producing no clinically evident disease. In some individuals, the virus may reactivate and travel along peripheral or cranial sensory pathways to the nerve endings, producing the pain and skin lesions characteristic of shingles. The reason for reactivation in only some individuals is not fully understood, but a theory is that a decrease in cell-mediated immunity allows the virus to multiply in the ganglia and spread to the corresponding sensory nerves, producing clinical disease.1 Patients with malignant disease (particularly lymphoma) undergoing immunosuppressive therapy (chemotherapy, steroids, radiation) or with chronic diseases generally have debilitated conditions and are more likely than the healthy population to have acute herpes zoster develop.2 These patients all have in common a decreased cell-mediated immune response, which may be the reason for the propensity for shingles. This may also explain why the incidence rate of shingles increases dramatically in patients older than 60 years and is relatively uncommon in persons younger than age 20 years.
Signs and Symptoms As viral reactivation occurs, ganglionitis and peripheral neuritis cause pain, which is generally localized to the segmental distribution of the posterior spinal or cranial ganglia affected. Approximately 52% of cases involve the thoracic dermatomes, 20% the cervical region, 17% the trigeminal nerve, and 11% the lumbosacral region.2 Rarely, the virus may attack the geniculate ganglion, resulting in facial paralysis, hearing loss, 268
Drug Therapy 269 Adjunctive Treatments 270
Complications 271 Conclusion 271
vesicles in the ear, and pain. This combination of symptoms is called the Ramsay Hunt syndrome.3 Herpetic pain may be accompanied by flu-like symptoms and generally progresses from a dull, aching sensation to unilateral, segmental, band-like dysesthesias and hyperpathia. Because the pain of herpes zoster usually precedes the eruption of skin lesions by 5 to 7 days, erroneous diagnosis of other painful conditions (e.g., myocardial infarction, cholecystitis, appendicitis, or glaucoma) may be made. Some pain specialists believe that in some immunocompetent hosts, when reactivation of virus occurs, a rapid immune response may attenuate the natural course of the disease and the rash may not appear. This segmental pain without rash is called zoster sine herpete and is, by necessity, a diagnosis of exclusion. In most patients, however, clinical diagnosis of shingles is readily made when the rash appears. Like chickenpox, the rash of herpes zoster appears in crops of macular lesions, which progress to papules and then to vesicles. At this point, should the diagnosis of herpes zoster be in doubt, it can be confirmed with isolation of the virus from vesicular fluid (differentiating it from localized herpes simplex infection) or with Tzanck smear of the base of the vesicle, which reveals multinucleated giant cells and eosinophilic intranuclear inclusions. As the disease progresses, the vesicles coalesce and crusting occurs. The area affected by the disease can be extremely painful, and the pain tends to be exacerbated by any movement or contact (e.g., with clothing or sheets). As healing takes place, the crusts fall away, leaving pink scars in the distribution of the rash that gradually become hypopigmented and atrophic. As a general rule, the quicker all the vesicles in a given patient appear, the quicker the rash heals. The clinical severity of the skin lesions of herpes zoster varies widely from patient to patient, although the severity of skin lesions and scarring tends to increase with age as does the duration of pain (Fig. 29.1). In most patients, the hyperesthesia and © 2011 Elsevier Inc. All rights reserved.
Chapter 29—Acute Herpes Zoster and Postherpetic Neuralgia 8%
92%
20 Years of Age 70 Years of Age
Fig. 29.1 Postherpetic neuralgia: pain 1 year after attack. 16%
84%
20 Years of Age 70 Years of Age
Fig. 29.2 Postherpetic neuralgia: pain beyond lesion healing.
pain generally resolve as the skin lesions heal; in some, however, pain may persist beyond lesion healing. This most common and feared complication of herpes zoster is called postherpetic neuralgia; the elderly are affected at a higher rate than the general population with acute herpes zoster (Fig. 29.2). The symptoms of postherpetic neuralgia can vary from a mild self-limited problem to a debilitating, constantly burning pain that is exacerbated by light touch, movement, anxiety, and temperature change. This unremitting pain may be so severe that it often completely devastates the patient's life and can lead to suicide. The desire to avoid this disastrous sequela to a usually benign self-limited disease dictates all therapeutic efforts for the patient with acute herpes zoster.
Treatment Basic Considerations The therapeutic challenge of the patient with acute herpes zoster is twofold: the relief of acute pain and symptoms, and the prevention of complications, including postherpetic neuralgia. The consensus of most pain specialists is that the earlier in the natural course of the disease that treatment is initiated, the less likely the development of postherpetic neuralgia.4 Because the older patient is at highest risk for postherpetic neuralgia, early and aggressive treatment for this group of patients is mandatory. Careful initial evaluation, including a thorough history and physical examination, is indicated to rule out occult malignant or systemic disease that may be responsible for the patient's immunocompromised state and to allow early recognition of changes in clinical status that may presage the development of complications, including myelitis or dissemination of the disease.
269
Inherent problems in assessment of the efficacy of a specific treatment are that the disease has many different clinical expressions and the natural history of the disease, and the incidence of complications, including postherpetic neuralgia, cannot be predicted reliably in any single patient. Most studies of the efficacy of a proposed treatment have failed to take these problems into account; therefore, only the most general conclusions may be reached.
Nerve Blocks Sympathetic neural blockade appears to be the treatment of choice to relieve the symptoms of acute herpes zoster and to prevent the occurrence of postherpetic neuralgia.5 Sympathetic nerve block appears to achieve these goals by blocking the profound sympathetic stimulation that is a result of the viral inflammation of the nerve and ganglion. If untreated, this sympathetic hyperactivity can cause ischemia from decreased blood flow of the intraneural capillary bed. If this ischemia is allowed to persist, endoneural edema forms, increasing endoneural pressure and causing a further reduction of endoneural blood flow with irreversible nerve damage. This damage appears to preferentially destroy large myelinated nerve fibers, which are metabolically more active, and to spare small fibers. Skin biopsy studies in patients with acute herpes zoster reveals a striking loss of epidermal-free nerve endings, which in all likelihood further contributes to the patient's pain.6 Noordenbos was first to report this phenomenon and correlate it with the pain symptomatology of herpes zoster. He postulated that large neural fibers modulate or inhibit entry of pain impulses into the central nervous system (CNS), whereas small fibers enhance entry of pain impulses into the CNS. Therefore, enhanced transmission of painful stimuli, and misinterpretation of the non-noxious stimuli of the small fibers as pain by the CNS, results if large fibers are preferentially destroyed. Interestingly, the theory of Noordenbos' “fiber dissociation” predated Melzack and Wall's gate control theory by 6 years. His theory may also explain the clinical finding of Winnie and others that sympathetic neural blockade is more efficacious when used early in the course of the disease by presumably interrupting the neural ischemia before irreversible large fiber changes occur.7 For patients with acute herpes zoster that involves the trigeminal nerve (Fig. 29.3) and the geniculate, cervical, and high thoracic regions, blockade of the stellate ganglion with a local anesthetic on a daily basis should be implemented immediately. For patients with acute herpes zoster that involves the thoracic, lumbar, and sacral regions, daily epidural neural blockade with local anesthetic should be implemented immediately (Fig. 29.4). As vesicular crusting occurs, the addition of steroids to the local anesthetic may decrease neural scarring and further decrease the incidence of postherpetic neuralgia. These sympathetic blocks should be continued aggressively until the patient is pain free and should be reimplemented at the return of pain. Failure to use sympathetic neural blockade immediately and aggressively, especially in the elderly, may sentence the patient to a lifetime of suffering.
Treatment Options
Drug Therapy
There are as many therapeutic approaches to the treatment of acute herpes zoster as there are clinicians treating the disease.
Opioid analgesics may be useful in relieving the aching pain that is often present during the acute stages of herpes zoster as
270
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
Fig. 29.3 Acute herpes zoster involving the trigeminal nerve.
Fig. 29.4 Acute herpes zoster involving the thoracic dermatome.
sympathetic nerve blocks are being implemented. These drugs are less effective in the relief of the neuritic pain that is often present. Careful administration of potent, long-acting narcotic analgesics (e.g., oral morphine elixir or methadone) on a time-contingent rather than an as-needed (prn) basis may represent a beneficial adjunct to the pain relief provided with sympathetic neural blockade. Because many patients with acute herpes zoster are elderly or have severe multisystem disease, close monitoring for the potential side effects of potent narcotic analgesics (e.g., confusion or dizziness, which may cause a patient to fall) is warranted. Daily dietary fiber supplementation and milk of magnesia should be started along with narcotic analgesics to prevent the side effect of constipation. Antidepressants may be useful adjuncts in the initial treatment of the patient with acute herpes zoster.8 On an acute basis, these drugs help alleviate the significant sleep disturbance that is commonly seen in this setting. In addition, the antidepressants may be valuable in helping ameliorate the neuritic component of the pain, which is treated less effectively with narcotic analgesics. After several weeks of treatment, the antidepressants may exert a mood-elevating effect that may be desirable in some patients. Care must be taken to observe closely for CNS side effects in this patient population. These
drugs may cause urinary retention and constipation that may be mistakenly attributed to herpes zoster myelitis. Anticonvulsants may also be of value as an adjunct to sympathetic neural blockade in the management of pain from acute herpes zoster. They may be particularly useful in relieving persistent paresthetic or dysesthetic pain. As with the narcotic analgesics and antidepressants, careful monitoring for CNS side effects is mandatory. Gabapentin at a bedtime dose of 300 mg is a reasonable starting place, with the dosage of this drug increased by 300 mg in divided doses every 48 to 72 hours as side effects allow. If carbamazepine is used, rigid monitoring for hematologic parameters, especially in patients undergoing chemotherapy or radiation therapy, is indicated. Phenytoin should not be used in patients with lymphoma because the drug may induce a pseudolymphoma-like state that is difficult to distinguish from the actual disease. Pregablin has also been shown to be efficacious in decreasing allodynia.9 Minor tranquilizers (e.g., diazepam) have a limited place in the adjunctive therapy of pain of acute herpes zoster. Although anxiety is often present in this setting, these drugs may actually increase pain perception. In addition, the addiction potential and CNS side effects limit their usefulness. Anxiety may be treated pharmacologically with hydroxyzine or, perhaps more appropriately, with behavioral interventions (e.g., monitored relaxation training and hypnosis). A limited number of antiviral agents, including famcyclovir, acyclovir, and perhaps interferon, have been shown to shorten the course of acute herpes zoster.10 Of these drugs, famciclovir and acyclovir appear to have fewer side effects. A difference of opinion exists as to whether these drugs prevent the occurrence of postherpetic neuralgia. They are probably useful in attenuating the disease in patients with immunosuppression and may provide symptomatic relief. Careful monitoring for side effects is mandatory with the use of these relatively toxic drugs. In the past, corticosteroids have been advocated as an adjunct in the treatment of acute herpes zoster. Proponents of this approach cite more rapid healing and a decreased incidence of postherpetic neuralgia. Other studies have been unable to confirm these findings. Local infiltration of affected skin areas with corticosteroid with or without local anesthetic may be of value as an adjunct to sympathetic neural blockade in decreasing localized areas of pain not amenable to other treatment modalities. Some authors believe that corticosteroids may increase the risk of dissemination in patients with immunosuppression if used before vesicular crusting. Our experience has not confirmed this to be the case.
Adjunctive Treatments Local application of ice packs to the lesions of acute herpes zoster may provide relief in some patients. Application of heat increases pain in most patients, presumably because of increased conduction of small fibers, but is beneficial in an occasional patient and may be worth trying if application of cold is ineffective. Transcutaneous electrical nerve stimulation and vibration may also be effective in a limited number of patients. The favorable risk-to-benefit ratio of all these methods makes them reasonable alternatives for patients who cannot or will not undergo sympathetic neural blockade. As a last resort, spinal cord stimulation may be considered in those patients in whom no other treatment methods have provided pain relief.
Chapter 29—Acute Herpes Zoster and Postherpetic Neuralgia
Topical application of aluminum sulfate as a tepid soak provides excellent drying of the crusting and weeping lesions of acute herpes zoster, and most patients find these soaks soothing. Zinc oxide ointment may also be used as a protective agent, especially during the healing phase, when temperature sensitivity is a problem. Topical lidocaine patches provide some patients with postherpetic neuralgia symptomatic relief, but this method should not be used on broken or inflamed skin or skin with active lesions.11 Topical capsaicin has also been advocated as a treatment for postherpetic neuralgia; however, experience has shown that this treatment is poorly tolerated by many patients.12,13 Disposable diapers can be used as an absorbent padding to protect healing lesions from contact with clothing and sheets.
Complications In most patients, acute herpes zoster is a self-limited disease. In the elderly and in patients with immunosuppression, however, complications may occur.2 Cutaneous and
271
visceral dissemination may range from a mild rash that resembles chickenpox to an overwhelming, life-threatening infection in those who already have severe multisystem disease. Myelitis may cause bowel, bladder, and lower-extremity paresis. Ocular complications from trigeminal-nerve involvement range from severe photophobia to keratitis with loss of vision.
Conclusion In view of the devastating effects of inadequately treated acute herpes zoster on the patient, the family, and society in terms of cost and lost productivity, healthcare professionals must initiate immediate and aggressive treatment for all patients with acute herpes zoster.
References Full references for this chapter can be found on www.expertconsult.com.
III
Chapter
30
Complex Regional Pain Syndrome Type I (Ref lex Sympathetic Dystrophy) Andreas Binder, Jörn Schattschneider, and Ralf Baron
CHAPTER OUTLINE Definition 273 History 273 Epidemiology 273 Incidence and Prevalence 273
Clinical Presentation 274 Spatial Distribution 274 Time Course 274 Stages 275 Psychology 275 Genetics 275
Pathophysiologic Mechanisms 275 Sensory Abnormalities and Pain 275 Autonomic Abnormalities 276 Denervation Supersensitivity 276 Central Autonomic Dysregulation 276 Neurogenic Inflammation 277 Motor Abnormalities 277 Sympathetically Maintained Pain 279 Definition 279 Studies on Patients 279 Summary of Pathophysiologic Mechanisms 280
Diagnosis 280 Diagnostic Tests 281 Validation of Clinical Diagnostic Criteria 282 Differential Diagnosis 282 Post-Traumatic Neuralgia 282
Treatment 283
Complex regional pain syndrome types I and II (CRPS I and CRPS II) share most of the same pathophysiologic, clinical, and therapeutic features. Therefore, all main information regarding CRPS in general is included in this chapter dealing with CRPS I. Specific information on CRPS II is added in Chapter 31. Until the 1990s, CRPSs were recognized as poorly defined pain disorders that mostly confused basic researchers, clinicians, and epidemiologists, rather than stimulating their scientific activities. The reasons for this confusion were that diagnostic criteria were defined vaguely, underlying pathophysiologic mechanisms were unknown, and therapeutic 272
Pharmacologic Therapy 283 Nonsteroidal Anti-Inflammatory Drugs 283 Opioids 283 Antidepressants 284 Sodium Channel Blocking Agents 284 γ-Aminobutyric Acid Agonists 285 Gabapentin 285 Corticosteroids 285 N-Methyl-d-Aspartate Receptor Blockers 285 Calcium-Regulating Drugs 285 Free Radical Scavengers 285 Miscellaneous Agents 285 Interventional Therapy at the Sympathetic Nervous System Level 285 Sympathetic Ganglion Blocks 285 Intravenous Regional Sympatholysis: Open Studies 285 Surgical Sympathectomy 286 Stimulation Techniques and Spinal Drug Application 286 Physical Therapy and Occupational Therapy 286 Psychological Therapy 287 Treatment Guidelines 287
Children 287 Prevention Studies 287 Prognosis 287 Conclusion 289 Acknowledgments 289
options were limited. No data on incidence, prognosis, and prevention were available, and research on mechanisms focused primarily on pain and controlled treatment studies were absent. However, insight into pathophysiologic mechanisms has progressed dramatically since the 1990s. Researchers became aware that CRPS I and II are not just neuropathic pain syndromes. Based on this notion, it has become obvious that multiple different pathophysiologic mechanisms may occur in different individual patterns.1 These consist of somatosensory changes (including pain) that interact with changes related to the sympathetic nervous system, peripheral inflammatory changes, and changes in the somatomotor system.2 © 2011 Elsevier Inc. All rights reserved.
Chapter 30—Complex Regional Pain Syndrome Type I (Reflex Sympathetic Dystrophy)
273
Definition The International Association for the Study of Pain (IASP) Classification of Chronic Pain redefined pain syndromes formerly known as reflex sympathetic dystrophy and causalgia. The term complex regional pain syndrome describes “a variety of painful conditions following injury which appears regionally having a distal predominance of abnormal findings, exceeding in both magnitude and duration the expected clinical course of the inciting event often resulting in significant impairment of motor function, and showing variable progression over time.”3 These chronic pain syndromes contain different additional clinical features including spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, and trophic signs. In CRPS I (reflex sympathetic dystrophy), minor injuries or fractures of a limb precede the onset of symptoms. CRPS II (causalgia) develops after injury to a major peripheral nerve.
History The American Civil War physician Weir Mitchell observed that approximately 10% of patients with traumatic partial peripheral nerve injuries in the distal extremity had a dramatic clinical syndrome that consisted of prominent, distal, spontaneous burning pain. In addition, patients reported exquisite hypersensitivity of the skin to light mechanical stimulation. Furthermore, movement, loud noises, or strong emotions could trigger their pain. The distal extremity showed considerable swelling, smoothness and mottling of the skin, and, in some cases, acute arthritis. In most cases, the limb was cold and sweaty. Weir Mitchell named this syndrome “causalgia.” He was emphatic that the sensory and trophic abnormalities spread beyond the innervation territory of the injured peripheral nerve and often were remote from the site of injury. The nerve lesions giving rise to this syndrome were always partial; complete transection did not cause it. Because of this and the peripheral signs of the disease, Weir Mitchell concluded that, in addition to disease of the nerve, some process in the skin or other peripheral tissue was responsible for the pain. After World War II, Leriche for the first time reported that sympathectomy dramatically relieved causalgia. This notion was supported by several large clinical series, primarily in wounded soldiers. Richards described the clinical features of causalgia and the effect of sympatholytic interventions in hundreds of cases. He repeatedly stressed the dramatic response of causalgia to sympathetic blockade: “One of the outstanding surgical lessons that was learned during World War II was that interruption of the appropriate sympathetic nerve fibres is almost invariably effective in the treatment of causalgia. When the sympathetic chain is blocked by a local anaesthetic, complete relief occurs almost immediately.” The finding that sympatholysis relieves causalgic pain gave rise to the concept of sympathetically maintained pain. In the years between World Wars I and II, the concept that sympathetic outflow could influence pain was extended to a group of patients without detectable nerve injury. These patients developed asymmetrical distal extremity pain and swelling (Fig. 30.1). The disorder had first been described by Sudeck early in the century. Precipitating events include fracture or minor soft tissue trauma, low-grade infection, frostbite,
Fig. 30.1 Clinical picture of patient with complex regional pain syndrome type I of the upper left extremity after distortion of the left wrist. (From Baron R: Complex regional pain syndromes. In McMahon SB, Koltzenburg M, editors: Wall and Melzack's textbook of pain, ed 5, London, 2006, Elsevier, pp 1011–1027.)
and burns, as well as stroke and myocardial infarction. The swelling and pain often develop at a site remote from the inciting injury, without any obvious local tissue-damaging process at the site of pain and swelling. This syndrome was named reflex sympathetic dystrophy because vasomotor (altered skin color and temperature) and sudomotor abnormalities (altered sweat production) are common, the pain and swelling are often spatially remote from the inciting injury, and patients typically obtain dramatic relief with sympathetic block.
Epidemiology Incidence and Prevalence A population-based study on CRPS I calculated an incidence of approximately 5.5 per 100,000 person-years at risk and a prevalence of approximately 21 per 100,000.4 In contrast, a European population-based study using a different diagnostic approach calculated a much higher incidence of 26.2 per 100,000 for CRPS in general.5 CRPS I develops more often than does CRPS II. Retrospective analyses revealed CRPS prevalences following fractures of between 0.03% and 37%.6,7 Estimations suggested an overall incidence of CRPS I of 1% to 2% after fractures, 12% after brain lesions, and 5% after myocardial infarction. However, the data for brain lesions and myocardial infarctions are relatively high and must be interpreted with some care because of the lack of uniform diagnostic criteria in the past. Preceding trauma such as fracture or surgery is the most common (≈40%) inciting event in CRPS I. However, in approximately 10% of the patients, CRPS develops after minor trauma, and in 5% to 10% of patients it develops spontaneously. No correlation exists between the severity of trauma and CRPS presentation.8 Female patients are more often affected than male patients, and the femaleto-male ratio ranges from 2:1 to 4:1. CRPS shows a distribution over all ages, with a mean age peak of 37 to 50 years and highest incidence rates at 61 to 70 years. The epidemiologic differences may reflect ethnicity, socioeconomic factors, and diagnostic criteria.
274
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
Clinical Presentation The most common precipitating event is trauma affecting the distal part of an extremity (65%), especially fracture, a postsurgical condition, contusion, and strain or sprain. Less common incidents are central nervous system (CNS) lesions such as spinal cord injuries and cerebrovascular accidents, as well as cardiac ischemia. Patients with CRPS I develop asymmetrical distal extremity pain and swelling without an overt nerve lesion (Table 30.1; see also Fig. 30.1). These patients often report a burning spontaneous pain felt in the distal part of the affected extremity. Characteristically, the pain is disproportionate in intensity to the inciting event. The pain usually increases when the extremity is in a dependent position. Stimulus-evoked pain is a striking clinical feature; these pains in clude mechanical and thermal allodynia or hyperalgesia. These sensory abnormalities often appear early, are most pronounced distally, and have no consistent spatial relationship with individual nerve territories or to the site of the inciting lesion. Typically, pain can be elicited by movement of and pressure on the joints (deep somatic hyperalgesia), even if these joints are not directly
Table 30.1 Signs and Symptoms of Complex Regional Pain Syndrome Duration
Sign or Symptom
2–6 mo (%)
>12 mo (%)
Total from 0–12 mo (%)
Pain
88
97
93
Increase of complaints after exercise
95
97
96
Neurologic
Hyperesthesia/allodynia
75
85
76
Coordination deficits
47
61
54
Tremor
44
50
49
Muscle spasm
13
42
25
Paresis
93
97
95
Sympathetic
Hyperhidrosis
56
40
47
Color difference
96
84
92
Temperature difference
91
91
92
Changed growth of hair
71
35
55
Changed growth of nails
60
52
60
Edema
80
55
69
Atrophy
Skin
37
44
40
Nails
23
36
27
Muscle
50
67
55
Bone (diffuse/spotty osteoporosis on radiograph)
41
52
38
Modified from Veldman PH, Reynen HM, Arntz IE, et al: Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients, Lancet 342:1012, 1993.
affected by the inciting lesion. Autonomic abnormalities include swelling and changes of sweating and skin blood flow. In the acute stages of CRPS I, the affected limb is often warmer than the contralateral limb. Patients with initially cold skin temperature (“cold” CRPS type) are thought to have an unfavorable course of the disease (see the later discussion of prognosis) and have been found to present with different clinical findings, such as increased incidence of dystonia, sensory loss, and cold-induced pain.9 Sweating abnormalities—either hypohidrosis or, more frequently, hyperhidrosis—are present in many patients with CRPS I. The acute distal swelling of the affected limb depends on aggravating stimuli. Because the swelling may diminish after sympathetic blocks, it is probably maintained by sympathetic activity. Trophic changes such as abnormal nail growth, increased or decreased hair growth, fibrosis, thin glossy skin, and osteoporosis may be present, particularly in chronic stages. Restrictions of passive movement are often present in patients with long-standing cases and may be related to both functional motor disturbances and trophic changes of joints and tendons. Weakness of all muscles of the affected distal extremity is often present. Small, accurate movements are characteristically impaired. Results of nerve conduction and electromyography studies are normal, except in patients in very chronic and advanced stages of the disorder. Approximately half of the patients have a postural or action tremor, which represents an increased physiologic tremor. In approximately 10% of cases, dystonia of the affected hand or foot develops.10
Spatial Distribution Predominantly, CRPS occurs in one extremity. Retrospective studies in large cohorts showed a distribution in the upper and lower extremity from 1:1 to 2:1. In 113 retrospectively reviewed cases, symptoms occurred in 47% of patients on the right side, in 51% on the left side, and in 2% bilaterally. Multiple extremities were affected in up to 7%.4,11–13
Time Course For therapeutic reasons, every effort should be undertaken to diagnose CRPS as early as possible. CRPS mostly starts acutely; that is, the cardinal symptoms may appear within hours or days. At the onset, the main symptoms of CRPS are spontaneous pain, generalized swelling, and difference in skin temperature on the symptomatic side. These early symptoms already develop in areas and tissues that are not affected by the preceding lesion. Thus, swelling and pain provide valuable information for an early diagnosis of CRPS. Before the onset of CRPS, pain is felt inside the area of the preceding lesion. After the onset of CRPS, however, the pain becomes diffuse and felt deep inside the distal extremity and the swelling generalizes, yet the initial pain may already have disappeared. To some extent, the tendency of symptoms to generalize may be a physiologic phenomenon in post-traumatic states that will disappear without any treatment. Exact differentiation between these physiologic diffuse posttraumatic reactions and the development of “real” CRPS is not possible at present.
Chapter 30—Complex Regional Pain Syndrome Type I (Reflex Sympathetic Dystrophy)
Stages A sequential progression of untreated CRPS has been repeatedly described. Each stage of CRPS (usually three are proposed) differs in patterns of signs and symptoms. Nevertheless, this concept has come into question. In 2002, the clinical validity of this concept was tested in 113 patients by Bruehl et al.12 Using a cluster analysis, the investigators identified 3 subgroups that could be differentiated by their symptoms and signs regardless of disease duration. The sequential concept relies on the course of untreated CRPS; however, so far all studies performed to test the clinical validity of this concept investigated patients already under treatment. Furthermore, vascular disturbances and skin temperature measurements indicated different thermoregulatory types, depending on time. In conclusion, it is questionable whether staging of CRPS is appropriate. A much more practical approach, one with direct therapeutic implications, is to grade CRPS according to the intensity of the sensory, autonomic, motor, and trophic changes as being mild, moderate, or severe (see later).
Psychology Most patients with CRPS exhibit significant psychological distress, most commonly depression and anxiety. Many patients become overwhelmed by the pain and associated symptoms and, without adequate psychosocial support, may develop maladaptive coping skills. Based on these symptoms, the tendency is to ascribe the origin of CRPS to emotional causes, and investigators have proposed that CRPS is a psychiatric illness. In fact, sometimes it is difficult to recognize the organic nature of the symptoms. However, when describing the clinical picture in the 1940s, Livingston was convinced: “The ultimate source of this dysfunction is not known but its organic nature is obvious and no one seems to doubt that these classical pain syndromes are real.” Covington14 drew the following conclusions about psychological factors in CRPS: 1. No evidence was found to support the theory that CRPS is a psychogenic condition. 2. Because anxiety and stress increase nociception, relaxation and antidepressive treatment are helpful. 3. The pain in CRPS is the cause of psychiatric problems and not the converse. 4. Maladaptive behavior by patients, such as volitional or inadvertent actions, is mostly the result of fear, regression, or misinformation and does not indicate a psychopathologic condition. 5. Some patients with conversion disorders and factitious diseases have been diagnosed incorrectly with CRPS. In summary, Covington concluded that the widely proposed “CRPS personality” is clearly unsubstantiated. This assumption was further strengthened when no differences in psychological patterns were found in patients with radius fracture who developed CRPS I in comparison with patients who recovered without developing CRPS.15 In a study supporting this view, an even distribution of childhood trauma, of pain intensity, and of psychological distress was confirmed in patients with CRPS in comparison with patients with other neuropathic pain and chronic back pain.16 Further studies demonstrated a high rate of psychiatric comorbidity, especially depression, anxiety, and personality disorders, in patients with CRPS. These findings are also present in other
275
patients with chronic pain and are more likely a result of the long and severe pain disease.17 Compared with patients with low back pain, patients with CRPS showed a higher tendency to somatization but did not show any other psychological differences.18 In 145 patients, 42% reported stressful life events in close relation to the onset of CRPS, and 41% had a previous history of chronic pain.19 Thus, stressful life events could be risk factors for the development of CRPS.
Genetics One of the unsolved features in human pain diseases is that a minority of patients develop chronic pain after seemingly identical inciting events. Similarly, in certain nerve lesion animal models, differences in pain susceptibility were found to result from genetic factors. The clinical importance of genetic factors in CRPS is not clear. A mendelian law does not seem to affect the incidence and prevalence, but familial occurrence has been described.20 Evidence indicates that certain genotypes are predisposing risk factors for the development of CRPS. A single nucleotide polymorphism of the alpha1-adrenoreceptor was identified as a risk factor for the development of CRPS I.21 Human leukocyte antigen (HLA) associations with different phenotypes showed an increase in A3, B7, and DR(2) major histocompatibility complex (MHC) antigens in a small group of patients with CRPS in whom resistance to treatment was associated with positivity of DR(2). In a cohort of 52 patients with CRPS, class I or II MHC antigens were typed. The frequency of HLA-DQ1 was found to be significantly increased compared with control frequencies.22 In patients with CRPS who progressed toward multifocal or generalized tonic dystonia, an association with HLA-DR13 was noted, and an association of fixed dystonia with HLA-B62 and HLA-DQ8 was reported.23,24 Furthermore, a different locus, centromeric in HLA class I, was found to be associated with the spontaneous development of CRPS, a finding suggesting an interaction between trauma severity and genetic factors that describe CRPS susceptibility.25 No associations have been identified for different cytokines, inflammatory neuropeptides, neutral endopeptidase, the SCNA9 sodium Na1.7 channel, and mutations of different dystonia predicting genes (DYT genes).
Pathophysiologic Mechanisms Sensory Abnormalities and Pain Based on numerous animal experimental findings, spontaneous pain and various forms of hyperalgesia at the distal extremity are thought to be generated by processes of peripheral and central sensitization. In patients with acute CRPS I, somatosensory profiling revealed heat and cold hyperalgesia in combination with warm and cold hypoesthesia, whereas in chronic CRPS I, thermal hyperalgesia declined and thermal hypoesthesia increased.26 Similar but minor deficits were found at the contralateral nonaffected extremity. In addition, up to 50% of patients with chronic CRPS I develop hypoesthesia and hypoalgesia in the entire half of the body or in the upper quadrant ipsilateral to the affected extremity. Systematic quantitative sensory testing has shown that patients with these generalized hypoesthesias have increased thresholds to mechanical, cold, warmth, and heat stimuli compared with the responses generated from the corresponding contralateral
276
Section III—Generalized Pain Syndromes Encountered in Clinical Practice
healthy body side. Patients with these extended sensory deficits have longer disease duration, greater pain intensity, a higher frequency of mechanical allodynia, and a greater tendency to develop changes in the somatomotor system than do patients with spatially restricted sensory deficits. These changed somatosensory perceptions are likely the result of changes in the central representation of somatosensory sensations in the thalamus and cortex. Accordingly, positron emission tomography (PET) studies demonstrated adaptive changes in the thalamus during the course of the disease.27 The magnetoencephalographic (MEG) first somatosensory (SI) responses were increased on the affected side, a finding indicating processes of central sensitization. Psychophysical and transcranial magnetic stimulation (TMS) studies suggested sensory and motor hyperexcitability within the CNS.28 Furthermore, MEG and functional magnetic resonance imaging (fMRI) studies uncovered networks of hyperalgesia and allodynia involving nociceptive, motor, and attention processing and demonstrated a shortened distance between little finger and thumb representations in the SI cortex on the painful side (Fig. 30.2).29–32 This latter cortical reorganization was reversible and correlated with pain reduction and improvement of tactile impairment.33–35 This cortical reorganization may not be CRPS specific, however, but may give a suitable hypothesis for the observed sensory features in CRPS.29 Using fMRI, Lebel et al36 demonstrated that patients who had recovered from CRPS still had significant differences in CNS reactivity to sensory stimuli. The dependency of these phenomena on structural or functional changes in the peripheral nerve system is not known. However, skin preparations from patients with CRPS I showed diminished axonal density37 and mixed decreased and increased innervation of epidermal and vascular structures and sweat glands.38 The relevance of these findings to distinct pathophysiologic mechanisms remains unclear.39
nerve are the result of peripheral impairment of sympathetic function and sympathetic denervation. During the first weeks after transection of vasoconstrictor fibers, vasodilatation is present within the denervated area. Later, the vasculature may develop increased sensitivity to circulating catecholamines, probably because of up-regulation of adrenoceptors.
Central Autonomic Dysregulation Sympathetic denervation and denervation hypersensitivity cannot completely account for vasomotor and sudomotor abnormalities in CRPS. First, patients with CRPS I have no overt nerve lesion, and, second, in CRPS II, the autonomic symptoms spread beyond the territory of the lesioned nerve. In fact, direct evidence indicates a reorganization of central autonomic control in these syndromes.2,40 Hyperhidrosis, for example, is found in many patients with CRPS. Resting sweat output and thermoregulatory and axon reflex sweating are increased in patients with CRPS I.41 Increased sweat production cannot be explained by a peripheral mechanism because, unlike blood vessels, sweat glands do not develop denervation supersensitivity. Moreover, exaggerated CGRP levels may enhance sweat gland activation.42 To study cutaneous sympathetic vasoconstrictor innervation in patients with CRPS I, Baron and Wasner et al43–45 analyzed central sympathetic reflexes induced by thermoregulatory (whole-body warming, cooling) and respiratory stimuli. Sympathetic effector organ function (i.e., skin temperature and skin blood flow) was measured bilaterally at the extremities by infrared thermometry and laser Doppler flowmetry. Under normal conditions, these reflexes do not show interside differences. In patients with CRPS, three distinct vascular regulation patterns were identified related to the duration of the disorder: 1. In the warm regulation type (acute stage, 30%
Normal
Preganglionic and postganglionic lesion
Reduced >30%
Absent or reduced >N9 amplitude reduction
Table 59.4 Differential Diagnosis of Nerve versus Muscle Involvement in Brachial Plexopathy Abnormal Electrodiagnostic Study
Involved Muscles on Electromyography
Motor Nerve
Sensory Nerve
Upper trunk
Axillary Musculocutaneous Suprascapular
Lateral antebrachial cutaneous (terminal branch of musculocutaneous) Radial: thumb Median: first or second digit
Deltoid Biceps Brachioradialis Supraspinatus Infraspinatus Teres minor
Middle trunk
Radial
Radial: posterior antebrachial cutaneous Median: third digit
Triceps Pronator teres Flexor carpi radialis Extensor carpi radialis
Lower trunk
Median Ulnar Radial
Ulnar: fifth digit Ulnar: dorsal cutaneous nerve Medial antebrachial cutaneous
All muscles supplied by ulnar nerve; hand muscles supplied by median nerves Distal muscles supplied by radial nerve: extensor indicis, carpi ulnaris, and pollicis brevis
Lateral cord
Musculocutaneous
Lateral antebrachial cutaneous (terminal branch of musculocutaneous) Median: first, second, or third digit
Biceps Pronator teres Flexor carpi radialis
Posterior cord
Radial Axillary
Radial: posterior antebrachial cutaneous Radial: thumb
All muscles supplied by radial nerve in arm and forearm Latissimus dorsi Deltoid Teres major
Medial cord
Median Ulnar
Ulnar: fifth digit Ulnar: dorsal cutaneous nerve Medial antebrachial cutaneous
All hand muscles supplied by ulnar and median nerves All ulnar forearm muscles
540
Section IV—Regional Pain Syndromes
tendon. The use of appropriate orthoses to prevent contracture, maintain proper position, or improve functional gain is usually tailored to the patient's need. Rehabilitation therapy also addresses various activities of daily living with the use of adaptive equipment and functional orthoses. Recreational therapy provides compensatory techniques for arm use in various leisure activities. Rehabilitation therapy for the child with neonatal brachial plexopathy begins in infancy. Gentle range-of-motion exercises are started in the first month. Parents are taught different exercises, as well as how to give care without worsening the injury. A wrist extension splint is necessary to prevent contracture. Edema control, with retrograde massage, compressive garments, and elevation, is important in postradiation plexopathy and in some cases of recurrent neoplastic plexopathy.
Surgery Surgical exploration and repair of brachial plexus lesions are technically feasible, and favorable outcomes can be achieved if patients are thoroughly evaluated and appropriately selec ted.16 Surgery is indicated when the deficit does not improve with conservative treatment, except in clean, lacerating wounds with neural symptoms, for which immediate surgical exploration and repair may be indicated. For traumatic plexopathy, surgery gives better results when performed by 3 months after the injury. If this approach fails, tendon transfer or osteotomy can improve function.17 Common tendon transfers include triceps or pectoralis major or latissimus dorsi to biceps procedures and may be good options for patients with an encapsulated primary neoplasm. Surgical procedures varying from placement of spinal cord stimulators, morphine pump implantation, or creation of a dorsal root entry zone (DREZ) lesion may be used for pain control in brachial plexopathy.18
Pharmacologic Treatment Nonsteroidal anti-inflammatory agents, antiepileptic agents, tricyclic antidepressants, opiates, muscle relaxants, and antispasticity medications including botulinum A or B are used in various combinations to help reduce pain, paresthesias, muscle spasms, and spasticity.
Box 59.1 Organizations Brachial Plexus Palsy Foundation c/o 210 Springhaven Circle Royersford, PA 19468 email:
[email protected]; website: http://membrane.com/bpp telephone: 610-792-4234 National Institute on Disability and Rehabilitation Research (NIDRR) 600 Independence Avenue, SW Washington, DC 20013-1492 website: http://www.ed.gov/offices/OSERS/NIDRR telephone: 202-205-8134 National Organization for Rare Disorders (NORD) P.O. Box 1968 (55 Kenosia Avenue) Danbury, CT 06813-1968 email:
[email protected]; website: http://www.rarediseases .org telephone: 203-744-0100; voice mail: 800-999-NORD (6673); fax: 203-798-2291 National Rehabilitation Information Center (NARIC) 4200 Forbes Boulevard, Suite 202 Lanham, MD 20706-4829 email:
[email protected]; website: http://www .naric.com telephone: 301-562-2400 or 800-346-2742; fax: 301-562-2401 United Brachial Plexus Network 1610 Kent Street Kent, OH 44240 email:
[email protected]; website: http://www.ubpn.org telephone: 866-877-7004
capsulitis, and fibrosis of the endoneural tube work against the functional recovery. The prognosis of complete lesions is poor because the unaffected neural fibers are not available for collateral sprouting. Connective tissue disruption in the lesion site causes fibrosis and impedes advancement of the axon that leads to a poor prognosis for recovery of function. The prognosis is best in patients with upper trunk lesions.
Complications Like any other peripheral nerve injury, brachial plexopathy of any origin can lead to complex regional pain syndrome type II (reflex sympathetic dystrophy). Myofascial pain syndromes, joint and muscle contracture, subluxation, and heterotopic ossification may complicate the recovery. Scoliosis from muscle imbalance is a possible complication in children. The sequelae commonly seen in children are the results of muscle imbalance or contractures and may include osseous deformities of the shoulder and elbow, dislocation of both shoulder and elbow, and dislocation of both the humeral and radial heads. Patients with postradiation brachial plexopathy are at risk for lymphangiitis and cellulitis. In general, the prognosis of lower trunk lesions is poor, for two reasons: (1) because C8-T1 roots have weak connective tissue support, these structures are more vulnerable to avulsion (preganglionic) injury compared with other roots; and (2) even in a postganglionic lesion, the target organs for motor and sensory nerves are farthest to reach. Muscle contracture, joint
Conclusion Brachial plexus injury represents a complex clinical challenge from both diagnostic and treatment standpoints. Nerve grows 1 mm per day, hence an average of 1 inch per month. Most postanesthetic or surgical brachial plexopathy improves rapidly. Supraclavicular brachial plexopathy is more common than infraclavicular plexopathy. Upper plexus lesions have a better prognosis than lower plexus lesions. Practitioners from multiple specialties, including physical medicine and rehabilitation, pain medicine, neurosurgery, orthopedics, plastic surgery, pediatrics, oncology, and radiation oncology, should be consulted as appropriate. A list of organizations to consult for additional information is provided in Box 59.1.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
60
IV
Cervical Myelopathy Yoshiharu Kawaguchi
CHAPTER OUTLINE Pathology of Compressive Cervical Myelopathy 541 Pathologic Change in the Spinal Cord 541 Causes of Spinal Cord Compression 542 Cervical Spondylosis 542 Ossification of the Posterior Longitudinal Ligament 544 Cervical Disk Herniation 545 Calcification of the Ligamentum Flavum 545 Rheumatoid Arthritis 546 Spinal Tumors 546 Epidural Abscess 547 Anomaly in the Cervical Spine 547 Destructive Spondyloarthropathy 548
Diagnosis of Cervical Myelopathy 548
Physical Examination 549 Reflex Change 550 Motor Weakness 550 Sensory Disturbance 550 Evaluation System 550 Radiologic Evaluation 550
Therapeutic Strategies for Cervical Compressive Myelopathy 555 Indications for Surgery 555 Surgical Approaches 555 Anterior Approach 555 Posterior Approach 556
Conclusion 557
Clinical Symptoms 548
Based on neurologic findings in cervical spine disease, the pathologic entity is divided into two categories, cervical myelopathy and cervical radiculopathy. As for cervical disk herniation (Fig. 60.1), when disk prolapse occurs in the central part of the spinal canal and the cervical spinal cord is involved, the patient usually has cervical myelopathy. Conversely, when disk prolapse develops in the lateral part of the spinal canal and the herniated disk compresses the spinal nerve, cervical radiculopathy may occur. Patients with cervical radiculopathy often complain of unilateral radicular pain in an upper extremity. In contrast, patients with cervical myelopathy rarely have pain. They have clumsiness or loss of fine motor skills in the hand, gait disturbance, and vesicoureteral disturbance. Thus, pain is treatable in patients with cervical radiculopathy. However, one fourth of the patients with cervical degeneration have both myelopathy and radiculopathy.1,2 Further, neck pain from degenerative change in the cervical spine may be associated with cervical myelopathy and radiculopathy. Neck pain is regarded as a nonspecific complaint in these patients. Cervical myelopathy implies spinal cord dysfunction in the cervical spine. The causes are numerous and are divided into extrinsic and intrinsic neurogenic conditions (Table 60.1). Extrinsic neurogenic conditions are caused by spinal cord compression. Structural abnormalities surrounding the spinal cord contribute to encroachment on the available space in the spinal canal and result in spinal cord compression. Investigators have reported that spinal cord compression entities are some of the most common conditions in myelopathic patients who are more than 55 years of age, because © 2011 Elsevier Inc. All rights reserved.
these abnormalities generally result from degeneration of the cervical spine.3 Intrinsic neurogenic conditions are caused by the primary spinal cord disorder. These intrinsic disorders are important in the differential diagnosis of compressive myelopathy.4 Patients with cervical myelopathy do not always complain of pain. However, they may feel a type of pain resembling electric shock when the neck is in extension or flexion. This symptom is known as Lhermitte's sign.5 This chapter reviews the pathology, diagnosis, and therapeutic strategy of compressive myelopathy in the cervical spine.
Pathology of Compressive Cervical Myelopathy Pathologic Change in the Spinal Cord In the degenerative stage of the cervical spine, spinal canal narrowing is caused by intervertebral disk bulging, deformity of the uncovertebral joint, hypertrophy of the facet joints, and hypertrophy of the ligamentum flavum (Fig. 60.2). In the presence of these degenerative changes, spinal cord compression may occur. Macroscopically, the spinal cord with myelopathy shows anteroposterior flatness and becomes atrophic as a result of compression. According to morphologic studies using computed tomography myelography (CTM), the spinal cord sometimes has either a boomerang shape or is triangular. Histopathologic studies have shown that damage to neuronal components is mild in the spinal cord with a boomerang shape, whereas such damage is marked in patients with a triangular spinal cord.6 Ono et al7 reported the 541
542
Section IV—Regional Pain Syndromes
A
B
Fig. 60.1 Patterns of neurologic impairment resulting from cervical disk herniation. A, The cause of cervical myelopathy. B, The cause of cervical radiculopathy.
Table 60.1 Causes of Cervical Myelopathy Extrinsic Neurologic Conditions
Cervical spondylotic myelopathy Ossification of the posterior longitudinal ligament (OPLL) Cervical disc herniation
c linicopathologic findings in five necropsy cases with cervical spondylotic myelopathy. These investigators found extensive destruction in both the gray matter and the white matter at the most damaged segment. Ogino et al8 revealed that in mild compression, limited demyelination and spongy degeneration are seen in the posterolateral white column, whereas in severe compression, extensive degeneration and infarction of the gray matter with diffuse degeneration of the lateral white columns are observed. Ito et al9 also noted marked atrophy and neuronal loss in the gray matter in severely degenerated white matter columns. Patients with severe cases usually have accompanying developmental spinal stenosis. These pathologic changes are localized not only at the most markedly compressed site, but also at the craniocaudal regions in addition to the compression. Ascending degenerative demyelination is consistently seen in the cuneate and gracilis fasciculi of the posterior white columns in the spinal cord cranial to the compression site. Distinct descending demyelination of the lateral corticospinal tract is generally observed in the caudal site of the spinal cord. The pathologic changes in the spinal cord vary depending on age and extent and duration of compression.
Rheumatoid arthritis (RA) Spinal tumors
Causes of Spinal Cord Compression
Epidural abscess
Various disorders have the potential for encroachment in the spinal canal.3,10–13 The conditions discussed in the following subsections increase the risk of spinal cord involvement.
Anomaly in the cervical spine Destructive spondyloarthropathy (DSA) Intrinsic Neurologic Conditions
Cervical Spondylosis
Viral infections
Cervical spondylotic myelopathy is the most common cause of spinal cord dysfunction in patients with compressive myelopathy (Fig. 60.3). Cervical spondylosis initially results from degeneration of the intervertebral disk. Disk
Neoplasms Vascular diseases Motor neuron diseases Radiation myelopathy Nutritional myelopathy Syringomyelia
Posterior 4
3
2
1 Anterior
Fig. 60.2 Causes of spinal canal narrowing resulting from degeneration of the cervical spine: intervertebral disk, uncovertebral joint, facet joint, and ligamentum flavum.
Fig. 60.3 Radiologic features of cervical spondylotic myelopathy.
egeneration increases mechanical stress at the end plate, and d this condition causes subperiosteal bone formation. By such a mechanism, osteophytes develop at the upper or lower edge of the vertebral body. Osteophytes at the posterior margin of the vertebral body, which is called posterior bony spur, have the potential risk of encroaching on the spinal cord, followed by deformity of the uncovertebral joint, hypertrophy of facet joints, and hypertrophy of the ligamentum flavum. These findings are termed spondylotic changes in the cervical spine. These spondylotic changes are often observed at multiple levels in the cervical spine. However, the presence of cervical spondylosis alone does not generally lead to myelopathy. The pathology of cervical myelopathy is multifactorial. The clinician should consider the context of static and dynamic mechanical factors as well as ischemic factors.14,15 STATIC MECHANICAL FACTORS The size of the spinal canal plays an important role in the development of cervical myelopathy.16,17 Spinal canal size is the distance between the posterior margin of the vertebral body and the anterior edge of the spinous process (Fig. 60.4). The normal spinal canal diameter from C3 to C7 is 17 to 18 mm in white persons and 15 to 17 mm in Japanese persons.6,18 The spinal canal size in patients with cervical myelopathy is smaller than in those without the disorder.18 A sagittal diameter of 12 mm14,15,19 (or 13 mm in some reports)13,20,21 or less is believed to be a critical factor in the development of cervical spondylotic myelopathy. Younger patients, less than 50 years of age, with cervical myelopathy usually have a developmentally narrow cervical spinal canal. The Pavlov ratio is also used to identify cervical spinal stenosis.22 This is the ratio of the anteroposterior diameter of the spinal canal to the anteroposterior diameter of the vertebral
Chapter 60—Cervical Myelopathy
543
body at the same level as measured on a lateral radiograph (Fig. 60.5). The merit of this measurement is that the ratio is not affected by variations in radiologic magnification. A normal ratio is 1.0, and a ratio of less than 0.82 indicates cervical spinal stenosis. The Torg ratio is the same as the Pavlov ratio. Torg described that a ratio of less than 0.8 indicates cervical stenosis.23 DYNAMIC MECHANICAL FACTORS In cervical spondylosis, movement of the cervical spine may have an impact on spinal cord compression. During extension of the cervical spine, the ligamentum flavum buckles and thus narrows the spinal canal. The spinal cord is compressed between the posterior margin of one vertebral body and the lamina or ligamentum flavum of the next caudal level. During flexion, spinal cord compression occurs by the posterior margin of caudal vertebral body and the lamina or ligamentum flavum of the cranial level. This mechanism has been called the “pincer effect” of spinal cord compression (Fig. 60.6).24 Dynamic magnetic resonance imaging (MRI) clearly shows the pathologic features of cervical cord compression in flexion and extension (Fig. 60.7). As for the pathomechanism of cervical myelopathy in older patients, retrolisthesis of C4 results from intervertebral disk degeneration, which is the likely cause the spinal cord compression.25,26 During flexion of the cervical spine, the spinal cord must lengthen or move anteriorly within the spinal canal, and the result is axial tension. Bulged disk or anterior osteophytes can stretch the spinal cord in flexion. Anterolisthesis of the vertebral body can cause spinal cord compression. These local conditions lead to the onset of myelopathy. Investigators have reported that some patients with athetoid cerebral palsy show evidence of cervical myelopathy at an early age (30 to 40 years old).27 This condition results
A
B
Fig. 60.5 The Pavlov ratio. The Pavlov ratio is measured by A/B.
A Fig. 60.4 Measurement of the spinal canal. The dotted lines and arrows show the width of the spinal canal.
B
Fig. 60.6 The pincer effect of the spinal cord in flexion (A) and extension (B).
544
Section IV—Regional Pain Syndromes
Fig. 60.7 Dynamic magnetic reson ance imaging (MRI) showing sagittal views of T2-weighted MRI in flexion (A) and extension (B). Spinal cord compression is marked in extension.
A
B
from excessive movement of the cervical spine. These typical cases show the importance of dynamic factors in cervical cord dysfunction. ISCHEMIC FACTORS Spinal cord compression leads to ischemia of the spinal cord.28 Histopathologic examination reveals the occurrence of ischemic injury in the gray matter and the white matter in patients with myelopathy.14 In addition, several animal models showed that disturbance in the vascular supply to the spinal cord plays an important role in the pathophysiology of spinal cord dysfunction.6
Ossification of the Posterior Longitudinal Ligament Ossification of the posterior longitudinal ligament (OPLL) often causes narrowing of the spinal canal as a result of the replacement of spinal ligamentous tissue by ectopic new bone formation (Fig. 60.8).29,30 This disease is more common among Japanese persons and other nonwhite ethnic groups than among white persons. The incidence of OPLL among Japanese people is reported to be 3%, whereas it is 0.2% to 1.8% in Chinese persons, 0.95% in Koreans, 0.12% in residents of the United States, and 0.1% in Germans.31 Although the origin of OPLL remains obscure, investigators have reported that genetic background is a contributory factor. Studies using molecular biology have revealed that the collagen 11 α 2 gene (COL11A2),32,33 the retinoic X receptorβgene (RXRb),34 the nucleotide pyrophosphatase gene (NPPS),35 and transforming growth factor-β3 (TGFβ3)36 may be responsible for OPLL. It is widely recognized that severe myelopathy and radiculopathy may be caused by OPLL. Matsunaga and Sakou37 reported that cervical myelopathy was seen in all patients with more than 60% of the spinal canal compromised by OPLL. These investigators also found that dynamic factors were important in patients with less than 60% of OPLL-related spinal canal compromise.37 Ossification in OPLL is classified as continuous type, segmental type, mixed type, and other type, according to the
Fig. 60.8 Radiologic features of ossification of the posterior longitudinal ligament (OPLL). This 46-year-old woman has mixedtype OPLL.
criteria proposed by the Investigation Committee on the Ossification of the Spinal Ligaments of the Japanese Ministry of Public Health and Welfare (Fig. 60.9).38 Among these types, cervical myelopathy frequently develops in patients with the continuous or mixed type of OPLL. The progression of OPLL is often observed in long-term follow-up after cervical laminoplasty, and OPLL can cause recurrent cervical myelopathy.39 The risk of OPLL progression after posterior surgery is highest in patients in their 40s who have continuous and mixed types of ossification.40,41
Chapter 60—Cervical Myelopathy
A
B
C
D
Fig. 60.9 Classification of ossification of the posterior longitudinal ligament by the Investigation Committee on the Ossification of the Spinal Ligaments, Japanese Ministry of Public Health and Welfare. A, Continuous type. B, Segmental type. C, Mixed type. D, Other type. Adapted from Tsuyama N, Terayama K, Ohtani K, et al: The ossification of the posterior longitudinal ligament (OPLL): the investigation committee on OPLL of the Japanese Ministry of Public Health and Welfare, J Jpn Orthop Assoc 55:425, 1981.
A
545
B
Cervical Disk Herniation Cervical disk herniation is one of the compressive lesions that may cause cervical myelopathy (Fig. 60.10). Investigators proposed that nuclear herniation or anulus protrusion compresses the spinal cord, but precise histopathologic examination revealed that disk herniation associated with the cartilaginous end plate is the predominant type of herniation in the cervical spine.42 Patients with myelopathy resulting from disk herniation are relatively young, compared with patients who have cervical spondylotic myelopathy. The spinal canal is narrower in patients with herniation, and this configuration leads to myelopathy. A history of cervical spinal trauma appears to be a predisposing factor for disk herniation.43 In some patients with the median or diffuse type of disk herniation, spontaneous regression of the herniated mass is observed on MRI.44 The symptoms often resolve during such regression, and,
Fig. 60.11 Radiologic features of calcification of the ligamentum flavum. Computed tomography image obtained at the C5-6 level.
Fig. 60.10 Radiologic features of cervical disk herniation. Centrally located disk herniation (arrows) compresses the spinal cord at the C5-6 level. Sagittal (A) axial (B) images.
therefore, conservative treatment can be an option for mild myelopathy caused by cervical disk herniation.45
Calcification of the Ligamentum Flavum A few cases have been reported in which calcification of the ligamentum flavum narrowed the cervical spinal canal and resulted in myelopathy (Fig. 60.11). In the literature, most cases are Japanese. Kokubun et al46 reported that 4% (11 patients) of 306 patients with cervical myelopathy in northern Japan had calcification of the ligamentum flavum. CT is the most useful diagnostic tool for detecting this disease. Although the cause of calcification of the ligamentum flavum is unknown, calcium phosphate deposition in the ligamentum flavum is observed. The calcification can be absorbed after administration of cimetidine or etidronate. Experience indicates that the calcification disappears after cervical laminoplasty.
546
Section IV—Regional Pain Syndromes
1
2 C1
C2 Fig. 60.12 Atlantoaxial su bluxation in rheumatoid arthritis. Fig. 60.14 cord.
Atlas dental interval and
space available for the spinal
Occipital bone
1
Hard palate
2 C1
3
4 C2 C3
Fig. 60.13 Vertical subluxation in rheumatoid arthritis. Sagittal computed tomography image.
Rheumatoid Arthritis Involvement of the cervical spine in rheumatoid arthritis (RA) has been well studied.47–52 Compression of the spinal cord may result from direct compression by synovial pannus or from indirect compression caused by cervical subluxation. Upper cervical lesions, identified as atlantoaxial subluxation (Fig. 60.12) and vertical subluxation (Fig. 60.13), can cause cervical myelopathy.47,48 The atlas dental interval (ADI) is a useful marker for the analysis of atlantoaxial subluxation. In patients with an ADI exceeding 5 mm, the space available for the spinal cord (SAC) becomes narrow, and these patients are at risk of developing cervical myelopathy (Fig. 60.14). Several methods for analysis of vertical subluxation have been reported (Fig. 60.15). McGregor's line connects the posterior margin of the hard palate to the most caudal point of the occiput. The tip of the odontoid should not project more than 4.5 mm above this line. Ranawat's baseline measurement is another method. Ranawat's line is from the center of the sclerotic ring of C2 to the line between the center of the anterior and posterior arches of C1. A distance of less than 13 mm
Fig. 60.15 Analysis of vertical subluxation: McRae's line, line, McGregor's line, and Ranawat's line.
Chamberlain's
is abnormal. Lower cervical lesions, such as subaxial subluxation (Fig. 60.16) and swan-neck or goose-neck deformity, also cause myelopathy.53 Although the cervical spine is affected in 36% to 86% of patients with RA, the incidence of myelopathy is reported to be 4.9% to 32%.47 Neck pain is the most common symptom in patients with RA and cervical spine involvement. Erosive changes along the apophyseal joints and surrounding soft tissues may be a source of pain. Cervical instability at C1-2 may cause secondary impingement of the posterior rami of the occipital nerve and may lead to occipitalgia.48 The Ranawat grading system provides useful information on the clinical status of patients with RA (Table 60.2).54 In patients with severe neck pain resulting from cervical instability or subluxation, fusion surgery is usually necessary.
Spinal Tumors Spinal tumors are classified as intramedullary, intradural extramedullary, and extradural. Meningioma, neurofibroma,
Chapter 60—Cervical Myelopathy
A
Fig. 60.16 Subaxial subluxation in rheumatoid arthritis. This 54year-old woman had anterior subluxation of C2, C4, and C6. A, Plain radiograph. B, T2-weighted sagittal magnetic resonance image.
B
Table 60.2 The Ranawat Criteria for Pain and Neural Assessment Pain Assessment
Grade 0: None Grade 1: Mild; intermittent, requiring only aspirin analgesia Grade 2: Moderate; a cervical collar was needed Grade 3: Severe; pain could not be relieved by either aspirin or collar Neural Assessment
Class I: No neurologic deficit
547
Metastasis to the cervical spine is another entity that may cause compression myelopathy, although such lesions are rare in the cervical spine.58,59 The most likely primary tumors to metastasize to the cervical spine are breast, prostate, and lung cancers. Because these metastases frequently occur in the vertebral bone, most cases of spinal metastasis are classified as extradural tumors. The symptoms of myelopathy are sometimes acute and gradually progressive. Neck pain is frequently observed in patients who have destructive changes in the cervical spine caused by the tumors. Kyphotic deformity resulting from vertebral collapse, direct tumor invasion in the epidural space, and insufficiency of the anterior spinal artery system may produce cervical myelopathy.
Class II: Subjective weakness, hyperreflexia, dysesthesias Class III: Objective weakness, long tract signs Class IIIa: Ambulatory (walking possible) Class IIIb: Nonambulatory (quadriparesis with resultant inability to walk or feed oneself) Adapted from Ranawat CS, O'Leary P, Pellici P, et al: Cervical spine fusion in rheumatoid arthritis, J Bone Joint Surg Am 61:1003, 1979.
neurilemoma, and schwannoma are common examples of intradural extramedullary tumors.55–57 Intradural extramedullary tumors may cause cervical myelopathy. Meningioma grows from the cells in the arachnoid. Neurofibroma, neurilemoma, and schwannoma usually arise from the dorsal sensory roots. Neurofibroma occurs in von Recklinghausen's disease and sometimes follows the nerve root out of the spinal canal, with a resulting dumbbell tumor. Intradural extramedullary tumors are typically eccentric and lead to Brown-Séquard–type myelopathy. Gadolinium-enhanced MRI is very useful for detecting intradural extramedullary tumors.
Epidural Abscess Spinal epidural abscess can cause a mass to develop in the spinal canal (Fig. 60.17) that can lead to acute myelopathy and quadriplegia.60–62 In patients with epidural abscess, fever and severe neck pain are usually observed. Staphylococcus aureus is the etiologic agent in more than 50% of cases of acute epidural abscess. Spondylodiskitis may be accompanied by epidural abscess as a local pathology, whereas epidural infection may occur hematogenously from a distant site.
Anomaly in the Cervical Spine Anomalies in the cervical spine are frequently seen at the craniovertebral junction or at the upper cervical spine. In most patients, the anomalies are usually found in childhood congenital malformations. However, abnormal structures in the cervical spine are sometimes found in adulthood. Cervical myelopathy can develop in patients with basilar impression, Arnold-Chiari malformation, and atlantoaxial instability, which is associated with Down's syndrome.63,64 Klippel-Feil
548
Section IV—Regional Pain Syndromes
syndrome and os odontoideum (Fig. 60.18) with instability also may cause myelopathy. Severe neck pain is less common in these conditions.
Destructive Spondyloarthropathy Destructive change in the cervical spine is often seen in patients undergoing long-term hemodialysis. The disease entity destructive spondyloarthropathy (DSA) was first reported by Kuntz et al in 1984.65 Radiologic features of this disease are disk space narrowing and irregularity of the cartilaginous end plate without osteophyte formation. The C56 level is involved in more than half these patients, but involvement of multiple levels is common. The prevalence
of DSA is 4% to 20% in patients undergoing hemodialysis and is higher in patients who undergo hemodialysis for more than 10 years.66 Causes of myelopathy are spinal cord compression resulting from spinal instability, intervertebral subluxation, intracanal amyloid deposition, and hypertrophy of the ligamentum flavum.67,68 In patients with marked destructive change and instability in the cervical spine, neck pain is frequently a symptom. Although the pathology of DSA has not been clearly elucidated, investigators have reported that hyperparathyroidism and amyloidosis play important roles in the progression of DSA.67
Diagnosis of Cervical Myelopathy Clinical Symptoms
Fig. 60.17 Spinal epidural abscess. This 69-year-old-man had acute onset of cervical myelopathy. The T2-weighted sagittal magnetic resonance image shows an epidural abscess (arrow) from C5-6 diskitis.
Fig. 60.18 Os odontoideum with instability. This 67year-old woman had moderate cervical myelopathy at the C1 level. A, Sagittal view on computed tomography. B, With T2-weighted sagittal magnetic resonance imaging, spinal cord atrophy is marked at the C1-2 level.
A
Clinical symptoms of cervical myelopathy vary from patient to patient. Thus, history taking is very important for the diagnosis. Symptoms depend on the stage of myelopathy and the impaired pattern of the spinal cord. In the upper extremities, numbness, paresthesia, and clumsiness are often observed. The typical manifestations of numbness and paresthesia represent a global and nondermatomal pattern in the upper extremities. Patients often complain of clumsiness. Their symptoms include difficulties with handwriting, manipulating buttons or zippers, and using a knife and fork or chopsticks. The “myelopathy hand,”69,70 which is defined as “loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers,” is one of the characteristic findings in patients with cervical myelopathy. In the lower extremities, subtle changes in gait and balance occasionally progress to spastic gait. Patients with cervical myelopathy have difficulties walking down stairs smoothly. These patients are often frightened to use steps without a handrail. Singh and Crockard71 reported that a simple walking test is useful to detect cervical myelopathy. These investigators found that both the time taken and the number of steps in a 30-m walk test in patients with cervical spondylotic myelopathy were significantly greater than in controls. Significant recovery in these parameters was reported after decompressive surgery. Patients occasionally complain of urinary urgency, hesitation, or frequency. In the advanced stage, they may have incontinence or retention of urine, although the incidence is very rare.
B
Neck pain is noted as a nonspecific symptom in patients with cervical myelopathy. Neck pain may be caused by degeneration of the intervertebral disk and facet joint in the cervical spine.15,72 Pain in the upper or lower extremities is also rarely found in patients with pure cervical myelopathy. Patients with both myelopathy and radiculopathy may have radiating pain in upper extremities. In contrast, Lhermitte's sign may be characteristic in patients with cervical myelopathy. Lhermitte's sign consists of a sensation resembling electricity that radiates from the head to the upper or lower extremities and is induced by forward flexion of the neck. The sign was first described by Babinski and Dubois and was emphasized by Lhermitte as a symptom of multiple sclerosis.5 The phenomenon is believed to be caused by the lesion in the posterior and lateral columns of the spinal cord. Investigators have reported that this sign is present in patients with cervical spondylosis, neoplasms, radiation myelopathy, and subacute combined degeneration,73,74 although the incidence of the sign is unclear in these disorders. Opinions diverge on the presenting symptoms of cervical myelopathy. Gorter75 reported that cervical myelopathy usually first manifests as a subtle gait disturbance. In contrast, Kokubun et al47 stated that the most common initial symptom is numbness or tingling in the upper extremities, especially in the hand. Although investigators have believed that these symptoms gradually worsen, one study suggested that most patients with mild myelopathy have a stable condition for a long time.45 Guidelines for the surgical management of cervical degenerative disease, published in the Journal of Neurosurgery Spine in 2009,76 state that the natural history of cervical spondylotic myelopathy is mixed. The disorder may manifest as a slow, stepwise decline, or the patient may note a long period of quiescence (class III). The classification of evidence is as follows: class I, evidence derived from well-designed, randomized controlled trials (RCTs); class II, evidence derived from RCTs with design problems or from well-designed cohort studies; and class III, evidence derived from case series or poorly designed cohort studies. In patients with severe or long-lasting symptoms of cervical spondylotic myelopathy, the likelihood of improvement with nonoperative treatment is low. Objectively measurable deterioration is rarely seen in patients less than 75 years of age with mild cervical spondylotic myelopathy.76 Patients with severe, progressive cervical myelopathy cannot walk without a cane, even on a flat road, at the late stage of the disorder. Bowel or bladder dysfunction accompanies extremely severe myelopathy. Several attempts have been made to classify the symptoms of spinal cord dysfunction in patients with cervical myelopathy. In 1966, Crandall and Batzdorf 77 devised a classification system based on the differential susceptibility of various spinal cord tracts (Table 60.3). In 1975, Hattori and Kawai78 categorized spinal cord symptoms into three types based on clinical experience (Fig. 60.19). Ferguson and Caplan79 categorized spondylosis with nerve involvement into four distinct but overlapping syndromes (lateral or radicular syndrome, medial or spinal syndrome, combined medial and lateral syndrome, and vascular syndrome) in 1985.
Physical Examination The most characteristic findings in cervical myelopathy are segmental signs and long tract signs. Segmental signs indicate
Chapter 60—Cervical Myelopathy
549
lower motor findings at the level of the compressive lesion. Long tract signs signify upper motor findings observed below the lesion. Neurologic findings vary, depending on the level and nature of compression. Further, cervical spondylotic myelopathy is frequently combined with lumbar spinal stenosis. This combination of disorders renders the neurologic findings more complex. Careful physical examination should be carried out to ascertain the presence or absence of cervical myelopathy.80,81 If myelopathy is present, the clinician will need to detect the precise lesion.82 The finding of myelopathy hand70,71 strongly
Table 60.3 Crandall and Batzdorf Classification of Cervical Myelopathy 1. Transverse Lesion Syndrome Patients with a transverse lesion, with involvement of the appropriate neurologic tracts (corticospinal, spinothalamic, posterior columns), have severe spasticity and frequent sphincter involvement, and one third exhibit Lhermitte's sign. 2. Motor System Syndrome Patients with motor system lesions (anterior horn cells, corticospinal tract) show spasticity but relatively innocuous or absent sensory disturbance. 3. Central Cord Syndrome Patients with central cord syndrome have severe motor and sensory disturbances, with greater expression in the upper extremities (Lhermitte's sign characterizes this group). 4. Brown-Séquard Syndrome Patients with Brown-Séquard syndrome have typical contralateral sensory deficits and ipsilateral motor deficits. 5. Brachialgia Cord Syndrome Patients with brachialgia cord syndrome demonstrate lower motoneuron and upper extremity involvement and upper motoneuron and lower extremity involvement. Adapted from Crandall PH, Batzdorf U: Cervical spondylotic myelopathy, J Neurosurg 25:57, 1966.
Type 1: Central cord type
Type II: Type I + posterolateral type
Type III: Type II + anterolateral type
Fig. 60.19 Classification of cervical myelopathy by Hattori and Kawai. (Adapted from Hattori S, Kawai S: Diagnosis of cervical spondylosis [in Japanese], Orthop Mook 6:13, 1979.)
550
Section IV—Regional Pain Syndromes
suggests the presence of cervical myelopathy. The diagnosis of myelopathy hand is made by two simple tests, the finger escape sign and the rapid grip and release test. The finger escape sign is positive when the patient is asked to hold all digits of the hand in an adducted and extended position and the two ulnar digits fall into flexion and abduction within 30 seconds. In the rapid grip and release test, a neurologically normal person can make a fist and rapidly release it 20 times in 10 seconds, but patients with cervical myelopathy are unable to do this with rapid motion. Hosono et al83 developed quantitative methods to evaluate the severity of myelopathy hand by the video-recorded 15-second test of rapid grip and release of fingers. The gait becomes wide-based and jerky. Patients have difficulty in toe walking and heel walking. These provocative tests are useful to detect subtle gait disturbance resulting from cervical myelopathy. Patients with cervical myelopathy have impaired proprioception below the lesion.84 Impairment in the lower extremities may lead to gait disturbance. A full neurologic examination is performed, with careful evaluation of reflex change, motor weakness, and sensory disturbance.
Reflex Change Reflex changes are extremely important in making a diagnosis of cervical myelopathy. Hyperreflexia is found as a long tract sign in the upper and lower extremities below the lesion. However, hyporeflexia in the upper extremity may result from a segmental sign of spinal cord compression. Further, hyporeflexia in the lower extremity may be accompanied by lumbar spinal stenosis. As for provocative tests, not many patients have clonus in their lower extremity, and this finding indicates the typical condition of hyperreflexia. Pathologic reflexes, such as Hoffman's reflex, Trömner's reflex, Wartenberg's reflex, and inverted radial reflex in the upper extremity and Babinski's reflex, Chaddock's reflex, and Oppenheimer's reflex in the lower extremity also indicate abnormal long tract signs consistent with spinal cord compression. One report noted a low incidence of hyperreflexia and provocative signs; thus, the absence of these signs does not preclude the diagnosis of cervical myelopathy.85 The scapulohumeral reflex86 is useful for detecting lesions cranial to the C3 vertebral body level. The reflex is hyperactive when elevation of the scapula or abduction of the humerus is found during tapping of the spine of the scapula or tapping of the acromion in a caudal direction. More than 95% of patients with high cervical spinal cord compression have a hyperactive scapulohumeral reflex.
Motor Weakness Generalized weakness and extremity weakness are found in some patients with cervical myelopathy. Muscle atrophy, muscle wasting, and fasciculation can be observed in the upper extremity of patients with cervical myelopathy. These findings are caused by lower motoneuron dysfunction and are regarded as segmental signs of a compressive lesion. Conversely the weakness in the lower extremity has been speculated to be caused by dysfunction of the corticospinal tract.
Sensory Disturbance The changes in senses of pain, touch and vibration, and proprioception are important to differentiate because the tracts of
each sensation vary. In cervical myelopathy, sensory change is global and ill-defined, compared with radiculopathy. A cervical line is typical for cervical myelopathy. This is the sensory change around the clavicle. Patients have sensory disturbance below the level of the clavicle and normal sensation above it. Investigators have speculated that the phenomenon of cervical line results from the distinct change of sensory lamination shown by Keegan's dermatome. Loss of vibration and proprioception signifies involvement of the posterior columns and is an indicator of poor prognosis of cervical myelopathy.84 Disturbance of proprioception is found in both upper and lower extremities.87,88
Evaluation System Various systems, including Odom's criteria89 and Nurick's score,90 have been suggested for evaluating the severity of cervical myelopathy. In 1975, the Japanese Orthopaedic Association (JOA)91 proposed a scoring system for cervical myelopathy as a basis for treatment of this disorder. In 1990, the JOA proposed a modified, 17-point scoring system (Table 60.4).92 This JOA system is reliable because of its high interobserver and intraobserver reliabilities,92 and it is used not only in Japan, but also in other countries. A patient-based scoring system for cervical spine disease was established in 2006 by the JOA (Table 60.5).93
Radiologic Evaluation X-ray studies, CT, three-dimensional CT, myelography, CTM, scintigraphy, MRI, and positron emission tomography (PET) are radiologic tools used in the evaluation of cervical myelopathy. Each imaging type has its own features and specificities. Thus, it is important to understand the purpose of the study before choosing an imaging modality. When patients are suspected of having cervical lesions, plain x-ray films should be taken at first. Plain x-ray films of the cervical spine in these patients include the following: the anteroposterior view; lateral views in neutral position, flexion, and extension; and oblique views.94 On the anteroposterior view, findings such as scoliotic deformity, tilting of cervical vertebrae, spondylotic change of uncovertebral joints (Luschka's joints), cervical ribs, and destructive changes are examined. Lateral views usually give the most useful information in patients with cervical myelopathy. Sagittal alignment, whether straight, lordotic, or kyphotic, is checked. Swan-neck deformity or goose-neck deformity can be observed in patients with RA. Destruction of the vertebral body may be caused by DSA or by metastasis from a malignant tumor. In the analysis of degenerative findings in the cervical spine, it is reasonable to categorize spinal canal findings as static factors or dynamic factors (previously described in this chapter). Static factors include the degree of disk space narrowing, the size of end-plate osteophyte, sagittal alignment, the size of the spinal canal, and ossified lesions such as OPLL and calcification of the ligamentum flavum. Dynamic factors can be determined by lateral views taken in flexion and extension. Instability and retrolisthesis or anterolisthesis of cervical vertebrae are checked on flexion and extension views. Foraminal stenosis is shown on oblique views. In contrast, the finding of a wide foramen may indicate the existence of a dumbbell
Table 60.4 Modified Japanese Orthopaedic Association Scoring System for Cervical Myelopathy* MOTOR FUNCTION
Fingers 0
Unable to feed oneself with any tableware including chopsticks, spoon, or fork, and/or unable to fasten buttons of any size
1
Can manage to feed oneself with a spoon and/or fork but not with chopsticks
2
Either chopstick feeding or writing is possible but not practical, and/or large buttons can be fastened
3
Either chopstick feeding or writing is clumsy but practical, and/or cuff buttons can be fastened
4
Normal
Shoulder and Elbow (Evaluated by MMT Score of the Deltoid or Biceps Muscles, Whichever Is Weaker) −2
MMT2 or below
−1
MMT3
−0.5 MMT4 0
MMT5
Lower Extremity 0
Unable to stand and walk by any means
0.5
Able to stand but unable to walk
1
Unable to walk without a cane or other support on a level
1.5
Able to walk without support but with a clumsy gait
2
Walks independently on a level but needs support on stairs
2.5
Walks independently when going upstairs, but needs support when going downstairs
3
Capable of fast but clumsy walking
4
Normal
SENSORY FUNCTION
Upper Extremity 0
Complete loss of touch and pain sensation
0.5
≤50% normal sensation and/or severe pain or numbness
1
>60% normal sensation and/or moderate pain or numbness
1.5
Subjective numbness of slight degree without any objective sensory deficit
2
Normal
Trunk 0
Complete loss of touch and pain sensation
0.5
≤50% normal sensation and/or severe pain or numbness
1
>60% normal sensation and/or moderate pain or numbness
1.5
Subjective numbness of slight degree without any objective sensory deficit
2
Normal
Lower Extremity 0
Complete loss of touch and pain sensation
0.5
≤50% normal sensation and/or severe pain or numbness
1
>60% normal sensation and/or moderate pain or numbness
1.5
Subjective numbness of slight degree without any objective sensory deficit
2
Normal
BLADDER FUNCTION 0
Urinary retention and/or incontinence
1
Sense of retention and/or dribbling and/or thin stream and/or incomplete continence
2
Urinary retardation and/or pollakiuria
3
Normal
*Total score for a healthy patient = 17. MMT, manual muscle test.
552
Section IV—Regional Pain Syndromes
Table 60.5 Japanese Orthopaedic Association Cervical Myelopathy Evaluation Questionnaire With regard to your health condition during the last week, please circle the number of one answer that best applies for each of the following questions. If your condition varies depending on the day or time, circle the number of the answer that applies when your condition was its worst. Q1-1. While in the sitting position, can you look up at the ceiling by tilting your head upward? 1. Impossible 2. Possible to some degree (with some effort) 3. Possible without difficulty Q1-2. Can you drink a glass of water without stopping despite the neck symptoms? 1. Impossible 2. Possible to some degree 3. Possible without difficulty Q1-3. While in the sitting position, can you turn your head toward the person who is seated to the side but behind you and speak to that person while looking at his or her face? 1. Impossible 2. Possible to some degree 3. Possible without difficulty Q1-4. Can you look at your feet when you go down the stairs? 1. Impossible 2. Possible to some degree 3. Possible without difficulty Q2-1. Can you fasten the front buttons of your blouse or shirt with both hands? 1. Impossible 2. Possible if I spend time 3. Possible without difficulty Q2-2. Can you eat a meal with your dominant hand using a spoon or fork? 1. Impossible 2. Possible if I spend time 3. Possible without difficulty Q2-3. Can you raise your arm? (Answer for the weaker side.) 1. Impossible 2. Possible up to shoulder level 3. Possible although the elbow and/or wrist is a little flexed 4. I can raise it straight upward Q3-1. Can you walk on a flat surface? 1. Impossible 2. Possible but slowly even with support 3. Possible only with the support of a handrail, a cane, or a walker 4. Possible but slowly without any support 5. Possible without difficulty Q3-2. Can you stand on either leg without the support hand? (Do you need to support yourself?) 1. Impossible with either leg 2. Possible on either leg for more than 10 seconds 3. Possible on both legs individually for more than 10 seconds Q3-3. Do you have difficulty going up stairs? 1. I have great difficulty 2. I have some difficulty 3. I have no difficulty Q3-4. Do you have difficulty with one of the following motions: bending forward, kneeling, or stooping? 1. I have great difficulty 2. I have some difficulty 3. I have no difficulty Q3-5. Do you have difficulty walking more than 15 minutes? 1. I have great difficulty 2. I have some difficulty 3. I have no difficulty Q4-1. Do you have urinary incontinence? 1. Always 2. Frequently 3. When retaining urine over a period of more than 2 hours 4. When sneezing or straining 5. No Q4-2. How often do you go to the bathroom at night? 1. Three times or more 2. Once or twice 3. Rarely
Table 60.5 Japanese Orthopaedic Association Cervical Myelopathy Evaluation Questionnaire—cont'd Q4-3. Do you have a feeling of residual urine in your bladder after voiding? 1. Most of the time 2. Sometimes 3. Rarely Q4-4. Can you initiate (start) your urine stream immediately when you want to void? 1. Usually not 2. Sometimes 3. Most of the time Q5-1. How is your present health condition? 1. Poor 2. Fair 3. Good 4. Very good 5. Excellent Q5-2. Have you been unable to do your work or ordinary activities as well as you would like? 1. I have not been able to do them at all. 2. I have been unable to do them most of the time. 3. I have sometimes been unable to do them. 4. I have been able to do them most of the time. 5. I have always been able to do them. Q5-3. Has your work routine been hindered because of the pain? 1. Greatly 2. Moderately 3. Slightly (somewhat) 4. Little (minimally) 5. Not at all Q5-4. Have you been discouraged and depressed? 1. Always 2. Frequently 3. Sometimes 4. Rarely 5. Never Q5-5. Do you feel exhausted? 1. Always 2. Frequently 3. Sometimes 4. Rarely 5. Never Q5-6. Have you felt happy? 1. Never 2. Rarely 3. Sometimes 4. Almost always 5. Always Q5-7. Do you think you are in decent health? 1. Not at all (my health is very poor) 2. Barely (my health is poor) 3. Not very much (my health is average) 4. Fairly (my health us better than average) 5. Yes (I am healthy) Q5-8. Do you feel your health will get worse? 1. Very much so 2. A little bit at a time 3. Sometimes yes and sometimes no 4. Not very much 5. Not at all On a scale of 0 to 10, with 0 meaning “no pain (numbness) at all” and 10 meaning “the most intense pain (numbness) imaginable,” mark a point between 0 and 10 on the lines below to show the degree of your pain or numbness when your symptom was at its worst during the week. If you feel pain or stiffness in your neck or shoulders, mark the degree. 0 10 If you feel tightness in your chest, mark the degree. 0 10 If you feel pain or numbness in your arms or hands, mark the degree. (If there is pain in both limbs, judge the worse of the two.) 0 10 If you feel pain or numbness from chest to toe, mark the degree. 0 10 Adapted from Fukui M, Chiba K, Kawakami M, et al: JOA back pain evaluation questionnaire (JOABPEQ)/JOA cervical myelopathy evaluation questionnaire (JOACMEQ): the report on the development of revised version April 16, 2007, J Orthop Sci 14:348, 2009.
554
Section IV—Regional Pain Syndromes
tumor. Further, the open-mouth anteroposterior view is used to detect lesions of the upper cervical spine. In 1970s and 1980s, myelography was the most useful and reliable tool for detecting lesions of the spinal canal. However, myelography was supplanted by the widespread use of MRI. CTM is clearly beneficial in its ability to detect atrophy of the spinal cord (Fig. 60.20). CT provides better information on bony lesions, such as bony spur and ossified ligament. Threedimensional CT is clinically useful not only in the diagnosis of myelopathy, but also in the decision process and safety promotion for surgical procedures in patients with cervical myelopathy. MRI has become the most important tool for detecting characteristic lesions in patients with cervical myelopathy.95 However, MRI is not indicated for everyone who is suspected to have cervical lesions. This imaging technique is recommended for patients who have obvious neurologic findings and persistent or worsening symptoms. The standard screening
Fig. 60.20 Spinal cord atrophy shown by computed tomography myelography. This 60-year-old man had ossification of the longitudinal ligament after cervical laminoplasty.
Fig. 60.21 High intensity in the spinal cord at the C5-6 level on T2-weighted sagittal (A) and axial (B) magnetic resonance images. The snake-eye appearance in the spinal cord is obvious on the axial image.
A
cervical spine MRI includes sagittal and axial sequences with T1- and T2-weighted images. The T1-weighted image provides superior spatial resolution and a survey of bone marrow signal intensity, whereas the T2-weighted study has the advantage of imaging the central canal and thecal sac. Because the cerebrospinal fluid and spinal cord are shown to be white and black, respectively, on the T2-weighted image, spinal cord compression is easily identified by the disappearance of cerebrospinal fluid. MRI can detect the extent of pathologic changes of the soft tissues, such as disk herniation and hypertrophy of the ligamentum flavum and posterior longitudinal ligament. Further, MRI is useful for visualizing various aspects of the spinal cord. The size and shape of the spinal cord are evident on both sagittal and transverse images. Long-lasting severe compression leads to spinal cord atrophy. Investigators have speculated that the size of the spinal cord is related to postoperative prognosis. In addition, MRI can show the intramedullary pathologic features of the spinal cord. The presence of high signal intensity on the T2-weighted image is considered to reflect a wide spectrum of pathologic changes of the spinal cord including reversible changes, such as edema, and irreversible changes, such as gliosis, myelomalacia, cystic necrosis, and syrinx formation (Fig. 60.21). Matsumoto et al96 reported that increased signal intensity is not related to a poor prognosis or the severity of myelopathy. In contrast, Mizuno et al97 examined the pathologic features of snake-eye appearance (a unique finding characterized as nearly symmetrical, round high signal intensity of the spinal parenchyma resembling the face of a snake; see Fig. 60.21) and noted that this finding revealed cystic necrosis of the spinal cord that led to poor recovery of upper extremity motor strength. Yukawa et al98 prospectively analyzed high signal intensity in the spinal cord on T2-weighted images. These investigators classified signal changes in the spinal cord into three grades: grade 0, none; grade 1, light (obscure); and grade 2, intense (bright). The result was that patients with greatest increased signal intensity in the spinal cord had the worst postoperative recovery.98 Therefore, the precise pathology of high signal intensity on T2-weighted images should be carefully analyzed. An attempt has been made to assess the utility of 18fluorodeoxyglucose (18FDG) PET in the evaluation of patients with
B
Chapter 60—Cervical Myelopathy
555
c ervical myelopathy. Uchida et al99 analyzed the glucose metabolic rate (standardized uptake value) in the spinal cord and found that postoperative neurologic improvement is correlated with the mean standardized uptake value.
be recommended to improve the clinical success rate in such cases. When the results of provocative diskography are positive, anterior diskectomy and fusion surgery are usually performed at the affected segment.2
Therapeutic Strategies for Cervical Compressive Myelopathy
Surgical Approaches
The therapeutic strategy for cervical myelopathy should be based on the patient's symptoms, the severity of the disorder, and the patient's general condition. Given that 5% of patients have a rapid onset of symptoms followed by a long period of quiescence, 20% show gradual but steady progression of signs and symptoms, and 75% show stepwise deterioration of clinical function with intervening variable periods of quiescent disease,2 careful observation is essential in the treatment of cervical compressive myelopathy. Emery15 noted that reevaluation every 6 to 12 months to assess deterioration of neurologic function or a change in symptoms may be appropriate during follow-up for patients with cervical compressive myelopathy. When the patient has a slight complaint, such as neck pain and mild myelopathy, conservative treatment should be considered. Conservative treatment consists of medication, cervical immobilization in a soft collar, active discouragement of high-risk activity, and avoidance of overloading, manipulation therapies, and vigorous or prolonged flexion and extension of the neck. When the patient complains of neck pain or radiculopathy mainly, narcotic analgesics, nonsteroidal anti-inflammatory agents, corticosteroids, muscle relaxants, and antidepressants are commonly recommended. A prospective randomized study by Kadanka and Bednarik et al100,101 revealed that surgery is not superior to conservative treatment for patients with mild or moderate forms of spondylotic cervical myelopathy, whereas surgery is more suitable for patients with a clinically worse status.
Indications for Surgery Patients with severe or progressive cervical myelopathy associated with concordant radiologic findings, such as spinal cord compression, are candidates for operative treatment. However, the clinician must consider the definition of severe myelopathy. A patient with spastic gait and myelopathy hand may be considered to have severe myelopathy, although no clear definition exists for the severity of this disease. Guidelines for the surgical management of cervical degenerative disease in the Journal of Neurosurgery Spine in 2009 stated that patients with more severe cervical spondylotic myelopathy (modified JOA score ≤ 12) should be considered for surgery, on a case-by-case basis.76 One study reported that 12 patients with severe disability showed significant improvement after surgical intervention; however, in patients with mild or moderate myelopathy, no difference between the operative group and the nonoperative group was evident at 12 and 24 months after treatment.102,103 Surgical intervention is not generally recommended when the sole symptom is neck pain, because surgical treatment is not always effective in patients whose predominant complaint is pain.2,72 However, in patients with severely limiting pain caused by cervical degenerative disease, surgical intervention may be considered.104 Provocative diskography may
With regard to the surgical management of cervical spondylotic myelopathy, controversy remains about whether the anterior or posterior technique is preferable because both techniques have been used successfully. The anterior option includes diskectomy with fusion and corpectomy with strut graft fusion techniques, which are performed with or without anterior instrumentation (plate or intervertebral cage) and cervical arthroplasty with artificial disk placement. The posterior option includes laminectomy, as well as laminoplasty with or without instrumentation (miniplate and ceramic spacer for opening the lamina or facet screw and screw and rod system for posterior fusion). Posterior foraminotomy can be added. The choice of approach is based on the local pathologic features, the patient's general condition, and the surgeon's skill. As for the local pathologic features of cervical myelopathy, the factors important in decision making are as follows: (1) the sagittal cervical alignment, (2) the width of the spinal canal, (3) the number of affected segments, (4) the location of the compressive abnormality, and (5) the presence of instability.2 The various surgical approaches, anterior cervical diskectomy, with fusion, anterior cervical corpectomy with fusion, laminectomy, laminoplasty, and laminectomy with arthrodesis, all provide near-term functional improvement in patients with cervical spondylotic myelopathy. The advantages, disadvantages, and possible early and late complications are described in Table 60.6.
Anterior Approach Anterior decompression and arthrodesis are performed through the anterior approach. This approach is advantageous for patients who have anterior compressive factors, such as bony spur behind the vertebral bodies, intervertebral disk herniation, and OPLL, because this approach allows direct decompression of the spinal cord. Further, in patients with cervical segmental instability, defined as excessive segmental motion according to the criteria proposed by White et al105 or anterolisthesis or retrolisthesis exceeding 3.5 mm,106 arthrodesis should be considered. Arthrodesis may also be effective for the management of axial pain. Studies have indicated that anterior fusion procedures provide good axial pain relief.2,19,72 However, the anterior approach is technically demanding, especially in patients with multilevel stenosis. Yonenobu et al107 reported that patients with one- or two-level involvement were managed with anterior cervical diskectomy or corpectomy and fusion, patients with involvement of four levels or more were managed with the posterior approach, and patients with involvement of three levels were managed with either the anterior or the posterior approach. When patients have a developmentally narrow spinal canal, posterior decompression is recommended because these patients generally have multilevel spinal stenosis. Autograft, allograft, titanium cage, polymethylmethacrylate (PMMA), hydroxyapatite, polyetheretherketone (PEEK), and recombinant human bone morphogenic protein-2 (rhBMP-2)
556
Section IV—Regional Pain Syndromes
Table 60.6 Advantages, Disadvantages, and Possible Early and Late Complications of Anterior and Posterior Surgical Approaches in Cervical Myelopathy Approach
Advantages
Disadvantages
Early Complications
Late Complications
Anterior approach
Direct decompression of the spinal cord Stabilization with fusion Correction of deformity Axial pain relief
Technically demanding Graft complication Need for a rigid brace after surgery
Dysphagia Recurrent laryngeal nerve palsy Bone graft dislodgment C5 palsy Horner's syndrome
Adjacent segment disease Loss of motion
Posterior approach
Not technically demanding Less need for a brace Avoidance of graft complications Applicable for multiple segments Applicable for developmental stenosis
Indirect decompression Not applicable for preoperative kyphosis
C5 palsy Postoperative axial pain Limited range of motion Shoulder stiffness
Late instability OPLL progression Postoperative kyphosis
OPLL, ossification of the posterior longitudinal ligament.
have been used for interbody grafting. These multiple strategies have been successful, and class II evidence supports the use of autograft, allograft, and titanium cage.108 Cervical spondylotic myelopathy has also been managed with cervical arthroplasty and the use of an artificial disk. Several types of artificial disks have been developed,109 and on the basis of biomechanical and clinical studies,110,111 favorable results have been reported.112 Cervical disk replacement seems to be successful in the management of single-level cervical spinal radiculopathy, but not myelopathy. Effectiveness during long-term follow-up is still uncertain. Strict selection criteria and adherence to scientific evidence are necessary.113 One of the disadvantages of the anterior approach is the long-term application of a rigid orthosis. Patients must wear a rigid brace until fusion is complete. Further, postoperative complications such as recurrent laryngeal nerve palsy, sympathetic nerve injury resulting in Horner's syndrome, dysphagia, and vertebral artery injury are associated with the anterior surgical approach. Dislodgment of grafted bone may occur in the postoperative period. During long-term follow-up, it is important to be aware of possible adjacent segment disease above or below the fusion levels.114
Posterior Approach Posterior surgery is divided into laminoplasty and laminectomy with posterior fusion. Laminectomy alone has become uncommon because many surgeons believe that postlaminectomy kyphosis is a possible complication. Because the spinal cord shifts dorsally after posterior decompressive surgery, posterior surgery causes indirect decompression of the spinal cord.115 Based on this background, posterior decompression is generally contraindicated for patients who have neutral or kyphotic cervical alignment. In fact, patients with lordotic alignment have better clinical results after cervical laminoplasty compared with patients with neutral or kyphotic alignment.116 Although the procedure has many modifications, cervical laminoplasty consists of two types, the French door type and the unilateral hinge type.117,118 No difference is reported in the postoperative results of these two types of laminoplasty. Because both of the posterior approaches are technically less demanding than the anterior approach, posterior surgery is indicated in patients with multilevel cervical stenosis.
Further, when patients have a developmentally narrow spinal canal, posterior decompression is recommended. In patients with cervical radiculopathy, posterior foraminotomy can be added at the affected level. When patients have cervical instability, segmental fusion with instrumentation can be considered. In particular, posterior fusion surgery is very effective in patients with RA and severe neck pain resulting from cervical instability.48,49 Procedures include occipitocervical fusion, occipitothoracic fusion, C1-2 fusion, cervical fusion, and cervical laminoplasty with posterior fusion. Fixation techniques using facet screws and pedicle screws or lateral mass screws with rod system fixation have been developed. Halo vest or rigid orthoses are required for posterior cervical fusion. In contrast, braces are less necessary after cervical laminoplasty. A soft collar is generally used for comfort after laminoplasty. A soft collar should be used for less than 1 month postoperatively. Based on data and experience,119 early muscle exercise with a short period (1 month) of soft collar use is beneficial postoperatively for patients who undergo cervical laminoplasty. Few complications are associated with the posterior surgical approach. However, when posterior instrumentation is used, especially fixation using pedicle screws, care must be taken not to penetrate the vertebral artery. Postoperative radiculopathy, motor palsy of the C5 nerve root, is a wellknown occasional complication of posterior decompression of the spinal cord. This complication can occur after anterior surgery. Postoperative C5 palsy is reported to occur in 5% to 8% of patients after surgery for cervical compressive myelopathy.120 No significant differences were noted between patients undergoing anterior decompression and fusion and laminoplasty, nor were distinctions apparent between the French door type and unilateral hinge type. Several causes, including a tethering effect of the nerve root and thermal or mechanical damage, have been suggested.121,122 However, the cause of this complication has not been clarified. The two mechanisms that may account for postoperative segmental motor paralysis are nerve root impairment and segmental spinal cord disorder. In a prospective study using MRI, Sakaura et al122 found that linear T2-weighted high-intensity areas in the spinal cord were significantly more likely to appear in the paralyzed segments after laminoplasty. Based on the findings, these investigators
Chapter 60—Cervical Myelopathy
proposed that some of the motor paralysis seen in these patients may be caused by spinal cord disease. Although definite preventive measures have not been developed, a previous report stated that foraminotomy and durotomy may be effective for releasing the tethering effect of the nerve root after laminoplasty.121 The prognosis is usually favorable, and investigators have reported that postoperative motor palsy spontaneously resolves within 12 months.121–123 Another common postoperative problem associated with the posterior approach is the presence of axial symptoms, such as axial pain and limited range of motion of the cervical spine. Regarding postoperative axial pain, the incidence was reported to be as high as 60% to 80% in early studies.124,125 However, the cause of this pain remains largely uncertain. Hosono et al126 reported that axial pain was prevented by avoiding inclusion of C7 in laminoplasty. This finding suggests that the pain originates from the neck muscle, because the C7 spinous process is connected to the scapula by the trapezius and rhomboideus minor muscles and has critically important biomechanical functions. Patients also complain of limited ROM of the neck after posterior surgery. The reduction in ROM is reported to range from 30% to 70% of preoperative ROM after cervical laminoplasty.127 Avoidance of postoperative laminar fusion and early mobilization after surgery are recommended.119
Conclusion 1. Patients with cervical myelopathy rarely have pain. However, neck pain from degenerative change in the cervical spine may be associated with cervical myelopathy.
557
2. Cervical myelopathy is caused by various pathologic conditions, such as cervical spondylosis, OPLL, cervical disk herniation, calcification of the ligamentum flavum, RA, spinal tumors, epidural abscess, anomaly of the cervical spine, and DSA. 3. The diagnosis of cervical myelopathy is based on history taking, physical examination, and radiologic evaluation. 4. The therapeutic strategy should be based on the patient's symptoms, severity of myelopathy, and general condition. 5. When patients complain of mild myelopathy and neck pain, conservative treatment, including medications (e.g., nonsteroidal anti-inflammatory drugs) and cervical immobilization should be provided, and therapeutic advice should be given. 6. Patients with severe or progressive cervical myelopathy associated with concordant radiologic findings are candidates for operative treatment. 7. Either an anterior or a posterior decompressive surgical procedure effectively improves symptoms of cervical myelopathy. 8. Both anterior and posterior approaches have specific advantages and disadvantages. 9. Anterior decompression and fusion may be effective for the management of axial pain when the patient has lesions at one or two intervertebral levels.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
61
Cervical Dystonia H. Michael Guo, James A. MacDonald, and Martin K. Childers
CHAPTER OUTLINE Historical Considerations 558 Pathogenesis 558 Clinical Presentation 559 Differential Diagnosis 560
Cervical dystonia (CD), one of the most common forms of focal dystonia, is characterized by simultaneous and sustained involuntary contraction of the cervical muscles that leads to twisting and repetitive head movements and abnormal postures.1,2 CD is also known as spasmodic torticollis and torsion dystonia. The prevalence of CD was reported to be 8.9 per million population in 1988.3 One study in Europe reported an annual prevalence for CD of 57 per million,4 and the Dystonia Medical Research Foundation estimated that no less than 300,000 people suffer from CD in North America. Patients with CD tend to be women in their fourth or fifth decades of life.5 In a study involving 266 patients, Chan et al6 found that the median age of onset was 41 years and the male-tofemale ratio was 1:1.9. Sixty-six percent to 75% of the patients with CD are believed to be disabled from the pain associated with this disorder.3,6–8 Dauer et al9 reported that CD is most often idiopathic, and it slowly develops over several years in patients 30 to 50 years old. Jankovic et al10 noted that approximately 12% of the patients with CD have a family history of the condition.
Historical Considerations As early as in the sixteenth century, the term torty colly was used by Rabelaris to elucidate wry neck.11 The term dystonia is attributed to the German neurologist Hermann Oppenheim who, in 1911, shortened the term dystonia musculorum deformans (reflecting the deforming nature of the syndrome). In his original article, Oppenheim (Fig. 61.1) described a childhood syndrome characterized by twisting of the torso, muscle spasms, jerky movements, and eventually progression of symptoms leading to fixed, contracted postures.12 Today, dystonia is defined as a clinical syndrome characterized by sustained, involuntary muscular contractions that frequently lead to twisting and repetitive movements or abnormal postures.2,13 Therefore, the term cervical dystonia refers to focal dystonia of the neck muscles that often leads to twisting or turning of the head and is more commonly known by the name torticollis or spasmodic torticollis. 558
Testing 560 Treatment 561 Complications and Pitfalls 563 Conclusion 563
Pathogenesis CD was described by Meige as a disorder originating in “the mind itself.” In the 1960s, psychiatrists postulated that the disorder resulted from castration anxiety or a symbolic “turning away from the world.” Thanks to modern imaging technology, electrophysiologic methods, and genetic analysis, the putative cause of CD has evolved from being a purely psychiatric disorder to a syndrome with links to a genetic origin and objective features. The pathogenesis of CD is still unknown, although evidence suggests a role for genetic factors. In 2001, a polymorphism in the dopamine D5 receptor (DRD5) gene was associated with CD in a British population, a finding suggesting that DRD5 is a susceptibility gene for CD.14 These findings were independently replicated by an Italian group of investigators who performed a large case-control study of the microsatellite deoxyribonucleic acid (DNA) region containing a polymorphism (CT/GT/GA)(n) at the DRD5 locus.15 The frequency of allele 4 was higher in the CD patients compared with controls, and this finding provided further evidence of an association between DRD5 and CD and supported the involvement of the dopamine pathway in the pathogenesis of CD. Several other lines of evidence point to a relationship between dopamine and CD. For example, primary torsion dystonia, a genetically heterogeneous group of movement disorders that includes CD, is inherited in an autosomal dominant fashion and is reported to be caused by a protein encoded by the DYT1 gene, torsion A, mutated in some forms of primary torsion dystonia. At least two other primary torsion dystonia gene loci have been mapped. The DYT6 locus on chromosome 8 is associated with a mixed phenotype, whereas the DYT7 locus on chromosome 18p is associated with adult-onset focal CD. A novel primary torsion dystonia locus (DYT13) was identified on chromosome 1 in a large Italian family with 11 affected members who displayed cervical, cranial, and upper limb dystonic symptoms.16 At present, 13 genes have been identified as causes for various forms of dystonia.17 In another line of research, electrophysiologic tests were used to evaluate three patients with hereditary dopa-responsive © 2011 Elsevier Inc. All rights reserved.
Chapter 61—Cervical Dystonia
559
Fig. 61.1 German neurologist Hermann Oppenheim and the title page of his original article describing cervical dystonia. (From Goetz CG, Chmura TA, Lanska DJ: History of dystonia: part 4 of the MDS-sponsored history of movement disorders exhibit, Barcelona, June, 2000, Mov Disord 16:339, 2001.)
dystonia, before and during treatment with levodopa.18,19 Results were compared with those in a group of 48 healthy subjects. In the patients before levodopa treatment, the soleus H-reflex recovery curve showed increased late facilitation and depressed late inhibition, a finding reflecting alterations in postsynaptic interneuronal activity. The inhibition of the H-reflex caused by vibration (presumably reflecting presynaptic inhibition) was depressed. Normalization of these test results occurred during levodopa treatment, concurrent with a clear clinical response. Because the H-reflex tests are thought to reflect mechanisms operating at the spinal level, the investigators concluded that spinal aminergic or dopaminergic systems are probably involved in dopa-responsive dystonia. Alternatively, patients with Parkinson's disease, when treated with levodopa, can develop dystonic symptoms (dyskinesias), and antipsychotic drugs that inhibit dopamine receptors are well known for their dystonic side effects. Hypothesized causes of CD include basal ganglia dysfunction, loss of motor cortex inhibition, and sensorimotor mismatch.20 Zhuang et al21 demonstrated abnormal firing rates within the basal ganglia in patients with dystonia. Those patients with focal dystonia had abnormal discharge rates in segmental distributions, whereas patients with generalized dystonia had involvement of the entire basal ganglia. The basal ganglia and its connections with the motor cortices are important in motor planning and movement. Disruption anywhere along the pathway from the basal ganglia to the motor cortex may lead to dystonia.22 Sensorimotor mismatch may also lead to the agonist and antagonist muscle contractions that occur in CD.23
Clinical Presentation Most patients with CD present with a combination of neck rotation (torticollis, the most common form), flexion (anterocollis), extension (retrocollis), side tilt (laterocollis), or lateral shift.24–26 These distinctive observable features of CD make the diagnosis fairly easy for the experienced clinician.27 Neck posturing may be static, but more commonly the head moves in a rhythmic or continuous pattern. Over time, sustained
Fig. 61.2 Touching the top or back of the head is one of the common sensory tricks in patients with cervical dystonia. (From Goetz CG, Chmura TA, Lanska DJ: History of dystonia: part 4 of the MDS-sponsored history of movement disorders exhibit, Barcelona, June, 2000, Mov Disord 16:339, 2001.)
a bnormal postures can result in permanent and fixed contractures. The duration of the disease is variable, ranging from months to decades. Sensory tricks (geste antagonistique) may temporarily improve symptoms. Sensory tricks commonly used by patients with CD include touching the chin, the back of the head, or the top of the head (Fig. 61.2).24 Symptoms of
560
Section IV—Regional Pain Syndromes
Table 61.1 Clues Suggesting Psychogenic Origin of Cervical Dystonia Movements
Abrupt onset Inconsistent movements (changing characteristics over time) Incongruous movements and postures (movements do not fit with recognized patterns or with normal physiologic patterns) Presence of additional types of abnormal movements that are not consistent with the basic abnormal movement pattern or are not congruous with a known movement disorder, particularly rhythmical shaking, bizarre gait, deliberate slowness carrying out requested voluntary movement, bursts of verbal gibberish, and excessive startle (bizarre movements in response to sudden, unexpected noise or threatening movement) Spontaneous remissions Movements that disappear with distraction Response to placebo, suggestion, or psychotherapy Presence as a paroxysmal disorder Dystonia beginning as a fixed posture Other Observations
False weakness False sensory complaints Multiple somatizations or undiagnosed conditions Self-inflicted injuries Obvious psychiatric disturbances Employment in the health profession or in insurance claims Presence of secondary gain, including continuing care by a “devoted” spouse Litigation or compensation pending Adapted from Fahn S: The varied clinical expressions of dystonia, Neurol Clin 2:541, 1984.
CD stabilize over time, and remission rates of 10% to 20% are reported, usually within the first few years. Symptoms of dystonia can spread to other parts of the body, most typically to the face, jaw, arms, or trunk.9 For example, in a study of 72 British patients who were followed up for 7 years, dystonia progressed to areas other than the neck (mainly the face and upper limbs in approximately one third of patients). Only 20% of patients experienced remission of symptoms.28 Patients with CD generally report insidious onset of symptoms that gradually worsen with time. Sleep helps relieve symptoms, whereas tasks such as driving, reading, or working at the computer exacerbate the unwanted movements. Stressful situations such as meeting others in social gatherings, giving a presentation, or concentrating on a difficult task also tend to make the symptoms worse. Because the diagnosis of CD depends on clinical examination without confirmatory laboratory tests, one of the most difficult tasks for the clinician treating these patients is to distinguish psychogenic CD from idiopathic CD. Sudden onset of symptoms or relentless progression of movements without abatement or change suggests a psychogenic disorder. Fahn listed “situations” (Table 61.1) that may provide clues to identifying a patient with psychogenic CD.13
Patients with CD do not attribute any particular head osition to discomfort.27 Myofascial trigger points are not presp ent. Patients with CD describe unpleasant sensations accompanied by “pulling” or “tugging.” Headaches are common25 and may respond to local injections with botulinum toxin (BoNT). Pain attributed to CD differs from pain described by patients with diskogenic pain or fibromyalgia. The severity of the pain is usually related to the intensity of the dystonia and muscle spasms.6 Jahanshahi et al28 reported progression of dystonic symptoms to extranuchal but still cervical innervated sites such as the hand, arm, oromandibular region in one third of 72 patients with adult-onset CD. Patients with CD may develop neck pain from the muscle contraction and muscle strain resulting from correcting the abnormal posture. The chronic abnormal posture may also lead to degenerative changes in the cervical spine, with consequent facet pain, radiculopathy, or spinal stenosis. Acute post-traumatic CD is different, and symptoms include immediate local pain followed by significant cervical range of motion, abnormal head and shoulder posture, and possible trapezius hypertrophy. Those changes often result in abnormal muscle contraction and pain,6,10 which contribute to functional limitations in these patients and interfere with activities of daily living.10 Rondot et al29 revealed that 99% of the 220 patients they studied had various functional difficulties. Dysphasia and subclinical swallowing motility disturbances were also reported in patients with CD.30 Permanent disability from the decreased cervical range of motion, involuntary movements, and intractable pain may occur in these patients.31 Although the diagnosis of CD is clinical, and inspection is usually enough, a thorough physical examination should be conducted to rule out “pseudodystonia,” caused by structural abnormalities,32 and secondary dystonia. Adolescents or children, particularly those patients with a sudden onset of symptoms, should be evaluated for other disorders. These disorders are discussed in the next paragraph.
Differential Diagnosis Torticollis is the observable feature of a twisted neck, and it may result from underlying causes other than CD.9 Therefore, the differential diagnosis (Table 61.2) includes other disease states associated with abnormal postures, movement disorders, alterations in the dopaminergic system, and neurodegenerative processes. Rarely, CD with dystonic components occurs in the context of Parkinson's disease. Head tremors may suggest an underlying cause of essential tremor but should not occur with the fixed abnormal postures seen in CD. Patients with acquired (congenital) CD of childhood should not display alternating hypertonia and hypotonia, and no palpable muscle hypertrophy or geste antagonistique should be present.
Testing A family history of movement disorders may suggest familial dystonia rather than idiopathic CD. Therefore, genetic tests based on DNA analysis for specific hereditary dystonias are available that use polymerase chain reaction to detect and amplify DNA in blood samples. However, no simple
Chapter 61—Cervical Dystonia
Table 61.2 Differential Diagnosis of Cervical Dystonia Idiopathic torsion dystonia Corticobasal ganglionic degeneration Cerebral palsy Huntington's disease Stroke Spinal cord ependymoma Wilson's disease Essential tremor Multiple sclerosis Myasthenia gravis Tardive dyskinesia Psychogenic torticollis Posterior fossa tumor Parkinson disease Multiple sclerosis Syrinx Congenital dystonia Side effects of psychogenic drugs Electrical injury
test confirms the diagnosis of CD or excludes a psychogenic component. Further research is needed before genetic testing becomes widely available in the clinic to identify patients at risk or to confirm a clinical diagnosis of idiopathic CD. Cervical radiographs may identify structural changes of the spine caused by scoliosis or spondylosis secondary to longstanding CD. Similarly, magnetic resonance imaging (MRI) of the cervical spinal cord is useful for determining the presence of spinal cord impingement secondary to bony changes from chronic CD. Contrast medium–enhanced swallowing studies can be performed in consultation with a speech pathologist to evaluate and treat patients for swallowing disorders that accompany CD. One treatment for CD, BoNT injection, may weaken the muscles surrounding the larynx. Thus, patients at risk for aspiration should be evaluated by a speech pathologist or a swallowing study before they are treated with BoNT. Brain imaging (by computed tomography or MRI) is indicated when the physical examination demonstrates findings consistent with an upper motoneuron syndrome, dementia, or pigmented corneal rings (e.g., Kayser-Fleischer rings seen in Wilson's disease). Electromyography (EMG) can help exclude the diagnosis in patients in whom the diagnosis is in question. For example, an EMG study of the sternocleidomastoid and splenius capitis muscles of eight patients with CD and of eight age-matched controls demonstrated that all control subjects but one showed a peak in splenius capitis EMG at 1 to 12 Hz, a finding that was absent in all subjects with CD.33 Frequency analysis between patients with CD and controls demonstrated differences suggesting that EMG may provide data to help distinguish CD from psychogenic torticollis. More commonly, EMG is used as a tool for mapping injection patterns for patients treated with BoNT. Identifying muscles by EMG, particularly those muscles deep to the surface that are contracting involuntarily, is useful before injection. The use of palpation alone to identify
561
tight or contracting muscles may bias the examiner to identify only the most superficial muscles, whereas the use of EMG can assist the clinician in identifying deeper muscles that can contribute to dystonic postures.27
Treatment In general, oral medications are not very effective for CD, and only a few have been systematically evaluated in clinical trials.34–36 Anticholinergic medications such as trihexyphenidyl or benztropine are worth a trial for patients with CD, but these medications are more useful in patients with generalized dystonias. Mexiletine was reported as helpful in the treatment of both CD and generalized dystonia.37,38 Glutamate receptor blockers such as amantadine, riluzole, and lamotrigine and spasmolytic agents such as clonazepam and baclofen have all been reported to be useful in some patients with CD.39,40 A subset of patients may respond to biofeedback training41 or muscle relaxation training. A soft cervical collar can reproduce the sensory tricks that reduce head turning, but effects usually wane after a few hours of wear. In patients who are refractory to all other conservative treatments, including BoNT injections, surgical resection of cervical muscles, peripheral selective denervation, or deep brain stimulation is a treatment option, and positive results are reported.42–55 Because many patients with CD find that specific postures, positions, or physical activities exacerbate symptoms, evaluation of workplace or household ergonomics can be helpful. Occupational or physical therapists can assist in the evaluation and make strategic recommendations for ergonomic aids. Patients often discover their own coping strategies to diminish physical stress, such as reducing the number of hours spent in front of a computer, working at a standing desk instead of a conventional desk, standing to the left or right of a person while carrying on a conversation, or making automobile seat adjustments. Patients with CD often seek treatment for pain other than for motor symptoms, and headache and neck pain are the main complaints. Therefore, it is advisable to examine new patients with neck pain or headache for physical findings consistent with CD. One theory27 attributed CD pain to the “relentless contraction of neck muscles” and theorized that one of the beneficial effects of BoNT is that it causes local muscle relaxation and thereby relieving pain. The most effective therapy for patients with CD is local injections of BoNT, the treatment supported by evidence-based reviews and meta-analysis.35,56–59 The United States Food and Drug Administration approved the indication for CD treatment in 2000. Three membrane proteins (collectively known as SNAREs)— synaptobrevin (Sbr), synaptosome-associated protein of molecular weight 25,000 (SNAP-25), and syntaxin—mediate the process of exocytosis of synaptic vesicles containing the neurotransmitter acetylcholine. Vesicle membrane fusion at the neuromuscular junction transfers the contents of secretory proteins and transmitters. SNARE proteins provide the substrate for at least one of the seven serotypes (A to G) of BoNT or tetanus toxin (TeTx), which are bacterial proteases that act to block neurotransmitter release.60 The family of BoNTs is also responsible for illness resulting from food contamination or wound infection. Botulinum neurotoxin type A (BoNT-A, Botox, Allergan, Inc., Irvine, CA; Dysport, Ipsen Pharmaceuticals, Boulogne-Billancourt, France) and type B (Myobloc, Solstice Neurosciences, San Francisco, CA)
562
Section IV—Regional Pain Syndromes
are produced by the anaerobic bacteria Clostridium botulinum, an organism found in soil and water. Only BoNT-A and BoNT-B are clinically available for therapeutic use in the United States. BoNT-A and BoNT-E cleave the carboxyl terminus of SNAP-25,61 whereas BoNT-B cleaves Sbr. The time course of functional motor recovery after synaptic BoNT intoxication differs among serotypes.61 Thus, the major assumption regarding the mechanism by which BoNTs decrease muscular contraction involves blocking acetylcholine release from presynaptic motor nerve terminal synapses. It is generally assumed that conditions such as dystonia and spasticity may be relieved subsequent to decreased muscular force in the areas injected, but this hypothesis has not been directly tested. Moreover, preclinical data may not necessarily apply to humans, because physiologic differences exist in the density, distribution, and morphology of the neuromuscular junction between species, age,62 and disease states.63,64 Indeed, chemodenervation by BoNT is generally considered the treatment of choice for patients with CD,65–67 and 63% of patients report benefit at 5 years.68 Jankovic and Schwartz69 followed up 202 of 232 patients who received BoNT injection for CD that was resistant to medical treatments. Seventy-one percent of those patients had improved symptoms, and 76% had almost complete relief of pain. Success is determined by the following clinical outcome measures: prevalence of complications (e.g., dysphagia),70 score on the Tsui scale,71–73 pain scores,72,74 the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS),57,75,76 and the relative cost of treatment.77 However, because neurologic impairments may have only a small impact on the functional health of patients with CD, other outcome measures that include disability, handicap, and global disease scales may increase the relative response rate of patients with CD who are treated with BoNT.73 The American Academy of Neurology78 performed an extensive evidencebased review in 2008 on the use of BoNT for the treatment of movement disorders. Academy investigators stated that level A evidence confirmed that BoNT should be offered for the treatment of CD by the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology.78 No clear guidelines are available for the appropriate dose of BoNT for the treatment of CD. The reason is that the most appropriate dose depends on several clinical and logistical considerations. First, the dose of BoNT should be individualized. Koller et al79 noted that fixed-dose fixed-muscle controlled studies of BoNT for the clinical management of CD did not produce the same effects as studies (or case reports) in which the dosages and muscles were individualized according to the patient. Second, clinicians should strive to administer the lowest effective dosage of BoNT for treatment of CD, to protect the patient from becoming immune to the agent's therapeutic effect.24,80 In general, patients should receive as few doses of toxin over the life span as possible, so long as their symptoms are manageable and until further studies of longterm effects of toxin therapy are completed. Because of the complexity of the neck, it is critical for the clinician to be familiar with anatomic landmarks, vital structures, and muscles for successful treatment of CD with BoNT injection. Attention should be paid to the following structures and organs when injecting BoNT: brachial plexus, carotid sheath, pharynx, esophagus, and apex of the lung. The muscles involved in various forms of CD are listed in Table 61.3. EMG guidance may play a role in determining dosage, in that
Table 61.3 Typical Muscle Involvement in Cervical Dystonia Type of Cervical Dystonia
Muscles Involved
Torticollis
Ipsilateral splenius/semispinalis capitis Contralateral sternocleidomastoid
Laterocollis
Ipsilateral sternocleidomastoid Ipsilateral splenius/semispinalis capitis Ipsilateral scalene complex Ipsilateral levator scapulae Ipsilateral posterior paravertebrals
Retrocollis
Bilateral splenius/semispinalis capitis Bilateral upper trapezius Bilateral deeper paravertebrals
Anterocollis
Bilateral sternocleidomastoid Bilateral scalene complex Bilateral submental complex
Shoulder elevation
Ipsilateral levator scapulae Ipsilateral trapezius
Adapted from Brashear A: Botulinum toxin type A in the treatment of patients with cervical dystonia, Biologics 3:1, 2009.
it may help with both effectively targeting affected muscles81 and also with targeting motor end plates within those muscles,82–84 thereby potentiating neurotoxin effects. However, when palpation alone is used to identify affected muscles, injection into either the midbelly or several sites of the muscle is generally recommended. Finally, conversion of equivalent units among BoNT serotypes (or even different formulations of the same serotype) may not be a simple matter of mathematical calculation.85 Two formulations of BoNT-A, marketed as Botox (Allergan, Inc.) and Dysport (Ipsen, Inc.), are available for clinical use. Although they are the same serotype, controversy exists regarding the conversion of units between available commercial formulations. Reviews65–67 suggested that 200 U Botox are roughly equivalent to 500 U Dysport (i.e., a 2:5 ratio or a conversion factor of 2.5), as indicated by results of a comparison trial.86 Only one formulation of BoNT-B, marketed as Myobloc, is commercially available for the treatment of patients with CD.57 Although it was not possible to make a definitive comparison between BoNT type A and type B for treatment of CD,87 Costa et al57,88 concluded in the Cochrane Review that single injections of BoNT type A and type B are effective and safe for treating CD and that further injection cycles continue to work for most patients, based on longterm uncontrolled studies. Table 61.4 lists published doses of BoNT-B for CD that range from 2500 to10,000 U. Fewer data are available on efficacy, safety, and dosing for BoNT-B. The Cochrane Review suggested that uncontrolled comparisons of BoNT-A and BoNT-B should be regarded “with suspicion.”57 Therefore, dosing conversions between A and B serotypes may be speculative. Another serotype, BoNT-F, may be a future option for patients who are immunoresistant to serotypes A and B, although less literature exists for BoNT-F.89,90 The effects of long-term treatment of CD with BoNT are not well studied. Three studies of long-term effects of BoNT-A in CD suggested that safety and efficacy persist over time. Brans et al91 reported improvements in disability, handicap, and perceived general health after 12 months of treatment.
Chapter 61—Cervical Dystonia
563
Table 61.4 Prospective Trials of Botulinum Neurotoxin in Cervical Dystonia Serotype
Product
Dose
Injection Site
Reference
55
30–250 U
SCM, trapezius, splenius capitis
Greene et al, 199094
7
50–100 U
SCM, trapezius
Jankovic and Orman, 198795
242
∼222 U
Splenius capitis, SCM, trapezius, scalenus
Jankovic and Schwartz, 199170
Botox
23
150 U
SCM, splenius capitis, trapezius
Lorentz et al, 199196
A
Botox
20
500 U
Active muscles
Moore and Blumhardt, 199197
A
Botox
35
152 U (SD ± 45)
One or more clinically indicated muscles
Odergren et al, 199898
A
Botox
54
NS
Individualized
Ranoux et al, 200282
A
Dysport
32
262–292 U
Individualized
Brans et al, 199671
A
Dysport
303
778 (SD ± 253)
SCM, trapezius, splenius capitis, levator scapulae
Kessler et al, 199992
A
Dysport
38
477 U (SD ± 131)
One or more clinically indicated muscles
Odergren et al, 199898
A
Dysport
75
500–1000 U
Splenius capitis and SCM
Poewe et al, 199872
A
Dysport
54
NS
Individualized
Ranoux et al, 200282
A
N/A
19
480 U
SCM, splenius capitis, trapezius
Blackie and Lees, 199099
A
N/A
20
100–140 U
SCM, splenius capitis, trapezius
Gelb et al, 1998100
B
Myobloc
109
5,000–10,000 U
2–4 cervical muscles
Brashear et al, 1999101
B
Myobloc
76
10,000 U
2–4 cervical muscles
Brin et al, 1999102
B
Myobloc
122
2,500–10,000 U
2–4 cervical muscles
Lew et al, 1997103
F
BoNT-F*
5
520–780 MU
Affected neck muscles
Houser et al, 199890
A
Botox
A
Oculinum
A
Botox
A
No. of Patients
*BoNT-F is not commercially available in the United States. SCM, sternocleidomastoid muscle; NS, not specified; SD, standard deviation.
Kessler et al92 reported disease severity improvement over 5 years, and Haussermann et al93 reported safety and efficacy data on BoNT treatment of 100 consecutive CD patients over 10 years. This line of evidence suggests that long-term treatment of CD with BoNT is both safe and effective, but further longitudinal studies will be required.
underlying swallowing disorder should be approached with caution when BoNT treatment is contemplated. Swallowing studies are helpful in determining proper nutritional strategies for patients at risk or for those patients who develop dysphagia after injections.
Complications and Pitfalls
Conclusion
Children or adults with fixed contractures of the neck caused by other problems (e.g., congenital torticollis) may be misdiagnosed with CD. Because a distinctive feature of CD is that the neck moves almost continually,27 patients with no active neck movement may not have true CD but rather a fixed contracture and will not respond to BoNT injections. Rarely, torticollis or torsion dystonia accompanies an upper motoneuron syndrome. In these cases when the neurologic examination reveals abnormalities, the patient should be referred to a neurologist or neurosurgeon for appropriate workup to determine the underlying cause. Finally, for patients with CD who are treated with BoNT injections, dysphagia can result from BoNT-induced weakening of the laryngeal muscles and may place the patient at risk for aspiration. Any patient with an
CD causes involuntary head turning or tilting, it may be painful, and it most often affects women in the third or fourth decade of life. The diagnosis is based on clinical examination and the finding of abnormal head and neck position. A diagnosis of idiopathic CD is made in the presence of an otherwise normal physical examination, normal family history, and normal results of laboratory and imaging studies. Local injection of BoNT is the treatment of choice for CD. Dysphagia is a potential complication of the injections.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
62
Degenerative Arthritis of the Shoulder Steven D. Waldman
CHAPTER OUTLINE Testing 566 Differential Diagnosis 566
The shoulder joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability to damage the joint cartilage.1 Osteoarthritis is the most common cause of shoulder pain and functional disability.2 It may occur following seemingly minor trauma or may be the result of repeated microtrauma. Pain around the shoulder and upper arm that is worse with activity is present in most patients suffering from osteoarthritis of the shoulder. Difficulty in sleeping is also common, as is progressive loss of motion (Fig. 62.1). Most patients presenting with shoulder pain secondary to osteoarthritis, rotator cuff arthropathy, and post-traumatic arthritis pain complain of pain that is localized around the shoulder and upper arm.3 Activity makes the pain worse, whereas rest and heat provide some relief. The pain is constant and characterized as aching. The pain may interfere with sleep. Some patients complain of a grating or popping sensation with use of the joint, and crepitus may be present on physical examination. In addition to the aforementioned pain, patients suffering from arthritis of the shoulder joint often experience a gradual decrease in functional ability with decreasing shoulder range of motion that render simple, everyday tasks such as combing hair, fastening a brassiere, or reaching overhead quite difficult.4 With continued disuse, muscle wasting may occur, and a frozen shoulder may develop (Fig. 62.2).
Treatment 568 Conclusion 569
Differential Diagnosis Osteoarthritis of the joint is the most common form of arthritis that results in shoulder joint pain (Table 62.1).6 However, rheumatoid arthritis, post-traumatic arthritis, and rotator cuff tear arthropathy are also common causes of shoulder pain secondary to arthritis. Less common causes of arthritis-induced shoulder pain include the collagen vascular diseases, infection,
Testing Plain radiographs are indicated in all patients who present with shoulder pain (Fig. 62.3).5 Based on the patient's clinical presentation, additional testing, including complete blood count, erythrocyte sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance imaging scan of the shoulder is indicated if rotator cuff tear is suspected (Fig. 62.4). Radionuclide bone scan is indicated if metastatic disease or primary tumor involving the shoulder is being considered. 566
Fig. 62.1 Range of motion of the shoulder can precipitate the pain of osteoarthritis of the shoulder. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 75.)
© 2011 Elsevier Inc. All rights reserved.
Chapter 62—Degenerative Arthritis of the Shoulder
567
Fig. 62.2 Adhesive capsulitis: Arthrography. A, Frontal radiograph obtained after the injection of 5 mL of radiopaque contrast material into the glenohumeral joint reveals a tightappearing articulation with lymphatic filling (arrow). No axillary pouch is seen. B, In a second patient, incomplete opacification of the glenohumeral joint is indicative of adhesive capsulitis. (From
A
B
Fig. 62.3 Osteoarthritis of the shoulder. The radiograph shows all the features of a “hypertrophic” form of osteoarthritis of the glenohumeral joint, with joint space narrowing, subchondral sclerosis, large cysts in the glenoid, and the massive inferior osteophytosis that is characteristic of this condition. (From Klippel JH, Dieppe PA: Rheumatology, ed 2, London, 1998, Mosby.)
villonodular synovitis, and Lyme disease. Acute infectious arthritis is usually accompanied by significant systemic symptoms including fever and malaise. This form of arthritis should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics, rather than injection therapy. The collagen vascular diseases generally manifest with polyarthropathy rather than monoarthropathy limited to the shoulder joint, although shoulder pain secondary to collagen vascular disease responds exceedingly well to the intra-articular injection technique described in the next section.
Treatment Initial treatment of the pain and functional disability associated with osteoarthritis of the shoulder should include a combination of the nonsteroidal anti-inflammatory drugs
Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 3108.)
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. The local application of heat and cold may also be beneficial. For patients who do not respond to these treatment modalities, an intra-articular injection of local anesthetic and steroid may be a reasonable next step.7 Intra-articular injection of the shoulder is performed by placing the patient in the supine position and preparing with antiseptic solution the skin overlying the shoulder, subacromial region, and joint space. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2 inch 25-gauge needle, and strict aseptic technique is used. With strict aseptic technique, the midpoint of the acromion is identified, and at a point approximately 1 inch below the midpoint, the shoulder joint space is identified. The needle is then carefully advanced through the skin and subcutaneous tissues, through the joint capsule, and into the joint (Fig. 62.5). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and is redirected superiorly and slightly more medially. Once the joint space is entered, the contents of the syringe are gently injected. The clinician should feel little resistance to the injection. If resistance is encountered, the needle is probably located in a ligament or tendon and should be advanced slightly into the joint space until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The major complication of intra-articular injection of the shoulder is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients will complain of a transient increase in pain following intra-articular injection of the shoulder joint, and patients should be warned of this possibility.
Conclusion Osteoarthritis of the shoulder is a common condition encountered in clinical practice. It must be separated from other causes of shoulder pain including rotator cuff tears. Intra-articular injection of the shoulder is extremely effective in the treatment of pain secondary to the aforementioned causes of arthritis of the shoulder joint. Coexisting bursitis
568
Section IV—Regional Pain Syndromes
Fig. 62.4 Full thickness rotator cuff tears: Glenohumeral joint arthography. These coronal sections were prepared after air arthography of the glenohumeral joint in cadavers of older persons. A and B, On a corresponding radiograph and photograph, note the irregular and torn rotator cuff (arrowheads), allowing communication of the glenohumeral joint (solid arrows) and the subacromial (subdeltoid) bursa (open arrows). C and D, In a different cadaver, note the irregular rotator cuff (arrowheads) with communication of the glumohumeral joint (solid arrows) and the subacromial (subdeltoid) bursa (open arrows). The articular cartilage is eroded. (From Resnick D: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 3090.)
A
B
D
C
Table 62.1 Causes of Shoulder Pain Localized Bony or Joint Space Disorders
Periarticular Disorders
Fracture Primary bone tumor Primary synovial tissue tumor Joint instability Localized arthritis Osteophyte formation Joint space infection Hemarthrosis Villonodular synovitis intra-articular foreign body
Bursitis Tendinitis Rotator cuff tear Impingement syndromes Adhesive capsulitis Joint instability Muscle strain Periarticular infection not involving joint space
Systemic Disease
Sympathetically Mediated Pain
Pain Referred from Other Body Areas
Rheumatoid arthritis Collagen vascular disease Reiter's syndrome Gout Other crystal arthropathies Charcot's neuropathic arthritis
Causalgia Reflex sympathetic dystrophy Shoulder-hand syndrome Dressler's syndrome Postmyocardial infarction adhesive capsulitis of the shoulder
Brachial plexopathy Cervical radiculopathy Cervical spondylosis Fibromyalgia Myofascial pain syndromes such as scapulocostal syndrome Parsonage-Turner syndrome (idiopathic brachial neuritis) Thoracic outlet syndrome Entrapment neuropathies Intrathoracic tumors Pneumothorax Subdiaphragmatic disorders such as subscapular hematoma of the spleen with positive Kerr's sign
Adapted from Waldman SD: Physical diagnosis of pain, ed 2, Philadelphia, 2010, Saunders, p 42.
Chapter 62—Degenerative Arthritis of the Shoulder
Worn arthritic cartilage
Glenoid fossa
and tendinitis may also contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot steroid. The foregoing technique is a safe procedure if careful attention is paid to the clinically relevant anatomy of the areas to be injected. Care must be taken to use sterile technique to avoid infection and universal precautions to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately following injection. The use of physical modalities, including local heat and gentle range-of-motion exercises, should be introduced several days after the patient undergoes the injection for shoulder pain. Vigorous exercises should be avoided because they will exacerbate the patient's symptoms. Simple analgesics and nonsteroidal anti-inflammatory agents or a COX-2 inhibitor may be used concurrently with this injection technique.
References Full references for this chapter can be found on www.expertconsult.com.
Fig. 62.5 Injection technique for intra-articular injection of the shoulder. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 58.)
569
IV
Chapter
63
Disorders of the Rotator Cuff D. Ross Henshaw and Edward V. Craig
CHAPTER OUTLINE Historical Considerations 570 Clinical Presentation 571 History 571 Physical Examination 571
Diagnosis 575 Plain Radiology 575
Disorders of the rotator cuff, ranging from tendon inflammation to rupture, are a common source of anterior shoulder pain. The etiology of rotator cuff disease is a subject of debate between those who believe in extrinsic causes of cuff injury and those who favor intrinsic causes. Although many extrinsic and intrinsic mechanisms have been described, the actual cause in each patient is likely multifactorial. Whatever the origin, cuff disorders from tendinosis to tearing have certain characteristic clinical and radiographic features that aid in diagnosis. Both operative and nonoperative treatments have their place in the definitive treatment of cuff disorders.
Historical Considerations The rotator cuff is a composite of four tendons that insert circumferentially on the proximal humerus and is one of the largest tendinous structures in the body (Fig. 63.1). The unconstrained bony architecture of the glenohumeral joint allows for the highest range of motion of any joint, and it sacrifices stability to do so. Along with labroligamentous restraints, the rotator cuff contributes to maintaining a delicate balance between mobility and stability by providing crucial dynamic stability throughout the arch of motion. These demands make the rotator cuff susceptible to overload and failure. The diagnosis and treatment of shoulder disorders were first described by Codman in his text The Shoulder, which represented 25 years of dedication to understanding and treating painful and stiff shoulders.1 In 1941, Bosworth2 described the supraspinatus syndrome, and our understanding of this was amplified by McLaughlin in 1944.3 Other investigators focused on the biceps tendon as a source of shoulder pain.4,5 However, until Neer6 introduced his concept of “impingement syndrome” in 1972, the etiology and treatment of shoulder pain were poorly understood, and the condition was often unsuccessfully treated. Neer's landmark articles clarified the source of rotator cuff injuries and how to treat them. He described the concept of primary impingement as an external source of mechanical injury to the rotator cuff, its pathologic 570
Ultrasound 575 Magnetic Resonance Imaging 575
Treatment 576 Nonoperative Management 576 Operative Management 577
Conclusion 578
stages, clinical diagnosis, and surgical treatment. Narrowing of the supraspinatus outlet is most frequently the result of anterolateral subacromial spurring; however, hypertrophy of the coracoacromial ligament, acromioclavicular joint spurring, or greater tuberosity malunion can also lead to impingement with mechanical cuff abrasion.7–9 Neer's concept of the acromion as a primary cause of cuff injury unified much of the thinking on rotator cuff surgery and led to anterior acromioplasty as the definitive surgical treatment. This operation has reported success rates ranging from 80% to 90%. However, disappointing results obtained with young athletes who throw overhand after acromioplasty and improved understanding of shoulder biomechanics led several investigators to offer alternative explanations to primary impingement as the cause of shoulder pain in athletes. Overuse syndromes are common in unconditioned athletes and occur when repetitive eccentric contractions lead to microtrauma within the tendon and inflammation.10,11 Secondary impingement occurs in athletes who use their shoulders repetitively at the extremes of motion, a situation that leads to gradual attenuation of static stabilizers and may result in instability. This microinstability causes the humeral head to sublux anteriorly and superiorly, thus creating secondary impingement as the cuff is compressed on the undersurface of the coracoacromial arch.12,13 Internal impingement is another source of rotator cuff injury. This entity, as described by Jobe et al,14 occurs when anterior subluxation leads to contact and abrasion of the undersurface of the supraspinatus tendon against the posterosuperior glenoid labrum. Impingement occurs within the joint rather than in the subacromial space.14 Treatment of these injuries in throwers thus focuses on reducing inflammation and, if necessary, on correcting the instability through either strengthening of scapular stabilizers and rotator cuff or retensioning of the capsuloligamentous complex. In contrast to the theory of an extrinsic, mechanical cause of rotator cuff disease, Codman1 was the first to introduce the concept of an intrinsic tendon degeneration as a source of © 2011 Elsevier Inc. All rights reserved.
Chapter 63—Disorders of the Rotator Cuff Clavicle Subscapularis m. Coracoid process
History Coracoacromial lig.
Acromion Acromioclavicular lig.
Supraspinatus m. Infraspinatus m.
571
Spine of scapula
Fig. 63.1 A superior view of the rotator cuff shows the four cuff tendons inserting circumferentially around the proximal humerus: subscapularis, supraspinatus, infraspinatus, and teres minor. The coracoclavicular liga ment and the acromion are also labeled.
rotator cuff disorders. From his anatomic dissections, Codman observed a “critical” zone near the insertion of the rotator cuff on the greater tuberosity of the proximal humerus that was both hypovascular and the common location of tears. Further work by Rathbun and Macnab15 on the vascularity of the rotator cuff supported this observation and led some investigators to emphasize primary anatomic pathologic features of the tendon itself that make the tendon prone to degeneration and tears. This finding contrasted with the concept by Neer of mechanical impingement as the primary cause of rotator cuff injuries. However, changes within the cuff can occur without accompanying stenosis of the subacromial space. Uhtoff et al16 showed that most tears begin inside the joint on the articular surface, rather than externally in the subacromial space. Ozaki et al17 looked at 200 anatomic shoulder specimens and correlated pathologic changes on the undersurface of the acromion with cuff tears. Subacromial spurring was present only with cuff tears, and, with partial tears, the acromion was almost always nonpathologic. These investigators concluded that primary cuff degeneration leads to tendon rupture. Nirschl and Pettrone18 called this degeneration angiofibroblastic hyperplasia and theorized that it led to diminished tissue perfusion. More recently, Yuan et al19 showed apoptotic cells in areas of tendon degeneration, a finding implicating uncontrolled apoptosis in the pathogenesis of intrinsic rotator cuff degeneration. Although the primary etiology of rotator cuff disease may still be debated, it is likely that for each individual patient the cause is multifactorial and probably includes some component of extrinsic and intrinsic injury. If the origin is multifactorial, then treatments should be tailored toward whichever cause is thought to dominate the clinical picture.
Clinical Presentation Rotator cuff disease usually manifests as anterior shoulder pain. The signs and symptoms, however, can often be vague and difficult to interpret. The diagnosis of rotator cuff injury therefore requires a systematic approach, including history of presentation, physical examination, and d iagnostic testing.
Patients with rotator cuff disorders most often present complaining of pain with an insidious onset and progressive course. These patients often have no history of trauma and frequently cannot clearly define when the pain started. Night pain, when present, is frequently associated with tendon tearing. Other symptoms include crepitus, catching, clunking, weakness, and loss of motion. Although weakness with loss of motion is characteristic of rotator cuff tears, this condition needs to be differentiated from strength deficiencies resulting from pain inhibition. The pain most commonly radiates to the anterolateral aspect of the shoulder to the deltoid insertion. However, significant overlap with other shoulder conditions occurs in this region. Labral injury, biceps inflammation, glenohumeral arthritis, joint stiffness, and acromioclavicular arthropathy can also cause shoulder pain. Radicular pain with motion crossing the elbow to the hand and wrist may indicate lower cervical involvement. However, C5 root involvement may manifest as isolated shoulder pain. It is essential to have a high index of suspicion for cervical spine disease as a cause of the painful shoulder. The age, occupation, and handedness of the patient and the onset, duration, timing, severity, quality, exacerbation, and relief of symptoms are important differentiating factors. Younger patients should be asked about their sports and activities and the relation of their symptoms to specific activities. A younger patient is more likely to have an underlying instability, whereas an older patient is more likely to have a mechanical or degenerative source of pain. Therapeutic history, whether with pain medication, physical therapy, or corticosteroid injections, should also be elicited to determine whether conservative therapy has been exhausted. Previous surgical treatment can also have an important impact on diagnosis and future management.
Physical Examination The physical examination includes inspection, palpation, range of motion, and special provocative testing. The cervical spine, elbow, wrist, hand, and neurovascular status should also be thoroughly assessed as potential pathologic sources. Cervical spine disease, particularly when it involves the C5 root, may manifest as shoulder pain. This is particularly true if neck pain with palpation, range of motion, and provocative maneuvers such as a Spurling test duplicates and reproduces the patient's presenting symptoms. Unlike in a patient who has a cuff tear, C5 root involvement may produce biceps weakness, and this may be a distinguishing feature. Visual inspection of both shoulders should be performed on every patient. The shoulders are examined from the front and back in a search for previous scars, discoloration, swelling, deformity, asymmetry, muscle atrophy, acromioclavicular prominence, and biceps rupture (Fig. 63.2). Scapular winging may accompany underlying scapulothoracic dysfunction and can be related to shoulder instability, muscle fatigue, muscle imbalance, scoliosis, kyphosis, and neurologic injury. The bony prominences of the neck, scapula, acromion, acromioclavicular joint, clavicle, and sternoclavicular joints are palpated. Acromioclavicular joint pain is an often overlooked but common source of anterior shoulder pain. Tenderness over the greater tuberosity and in the bicipital groove can be helpful to differentiate between bicipital and cuff inflammation. Pain in the suprascapular notch or the quadrilateral
572
Section IV—Regional Pain Syndromes
space may be associated with suprascapular and axillary nerve entrapment, respectively. Range of motion should be performed with the patient in the standing and supine positions in all planes, and the painful and nonpainful extremities should be compared. In the supine position, compensatory movements of the scapula and torso are removed and give a more precise measurement of range of motion. Discrepancies between active and passive range of motion may be secondary to pain inhibition, cuff tears, glenohumeral arthritis, volitional factors, muscle disease, and neurogenic factors. Patients with rotator cuff tears frequently have less range of motion actively than passively because of weakness. This situation differs from the loss of motion in arthritis and stiffness resulting from capsular contraction or inflammation, in which patients frequently have both active and passive reduced mobility. Excessive passive external rotation may indicate subscapularis rupture. However, in throwing athletes, excessive external rotation and decreased internal rotation are common and are secondary to stretched anterior structures and a contracted posterior capsule. Muscle strength testing of the deltoid, teres minor, infraspinatus, supraspinatus, subscapularis, and biceps should be conducted. However, these tests may be unreliable in the presence of pain. Several tests enable the examiner to isolate the individual muscles of the rotator cuff and to record results separately.20 Because the subscapularis is less frequently torn than the supraspinatus tendon, the diagnosis is often overlooked and may be delayed. Two reliable clinical tests for subscapularis function are available. For the liftoff test described by Gerber and Krushell,21 the arm is internally rotated, and the hand rests on the lower back or buttock. The patient then pushes his or her hand away in the horizontal plane, a maneuver that isolates the subscapularis.21 This test can be inaccurate when the patient recruits the triceps to move the hand away. To avoid
Fig. 63.2 Examination of both shoulders from behind the patient may reveal muscle asymmetry. In this patient, atrophy of the supraspinatus and infraspinatus muscles is present, as evidenced by wasting in the infraspinatus and supraspinatus fossae (arrows) on the right as compared with the left side.
this situation, a modification of the test can be done in which the examiner holds the patient's hand away from the small of the back and asks the patient to maintain the position. If the patient cannot do this, weakness or a tear of the subscapularis is suspected. Because the liftoff test is painful for many patients, the belly-press test may be used, as described by Tokish et al.22 With this test, the patient places his or her hands on the abdomen and rotates the elbows forward with and without resistance. The subscapularis is responsible for the ability to press against the abdomen and push the elbows away from the body. An inability to do this suggests tendon discontinuity. Jobe and Bradley23 described a useful test to isolate supraspinatus strength. Both arms are abducted to 90 degrees in the scapular plane and then are fully pronated to point the thumbs toward the ground. Side-to-side comparison to resisted downward force gives an accurate indication of function. Pain and weakness are indicators of partial- or full-thickness tears. The infraspinatus and teres minor are external rotators contributing approximately 90% and 10% rotational force, respectively. Their strength is best measured with the arm at the side in 0 degrees of abduction and the elbow flexed to 90 degrees. In this position, the patient externally rotates his or her hand and forearm against resistance. Weakness suggests a tear. This maneuver is perhaps the best clinical test for cuff discontinuity. This test is particularly useful because both arms may be simultaneously tested and compared. The hornblower's sign or drop sign is an attempt to isolate the teres minor (Fig. 63.3). The patient's arm is placed in 90 degrees of abduction and 90 degrees of forward elevation in maximal external rotation, and the patient is asked to maintain the position of the arm.24 Insufficient strength of the muscle or tendon is suggested if the patient cannot maintain this position. Assessing each muscle individually enables the examiner to determine the size and location of a tear. Complete ruptures of four tendons are rare. Most commonly, tears originate in the supraspinatus and enlarge to involve the tendons of the infraspinatus and teres minor. Small tears of the supraspinatus cause pain and weakness with the Jobe test, but external rotation usually remains strong. Patients with large tears involving
Fig. 63.3 Hornblower's sign. The inability to hold the forearm in 90 degrees of abduction indicates injury of the teres minor tendon.
Chapter 63—Disorders of the Rotator Cuff
the supraspinatus and infraspinatus have positive Jobe signs and weak external rotation, but an intact hornblower's sign. Patients with massive tears have weakness in the supraspinatus and infraspinatus, and because the teres is involved, they will not be able to hold the arm in the 90/90-degree position in maximal external rotation. Patients with massive cuff tears often use accessory muscles to elevate their arms. A common physical finding is the shrug sign, in which the patient activates the trapezius and deltoid when attempting forward elevation (Fig. 63.4). Less common are isolated subscapularis
Fig. 63.4 Shrug sign. With massive rotator cuff tears, patients recruit accessory muscles when attempting forward elevation. When this patient tries to elevate her arm, her shoulder shrugs as her trapezium and deltoid fire to compensate for a massive cuff tear.
A
573
tears, and patients often report a history of prior surgery or trauma. These patients have intact supraspinatus, infraspinatus, and teres minor strength with isolated subscapularis weakness and excessive external rotation. After the shoulder musculature has been assessed, provocative tests can be used to identify specific disorders.20 These tests include maneuvers that reproduce pain associated with impingement, instability, labral disease, and bicipital involvement. Not all of these tests are applicable for each patient, and the history and physical findings guide the examiner's choice of tests. Impingement signs are not specific and point only to the cause of pain within the subacromial space (subacromial spurs, bursitis, or cuff tear). In his description of impingement lesions, Neer described his classic impingement maneuver. While the scapula is stabilized, the arm is elevated in the plane of the scapula. As the arm reaches the limit of forward elevation, the greater tuberosity is jammed underneath the acromion and thus produces pain. Hawkins and Hobeika25 described another test for subacromial inflammation. With the arm at 90 degrees of forward elevation and slight adduction, and with the elbow flexed at 90 degrees, the shoulder is internally rotated, a maneuver that impales the greater tuberosity under the acromion.25 In the presence of cuff disease, this maneuver may elicit pain (Fig. 63.5). A simple adjunct used to confirm the location is the injection test. Local anesthetic is injected into the subacromial space, and the Neer and Hawkins tests are repeated. Significant reduction or elimination of pain within the subacromial space confirms that the pain originates in the subacromial space. If the patient reports pain relief, range of motion and muscle testing should be repeated. Weakness resulting from pain inhibition is minimized, and range of motion is improved. In this way, this test is highly effective at both localizing the source of pain and differentiating between weakness resulting from
B
Fig. 63.5 Neer and Hawkins tests. For the Neer test (A), the scapula is stabilized and the arm is elevated in the plane of the scapula. As the arm reaches the limit of forward elevation, the greater tuberosity is jammed underneath the acromion and thus produces pain. The Hawkins test (B) is performed with the arm at 90 degrees of forward elevation, in slight adduction; with the elbow flexed at 90 degrees, the shoulder is internally rotated, a maneuver than impales the greater tuberosity under the acromion.
574
Section IV—Regional Pain Syndromes
pain and weakness secondary to rotator cuff tear. Internal impingement can be assessed with Jobe's relocation test.14 With the patient supine, the arm is placed in the abducted externally rotated position (the same as for testing anterior apprehension when instability is suspected). The result of the test is positive if the patient experiences pain or discomfort. This position puts the undersurface of the supraspinatus in contact with the posterosuperior labrum, the site of internal impingement. This pain can be relieved with gentle posterior pressure placed on the anterior aspect of the arm to minimize
Fig. 63.6 Patients with anterior instability often feel a sense of instability and apprehension when the arm is placed in 90 degrees of abduction and 90 degrees of external rotation.
A
contact. When the examiner's hand is withdrawn, the contact and pain return. The most common direction of clinical instability is anterior. The anterior apprehension sign is performed by placing the patient's arm at 90 degrees of abduction and 90 degrees of external rotation. In this position, the patient may feel the sensation of shoulder subluxation anteriorly. The examiner should beware that patients often refuse to let the arm be put in this compromising position and are thus “apprehensive” about this arm position (Fig. 63.6). Other assessments of instability are the load and shift sign and the sulcus sign (Fig. 63.7). For the load and shift sign, the examiner places axial pressure along the humerus with one hand to center the humeral head and with the other hand translates the humerus anteriorly and posteriorly. Laxity is graded from 1 to 3. Grade 1 laxity is translation of the humeral head to the rim. For grade 2 laxity, the humeral head translates over the rim but is reducible. Grade 3 laxity manifests as translation over the rim and a humeral head that remains dislocated after pressure is removed. Inferior traction on the arm tests inferior translation and is noted by the presence of a sulcus under the lateral acromion: the sulcus sign. Anterior instability is called unidirectional if the instability is in one plane, and multidirectional laxity is increased translation in two or more directions when compared with the normal side. Generalized ligamentous laxity is not uncommon and should be assessed in every patient with multidirectional instability. Laxity should also be distinguished from instability. Many asymptomatic patients have loose or lax shoulders, but unless laxity causes pain or discomfort, it is not considered to reflect clinical instability. Instability therefore is symptomatic laxity. Involvement of the superior labrum and biceps anchor is best evaluated with the O'Brien active compression test.26
B
Fig. 63.7 In the load and shift maneuver, an axial load is placed along the humerus, and the humeral head is then shifted anteriorly and posteriorly (A). Inferior traction of the arm causing inferior subluxation produces a sulcus under the acromion (B).
The patient's arm is flexed, with the elbow kept straight and adducted to 15 degrees. In full pronation with the patient's palm facing down, an inferior force is applied to the arm. In the presence of superior labral disease, this position will elicit pain; and when the arm is fully supinated with the palm upward, the pain with downward pressure is relieved. In internal rotation with arm adduction, the biceps anchor is impinged by the humeral head; and with supination, which externally rotates the humeral head, the biceps pressure is relieved. Acromioclavicular disease is often overlooked as a common cause of failed rotator cuff treatment. The clinical diagnosis is usually not difficult because most patients are “point tender” over the joint. To test this source of pain, the examiner palpates the joint with one finger and with the other hand adducts the shoulder. It is also useful to palpate both the involved and uninvolved acromioclavicular joints simultaneously to compare the degree of tenderness. This maneuver often reproduces acromioclavicular symptoms.
Diagnosis Studies such as plain radiography, ultrasound, and magnetic resonance imaging (MRI) can be extremely helpful to confirm the clinical diagnosis of rotator cuff disease and in some cases to rule out other pathologic conditions. In some cases, these diagnostic studies can also help to determine the severity of the disease, the size of tears, and prognosis.
Plain Radiology Five standard radiographs are recommended for every patient with shoulder pain. These include a “true” anteroposterior view to evaluate the integrity of the glenohumeral joint articulation and anteroposterior views with the arm in internal and external rotation to show Hill-Sachs lesions and greater tuberosity sclerosis, respectively. Hill-Sachs and reverse Hill-Sachs lesions are indicative of anterior and posterior instability, respectively. With the patient's arm in external rotation, the greater tuberosity is rotated orthogonal to the x-ray, to allow better evaluation of its bony contour and to assess for the presence of sclerosis indicative of chronic injury from tendinosis or tear. The anteroposterior views also show resting state glenohumeral articulation. In patients with chronic large cuff tears, the centering effect of the cuff is lost, and the humeral head may migrate superiorly, thus decreasing the acromial humeral interval, which is normally 7 to 10 mm.27 An “outlet” view, which is a lateral view taken with 10 degrees of caudal tilt, allows evaluation of acromial morphology (Fig. 63.8) [online only]. In 1986, Bigliani and April7 described three types of acromial morphology: type 1 is smooth, type 2 is curved, and type 3 is hooked. Impingement and tears are more likely with curved and hooked acromions. Moreover, the presence of acromial spurring and calcification of the coracoacromial ligament can also be seen and indicate impingement. Finally, axillary radiographs show articular congruity and integrity of the glenoid bony architecture.
Chapter 63—Disorders of the Rotator Cuff
575
to develop and refine shoulder sonography, primarily because the shoulder is a common site of symptoms and clinical evaluation is challenging. Ultrasound is rapid, inexpensive, and comprehensive, and comparison with the asymptomatic shoulder is possible. Dramatic improvements since 2000 include newer high-resolution transducers, advances in the understanding of the technique of shoulder sonography, and more widespread agreement of the findings seen in patients with rotator cuff tears. All these factors have contributed to making the examination easier to perform and to interpret (Fig. 63.9). Ultrasound has evolved into a mature modality for evaluating rotator cuff tears and bicipital inflammation.30,31 Yamaguchi et al30 and Middleton et al31 reported their results of 100 shoulders evaluated preoperatively with ultrasound as compared with their arthroscopic findings. These investigators reported 100% sensitivity and 85% specificity, with an overall accuracy of 96% for full-thickness rotator cuff tears. Ultrasound, however, was less sensitive in detecting partial-thickness tears and biceps tendon ruptures. Although ultrasound has become a more sensitive and accurate diagnostic tool, its use is still not widespread, and results depend on the operator's experience.
Magnetic Resonance Imaging MRI is the modality of choice for assessing rotator cuff integrity. MRI is a noninvasive tool offering multiplanar analysis of not only the rotator cuff muscles and tendons but also the cartilage, cortical and medullary bone, and labral and acromioclavicular disease. Although sensitivities approach 100% and specificity is 95% for detecting full-thickness tears, MRI is less reliable for diagnosing partial-thickness tears. The size, shape, and amount of retraction and muscle atrophy are characterized by MRI and determine the repair potential (Fig. 63.10). The use of higher-resolution magnetic fields and improved pulse sequencing has made MRI arthrography with gadolinium contrast less routine.32 However, MRI arthrography may be useful in some instances for the identification of labral tears.
Ultrasound The potential use of ultrasound to evaluate rotator cuff disease has been recognized since the early 1980s.28,29 Even though sonography of the rotator cuff is more difficult than ultrasound imaging of other large tendons, a concerted effort has been made
Fig. 63.9 Ultrasound has evolved into a useful tool for evaluating rotator cuff disorders. This image depicts a normal rotator cuff. Note the deltoid (d), supraspinatus (ss), and humeral head (hh).
576
Section IV—Regional Pain Syndromes
Treatment
Nonoperative Management
The cause of rotator cuff disease is multifactorial, and the disorder affects patients of different ages and activity levels. Therefore, treatment should be individualized and tailored to meet the demands of each individual patient. Specifically, the physician should consider the patient's age, disability, and expectations and should carefully review the risks and benefits of both nonsurgical and surgical treatment. For instance, the incidence of cuff tears in patients who are more than 60 years old has been reported as high as 40%, and not all these patients are symptomatic.30 An active, healthy patient with acute rotator cuff tear should have acute surgical repair to restore function and to prevent retraction and secondary muscle atrophy, which can make repair more difficult and can adversely affect prognosis. Patients with chronic (≥3 months) symptomatic cuff tears who do not have precluding medical conditions should also have their tears repaired.
The effectiveness of nonoperative management was recognized by Neer, who found that many patients with impingement responded to nonoperative management. Nonoperative management may also improve symptoms in patients with cuff tears; however, complete pain relief is uncommon without surgical intervention.33 The principles of rehabilitation are to allow healing of inflamed tissue, to maintain motion, and to restore function. Generally, the earlier a rehabilitation program is begun, the more successful it is likely to be. Various nonoperative rotator cuff programs have been described, and all emphasize phases of therapy and recovery. Wirth et al33 described three phases of rotator cuff therapy: pain control, range of motion, and muscle strengthening. A fourth phase should also include modification of work or sport to avoid reinjury.33 Pain control and reduction of inflammation are the primary goals of the first phase. They are accomplished by rest and working with the therapist to avoid aggravating activities. This may involve avoiding overhead activities, and for athletes it may involve changing throwing mechanics or technique. For the worker who must work over his or her head, it may involve changing the work environment or, if that is not possible, job retraining or vocational change. Pain modification techniques such as cryotherapy, infrared therapy, ultrasound, transcutaneous electric nerve stimulation, and acupuncture can provide symptomatic relief. A course of nonsteroidal anti-inflammatory medication can be helpful, but these drugs should be used with caution in older patients and in those with peptic ulcer disease or hypertension. Subacromial corticosteroid injections can also be useful in patients with refractory cases, but this treatment should be limited to two to three injections spaced 2 to 3 months apart because of the possible adverse effects of catabolic steroids on tendons. After the patient's pain has been adequately controlled, the second phase begins with gentle stretching programs and restoration of range of motion to match that of the unaffected shoulder. The goal is to stretch out all area of tightness, with particular emphasis on the posterior capsule. Exercises progress variably from pendulum and wall walking to pulleys and often achieve capsular stretching. When near-normal passive flexibility of the shoulder is restored, the third phase, focusing on muscle strengthening, is initiated. Scapular strengthening is an essential and often overlooked component of shoulder therapy and should be initiated early. Internal and external rotator strengthening exercises are carried out with the arm at the side to strengthen the anterior and posterior cuff muscles while avoiding the position of impingement, as can occur with flexion and abduction exercises. These strengthening exercises are most conveniently performed using rubber tubing anchored to a door knob. The resistance is increased as the patient's muscle strength improves. Deltoid and supraspinatus strengthening exercises are added when they can be performed comfortably. The role of strength is in part to augment the resting tension of the humeral head “depressors” and, in effect, dynamically open the subacromial space. Finally, to return the patient to the comfortable pursuit of normal activities, analysis and modification of working environment or recreational techniques should be made, when necessary. Modifications include simple aids such as the use of a stepstool for patients needing to reach for high items. For throwing athletes, modification of body mechanics may prevent relapse
A
B Fig. 63.10 Magnetic resonance imaging evaluation of rotator cuff tears. A, Partial-thickness tear is demonstrated by high signal intensity through the articular half of the supraspinatus tendon (lines). The intact tendon has characteristic low signal intensity and is shown inserting onto the greater tuberosity. B, Full-thickness tear is demonstrated by the lowsignal tendon that is detached from its insertion and is retracted medially (arrows).
Chapter 63—Disorders of the Rotator Cuff
and may return the athlete to the previous level of competition. When a patient's occupation requires vigorous or repeated use of the shoulder in provocative positions, job retraining may be required.
Operative Management Surgical intervention is generally reserved for rotator cuff disease refractory to a 3- to 6-month period of conservative therapy. The precise surgical technique depends on the cause of rotator cuff injury and disease. Impingement and cuff tears caused by a narrowed subacromial space benefit from decompression or widening of the subacromial space through anterior acromial resection, whereas restoration of capsuloligamentous restraint is required for disorders secondary to instability. Arthroscopic surgery has permitted more accurate diagnosis and treatment of shoulder injuries. Because techniques and instrumentation have improved, most rotator cuff tears can be successfully treated arthroscopically. Traditional open procedures are gradually being replaced by arthroscopic techniques, but the type of procedure chosen depends both on the nature and severity of the disorder and, to some extent, the surgeon's experience and preference. The initial aims of surgical treatment are to relieve pain and to restore functional deficits. With arthroscopic techniques, less tissue injury occurs, with resulting improvements in postoperative pain and therapy. Classic impingement syndrome caused by a subacromial spur, thickened coracoacromial ligament, or other lesion is best treated with arthroscopic subacromial decompression. Decompression as described by Neer involved an open procedure with removal of up to 1 cm of anterolateral acromion.6 Modern arthroscopic techniques allow for accurate diagnosis of the source, location, and removal of the offending lesion (Fig. 63.11). Arthroscopic subacromial decompression has been shown to have success rates equal to those of open procedures, with faster recovery time.34 Another advantage of arthroscopic surgery is the ability to view both sides of the rotator cuff. In cases of impingement caused by subtle instability, capsular laxity or labral injury may be identified and treated. For partial- and full-thickness rotator cuff tears, surgical intervention is also based on treating both the cause of the injury and the tear itself. Decompression should be performed for impingement-associated tears, whereas a stabilization
A
B
577
procedure may be necessary to treat tears associated with microinstability. The treatment of partial-thickness tears is controversial, and no clear guidelines exist. In general, tears involving than 50% of the thickness are treated with decompression and débridement, and those involving more than 50% are treated by resecting the damaged tendon and repairing the defect as though the tear were full thickness (Fig. 63.12) [online only].35–38 Treatment of full-thickness tears is moving progressively more toward entirely arthroscopic techniques (Fig. 63.13). Arthroscopically assisted, mini-open procedures are also widely used as surgeons transition toward less invasive surgery (Fig. 63.14). As always, the choice of treatment is multifactorial, depending on the size, location, chronicity, and quality of the muscle and tendon. Many surgeons have reported success with mini-open and arthroscopic repairs that are equal or superior to open repair.39,40 The goal of surgery is to relieve pain. This can usually be achieved even in patients with large tears. However, improved strength and function, although desirable and often achievable, are less predictable than pain relief because tear size, quality of tissue, biologic healing potential, and irreversible muscle atrophy are not controllable.41
Fig. 63.11 Subacromial impingement. Arthroscopic evaluation of the subacromial space shows a subacromial spur (a) and fraying of the rotator cuff underneath (b).
C
Fig. 63.13 Example of a full-thickness tear and a subacromial spur (A) treated with arthroscopic acromioplasty (B) and rotator cuff repair (C).
578
Section IV—Regional Pain Syndromes
A
B
Fig. 63.14 Mini-open cuff repair. A and B, In arthroscopy-assisted rotator cuff repair, bursectomy, acromioplasty, and cuff mobilization can be achieved with arthroscopic techniques. Through a mini-open incision, the cuff is repaired to the greater tuberosity.
Conclusion Disorders of the rotator cuff are a common cause of anterior shoulder pain. Although the primary etiology of rotator cuff disease may still be debated, it is likely that for each individual patient the cause is multifactorial and probably includes some components of extrinsic and intrinsic injury. If the origin is multifactorial, then treatments should be tailored toward whichever cause is thought to dominate the clinical picture. A careful history and physical examination are crucial for diagnosing the source of injury. The age, occupation, and handedness of the patient and the onset, duration, timing, severity, quality, exacerbation, and relief of symptoms are important differentiating factors. Night pain and weakness are associated with tendon tears. Younger patients should be asked about their sports and activities and the relation of their symptoms to specific activities. A younger patient is more likely to have an underlying instability, whereas an older patient is more likely to have a mechanical or degenerative source of pain. Physical examination can test for specific cuff muscle weakness and
intra-articular disease, as opposed to extra-articular sources of pain. Radicular pain from the cervical spine should always be considered as a source of shoulder symptoms. Adjunctive studies including plain radiographs and MRI are an integral part of the evaluation and help determine the source and extent of injury. Ultrasound is also a useful, noninvasive method for diagnosing rotator cuff disease. Treatment is tailored to each individual patient's pathologic process. Although nonoperative modalities such as physical therapy, anti-inflammatory agents, and corticosteroid injections are successful, some patients require operative intervention. Both open and arthroscopic surgical procedures are highly successful for treating rotator cuff disease. Arthroscopy has improved clinicians' ability to define the pathologic features and treat many lesions more precisely, and it has become the technique of choice for most shoulder specialists.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
64
IV
Acromioclavicular Joint Pain Steven D. Waldman
CHAPTER OUTLINE Signs and Symptoms 579 Testing 579 Differential Diagnosis 579
The acromioclavicular joint is a common source of shoulder pain (Fig. 64.1).1 This joint is vulnerable to injury from acute trauma and repeated microtrauma. Acute injuries frequently take the form of falls directly onto the shoulder when playing sports or falling from bicycles. Repeated strain from throwing injuries or working with the arm raised across the body also may result in trauma to the joint. After trauma, the joint may become acutely inflamed; if the condition becomes chronic, arthritis and osteolysis of the acromioclavicular joint may develop.2
Signs and Symptoms A patient with acromioclavicular joint dysfunction frequently complains of pain when reaching across the chest (Fig. 64.2). Often the patient is unable to sleep on the affected shoulder and may complain of a grinding sensation in the joint, especially on first awakening. Physical examination may reveal enlargement or swelling of the joint with tenderness to palpation. Downward traction or passive adduction of the affected shoulder may cause increased pain (Fig. 64.3). If the ligaments of the acromioclavicular joint are disrupted, these maneuvers may reveal joint instability.
Testing Plain radiographs of the joint may reveal narrowing or sclerosis of the joint consistent with osteoarthritis. Magnetic resonance imaging is indicated if disruption of the ligaments is suspected. The injection technique described subsequently is both a diagnostic and a therapeutic maneuver. If polyarthritis is present, screening laboratory testing, including complete blood count, erythrocyte sedimentation rate, and antinuclear antibody testing, should be performed.
Differential Diagnosis Osteoarthritis of the acromioclavicular joint is a frequent cause of shoulder pain. This condition is usually the result of trauma. Rheumatoid arthritis and rotator cuff tear arthropathy also are common causes of shoulder pain that may mimic © 2011 Elsevier Inc. All rights reserved.
Treatment 579 Conclusion 581
the pain of acromioclavicular joint pain and may confuse the diagnosis.3 Less common causes of arthritis-induced shoulder pain include collagen vascular diseases, infection, and Lyme disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should be recognized easily by the astute clinician and treated appropriately with culture and antibiotics, rather than by injection therapy. The collagen vascular diseases generally manifest with polyarthropathy, rather than with monoarthropathy limited to the shoulder joint, although shoulder pain secondary to collagen vascular disease responds well to the intra-articular injection technique described subsequently.
Treatment Initial treatment of pain and functional disability associated with the acromioclavicular joint should include a combination of the nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. The local application of heat and cold also may be beneficial. For patients who do not respond to these treatment modalities, an intra-articular injection of local anesthetic and steroid may be a reasonable next step.4 Intra-articular injection of the acromioclavicular joint is performed by placing the patient in the supine position and preparing with antiseptic solution of the skin overlying the superior shoulder and distal clavicle. A sterile syringe containing 1 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch 25-gauge needle, and strict aseptic technique is used. With strict aseptic technique, the top of the acromion is identified, and at a point approximately 1 inch medially, the acromioclavicular joint space is identified. The needle is carefully advanced through the skin and subcutaneous tissues, through the joint capsule, and into the joint (Fig. 64.4). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and is redirected slightly more medially. After the joint space is entered, the contents of the syringe are gently injected. Some resistance to injection should be felt because the joint space 579
580
Section IV—Regional Pain Syndromes .
.
. and . . . and .
.
.
. . . .
.
. and
.
. .
.
. and . . . and .
. . .
.
. and . . .
. .
.
.
.
Fig. 64.1 Acromioclavicular joint. (From Kang HS, Ahn JM, Resnick D: Shoulder. In MRI of the extremities, ed 2, Philadelphia, 2002, Saunders, p 8.)
is small, and the joint capsule is dense. If significant resistance is encountered, the needle is probably in a ligament and should be advanced slightly into the joint space until the injection proceeds with only limited resistance. If no resistance is encountered on injection, the joint space is probably not intact, and magnetic resonance imaging is recommended. The needle is removed, and a sterile pressure dressing and ice pack are placed at the injection site.
The major complication of intra-articular injection of the acromioclavicular joint is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients complain of a transient increase in pain after intra-articular injection of the shoulder joint, and patients should be warned of this possibility. This injection technique is extremely effective in the treatment of pain secondary to the foregoing causes of arthritis of
Chapter 64—Acromioclavicular Joint Pain
581
Acromioclavicular lig.
Fig. 64.2 A patient with acromioclavicular joint dysfunction frequently complains of pain when reaching across the chest. (From Waldman SD: Acromioclavicular joint pain. In Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 78.)
Fig. 64.4 Injection technique for acromioclavicular joint pain. (From Waldman SD: Acromioclavicular joint pain. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 63.)
the acromioclavicular joint. Coexistent bursitis and tendinitis also may contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot steroid.2 This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection and universal precautions to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after injection. The use of physical modalities, including local heat and gentle range- of-motion exercises, should be introduced several days after the patient undergoes this injection technique for shoulder pain. Vigorous exercises should be avoided because they exacerbate the patient's symptoms. Simple analgesics and NSAIDs or COX-2 inhibitors may be used concurrently with this injection technique.
Conclusion Acromioclavicular joint pain is commonly encountered in clinical practice. It may manifest as an independent diagnosis after trauma to the shoulder, but more frequently it is a component of more complex shoulder dysfunction, including impingement syndromes and rotator cuff disease. Careful physical examination and confirmatory radiographic imaging usually confirm the diagnosis. If conservative treatment fails, injection of the acromioclavicular joint with local anesthetic and steroid is a reasonable next step. Fig. 64.3 The chin adduction test for acromioclavicular joint dysfunction. (From Waldman SD: Physical diagnosis of pain: an atlas of signs
References
and symptoms, Philadelphia, 2006, Saunders, p 105.)
Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
65
Subdeltoid Bursitis Steven D. Waldman
CHAPTER OUTLINE Signs and Symptoms 582 Testing 582 Differential Diagnosis 582
Inflammation of the subdeltoid bursa is a common cause of shoulder pain and functional disability.1 The subdeltoid bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the shoulder when playing sports or falling from bicycles. Repeated strain from throwing injuries, bowling, carrying a heavy briefcase, working with the arm raised across the body, rotator cuff injuries, or repetitive motion associated with assembly line work may result in inflammation of the subdeltoid bursa. The subdeltoid bursa lies primarily under the acromion and extends laterally between the deltoid muscle and the joint capsule under the deltoid muscle. It may exist as a single bursal sac or in some patients may exist as a multisegmented series of sacs that may be loculated (Fig. 65.1). If the inflammation of the subdeltoid bursa becomes chronic, calcification of the bursa may occur. The patient suffering from subdeltoid bursitis frequently complains of pain with any movement of the shoulder, but especially with abduction.2 The pain is localized to the subdeltoid area, with referred pain often noted at the insertion of the deltoid at the deltoid tuberosity on the upper third of the humerus (Fig. 65.2). Often, the patient is unable to sleep on the affected shoulder and may complain of a sharp, catching sensation when abducting the shoulder, especially on first awakening.
Signs and Symptoms Physical examination may reveal point tenderness over the acromion, and occasionally swelling of the bursa gives the affected deltoid muscle an edematous feel.1 Passive elevation and medial rotation of the affected shoulder reproduce the pain, as do resisted abduction and lateral rotation. Sudden release of resistance during this maneuver markedly increases the pain. Rotator cuff tear may mimic or coexist with subdeltoid bursitis and may confuse the diagnosis (see the later section on differential diagnosis). 582
Treatment 582 Conclusion 584
Testing Plain radiographs of the shoulder may reveal calcification of the bursa and associated structures consistent with chronic inflammation (see Fig. 65.1). Magnetic resonance imaging scan is indicated if tendinitis, partial disruption of the ligaments, or rotator cuff tear is suspected. Based on the patient's clinical presentation, additional testing including complete blood count, erythrocyte sedimentation rate, and antinuclear antibody testing may be indicated. Radionucleotide bone scan is indicated if metastatic disease or primary tumor involving the shoulder is being considered. The injection technique described later serves as both a diagnostic and a therapeutic maneuver.
Differential Diagnosis Subdeltoid bursitis is one of the most common forms of arthritis that results in shoulder joint pain. However, osteoarthritis, rheumatoid arthritis, post-traumatic arthritis, and rotator cuff tear arthropathy are also common causes of shoulder pain secondary to arthritis. Less common causes of arthritis-induced shoulder pain include the connective tissue diseases, infection, villonodular synovitis, and Lyme disease.3,4 Acute infectious arthritis is usually accompanied by significant systemic symptoms including fever and malaise and should be easily recognized by the astute clinician and treated appropriately with culture and antibiotics, rather than by injection therapy. The connective tissue diseases generally manifest with polyarthropathy rather than monoarthropathy limited to the shoulder joint, although shoulder pain secondary to connective tissue disease responds exceedingly well to the injection technique described subsequently.
Treatment Initial treatment of the pain and functional disability associ ated with osteoarthritis of the shoulder should include a combination of the nonsteroidal anti-inflammatory drugs
© 2011 Elsevier Inc. All rights reserved.
Fig. 65.1 Abnormalities of bursae in rheumatoid arthritis. Subdeltoid-subacromial bursitis. T2-weighted (TR/TE, 2000/80) coronal oblique spin-echo magnetic resonance image reveals a markedly distended bursa (arrows). Note the increase in signal intensity of fluid in the joint and in the bursa; however, regions of low signal density remain in the bursa. At surgery, these areas were found to be small fibrous nodules, or rice bodies. Also note the tear of the supraspinatus tendon (arrowhead), which may represent a complication of rheumatoid arthritis. (Courtesy of J Hodler, MD, Zurich, Switzerland. From Resnick D, Kransdorf
Chapter 65—Subdeltoid Bursitis
583
Fig. 65.2 Abduction of the shoulder exacerbates the pain of subdeltoid bursitis. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 82.)
MJ, editors: Bone and joint imaging, ed 3, Philadelphia, 2004, Saunders, p 214.)
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. The local application of heat and cold may also be beneficial. For patients who do not respond to these treatment modalities, an intra-articular injection of local anesthetic and steroid may be a reasonable next step.5 Injection of the subdeltoid bursa is performed by placing the patient in the supine position; proper preparation with antiseptic solution of the skin overlying the superior shoulder, acromion, and distal clavicle is performed. A sterile syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 11⁄2-inch 25-gauge needle, and strict aseptic technique is used. With strict aseptic technique, the lateral edge of the acromion is identified, and at the midpoint of the lateral edge, the injection site is identified. At this point, the needle is carefully advanced in a slightly cephalad trajectory through the skin and subcutaneous tissues beneath the acromion capsule into the bursa (Fig. 65.3). If bone is encountered, the needle is withdrawn into the subcutaneous tissues and is redirected slightly more inferiorly. After the bursa has been entered, the contents of the syringe are gently injected while the operator slowly withdraws the needle. Resistance to injection should be minimal unless calcification of the bursal sac is present. Calcification of the bursal sac is identified as resistance to needle advancement with an associated gritty feel. Significant calcific bursitis may ultimately require surgical excision to effect complete relief of symptoms.
Deltoid m. displaced Inflamed subdeltoid bursa Supraspinatus m.
Fig. 65.3 Technique for subdeltoid bursa injection. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 110.)
The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The major complication of injection of the subdeltoid bursa is infection. This complication should be exceedingly rare if strict aseptic technique is followed. Approximately 25% of patients complain of a transient increase in pain following injection of the subdeltoid bursa, and patients should be warned of this possibility.
584
Section IV—Regional Pain Syndromes
This injection technique is extremely effective in the treatment of pain secondary to subdeltoid bursitis. Coexistent arthritis and tendinitis may also contribute to shoulder pain and may require additional treatment with more localized injection of local anesthetic and depot steroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection and to use universal precautions to avoid risk to the operator. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately following injection. The use of physical modalities including local heat and gentle range-ofmotion exercises should be introduced several days after the patient undergoes this injection technique for shoulder pain. Vigorous exercises should be avoided because they exacerbate the patients' symptoms. Simple analgesics and NSAIDs may be used concurrently with this injection technique.
Conclusion The pain of subdeltoid bursitis is commonly encountered in clinical practice. It may manifest as an independent diagnosis following trauma to the shoulder, but more frequently it occurs as a component of more complex shoulder dysfunction including arthritis, impingement syndromes, and rotator cuff disease. Careful physical examination combined with confirmatory radiographic imaging usually confirms the diagnosis. If conservative treatment fails, injection of the subdeltoid bursa with local anesthetic and steroid is a reasonable next step.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
66
IV
Biceps Tendinitis Robert Trout
CHAPTER OUTLINE Historical Considerations 585 Signs and Symptoms 585 Testing 585 Differential Diagnosis 586
Historical Considerations The role of the biceps tendon in shoulder pain was controversial in the literature for most of the twentieth century. The earliest descriptions of bicipital tendinitis as a clinical entity were a series of articles by Meyer in the 1920s,1,2 in which he reported spontaneous subluxations and degeneration of the tendon. Many investigators remained skeptical regarding the concept of the biceps tendon as a primary source of pain in the shoulder, and numerous articles were published that either supported or refuted the idea.3,4 In hindsight, both groups may have been partly correct. In the 1970s, Neer5 was the first to describe biceps tendinitis as a secondary manifestation of impingement syndrome. Thus, the biceps tendon does not usually act as a primary pain generator in the shoulder, but rather acts in association with other shoulder diseases, most notably rotator cuff disorders. Numerous later studies supported this finding and eventually led to the classification of primary and secondary bicipital tendinitis.6,7 Secondary tendinitis, occurring in association with other underlying shoulder problems, is the most common type and may account for approximately 95% of cases.8 Primary tendinitis, in which the patient has an isolated problem of the biceps tendon, is often seen in younger patients and may be related to abnormality of the bicipital groove, possibly from previous trauma. These patients are at high risk for eventual rupture of the tendon. Initially, articles focused on tenodesis of the tendon as the definitive treatment of the problem.9 However, this approach eventually fell out of favor because of the high failure rate.10 More recently, arthroscopy was combined with tenodesis and acromioplasty, with better results. However, the main focus has been on early conservative treatment, with surgery considered in selected cases only.
Signs and Symptoms Although tendinitis implies an inflammatory condition, biceps tendinitis is usually a primarily degenerative problem because the tendon is subject to wear and tear under the coracoacromial arch, similar to the process observed in the rotator © 2011 Elsevier Inc. All rights reserved.
Treatment 587 Complications and Pitfalls 587 Conclusion 587
cuff (Fig. 66.1).5 The most common symptom is pain in the anterior shoulder that may radiate to the biceps muscle and worsen with overhead activities. Patients often report significant nighttime pain. Usually, they have no history of a specific traumatic event. Throwing athletes, in particular, also develop instability of the biceps tendon. They experience an audible pop or snap while moving through their throwing motion. On physical examination, the most common finding is point tenderness in the bicipital groove. The point of tenderness should move as the shoulder is passively internally and externally rotated. Other provocative tests that are specific for bicipital tendinitis include the Speed test and the Yergason test. In the Speed test, the patient holds the elbow in extension with the forearm supinated and then flexes the shoulder against resistance, thus reproducing the patient's pain (Fig. 66.2).8 When performing the Yergason test, the patient supinates the forearm against resistance with the forearm flexed (Fig. 66.3). A positive test result occurs when pain refers to the bicipital groove.8 Instability should be evaluated by placing the arm in abduction and external rotation and then slowly bringing it down to the patient's side. A palpable snap signifies a positive test result as the tendon subluxes. Because of the high percentage of other common shoulder disorders that occur in association with bicipital tendinitis, a full shoulder examination should always be performed. This examination should include passive and active range of motion, subdeltoid bursal and acromioclavicular joint tenderness, and other provocative testing for impingement syndrome and rotator cuff tears.
Testing Initial testing consists of plain films of the shoulder. These radiographs are usually unremarkable, but they can detect glenohumeral arthritis, fracture, or articular abnormalities from previous trauma. In addition, calcific tendinitis of the biceps tendon has been reported rarely and may be visible on plain films. If this finding is present, arthroscopic débridement of the tendon may be required.11 A biceps groove view can also be performed to evaluate for spurring of the groove, which many predispose a patient to primary tendinitis. 585
586
Section IV—Regional Pain Syndromes Coracoid process
Acromion
Damaged tendon
Biceps brachii long head Biceps brachii short head
Fig. 66.1 The long head of the biceps may be subjected to wear and tear under the acromion arch.
Fig. 66.3 The Yergason test for biceps tendon impingement.
may detect full-thickness tendon tears, but they lack sensitivity for partial-thickness tears, particularly if the joint does not adequately fill with contrast material. These methods are also invasive. Ultrasound is noninvasive and inexpensive and may have a role in initial testing. Ultrasound is able to reveal both rotator cuff and bicipital tendon tears. However, its sensitivity varies widely among institutions because the technique is highly operator dependent. Ultrasound is also unable to reveal labral disease. Rarely, primary tendinitis may occur secondary to a generalized inflammatory or autoimmune condition. If the patient's shoulder symptoms are accompanied by signs of synovitis or arthritis in other joints, routine laboratory tests should also be considered including erythrocyte sedimentation rate, antinuclear antibody, and rheumatoid factor.
Differential Diagnosis
Fig. 66.2 The Speed test for biceps tendon impingement.
For patients with persistent symptoms or when tendon rupture is suspected, magnetic resonance imaging (MRI) is the most sensitive and specific test. Although MRI is expensive, it is the standard for imaging of the joint and surrounding tendons. It can elucidate both edema and full and partial tears of the biceps tendon while also identifying rotator cuff and labral disorders. For patients unable to undergo an MRI scan, other possible alternatives include computed tomography (CT) scan, ultrasound, and arthrography. CT is useful to evaluate for bony lesions when ruling out other possible causes of pain, such as humeral fractures or acromioclavicular joint disease, but this imaging technique cannot adequately detect soft tissue damage. As a result, it has only limited use during attempts to make a definitive diagnosis. Arthrography and CT arthrography
The temptation to diagnose a case of anterior shoulder pain rapidly as tendinitis should be resisted because biceps tendinitis is often secondary to other types of shoulder disorders such as impingement syndrome and rotator cuff disorders. Table 66.1 lists the differential diagnosis of bicipital tendinitis. Patients with other neuropathic and neoplastic conditions may also exhibit radiating or referred pain to the anterior shoulder that may mimic a simple case of tendinitis. Fortunately, these problems can usually be identified with an adequate history and physical examination. Impingement syndrome is typified by the “painful arc” of 60 to 120 degrees of active abduction. A helpful test is the Neer sign, in which the patient's pronated arm is brought into full flexion, thus causing impingement under the acromion and reproducing the painful symptoms. Patients with adhesive capsulitis and glenohumeral osteoarthritis exhibit decreased passive and active range of motion in all planes. Some patients with long-standing bicipital tendinitis may eventually develop adhesive capsulitis. Clicking of the shoulder with overhead movements or a positive clunk sign may indicate labral disease. Provocative tests, such as the Hawkins test, may identify a rotator cuff
Chapter 66—Biceps Tendinitis
587
Table 66.1 Differential Diagnosis of Bicipital Tendinitis Bicipital rupture Impingement syndrome/rotator cuff tear Glenohumeral arthritis Adhesive capsulitis Acromioclavicular joint arthritis Cervical radiculopathy Brachial plexitis Autoimmune/systemic inflammatory disorders Pancoast's tumor/metastatic disease
isorder by eliciting pain when the patient's arm is raised to d 90 degrees and the shoulder is then internally rotated. Pain that localizes more to the top of the shoulder may be an indication of acromioclavicular joint arthritis and often worsens with abduction of greater than 120 degrees. This pain can be reproduced with the cross-arm test, in which the patient raises the arm to 90 degrees and then actively adducts it. Pain radiating distal to the elbow or other associated symptoms of numbness and paresthesias are typical of a radicular origin or brachial plexitis. Radicular pain is often exacerbated by coughing or sneezing, whereas a common presentation of brachial plexitis is acute pain followed within 2 weeks by weakness in the upper extremity. If these diagnoses are suspected, electrodiagnostic studies or cervical imaging may be considered.
Treatment Initial treatment for both primary and secondary bicipital tendinitis is conservative, with rest, icing, and anti-inflammatory medications. Several studies advocated the use of subacromial and glenohumeral steroid injections. This approach is logical given the high incidence of associated impingement syndrome and that the tendon of the long head is intra-articular. For patients with primary tendinitis, injection into the biceps tendon sheath can be beneficial (Fig. 66.4). The technique for this injection is not difficult, but the procedure should be performed carefully to avoid direct injection into the tendon, which can increase the potential for tendon rupture. The patient is placed in the supine position with the shoulder externally rotated 45 degrees. Doses for the injection can vary among specialties, particularly between surgeons and nonsurgeons.12 However, in a typical injection, a small volume of fluid is used, with 1.0 mL of 0.25% bupivacaine and 40 mg methylprednisolone in a sterile syringe attached to a 11⁄2-inch 25-gauge needle. The insertion of the bicipital tendon is found by first identifying the coracoid process and then palpating the lesser tuberosity slightly lateral to it. The needle is slowly advanced until it hits bone, and then it is withdrawn 1 to 2 mm. The medication is injected, and the operator should feel a small amount of resistance. If no resistance is felt, the needle is probably in the joint space. If resistance is significant, the needle may be within the tendon itself and should be withdrawn slightly.13 Once symptoms improve, physical therapy is initiated with range-of-motion exercises progressing to rotator cuff
Fig. 66.4 Injection technique for relieving the pain of biceps tendinitis.
strengthening for patients with impingement syndrome. For patients with significant instability or with recalcitrant symptoms despite appropriate treatment, referral to an orthopedist may be needed for possible arthroscopy of the shoulder with or without tenodesis of the tendon.
Complications and Pitfalls The most likely pitfall that should be avoided is bicipital tendon rupture. Most tendon ruptures occur in tendons previously degenerated and frayed from prolonged wear and tear under the acromial arch. These patients are most often older and will give a history of chronic shoulder pain that improved after a sudden and brief episode of severe pain in the anterior shoulder. A large amount of bruising may be present, as well as a palpable lump in the biceps region. Tendon rupture purely secondary to acute trauma is rare. Complications after injection, such as infection and hematoma, are rare if proper aseptic technique is used. The incidence of hematoma can be reduced by applying direct pressure immediately after the injection and by taking extra precautions with patients who take anticoagulants or have clotting disorders.
Conclusion Bicipital tendinitis is a common cause of anterior shoulder pain that is seen mostly in individuals who have some other type of intra-articular disorder or abnormality. Patients exhibit tenderness at the insertion of the tendon, and they report increased pain with active shoulder movements, most signi ficantly flexion. Radiographs are most often unremarkable, although an MRI scan may demonstrate an inflamed or degenerated tendon and rule out other problems such as labral disease or rotator cuff tear. Response to conservative treatment is generally excellent with anti-inflammatory medication, relative rest, injections, and gradual return to activity with physical therapy.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
67
Scapulocostal Syndrome Bernard M. Abrams
CHAPTER OUTLINE Historical Considerations 588 The Clinical Syndrome: Signs, Symptoms, and Physical Findings 588 Clinically Relevant Anatomy 589
The scapulocostal syndrome, also known as the levator scapulae syndrome, is a common painful musculoskeletal syndrome that mainly affects the posterior shoulder area; however, because of the pattern of pain radiation, it can mimic numerous other conditions including cervical radicular pain, intrinsic shoulder joint disease, and even visceral pain. This syndrome can be diagnosed clinically with a careful history and physical examination. No blood test abnormalities or neurophysiologic or imaging abnormalities are associated with the syndrome, but these tests may be useful in eliminating other entities from diagnostic consideration.
Historical Considerations The scapulocostal syndrome was first described by Michele et al in 1950.1 These investigators pointed out that, during the preceding 3 years, 30% of all middle-aged individuals presenting with shoulder complaints had this syndrome. Michele et al also described the syndrome's protean manifestations and pain radiation patterns. They noted that pain could radiate to the occiput or spinous processes of C3 and C4, it could appear to originate at the root of the neck and radiate into the shoulder joint, or it could radiate down the arm into the hand, usually along the posteromedial aspect of the upper arm and along the ulnar distribution in the forearm and hand. These investigators pointed out that the pain alternatively could radiate along the course of the fourth and fifth intercostal nerves and could mimic angina pectoris on the left and cholecystitis on the right. Finally, the patient could present with any combination of the foregoing symptoms and signs (Fig. 67.1). After some initial interest in this syndrome between 1956 and 1968,2–5 interest languished until the 1980s and early 1990s, when attention turned to the anatomy of this region.
The Clinical Syndrome: Signs, Symptoms, and Physical Findings The hallmark of the scapulocostal syndrome is pain. The pain may be localized to the medial superior border of the scapula, or it may radiate up into the neck and cause headache. It can 588
Differential Diagnosis 590 Treatment 591 Complications and Pitfalls 592 Conclusion 592
also cause pain into the root of the shoulder that simulates rotator cuff syndrome or other shoulder disorders. It can radiate around the chest wall or down the arm, usually in an ulnar nerve distribution. The characteristic pattern is that of acute pain localized in the upper trunk. The patient may complain of radicular-type pain, with or without sensory features.4,6 Although weakness of the arm and shoulder may be offered as complaints, this weakness is usually a result of guarding, without atrophy or neurophysiologic evidence of denervation on electromyography. The pain has been described variously as aching, burning, or gnawing, and rarely as sharp or radicular. The symptoms may be intermittent, but a nagging, constant quality is not uncommon. Insomnia is a frequent complaint because patients cannot find a comfortable sleeping position. The original article by Michele et al1 cited an equal distribution between the sexes. Since that time, most observers have noted a female predominance, as well as a predo minance in the dominant shoulder. Clerical occupation, rounded shoulders, large and pendulous breasts, and the carrying of personal items including handbags are often implicated. Russek7 classified the syndrome into three types: (1) primary, probably postural in origin; (2) secondary, a complication of preexisting neck or shoulder lesions; and (3) static, occurring in severely disabled patients who are unable to control the scapulothoracic relationship. Muscular, reflex, or sympathetic, or sensory findings are usually absent in the examination. The classic finding is a trigger point elicited by digital pressure at the medial scapular border in a line extending from the scapular spine. This trigger point (Fig. 67.2) may be missed (both diagnostically and therapeutically), unless the arm is adducted, with the palm of the affected hand flat on the opposite shoulder and crossing in front of the chest (Fig. 67.3). Alternatively, extension and internal rotation of the arm also elicit the pain (Fig. 67.4) Secondary trigger points may be found in the trapezius and rhomboid muscles (Fig. 67.5).1 Diffuse tenderness over the chest wall is usually mild. © 2011 Elsevier Inc. All rights reserved.
Chapter 67—Scapulocostal Syndrome
589
A B C D E
Fig. 67.3 Location of the trigger point area of tenderness when the scapula has been retracted from the posterior chest wall. (Adapted from Michele AA, Davies JJ, Krueger FJ, et al: Scapulocostal syndrome [fatigue-postural paradox], N Y J Med 50:1353, 1950.)
Fig. 67.1 Patterns of pain radiation. A, The pain radiates into the occiput. B, The pain is originating at the root of the neck and radiates into the shoulder joint. C and D, The pain radiates along the posteromedial aspect of the upper arm and the ulnar distribution of the forearm. Traction on the lower trunk of the brachial plexus as it passes over the first rib produces pain and numbness in the ulnar distribution of the hand and fingers. E, The pain may radiate into the fourth and fifth thoracic nerves because of the exaggerated lumbar lordosis. (Adapted from Michele AA, Davies JJ, Krueger FJ, et al: Scapulocostal syndrome [fatigue-postural paradox], N Y J Med 50:1353, 1950.)
Fig. 67.2 The trigger point. (Adapted from Ormandy L: Scapulocostal syndrome, Va Med Q 121:105, 1994.)
Fig. 67.4 Deep pressure over the superior medial angle of the scapula with compression of the posterior chest wall in conjunction with backward extension of the internally rotated arm. (Adapted from Michele AA, Davies JJ, Krueger FJ, et al: Scapulocostal syndrome [fatigue-postural paradox], N Y J Med 50:1353, 1950.)
Consistent biochemical, rheumatologic, radiologic, or neurophysiologic (electromyographic) findings have not been reported. One study reported increased heat emission from the upper medial angle of the affected shoulder on thermography in more than 60% of patients.8 Reproduction of the pain by palpation and relief by local anesthetic infiltration are the essential elements of this syndrome.
Clinically Relevant Anatomy The constant location of the pain in the deep trigger point seems to indicate that the levator scapulae muscle is involved in this syndrome (Fig. 67.6). Considerable controversy exists about the constancy of a bursa in connection with the levator scapulae,
590
Section IV—Regional Pain Syndromes
Levator scapulae m.
Fig. 67.5 Digital pressure underneath midbelly of the descending fibers of the trapezius toward the anterior surface of the superior medial angle of the scapula. Reinforcement by internal rotation and backward flexion of the arm. (Adapted from Michele AA, Davies JJ, Krueger FJ, et al: Scapulocostal
Fig. 67.6 Levator scapulae. Origin: transverse process of C1-C4 vertebrae; insertion: vertebral border of scapula between the medial angle and root of the spine. (Adapted from Quiring DP, Boyle BA, Boroush EL, et al: The extremities, with 106 engravings, Philadelphia, 1945, Lea & Febiger.)
syndrome [fatigue-postural paradox], N Y J Med 50:1353, 1950.)
Table 67.1 Three Layers of the Scapulothoracic Articulation Structure
Superficial
Intermediate
Deep
Muscles
Latissimus dorsi Trapezius
Levator scapulae Rhomboid minor Rhomboid major
Subscapularis Serratus anterior
Bursae
Inferior angle (number 1) 4 of 8 specimens
Superomedial angle (number 2) 8 of 8 specimens
Serratus space (number 3) 8 of 8 specimens Subscapularis space (number 4) 5 of 8 specimens
Nerves
Spinal accessory
From Williams GR, Shakil M, Klimkiewicz J, et al: Anatomy of the scapulothoracic articulation, Clin Orthop Relat Res 359:237, 1999.
which may be inserted in two layers enfolding the medial border of the scapula, with a second bursa found in the areolar tissue between the two layers.8 Williams et al9 undertook a dissection of four frozen human cadavers and also noted that the surgical anatomy of the scapulothoracic region was described infrequently. These investigators pointed out that the scapulothoracic articulation had three layers (Table 67.1).9 They described a superficial layer composed of the trapezius and latissimus dorsi muscles and an inconsistent bursa, which they found in four of eight specimens, between the inferior angle of the scapula and the superior fibers of the latissimus dorsi. These investigators then observed that the intermediate layer contained the rhomboid minor, rhomboid major, and levator scapulae muscles, along with the spinal accessory nerve, and a consistent bursa found in eight of eight specimens, between the superior medial scapula and the overlying trapezius. The deep layer consisted
of the serratus anterior and subscapularis muscles in addition to two bursae. One of the two bursae was consistently located between the serratus anterior muscle and the thoracic cage, whereas the other was inconsistently located between the serratus anterior and subscapularis muscles. These relationships probably account for the clinical finding that turning the head opposite the affected limb reproduces the pain.
Differential Diagnosis The differential diagnosis of pain in and about the scapula is extensive. Shoulder problems including rotator cuff disease, adhesive capsulitis, instability or arthritis of the glenohumeral joint, and vascular or neurogenic thoracic outlet syndrome may be at play.10 The pain in these individuals is generally exacerbated by scapulothoracic movement, as well as by movements
at the glenohumeral joint. Restriction of range of motion is frequent. Imaging of the shoulder with plain radiographs generally shows degenerative changes. Findings on magnetic resonance imaging or computed tomography arthrography may be definitive. An entity known as the “snapping scapula” has been used to describe the clinical situation of tenderness at the superomedial angle of the scapula, painful scapulothoracic motion, and scapulothoracic crepitus.10 Causes of snapping scapula include scapular exostosis, malunion of scapula or rib fracture, and Sprengel's deformity.11,12 Cervical radiculopathy can produce an aching pain into the scapula (protopathic pain), especially with C7 radiculopathy, which is associated with sharp (epicritic) pain down into the appropriate segment of the upper limb. In the case of C7 radiculopathy, pain usually descends the posterior aspect of the upper arm (triceps muscle) into the middle finger and is associated with weakness of the triceps and wrist extensors, diminution of the triceps reflex, and hypesthesia in the C7 dermatome. Suprascapular nerve entrapment may produce deep, poorly circumscribed pain.13 Because the suprascapular nerve is a motor nerve, the pain resulting from its irritation is deep and poorly circumscribed. This pain is roughly localized to the posterior and lateral aspects of the shoulder. When patients have an appreciable traction stress element on the upper trunk, they also have pain down the radial nerve axis. If the neuropathy has been present for a sufficient time, atrophy of the supraspinatus and infraspinatus muscles will be visible and palpable. This weakness is confirmed when patients have difficulty in initiating abduction and rotation at the glenohumeral joint. Most cases of suprascapular neuropathy are associated with an earlier motion impediment at this joint. Deep pressure toward the region of the suprascapular notch is painful. Motion of the scapula causes pain. The cross-body adduction test, performed by adducting the extended arm passively across the midline, is extremely painful because it lifts the scapular nerve away from the thoracic nerve and thereby tenses the suprascapular nerve. A suprascapular nerve block may be necessary for diagnosis. The region involved is somewhat lateral to the medial superior scapular border (at least three to four finger breadths in an average-sized person), so the tender area is clearly differentiated from the medial angle of the scapula where the levator scapulae muscle inserts in the scapulocostal syndrome (Fig. 67.7).
Chapter 67—Scapulocostal Syndrome
591
Suprascapular n. Branch to supraspinatus m. Branch to infraspinatus m. Branch to acromio-clavicular j. Branch to shoulder joint capsule 3-4 finger breadths Suprascapular notch
Fig. 67.7 Suprascapular nerve: motor and joint distribution. (Adapted from Kopell HP, Thomspon WAL: Suprascapular entrapment neuropathy, Surg Gynecol Obstet 109:92, 1959.)
Treatment Nonoperative treatment is sometimes successful in these patients. This treatment consists of activity modification, physical therapy, use of systemic anti-inflammatory medications, and injection into the region of the medial superior scapular border. Mixtures of 2 to 8 mL of plain 1% lidocaine HCl, in addition to 1 mL of betamethasone, followed by physical therapy exercises, have been advocated (Fig. 67.8).14 Ormandy14 treated 190 patients, 43% with one block, 40% with two blocks, and 17% with three blocks. On completion of treatment, approximately 98% of patients were relieved of pain and returned to their original occupations. Fourie15 invoked the serratus posterior superior muscle, a member of the third muscle layer of the back. He used 1 mL of steroid and 1.8 mL of local anesthetic. In his report of 201 cases, conservative treatment was successful in
Fig. 67.8 Infiltration of the subscapular region. (Adapted from Ormandy L: Scapulocostal syndrome, Va Med Q 121:105, 1994.)
95.9% of patients. Very few writers on this subject mention that the arm needs to be cross-adducted or internally rotated and extended to move the scapula out of the way and expose the levator scapulae muscle at its insertion into the medial border of the scapula. If this maneuver is done, success is much more likely. The recommended approach is to use a 25-gauge needle at a 90-degree angle to reach underneath the scapula, to place the needle in the most lateral excursion of the scapula, and then to infiltrate while withdrawing the needle toward the medial superior scapula border.
592
Section IV—Regional Pain Syndromes
Surgical options for patients who do not respond to nonoperative management include scapulothoracic bursectomy, excision of the superomedial angle of the scapula, and combined bursectomy and superior angle resection.9,16,17 One report described the operative treatment of scapulothoracic bursitis in professional baseball pitchers, four of whom were operated on and returned to their pitching careers.18 Endoscopic surgery has also been performed in the scapulothoracic region.19,20 Results of surgery have been reported infrequently and inconsistently.9
Complications and Pitfalls The major pitfall is a failure to diagnose this common and easily overlooked syndrome. A thorough history and a few simple physical diagnostic maneuvers involving the crossed adduction of the affected arm with palpation should be sufficient to make the diagnosis. Treatment can be unsuccessful if a similar posture for injection is not maintained, because one would be attempting to inject through the scapula itself, to reach the levator scapulae insertion or the putative bursa in this area. Once the clinician attempts to inject in this area, the possibility of pneumothorax should be kept in mind at all times, and the patient should be warned of this possibility and its potential consequences, including traction pneumothorax. Patients should be instructed to go the emergency
room with any chest pain on inspiration. Operative techniques have their own associated risks and morbidity. However, inconclusive results up to this point have clouded the issue.
Conclusion Scapulocostal syndrome is a common occurrence, especially in posturally compromised, middle-aged individuals, usually women, in particular persons with desk jobs or those whose vocations force them to extend their arms in front of them for prolonged periods. This syndrome has no definitive biologic markers. The differential diagnosis rests largely on ruling out cervical radiculopathy, intrinsic shoulder disease, osseous disease of the bony skeleton, and other afflictions of the scapula, including the snapping scapula syndrome and Sprengel's deformity. Scapulocostal syndrome is easily diagnosed and may be treated with a relative degree of success by injection therapy, which should be combined with physical therapy and alteration of lifestyle. Surgical treatment may be considered in refractory cases, but whether it is successful remains largely controversial.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
68
Tennis Elbow Steven D. Waldman
CHAPTER OUTLINE Signs and Symptoms 594 Testing 594 Differential Diagnosis 594
Tennis elbow, also known as lateral epicondylitis, is caused by repetitive microtrauma to the extensor tendons of the forearm.1 The pathophysiology of tennis elbow is initiated by micro-tearing at the origin of extensor carpi radialis and extensor carpi ulnaris (Fig. 68.1).2 Secondary inflammation may occur and can become chronic as the result of continued overuse or misuse of the extensors of the forearm. Coexisting bursitis, arthritis, and gout may also perpetuate the pain and disability of tennis elbow. Tennis elbow occurs in patients engaged in repetitive activities that include hand grasping (e.g., politicians shaking hands) or high-torque wrist turning (e.g., scooping ice cream at an ice cream parlor) (Fig. 68.2). Tennis players develop tennis elbow by two separate mechanisms: (1) increased pressure grip strain as a result of playing with too heavy a racquet and (2) making backhand shots with a leading shoulder and elbow rather than keeping the shoulder and elbow parallel to the net (Fig. 68.3). Other racquet sport players are also susceptible to the development of tennis elbow.
Signs and Symptoms The pain of tennis elbow is localized to the region of the lateral epicondyle. It is constant and is made worse by active contraction of the wrist. Patients note the inability to hold a coffee cup or a hammer. Sleep disturbance is common. On physical examination, patients report tenderness along the extensor tendons at, or just below, the lateral epicondyle.1 Many patients with tennis elbow have a bandlike thickening within the affected extensor tendons. Elbow range of motion is normal. Grip strength on the affected side is diminished. Patients with tennis elbow demonstrate a positive response to the tennis elbow test. The test is performed by stabilizing the patient's forearm and then having the patient clench his or her fist and actively extend the wrist. The examiner then attempts to force the wrist into flexion (Fig. 68.4). Sudden, severe pain is highly suggestive of tennis elbow.
Treatment 594 Side Effects and Complications 596 Conclusion 596
elbow, to rule out joint mice and other occult bony disorders. Based on the patient's clinical presentation, additional testing including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. Magnetic resonance imaging scan of the elbow is indicated if joint instability is suspected or if the patient's pain fails to respond to traditional treatment modalities (Fig. 68.5). The injection technique described subsequently serves as both a diagnostic and a therapeutic maneuver.
Differential Diagnosis Radial tunnel syndrome and occasionally C6-7 radiculo pathy can mimic tennis elbow. Radial tunnel syndrome is an entrapment neuropathy that results from entrapment of the radial nerve below the elbow. Radial tunnel syndrome can be distinguished from tennis elbow in that, in radial tunnel syndrome, the maximal tenderness to palpation is distal to the lateral epicondyle over the radial nerve, whereas in tennis elbow, the maximal tenderness to palpation is over the lateral epicondyle.3 The most common nidus of pain from tennis elbow is the bony origin of the extensor tendon of extensor carpi radialis brevis at the anterior facet of the lateral epicondyle. Less commonly, tennis elbow pain can originate from the extensor carpi radialis longus at the supracondylar crest or, rarely, more distally at the point where the extensor carpi radialis brevis overlies the radial head. As mentioned earlier, bursitis may accompany tennis elbow. The olecranon bursa lies in the posterior aspect of the elbow joint and may also become inflamed as a result of direct trauma or overuse of the joint. Other bursae susceptible to the development of bursitis exist between the insertion of the biceps and the head of the radius, as well as in the antecubital and cubital area.4
Testing
Treatment
Electromyography helps to distinguish cervical radiculopathy and radial tunnel syndrome from tennis elbow. Plain radiographs are indicated in all patients who present with tennis
Initial treatment of the pain and functional disability associated with tennis elbow should include a combination of the nonsteroidal anti-inflammatory agents or cyclooxygenase-2
594
© 2011 Elsevier Inc. All rights reserved.
.
. .
.
.
. .
. .
.
.
.
.
and .
. and . .
. .
.
.
. .
.
.
.
Fig. 68.1 Anatomy of the lateral epicondyle. (From Kang SH, Ahn JM, Resnick D: MRI of the extremities, ed 2, Philadelphia, 2002, Saunders, 2002, p 87.)
Improper wrist position
Ca
rri c
o&
Sh ave ll
Fig. 68.2 The pain of tennis elbow is localized to the lateral epicondyle.
Fig. 68.3 Improper wrist position causes tennis elbow syndrome.
(From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 110.)
(From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 138.)
596
Section IV—Regional Pain Syndromes
inhibitors and physical therapy. The local application of heat and cold may also be beneficial. Any repetitive activity that may exacerbate the patient's symptoms should be avoided.5 For patients who do not respond to these treatment modalities, the following injection technique may be a reasonable next step.6 Injection technique for tennis elbow is performed by placing the patient in a supine position with the arm fully adducted at the patient's side and the elbow flexed with the dorsum of the hand resting on a folded towel to relax the affected tendons. A total of 1 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the posterolateral aspect of the joint, the lateral epicondyle is identified. Using strict aseptic technique, the operator inserts a 1-inch 25-gauge
needle perpendicular to the lateral epicondyle through the skin and into the subcutaneous tissue overlying the affected tendon (Fig. 68.6). If bone is encountered, the needle is withdrawn into the subcutaneous tissue. The contents of the syringe are then gently injected. Little resistance to injection should be felt. If resistance is encountered, the needle is probably in the tendon and should be withdrawn until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.
Side Effects and Complications The major complication associated with tennis elbow is rupture of the affected inflamed tendons, either from repetitive trauma or from injection directly into the tendon. Inflamed and previously damaged tendons may rupture if they are directly injected, and the needle position should be confirmed outside the tendon before injection, to avoid this complication. Another complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is followed. The ulnar nerve is especially susceptible to damage at the elbow, and care must be taken to avoid this nerve when injecting the elbow. Approximately 25% of patients will complain of a transient increase in pain following this injection technique, and patients should be warned of this possibility.
Conclusion
Fig. 68.4 Test for eliciting the pain of tennis elbow. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 239.)
This injection technique is extremely effective in the treatment of pain secondary to tennis elbow. Coexistent bursitis and tendinitis may also contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot steroid. This technique is a safe procedure if careful attention is paid to the clinically relevant
Fig. 68.5 A 53-year-old stoker with persistent pain in his right elbow for 2 years. In these magnetic resonance images, a high T2 signal focus was found in the origin of the extensor carpi radialis brevis in the coronal and oblique planes (arrows). Intra-articular effusion was observed. Left image, T2; center image, T1; right image, T2 oblique.
Chapter 68—Tennis Elbow
anatomy of the areas to be injected. The use of physical modalities including local heat, as well as gentle range-ofmotion exercises, should be introduced several days after the patient undergoes this injection technique for tennis elbow pain. A Velcro band placed around the extensor tendons may also help relieve the symptoms of tennis elbow. Vigorous exercises should be avoided because they will exacerbate the patient's symptoms. Simple analgesics and nonsteroidal anti-
597
inflammatory agents may be used concurrently with this injection technique. As mentioned earlier, cervical radiculopathy and radial tunnel syndrome may mimic tennis elbow and must be ruled out to treat the underlying disorder effectively.
References Full references for this chapter can be found on www.expertconsult.com.
Radial n. Head of radius
Extensor carpi radialis longus m. Extensor carpi radialis brevis m.
Fig. 68.6 Injection technique for relieving the pain of tennis elbow. (From Waldman Inflamed and torn t.
SD: Atlas of pain management injection techniques, Philadelphia, 2000, Saunders, p 83.)
IV
Chapter
69
Golfer's Elbow Steven D. Waldman
CHAPTER OUTLINE Signs and Symptoms 598 Testing 598 Differential Diagnosis 598
Although 15 times less common than tennis elbow, golfer's elbow remains one of the most common causes of elbow and forearm pain.1 Golfer's elbow, also known as medial epicondylitis, is caused by repetitive microtrauma to the flexor tendons of the forearm in a manner analogous to tennis elbow.2 The pathophysiology of golfer's elbow is initiated by micro-tearing at the origin of the pronator teres, flexor carpi radialis, flexor carpi ulnaris, and the palmaris longus. Secondary inflammation may occur and can become chronic as the result of continued overuse or misuse of the flexors of the forearm. The most common nidi of pain from golfer's elbow are the bony origin of the flexor tendon of flexor carpi radialis and the humeral heads of the flexor carpi ulnaris and pronator teres at the medial epicondyle of the humerus (Fig. 69.1). Less commonly, golfer's elbow pain can originate from the ulnar head of the flexor carpi ulnaris at the medial aspect of the olecranon process. Coexisting bursitis, arthritis, and gout may also perpetuate the pain and disability of golfer's elbow.3 Golfer's elbow occurs in patients engaged in repetitive flexion activities that include throwing baseballs or footballs, carrying heavy suitcases, and driving golf balls (Fig. 69.2). These activities have in common repetitive flexion of the wrist and strain on the flexor tendons resulting from excessive weight or sudden arrested motion. Many of the activities that can cause tennis elbow can also cause golfer's elbow.1
Signs and Symptoms The pain of golfer's elbow is localized to the region of the medial epicondyle (see Fig. 69.1). It is constant and is made worse with active contraction of the wrist. Patients note the inability to hold a coffee cup or a hammer. Sleep disturbance is common. On physical examination, the patient reports tenderness along the flexor tendons at or just below the medial epicondyle. Many patients with golfer's elbow have a bandlike thickening within the affected flexor tendons. Elbow range of motion is normal. Grip strength on the affected side is diminished. Patients with golfer's elbow demonstrate a positive response to the golfer's elbow test.2 The test is performed by stabilizing the patients forearm and then having the patient 598
Treatment 598 Side Effects and Complications 599 Conclusion 600
actively flex the wrist (Fig. 69.3). The examiner then attempts to force the wrist into extension. Sudden, severe pain is highly suggestive of golfer's elbow.
Testing Plain radiographs are indicated in all patients who present with golfer's elbow to rule out joint mice and other occult bony disorders. Based on the patient's clinical presentation, additional testing including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. Magnetic resonance imaging scan of the elbow is indicated if joint instability is suspected. Electromyography is indicated to diagnose entrapment neuropathy at the elbow and to help distinguish golfer's elbow from cervical radiculopathy. The injection technique described subsequently serves as a diagnostic and a therapeutic maneuver.
Differential Diagnosis Occasionally, C6-7 radiculopathy can mimic golfer's elbow. The patient suffering from cervical radiculopathy usually has neck pain and proximal upper extremity pain in addition to symptoms below the elbow. Electromyography helps to distinguish radiculopathy from golfer's elbow. Bursitis, arthritis, and gout may also mimic golfer's elbow and may confuse the diagnosis. The olecranon bursa lies in the posterior aspect of the elbow joint and may also become inflamed as a result of direct trauma or overuse of the joint. Other bursae susceptible to the development of bursitis exist between the insertion of the biceps and the head of the radius, as well as in the antecubital and cubital area (Fig. 69.4).
Treatment Initial treatment of the pain and functional disability associated with golfer's elbow should include a combination of the nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 inhibitors and physical therapy.4 The local application of heat and cold may also be beneficial. Any repetitive © 2011 Elsevier Inc. All rights reserved.
Chapter 69—Golfer's Elbow
599
Brachials m.
. .
.
. .
.
and .
. and .
.
.
. . . .
. .
Fig. 69.1 Anatomy of the medial epicondyle. (From Kang SH, Ahn JM, Resnick D: MRI of the extremities, ed 2, Philadelphia, 2002, Saunders, p 91.)
A total of 1 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the medial aspect of the joint, the medial epicondyle is identified. Using strict aseptic technique, the operator inserts a 1-inch, 25-gauge needle perpendicular to the medial epicondyle through the skin and into the subcutaneous tissue overlying the affected tendon (Fig. 69.5). If bone is encountered, the needle is withdrawn into the subcutaneous tissue. The contents of the syringe are then gently injected. Little resistance to injection should be felt. If resistance is encountered, the needle is probably in the tendon and should be withdrawn until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.
Side Effects and Complications Fig. 69.2 The pain of golfer's elbow occurs at the medial epicondyle. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 114.)
activity that may exacerbate the patient's symptoms should be avoided. For patients who do not respond to these treatment modalities, the following injection technique may be a reasonable next step.5 Injection for golfer's elbow is carried out by placing the patient in a supine position with the arm fully adducted at the patient's side and the elbow fully extended with the dorsum of the hand resting on a folded towel to relax the affected tendons.
The major complications associated with this injection technique are related to trauma to the inflamed and previously damaged tendons. Such tendons may rupture if they are directly injected, and the needle position should be confirmed outside the tendon before injection, to avoid this complication. Another complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is followed. The ulnar nerve is especially susceptible to damage at the elbow, and care must be taken to avoid this nerve when injecting the elbow. Approximately 25% of patients will complain of a transient increase in pain following intra-articular injection of the elbow joint, and patients should be warned of this possibility.
600
Section IV—Regional Pain Syndromes
Patient Examiner
Inflamed epicondyle
Fig. 69.3 Test for eliciting the pain of golfer's elbow. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 149.)
Frayed and inflamed t. Pronator teres m.
Ulnar n.
Flexor carpi ulnaris m.
Medial epicondyle
Cubital bursa
Flexor carpi ulnaris m.
Fig. 69.4 Proper needle placement for injection for cubital bursitis. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 92.)
This injection technique is extremely effective in the treatment of pain secondary to golfer's elbow. Coexisting bursitis and tendinitis may also contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot steroid. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy of the areas to be injected. The use of physical modalities including local heat, as well as gentle range-of-motion exercises, should be introduced several days after the patient undergoes this injection technique for elbow pain. A Velcro band placed around the flexor tendons may also help relieve the symptoms of golfer's elbow. Vigorous exercises should be avoided because they will exacerbate the patient's symptoms. Simple analgesics and NSAIDs may be used concurrently with this injection technique. As mentioned earlier, cervical radiculopathy may mimic golfer's elbow and must be ruled out to treat the underlying disorder effectively.
Conclusion Golfer's elbow is a common cause of elbow and forearm pain encountered in clinical practice. This painful condition
Palmaris longus m.
Fig. 69.5 Injection technique for relieving the pain of golfer's elbow syndrome. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 150.)
f requently coexists with other elbow disorders including tendinitis, lateral epicondylitis, and bursitis. Entrapment neuropathy may also complicate the clinical picture. Identification of the activities responsible for the pathophysiology of golfer's elbow is paramount if rapid relief of pain and functional disability are to be achieved.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
70
IV
Olecranon and Cubital Bursitis Steven D. Waldman
CHAPTER OUTLINE Olecranon Bursitis 601 Clinically Relevant Anatomy 601 Signs and Symptoms 601 Testing 602 Differential Diagnosis 603 Treatment 603
Cubital Bursitis 603 Clinically Relevant Anatomy 604 Signs and Symptoms 604 Testing 604 Differential Diagnosis 604 Treatment 605
Conclusion 605
Olecranon bursitis and cubital bursitis are common causes of elbow pain encountered in clinical practice. Bursae are formed from synovial sacs that exist to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid, with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and, on rare occasions, infected. Although intrapatient variability is significant with regard to the number, size, and location of bursae, anatomists have been able to identify some clinically relevant bursae, including the olecranon and cubital bursae. The olecranon bursa lies in the posterior aspect of the elbow, whereas the cubital bursa lies in the anterior aspect. Both may exist as a single bursal sac or, in some patients, as a multisegmented series of sacs that may be loculated.
Olecranon Bursitis Olecranon bursitis may develop gradually as a result of repetitive irritation of the olecranon bursa or acutely in response to trauma or infection.1 The swelling associated with olecranon bursitis may, at times, be quite impressive, and the patient may complain about difficulty in wearing a longsleeved shirt (Fig. 70.1). The olecranon bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the elbow when playing sports such as hockey or falling directly onto the olecranon process. Repeated pressure from leaning on the elbow to arise from bed or from working long hours at a drafting table may result in inflammation and swelling of the olecranon bursa (Fig. 70.2). Gout or bacterial infection may rarely precipitate acute olecranon bursitis.2 If the inflammation of the olecranon bursa becomes chronic, calcification of the bursa with residual nodules called gravel may occur. © 2011 Elsevier Inc. All rights reserved.
Clinically Relevant Anatomy The elbow joint is a synovial hinge-type joint that serves as the articulation of the humerus, radius, and ulna (Fig. 70.3). The joint's primary function is to position the wrist to optimize hand function. The joint allows flexion and extension at the elbow as well as pronation and supination of the forearm. The joint is lined with synovium. The entire joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and medially to form the radial collateral ligament (Fig. 70.4). These dense ligaments, coupled with the elbow joint's deep bony socket, makes this joint extremely stable and relatively resistant to subluxation and dislocation. The anterior and posterior joint capsule is less dense and may become distended in the presence of joint effusion. The elbow joint is innervated primarily by the musculocutaneous and radial nerves. The ulnar and median nerves provide varying degrees of innervation. At the middle of the upper arm, the ulnar nerve courses medially to pass between the olecranon process and the medial epicondyle of the humerus. The nerve is susceptible to entrapment and trauma at this point. At the elbow, the median nerve lies just medial to the brachial artery and is occasionally damaged during brachial artery cannulation for blood gas determination.
Signs and Symptoms The patient suffering from olecranon bursitis frequently complains of pain and swelling during any movement of the elbow, but especially extension. The pain is localized to the olecranon area, and referred pain is often noted above the elbow joint.3 The patient is frequently more concerned about the swelling around the bursa than about the pain. Physical examination reveals point tenderness over the olecranon and swelling of the bursa that can be quite extensive (see Figs. 70.1 and 70.2).4 Passive flexion and resisted extension of the elbow reproduce the pain, as does any pressure over the bursa. Fever and 601
602
Section IV—Regional Pain Syndromes
chills usually accompany infection of the bursa. If infection is suspected, aspiration, Gram stain, and culture of the bursa followed by treatment with appropriate antibiotics are indicated on an emergency basis. Humerus
Testing The diagnosis of olecranon bursitis is usually made on clinical grounds alone. Plain radiographs of the posterior elbow are indicated if the patient has a history of elbow trauma or if arthritis of the elbow is suspected. Plain radiographs may also reveal calcification of the bursa and associated structures consistent with chronic inflammation (Fig. 70.5). Magnetic resonance imaging (MRI) scan is indicated if infection or joint instability is suspected (Fig. 70.6). Complete blood count and an automated chemistry profile including uric acid, sedimentation rate, and antinuclear antibody are indicated if collagen vascular disease is suspected. When infection is considered, aspiration, Gram stain, and culture of bursal fluid are indicated on an emergency basis.
Radial fossa Coronoid fossa Lateral epicondyle Capitulum
Medial epicondyle Trochlea
Coronoid process
Radius
Radial notch
Ulna
Fig. 70.3 Clinically relevant anatomy of the elbow. The elbow joint is a synovial hinge-type joint that serves as the articulation of the humerus, radius, and ulna.
Fig. 70.1 Olecranon bursitis in early rheumatoid arthritis. (From Groff GD: Olecranon bursitis. In Klippel JH, Dieppe PA, editors: Rheumatology, ed 2, London, 1998, Mosby, p 4.14.3.)
Humerus
Articular capsule
Radial collateral lig.
Medial epicondyle
Annular lig. Ulnar collateral lig. Radius Ulna
Fig. 70.2 Olecranon bursitis is often caused by repeated pressure on the elbow. (From Waldman SD: Olecranon bursitis. In Atlas of common pain syndromes, ed 2, Philadelphia, 2007, Saunders, p 131.)
Fig. 70.4 The entire elbow joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and medially to form the radial collateral ligament.
Chapter 70—Olecranon and Cubital Bursitis
Differential Diagnosis
or cyclooxygenase-2 (COX-2) inhibitors, and an elbow protector to prevent further trauma is a reasonable first step in the treatment of patients suffering from olecranon bursitis. If the patient does not experience rapid improvement, the following injection technique is a logical next step.5 The patient is placed in a supine position with the arm fully adducted at the patient's side and the elbow flexed with the palm of the hand resting on the patient's abdomen. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. After sterile preparation of skin overlying the posterior aspect of the joint, the olecranon process and overlying bursa are identified. Using strict aseptic technique, the operator inserts a 1-inch, 25-gauge needle through the skin and subcutaneous tissues directly into the bursa in the midline (Fig. 70.7). If bone is encountered, the needle is withdrawn into the bursa. After entering the bursa, the operator gently injects the contents of the syringe. Resistance to injection should be minimal. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.
Olecranon bursitis is usually a straightforward clinical diagnosis. Occasionally, rheumatoid nodules or gouty arthritis of the elbow may confuse the clinician. Synovial cysts of the elbow may also mimic olecranon bursitis. Coexisting tendinitis, (e.g., tennis elbow and golfer's elbow) may require additional treatment.
Treatment A short course of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs)
603
Cubital Bursitis
A
B
Fig. 70.5 Septic bursitis. A, Olecranon bursitis. Note olecranon swelling (arrows) and soft tissue edema resulting from Staphylococcus aureus infection. Previous surgery and trauma are the causes of the adjacent bony abnormalities. B, Prepatellar bursitis. This 28-year-old carpenter who had worked on his knees for prolonged periods developed tender swelling in front of the knee (arrows). Inflammatory fluid that was culture positive for S. aures was recovered from the bursa. (From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 2438.)
B
A
The cubital bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the anterior aspect of the elbow. Repetitive movements of the elbow, including throwing javelins and baseballs, may result in inflammation and swelling of the cubital bursa. Gout or rheumatoid arthritis may rarely precipitate acute cubital bursitis. If the inflammation of the cubital bursa becomes chronic, calcification of the bursa may occur. The patient suffering from cubital bursitis frequently complains of pain and swelling with any movement of the elbow (Fig. 70.8). The pain is localized to the cubital area, and referred pain is often noted in the forearm and hand. Physical examination reveals point tenderness in the anterior aspect of the elbow over the cubital bursa and swelling of the bursa. Passive extension and resisted flexion of the shoulder reproduce the pain, as does any pressure over the bursa. Plain radiographs of
Fig. 70.6 Septic olecranon bursitis. A sagittal multiplanar gradient (MPGR; TR/TE, 500/11; flip angle, 15 degrees) magnetic resonance imaging (MRI) scan (A) reveals abnormal high signal intensity in the region of the olecranon bursa with bone involvement (arrow), also of high signal intensity. A transaxial fat-suppressed fast spin echo (TR/TE, 5000/108) MRI scan (B) confirms bone involvement (arrow). (From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 2439.)
604
Section IV—Regional Pain Syndromes
Humerus
Radius Ulna Olecranon Inflamed and cystic bursa
Fig. 70.7 Injection technique for olecranon bursitis pain. (From Waldman SD: Olecranon bursitis pain. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 181.)
hand function. The joint allows flexion and extension at the elbow, as well as pronation and supination of the forearm. The joint is lined with synovium. The entire joint is covered by a dense capsule that thickens medially to form the ulnar collateral ligament and medially to form the radial collateral ligaments (see Fig. 70.4). These dense ligaments coupled with the elbow joint's deep bony socket make this joint extremely stable and relatively resistant to subluxation and dislocation. The anterior and posterior joint capsule is less dense and may become distended if joint effusion is present. The cubital fossa lies in the anterior aspect of the elbow joint and is bounded laterally by the brachioradialis muscle and medially by the pronator teres. The cubital fossa contains the median nerve, which is susceptible to irritation and compression from a swollen, inflamed cubital bursa. The elbow joint is innervated primarily by the musculocutaneous and radial nerves. The ulnar and median nerves provide varying degrees of innervation. At the middle of the upper arm, the ulnar nerve courses medially to pass between the olecranon process and the medial epicondyle of the humerus. The nerve is susceptible to entrapment and trauma at this point. At the elbow, the median nerve lies just medial to the brachial artery and is occasionally damaged during brachial artery cannulation for blood gas measurement. The median nerve may also be injured during injection of the cubital bursa.
Signs and Symptoms The patient suffering from cubital bursitis frequently complains of pain and swelling with any movement of the elbow, but especially flexion. The pain is localized to the cubital fossa, and referred pain is often noted above the elbow joint.6 The patient is frequently more concerned about the swelling around the bursa than about the pain. Physical examination reveals point tenderness over the cubital bursa and swelling of the bursa that, at times, can be quite extensive.6 Passive extension and resisted flexion of the elbow reproduce the pain, as does any pressure over the bursa. Fever and chills usually accompany infection of the bursa. When infection is suspected, aspiration, Gram stain, and culture of the bursa followed by treatment with appropriate antibiotics are indicated on an emergency basis.
Testing
the posterior elbow may reveal calcification of the bursa and associated structures consistent with chronic inflammation.
The diagnosis of cubital bursitis is usually made on clinical grounds alone. Plain radiographs of the posterior elbow are indicated if the patient has a history of elbow trauma or if arthritis of the elbow is suspected. Plain radiographs may also reveal calcification of the bursa and associated structures consistent with chronic inflammation. MRI scan is indicated if infection or joint instability is suspected. Complete blood count and an automated chemistry profile including uric acid, sedimentation rate, and antinuclear antibody testing are indicated if collagen vascular disease is suspected. When infection is considered, aspiration, Gram stain, and culture of bursal fluid are indicated on an emergency basis.
Clinically Relevant Anatomy
Differential Diagnosis
The elbow joint is a synovial hinge-type joint that serves as the articulation of the humerus, radius, and ulna (see Fig. 70.3). The joint's primary function is to position the wrist to optimize
Cubital bursitis is usually a straightforward clinical diagnosis. Occasionally, rheumatoid nodules or gouty arthritis of the elbow may confuse the clinician. Synovial cysts of the
Fig. 70.8 A patient suffering from cubital bursitis complains of pain and swelling on movement of the elbow. (From Waldman SD: Cubital bursitis. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 92.)
Chapter 70—Olecranon and Cubital Bursitis
605
Brachial a. Median n.
Brachialis m.
Ca rr
ico
&S
ha vel l
Biceps brachii m.
Cuboidal bursa
Extensor carpi radialis m.
Radial a.
Brachioradialis m.
elbow may also mimic cubital bursitis. Coexistent tendinitis (e.g., tennis elbow and golfer's elbow) may require additional treatment.
Treatment A short course of conservative therapy consisting of simple analgesics, NSAIDs or COX-2 inhibitors, and an elbow protector to prevent further trauma is a reasonable first step in the treatment of patients suffering from cubital bursitis. If the patient does not experience rapid improvement, the following injection technique is a logical next step.7,8 The patient is placed in a supine position with the arm fully adducted at the patient's side and the elbow extended with the dorsum of the hand resting on a folded towel. A total of 2 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 5-mL sterile syringe. The clinician identifies the pulsations of the brachial artery at the crease of the elbow. After preparation of the skin with antiseptic solution, a 1-inch, 25-gauge needle is inserted just lateral to the brachial artery at the crease and is slowly advanced in a slightly medial and cephalad trajectory through the skin and subcutaneous tissues (Fig. 70.9). If bone is encountered, the needle is withdrawn into the subcutaneous tissue. The contents of the syringe are then gently injected. Resistance to injection should be minimal. If resistance is encountered, the needle is probably in the tendon and should be withdrawn until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.
Medial epicondyle Pronator teres m. Flexor carpi radialis m. Palmaris longus m. Aponeurotic extension of biceps m.
Flexor carpi ulnaris m.
Fig. 70.9 Injection technique for cubital bursitis pain. (From Waldman SD: Cubital bursitis pain. In Atlas of
Flexor digitorum superficialis m.
pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 189.)
Injection of the cubital bursa at the elbow is a relatively safe block. The major complications are inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the median nerve. This technique can safely be performed in patients receiving anticoagulants with the use of a 25- or 27-gauge needle, albeit at an increased risk of hematoma, if the clinical situation dictates a favorable risk-tobenefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately following injection. The application of cold packs for 20-minute periods following the block also decreases the amount of postprocedure pain and bleeding.
Conclusion Olecranon bursitis and cubital bursitis are common causes of elbow pain encountered in clinical practice. Coexistent tendinitis and epicondylitis often contribute to elbow pain and may require additional treatment with more localized injection of local anesthetic and depot steroid. Failure to treat olecranon and cubital bursitis adequately may result in the development of chronic pain and loss of range of motion of the affected elbow.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
71
Entrapment Neuropathies of the Elbow and Forearm Steven D. Waldman
CHAPTER OUTLINE Tardy Ulnar Palsy 606 Signs and Symptoms 606 Testing 606 Differential Diagnosis 607 Treatment 608 Complications and Pitfalls 608
Pronator Syndrome 609 Signs and Symptoms 609 Testing 610 Differential Diagnosis 610
Entrapment neuropathies of the elbow and forearm provide significant diagnostic and therapeutic challenges to the clinician. Although reasonably common in clinical practice, these disorders are frequently misdiagnosed and mistreated. This chapter provides the clinician with a concise review of these clinical syndromes and presents a step-by-step guide to treatment.
Tardy Ulnar Palsy Ulnar nerve entrapment at the elbow is one of the most common entrapment neuropathies encountered in clinical practice.1 Causes include compression of the ulnar nerve by an aponeurotic band that runs from the medial epicondyle of the humerus to the medial border of the olecranon, direct trauma to the ulnar nerve at the elbow, and repetitive elbow motion (Fig. 71.1). Ulnar nerve entrapment at the elbow is also called tardy ulnar palsy, cubital tunnel syndrome, and ulnar nerve neuritis. This entrapment neuropathy manifests as pain and associated paresthesias in the lateral forearm that radiate to the wrist and to the ring and little fingers (Fig. 71.2). Some patients suffering from ulnar nerve entrapment at the elbow may also notice pain referred to the medial aspect of the scapula on the affected side. Untreated, ulnar nerve entrapment at the elbow can result in a progressive motor deficit and, ultimately, flexion contracture of the affected fingers. The onset of symptoms usually occurs after repetitive elbow motion or results from repeated pressure on the elbow, such as using the elbows to arise from bed. Direct trauma to the ulnar nerve as it enters the cubital tunnel may also cause a similar clinical presentation. Patients with vulnerable nerve syndrome 606
Treatment 610 Complications and Pitfalls 610
Anterior Interosseous Syndrome 611 Clinically Relevant Anatomy 611 Treatment 612 Complications and Pitfalls 613
Radial Tunnel Syndrome 613 Clinically Relevant Anatomy 614 Treatment 614
Conclusion 614
(e.g., patients with diabetes or alcoholism) are at greater risk for the development of ulnar nerve entrapment at the elbow (Fig. 71.3).
Signs and Symptoms Physical findings include tenderness over the ulnar nerve at the elbow. A positive Tinel sign over the ulnar nerve as it passes beneath the aponeuroses is usually present. Weakness of the intrinsic muscles of the forearm and hand that are innervated by the ulnar nerve may be identified by careful manual muscle testing, although early in the evolution of cubital tunnel syndrome, the only physical finding other than tenderness over the nerve may be the loss of sensation on the ulnar side of the little finger. Muscle wasting of the intrinsic muscles of the hand can best be identified by viewing the hand with the palm down. The Tinel sign at the elbow is often present when the ulnar nerve is stimulated.
Testing Electromyography with nerve conduction velocity testing is an extremely sensitive test. The skilled electromyographer can diagnose ulnar nerve entrapment at the elbow with a high degree of accuracy, as well as help sort out other neuropathic causes of pain that may mimic ulnar nerve entrapment at the elbow including radiculopathy and plexopathy. Plain radiographs are indicated in all patients who present with ulnar nerve entrapment at the elbow to rule out occult bony disease. If surgery is contemplated, a magnetic resonance imaging (MRI) scan of the affected elbow may help further delineate that pathologic process responsible for the nerve entrapment © 2011 Elsevier Inc. All rights reserved.
Chapter 71—Entrapment Neuropathies of the Elbow and Forearm
607
Ulnar n.
Medial epicondyle
Ulnar collateral lig.
Flexor carpi ulnaris
Fig. 71.1 The causes of ulnar nerve entrap ment at the elbow include compression of the ulnar nerve by an aponeurotic band that runs from the medial epicondyle of the humerus to the medial border of the olecranon, direct trauma to the ulnar nerve at the elbow, and repetitive elbow motion.
Superficial br. Deep br.
Ulnar n.
Fig. 71.3 The ulnar nerve is susceptible to compression at the elbow. (From Waldman SD: Ulnar nerve entrapment at the elbow. In Atlas of common pain syndromes, ed 2, Philadelphia, 2007, Saunders, p 125.)
(e.g., bone spur, tumor, or aponeurotic band thickening) (Fig. 71.4). If Pancoast's tumor or other tumors of the brachial plexus are suspected, chest radiographs with apical lordotic views may be helpful. Screening laboratory testing consisting of complete blood count, erythrocyte sedimentation rate, antinuclear antibody testing, and automated blood chemistry testing should be performed if the diagnosis of ulnar nerve entrapment at the elbow is in question, to help rule out other causes of the patient's pain. The injection technique described subsequently serves as both a diagnostic test and a therapeutic maneuver.2 Fig. 71.2 Ulnar nerve entrapment at the elbow manifests as pain and associated paresthesias in the lateral forearm that radiate to the wrist and to the ring and little fingers. (From Waldman SD: Cubital tunnel syndrome. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 196.)
Differential Diagnosis Ulnar nerve entrapment at the elbow is often misdiagnosed as golfer's elbow, and this error accounts for the many patients whose “golfer's elbow” fails to respond to conservative measures.3
608
Section IV—Regional Pain Syndromes
Superficial br. Deep br.
Radius Ulna Ulnar n.
Fig. 71.4 Entrapment of the ulnar nerve: cubital tunnel syndrome. A lipoma (arrow) adjacent to the ulnar nerve (arrowhead) is well shown in these transverse intermediate-weighted (TR/TE 2000/20) spin-echo magnetic resonance images. The lipoma led to clinical findings of ulnar nerve entrapment in this 36-year-old man. (Courtesy of Z. Rosenberg, MD, New York.)
Ulnar nerve entrapment at the elbow can be distinguished from golfer's elbow in that in cubital tunnel syndrome, the maximal tenderness to palpation is over the ulnar nerve 1 inch below the medial epicondyle, whereas in golfer's elbow, the maximal tenderness to palpation is directly over the medial epicondyle. Ulnar nerve entrapment at the elbow should also be differentiated from cervical radiculopathy involving the C7 or C8 roots. Cervical radiculopathy and ulnar nerve entrapment may coexist as the double-crush syndrome. The double-crush syndrome is seen most commonly with median nerve entrapment at the wrist or carpal tunnel syndrome.4
Treatment A short course of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors, and splinting to avoid elbow flexion is indicated in patients who present with ulnar nerve entrapment at the elbow. If the patient does not experience marked improvement in symptoms within 1 week, careful injection of the ulnar nerve at the elbow with the following technique is a reasonable next step.2 Ulnar nerve injection at the elbow is carried out by placing the patient in the supine position with the arm fully adducted at the patient's side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total of 5 to 7 mL of local anesthetic is drawn up in a 12-mL sterile syringe. A total of 80 mg of depot steroid is added to the local anesthetic with the first block, and a 40-mg dose of depot steroid is added with subsequent blocks. The clinician then identifies the olecranon process and the medial epicondyle of the humerus. The ulnar nerve sulcus between these two bony landmarks is then identified. After preparation of the skin with antiseptic solution, a 5⁄8-inch,
Medial epicondyle Aponeurotic band Fig. 71.5 Injection technique for relieving pain resulting from ulnar nerve entrapment at the elbow. (From Waldman SD: Cubital tunnel syndrome. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 199.)
25-gauge needle is inserted just proximal to the sulcus and is slowly advanced in a slightly cephalad trajectory (Fig. 71.5). As the needle advances approximately 1⁄2 inch, strong paresthesia in the distribution of the ulnar nerve is elicited. The patient should be warned that paresthesia will occur and to say “there!!!!” as soon as the paresthesia is felt. After paresthesia is elicited and its distribution is identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the ulnar nerve remains, a total of 5 to 7 mL of solution is slowly injected, and the patient is monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is slowly injected in a fanlike manner just proximal to the notch, with care taken to avoid intravascular injection. If the patient does not respond to the aforementioned treatments or if the patient is experiencing progressive neurologic deficit, strong consideration to surgical decompression of the ulnar nerve is indicated. As mentioned earlier, MRI scanning of the affected elbow should help to clarify the disorder responsible for compression of the ulnar nerve.
Complications and Pitfalls Failure to identify and treat ulnar nerve entrapment at the elbow promptly can result in permanent neurologic deficit. It is also important to rule out other causes of pain and
Chapter 71—Entrapment Neuropathies of the Elbow and Forearm
609
Enlarged pronator teres m. Median n.
Pronator teres m. (cut): Humeral head Ulnar head Pronator teres m. (cut)
Flexor digitorum superficialis m.
Fig. 71.6 The symptoms of pronator syndrome result from compression of the median nerve by the pronator teres muscle. (From Waldman SD: Pronator syndrome. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 87.)
Fig. 71.7 The onset of pronator syndrome usually occurs after repetitive elbow motions such as chopping wood, sculling, or cleaning fish, although occasionally the onset is more insidious, without apparent antecedent trauma. (From Waldman SD: Pronator syndrome. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 187.)
umbness that may mimic the symptoms of ulnar nerve n entrapment at the elbow, such as Pancoast's tumor, to avoid harm to the patient. Ulnar nerve block at the elbow is a relatively safe block. The major complications are inadvertent intravascular injection into the ulnar artery and persistent paresthesia secondary to needle trauma to the nerve. Care should be taken to inject just proximal to the sulcus slowly, to avoid additional compromise of the nerve because, as the nerve passes through the ulnar nerve sulcus, it is enclosed by a dense fibrous band.
Pronator Syndrome Entrapment of the median nerve in the forearm occurs at several sites. The median nerve may be entrapped at the lacertus fibrosus, at the lateral edge of the flexor digitorum superficialis, by fibrous bands of the superficial head of the pronator teres muscle, or, most commonly, by the pronator teres muscle itself (Fig. 71.6). Compression of the median nerve by the pronator teres muscle is called pronator syndrome.5 The onset of symptoms usually occurs after repetitive elbow
motions such as chopping wood, sculling, or cleaning fish, although occasionally the onset is more insidious, without apparent antecedent trauma (Fig. 71.7). Clinically, pronator syndrome manifests as a chronic aching sensation localized to the forearm with pain occasionally radiating into the elbow. Patients with pronator syndrome may complain about a tired or heavy sensation in the forearm during minimal activity, as well as clumsiness of the affected extremity. The sensory symptoms of pronator syndrome are identical to those of carpal tunnel syndrome. However, in contradistinction to carpal tunnel syndrome, nighttime symptoms are unusual in pronator syndrome.5
Signs and Symptoms The physical findings of pronator syndrome include tenderness over the forearm in the region of the pronator teres muscle. Unilateral hypertrophy of the pronator teres muscle may be identified. A positive Tinel sign over the median nerve as it passes beneath the pronator teres muscle may also be present. Weakness of the intrinsic muscles of the forearm and hand that are innervated by the median nerve may be identified
610
Section IV—Regional Pain Syndromes
Fig. 71.9 Median nerve anatomy. Transverse T1-weighted (TR/TE 500/20) spin-echo magnetic resonance image at the level of the proximal portion of the forearm of an extended elbow shows the following: the median nerve (straight white arrow) located between the two heads of the pronator teres (p) muscles; the ulnar nerve (curved white arrow) between the flexor digitorum profundus (fd), flexor digitorum superficialis (fs), and flexor carpi ulnaris (fu) muscles; and the radial nerve (black arrow) between the two heads of the supinator (s) muscle. (From Kim YS, Yeh LR, Trudell D, et al: MR imaging of the major nerves about the elbow: cadaveric study examining the effect of flexion and extension of the elbow and pronation and supination of the forearm, Skeletal Radiol 27:419, 1998.)
Fig. 71.8 A positive pronator syndrome test result is highly indicative of pronator syndrome. (From Waldman SD: Pronator syndrome. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 88.)
with careful manual muscle testing. A positive pronator syndrome test result, characterized by pain on forced pronation of the patient's fully supinated arm, is highly suggestive of compression of the median nerve by the pronator teres muscle (Fig. 71.8).
Testing Electromyography helps to distinguish cervical radiculopathy, thoracic outlet syndrome, and carpal tunnel syndrome from pronator syndrome. Plain radiographs are indicated in all patients who present with pronator syndrome, to rule out occult bony disease. Based on the patient's clinical presentation, additional testing including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. MRI scan of the forearm is indicated if a primary elbow disorder or a space-occupying lesion is suspected (Fig. 71.9). The injection of the median nerve at the elbow serves as both a diagnostic test and a therapeutic maneuver.
Differential Diagnosis Median nerve entrapment by the ligament of Struthers manifests clinically as unexplained persistent forearm pain caused by compression of the median nerve by an aberrant ligament that runs from a supracondylar process to the medial epicondyle. Clinically, this disorder is difficult to distinguish from pronator syndrome. The diagnosis is made by electromyography and nerve conduction velocity testing, which demonstrate compression of the median nerve at the elbow, combined with the radiographic finding of a supracondylar process.
Both of these entrapment neuropathies can be differentiated from isolated compression of the anterior interosseous nerve that occurs some 6 to 8 cm below the elbow. These syndromes should also be differentiated from cervical radiculopathy involving the C6 or C7 roots that may, at times, mimic median nerve compression. Cervical radiculopathy and median nerve entrapment may coexist as the double-crush syndrome. The double-crush syndrome is seen most commonly with median nerve entrapment at the wrist or carpal tunnel syndrome. Thoracic outlet syndrome may also cause forearm pain and be confused with pronator syndrome. However, the pain of thoracic outlet syndrome radiates into the ulnar rather than the median portion of the hand.
Treatment Use of NSAIDs or COX-2 inhibitors represents a reasonable first step in the treatment of pronator syndrome. The administration of tricyclic antidepressants (e.g., nortriptyline, at a single bedtime dose of 25 mg, with upward titration as side effects allow) is useful, especially if sleep disturbance is also present. Avoidance of repetitive trauma thought to contribute to this entrapment neuropathy is also important. If these maneuvers fail to produce rapid symptomatic relief, injection of the median nerve at the elbow with local anesthetic and steroid is a reasonable next step (Fig. 71.10).6 If symptoms continue to persist, surgical exploration and release of the median nerve will be indicated.
Complications and Pitfalls Median nerve block at the elbow is a relatively safe block. The major complications are inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in patients
Chapter 71—Entrapment Neuropathies of the Elbow and Forearm
Biceps brachii m.
611
Brachial a. Median n.
Lig. of Struthers Brachialis m.
Medial epicondyle Extensor carpi radialis m.
Enlarged pronator teres m. Palmaris longus m.
Radial a.
Aponeurotic extension of biceps Flexor carpi radialis m.
Brachioradialis m.
receiving anticoagulants by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately following injection. The application of cold packs for 20-minute periods following the block also decreases the amount of postprocedure pain and bleeding.
Anterior Interosseous Syndrome Anterior interosseous syndrome is characterized by pain and muscle weakness secondary to median nerve compression syndrome below the elbow by the tendinous origins of the pronator teres muscle and flexor digitorum superficialis muscle of the long finger or by aberrant blood vessels (Fig. 71.11). The onset of symptoms is usually after acute trauma to the forearm or following repetitive forearm and elbow motions such as using an ice pick. An inflammatory origin analogous to that of Parsonage-Turner syndrome has also been suggested as a cause of anterior interosseous syndrome. Clinically, anterior interosseous syndrome manifests as an acute pain in the proximal forearm.7 As the syndrome progresses, patients with anterior interosseous syndrome may complain about a tired or heavy sensation in the forearm during minimal activity, as well as the inability to pinch items between the thumb and index fingers because of paralysis of the flexor pollicis longus and flexor digitorum profundus muscles (see Fig. 71.11). Physical findings include the inability to flex the interphalangeal joint of the thumb and the distal interphalangeal joint
Flexor carpi ulnaris m. Flexor digitorum superficialis m.
Fig. 71.10 Injection technique for relieving pain resulting from pronator syndrome. (From Waldman SD: Pronator syndrome. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 189.)
of the index finger because of paralysis of the flexor pollicis longus and flexor digitorum profundus muscles.8 Tenderness over the forearm in the region of the pronator teres muscle is seen in some patients suffering from anterior interosseous syndrome. A positive Tinel sign over the anterior interosseous branch of the median nerve approximately 6 to 8 cm below the elbow may also be present. The anterior interosseous syndrome should also be differentiated from cervical radiculopathy involving the C6 or C7 roots that may mimic median nerve compression. Furthermore, cervical radiculopathy and median nerve entrapment may coexist as the double-crush syndrome. The double crush syndrome is seen most commonly with median nerve entrapment at the wrist or carpal tunnel syndrome.
Clinically Relevant Anatomy The median nerve is composed of fibers from C5-T1 spinal roots. The nerve lies anterior and superior to the axillary artery. Exiting the axilla, the median nerve descends into the upper arm along with the brachial artery. At the level of the elbow, the brachial artery is just medial to the biceps muscle. At this level, the median nerve lies just medial to the brachial artery. As the median nerve proceeds downward into the forearm, it gives off numerous branches that provide motor innervation to the flexor muscles of the forearm, including the anterior interosseous nerve. These branches are susceptible to nerve entrapment by aberrant ligaments, muscle hypertrophy, and direct trauma. The nerve approaches the wrist overlying the radius. It lies deep to and between the tendons of the palmaris longus muscle and the flexor carpi radialis muscle at the wrist. The terminal branches of the median nerve provide
612
Section IV—Regional Pain Syndromes Muscle paralysis: Nerve compression: Normal
Pronator teres m.
Median n. Muscle paralysis
Pronator digitorum superficialis m. Flexor pollicis longus m.
Ant. interosseous branch of median n.
Flexor digitorum profundus m.
Fig. 71.11 Patients suffering from the anterior interosseous syndrome exhibit acute forearm pain and progressive weakness of pinch. (From Waldman SD: Anterior interosseous syndrome. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 107.)
sensory innervation to a portion of the palmar surface of the hand, as well as to the palmar surface of the thumb and the index, and middle fingers and the radial portion of the ring finger. The median nerve also provides sensory innervation to the distal dorsal surface of the index and middle fingers and the radial portion of the ring finger.
Treatment Use of the NSAIDs or COX-2 inhibitors represents a reasonable first step in the treatment of pronator syndrome. The administration of a tricyclic antidepressant (e.g., nortriptyline, at a single bedtime dose of 25 mg, with upward titration as side effects allow) is useful, especially if sleep disturbance is also present. Avoidance of repetitive trauma thought to contribute to this entrapment neuropathy is also important. If these maneuvers fail to produce rapid symptomatic relief, injection of the median nerve at the forearm with local anesthetic and steroid is a reasonable next step.7 If symptoms continue to persist, surgical exploration and release of the median nerve will be indicated. The patient is placed in a supine position with the arm fully adducted at the patient's side and the elbow slightly flexed with the dorsum of the hand resting on a folded towel. A total
of 5 to 7 mL of local anesthetic and 40 mg of methylprednisolone is drawn up in a 12-mL sterile syringe. The patient is then asked to flex his or her forearm against resistance to identify the biceps tendon at the crease of the elbow. A point 6 to 8 cm below the biceps tendon is then identified and marked with a sterile skin marker. After preparation of the skin with antiseptic solution, a 11⁄2inch, 25-gauge needle is inserted at the previously marked point and is slowly advanced in a slightly cephalad trajectory (Fig. 71.12). As the needle advances approximately 1⁄2 to 3 ⁄4 inch, strong paresthesia in the distribution of the median nerve is elicited. If no paresthesia is elicited and the needle contacts bone, the needle is withdrawn and is redirected slightly more medially until paresthesia is elicited. The patient should be warned that paresthesia will occur and to say “there!!!!” as soon as the paresthesia is felt. After paresthesia is elicited and its distribution is identified, gentle aspiration is carried out to identify blood. If the aspiration test result is negative and no persistent paresthesia into the distribution of the median nerve remains, a total of 5 to 7 mL of solution is slowly injected, and the patient is monitored closely for signs of local anesthetic toxicity. If no paresthesia can be elicited, a similar amount of solution is injected in a fanlike manner, with care taken not to inadvertently inject into the anterior interosseous artery.
Chapter 71—Entrapment Neuropathies of the Elbow and Forearm
613
Median n. Humerus
Brachial a.
Radial n. Radius Radial a. Ant. interosseous n.
Ulna
Ant. interosseous a.
Ulnar a.
Extensor carpi radialis brevis m.
Pronator quadratus m.
Fig. 71.12 Injection technique for relieving pain resulting from anterior interosseous syndrome. (From Waldman SD: Anterior interosseous
Fig. 71.13 The pain of radial tunnel syndrome is localized to the deep exterior muscle mass and may radiate proximally and distally into the upper arm and forearm. (From Waldman SD: Radial tunnel syndrome. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 102.)
syndrome. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 193.)
Complications and Pitfalls Median nerve block below the elbow is a relatively safe block. The major complications are inadvertent intravascular injection and persistent paresthesia secondary to needle trauma to the nerve. This technique can safely be performed in patients receiving anticoagulants by using a 25- or 27-gauge needle, albeit at increased risk of hematoma, if the clinical situation dictates a favorable risk-to-benefit ratio. These complications can be decreased if manual pressure is applied to the area of the block immediately following injection. The application of cold packs for 20-minute periods following the block also decreases the amount of postprocedure pain and bleeding.
Radial Tunnel Syndrome Radial tunnel syndrome is an entrapment neuropathy of the radial nerve that is often clinically misdiagnosed as resistant tennis elbow.9,10 In radial tunnel syndrome, the posterior interosseous branch of the radial nerve is entrapped by various mechanisms that share a similar clinical presentation.
These mechanisms include aberrant fibrous bands in front of the radial head, anomalous blood vessels that compress the nerve, and a sharp tendinous margin of the extensor carpi radialis brevis (see Fig. 71.11). These entrapments may exist alone or in combination. Regardless of the mechanism of entrapment of the radial nerve, the common clinical feature of radial tunnel syndrome is pain just below the lateral epicondyle of the humerus.9 The pain of radial tunnel syndrome may develop after an acute twisting injury or direct trauma to the soft tissues overlying the posterior interosseous branch of the radial nerve, or the onset may be more insidious, without an obvious inciting factor (Fig. 71.13). The pain is constant and is made worse by active supination of the wrist. Patients often note the inability to hold a coffee cup or hammer. Sleep disturbance is common. On physical examination, the patient will report tenderness to palpation of the posterior interosseous branch of the radial nerve just below the lateral epicondyle11 (Fig. 71.14). Elbow range of motion is normal. Grip strength on the affected side may be diminished. Patients with radial tunnel syndrome exhibit pain on active resisted supination of the forearm. Cervical radiculopathy and tennis elbow can mimic radial tunnel syndrome.10 Radial tunnel syndrome can
614
Section IV—Regional Pain Syndromes
Posterior interosseous n.
Lateral epicondyle
it supplies a motor branch to the triceps. Continuing its downward path, it gives off numerous sensory branches to the upper arm. At a point between the lateral epicondyle of the humerus and the musculospiral groove, the radial nerve divides into its two terminal branches. The superficial branch continues down the arm along with the radial artery and provides sensory innervation to the dorsum of the wrist and the dorsal aspects of a portion of the thumb, index, and middle finger. The deep posterior interosseous branch provides most of the motor innervation to the extensors of the forearm.
Treatment Fig. 71.14 Radial tunnel syndrome can be distinguished from tennis elbow by careful identification of the point of maximal tenderness. (From Waldman SD: Radial tunnel syndrome. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 103.)
be distinguished from tennis elbow in that in radial tunnel syndrome, the maximal tenderness to palpation is distal to the lateral epicondyle over the posterior interosseous branch of the radial nerve, whereas in tennis elbow, the maximal tenderness to palpation is over the lateral epicondyle (see Fig. 71.12). Electromyography helps to distinguish cervical radiculopathy and radial tunnel syndrome from tennis elbow. Plain radiographs are indicated to rule out occult bony disease in all patients who present with radial tunnel syndrome. Based on the patient's clinical presentation, additional testing including complete blood count, uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. MRI scan of the elbow is indicated if joint instability is suspected. The injection technique described here serves as both a diagnostic test and a therapeutic maneuver.12
Clinically Relevant Anatomy The radial nerve is made up of fibers from C5-T1 spinal roots. The nerve lies posterior and inferior to the axillary artery. Exiting the axilla, the radial nerve passes between the medial and long heads of the triceps muscle. As the nerve curves across the posterior aspect of the humerus,
Use of the NSAIDs or COX-2 inhibitors represents a reasonable first step in the treatment of pronator syndrome. The administration of the tricyclic antidepressants (e.g., nortriptyline, at a single bedtime dose of 25 mg, with upward titration as side effects allow) is also useful, especially if sleep disturbance is also present. Avoidance of repetitive trauma thought to contribute to this entrapment neuropathy is also important. If these maneuvers fail to produce rapid symptomatic relief, injection of the median nerve at the forearm with local anesthetic and steroid is a reasonable next step.7 If symptoms continue to persist, surgical exploration and release of the radial nerve will be indicated.
Conclusion The myriad and overlapping clinical presentations of the entrapment neuropathies at the elbow and forearm present a diagnostic challenge to the clinician. To make the correct diagnosis, a targeted history and physical examination are mandatory. Electromyography and nerve conduction studies combined with judicious use of diagnostic imaging techniques will help to confirm the diagnosis. Failure to diagnose and treat in a timely manner the entrapment neuropathies discussed here can lead to significant suffering and disability for the patient.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
72
Arthritis of the Wrist and Hand Richard M. Keating
CHAPTER OUTLINE General Considerations 616 Arthritis of the Wrist 616 Etiology 616 Clinical Features and Differential Diagnosis 616
General Considerations Pain in the wrist and hand is a relatively common symptom that patients bring to a clinician. The pain may emanate from any of the numerous bones or joints in the hand, from periarticular soft tissue sites (subcutaneous tissues, palmar fascia, tendon sheaths), from vascular structures, or from peripheral nerves. The pain may even be referred pain from anomalies in the cervical spine, thoracic outlet, shoulder, or elbow. Table 72.1 provides a list of the differential diagnoses of painful disorders of the wrist and hand, based on location. Many of these entities are discussed more fully in other chapters. As always, an accurate diagnosis depends on a detailed history and on a careful physical examination of the joints, the tenosynovial sheaths and periarticular structures, the cervical spine, and the nerve and blood supplies to the hand. Laboratory testing and imaging studies supplement the history and physical examination, to arrive at a correct diagnosis.1 The onset of many painful, nontraumatic hand disorders is often insidious, with the exception of crystalline disease, which usually has an abrupt onset. A history of unaccustomed, repetitive, or excessive hand activity is particularly important in the diagnosis of wrist, thumb, or finger arthritis or tenosynovitis when the cause is an overuse syndrome. A detailed occupational history is important for determining whether the hand tenosynovitis is work related, either as a cumulative trauma disorder or as an acute injury. A working knowledge of the anatomy of the wrist joint, the metacarpophalangeal (MCP) joints, the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints of the fingers, and the tendon sheaths (Figs. 72.1 and 72.2) is important for precise diagnosis. The back of the hand is called the dorsum, the palmar aspect is called the volar side, and each finger has three joints: the MCP, PIP, and DIP. The thumb has an MCP and an interphalangeal joint (IP) but no DIP joint. The base of the thumb, where the metacarpal bone meets the carpal row, is the carpometacarpal (CMC) joint. The ability to localize the area of pain accurately in the hand quickly narrows the differential diagnosis. For example, 616
Arthritis of the Metacarpophalangeal Proximal Interphalangeal, and Distal Interphalangeal Joints 618 Treatment 618
most pain in the CMC joint results from osteoarthritis (OA), whereas pain with swelling in the MCP joints is often a sign of rheumatoid arthritis (RA) or another inflammatory arthritis. Correct localization of the pain allows the clinician to make the correct diagnosis. Most disorders of the hand and wrist can be diagnosed without the need for laboratory analysis. Diagnostic studies may include a complete blood count, erythrocyte sedimentation rate, chemistry studies, and rheumatoid factor and antinuclear antibody determinations (if the overall history and physical examination suggest a diffuse connective tissue disease). Hand radiographs are useful for diagnosing certain forms of arthritis, if the arthritis has been present for long enough to result in bony changes. Synovial fluid analysis (if joint effusion is present) may be diagnostic of crystalline disease, and this analysis is also necessary to differentiate inflammatory from noninflammatory arthritis. Additional studies are sometimes required and may include skeletal scintigraphy, ultrasonography, nerve conduction studies, noninvasive vascular (Doppler) studies, arteriography, computed tomography, magnetic resonance imaging, arthrography, and even synovial biopsy.
Arthritis of the Wrist Etiology The radiocarpal (wrist) joint is a common site for inflammatory arthritides, such as RA, systemic lupus erythematosus (SLE), crystalline arthritis (gout and pseudogout), psoriatic arthritis (PsA), ankylosing spondylitis, reactive arthritis, and enteropathic arthritis.1 Primary OA of the wrist is rare, but the joint can be affected by secondary OA brought on by trauma, hemochromatosis, ochronosis, osteonecrosis, or past infection.
Clinical Features and Differential Diagnosis Arthritis of the wrist is associated with pain and stiffness just distal to the radius and ulna. Movements are often restricted, and crepitus may be appreciated with both active and passive © 2011 Elsevier Inc. All rights reserved.
Chapter 72—Arthritis of the Wrist and Hand
range of motion. Inflammatory arthritis is usually accompanied by joint capsule–based swelling (synovitis), along with reduced function and even deformity. Inflammatory arthritis effusions may be appreciated when pressure with one hand on one side of the joints produces a fluid wave transmitted to the second hand placed on the opposite side of the joint. Wrist deformities are common in RA and other chronic inflammatory arthritides. Findings may include volar subluxation of the carpus with a visible step opposite the radiocarpal joint, carpal collapse (loss of carpal height to less than half the length
Extensor pollicis longus (third compartment)
Extensor pollicis brevis Abductor pollicis longus
Table 72.1 Differential Diagnoses of Wrist and Hand Pain Articular Wrist MCP PIP DIP Periarticular Subcutaneous Palmar fascia Tendon sheath
Acute calcific periarthritis Ganglion Osseous
RA, SLE, crystalline disease RA, SLE, crystalline disease Nodal OA, RA, SLE, psoriatic arthritis Nodal OA, SLE, psoriatic arthritis RA nodule, gouty tophus, glomus tumor Dupuytren's contracture de Quervain's tenosynovitis Wrist volar flexor tenosynovitis Thumb or finger flexor tenosynovitis (trigger or snapping thumb or finger) Pigmented villonodular tenosynovitis (giant cell tumor of the tendon sheath) Wrist, MCP, and rarely PIP and DIP Attached to joint capsule, tendon sheath, or tendon
Vascular Vasospastic disorders (Raynaud's) Vasculitis
Abductor pollicis longus and extensor pollicis brevis (first compartment)
Extensor carpi radialis longus and extensor carpi radialis brevis (second compartment)
Referred radicular pain syndromes Shoulder-hand syndrome and causalgia
Cardiac
Angina pectoris
*Formerly called reflex sympathic dystrophy. DIP, distal interphalangeal; MCP, metacarpophalangeal; OA, osteoarthritis; PIP, proximal interphalangeal; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.
Extensor digiti minimi (fifth compartment) Extensor retinaculum Extensor carpi ulnaris tendon and sheath (sixth compartment)
ed 3, Philadelphia, 2003, Mosby, p 642.)
Digital flexor tendon sheaths
Common flexor tendon sheath Flexor pollicis longus tendon and sheath
Scleroderma, occupational vibration syndrome Digital ischemia and ischemic ulcers, SLE, RA
Referred Pain Cervical spine disorders Complex regional pain syndrome*
Extensor digitorum communis and extensor indicis proprius (fourth compartment)
Fig. 72.1 Extensor tendons and tendon sheaths of the wrist, fingers, and thumb. (From Hochberg M, Silman A, editors: Rheumatology,
Fractures, neoplasms, infection (osteomyelitis) Osteonecrosis including Kienböck's disease (lunate bone) and Preiser's disease (scaphoid bone)
Nerve Entrapment Syndromes Median nerve Carpal tunnel syndrome (at wrist) Pronator teres syndrome (at pronator teres) Anterior interosseous nerve syndrome Ulnar nerve Cubital tunnel syndrome (at elbow) Guyon canal (at wrist) Posterior interosseous Radial nerve palsy (spiral groove syndrome) Lower brachial plexus Thoracic outlet syndrome, Pancoast's tumor Cervical nerve roots Herniated cervical disk, tumors Spinal cord lesion Spinal tumors, syringomyelia
617
Flexor retinaculum Flexor superficialis and flexor profundus tendons
Flexor carpi radialis tendon and sheath
Fig. 72.2 Flexor tendon sheaths of the wrist, fingers, and thumb. (From Hochberg M, Silman A, editors: Rheumatology, ed 3, Philadelphia, 2003, Mosby, p 642.)
618
Section IV—Regional Pain Syndromes
of the third metacarpal), and radial deviation of the carpus from the axis of the wrist and hand. Chronic inflammatory arthritis of the distal radioulnar joint is associated with local swelling, painful restriction of pronation and supination, and often instability with dorsal subluxation of the ulnar head and a “piano key sign” on the distal ulna (it sits higher than the distal radius and can be easily moved up and down because of ligamentous laxity). Extensor wrist tenosynovitis, by contrast, manifests as a superficial, linear or oval, dorsal swelling localized to the distribution of the affected tendon sheath and extending well beyond the joint margins, seemingly to involve the entire dorsum of the hand. When the fingers are actively extended, the distal margin of the swelling moves proximally and folds inward, like a sheet being tucked under a mattress (the “tuck sign”). Tenosynovitis of the common flexor tendon sheath manifests as a swelling over the volar aspect of the wrist just proximal to the carpal tunnel (volar “hot dog sign”).1 Ganglia are mucinous structures with a jelly-like consistency on palpation that arise in the hand. They may be attached to various structures including the joint capsule, tendon sheath, or tendons themselves. The cause of ganglia is not known. Most ganglia are found on the dorsal aspect of the wrist. Often painless, they can sometimes interfere with smooth mechanical function. Although aspiration diminishes their size, they often recur following the procedure, and surgical excision is required.2
Fig. 72.3 Boutonnière deformity of the right ring finger. (From Hochberg M, Silman A, editors: Rheumatology, ed 3, Philadelphia, 2003, Mosby, p 644.)
Arthritis of the Metacarpophalangeal Proximal Interphalangeal, and Distal Interphalangeal Joints Inflammatory arthritis of the MCP and PIP joints is most often associated with RA and SLE. These same joints can be affected by PsA, but PsA may also affect the DIP joints, especially when the nails are affected by psoriasis. MCP synovitis produces diffuse, tender swelling of the joint that may obscure the valleys between the knuckles and that is sometimes referred to as “the mogul sign.”1 Swelling of the PIP joint produces a fusiform or spindle-shaped finger. To detect PIP or DIP joint effusion, compression of the joint by one hand produces ballooning or a hydraulic lift sensed by the other hand (“balloon sign”). Unlike PIP synovitis, dorsal knuckle pads are a subcutaneous tissue thickening that produces nontender thickening of the skin localized to the dorsal surface overlying the PIP joints. Both the PIP and DIP joints are commonly affected in primary “nodal” OA, which manifests as Bouchard's nodes and Heberden's nodes, respectively. Digital flexor tenosynovitis, by contrast, produces a linear tender swelling over the volar aspect of the finger (“sausage finger”), often associated with thickening, nodules, and fine crepitus of the flexor tendon sheath. Deformities of the MCP, PIP, and DIP joints are relatively common in inflammatory arthritis.1 MCP joint deformities include ulnar drift, volar subluxation (often visible as a step), and fixed flexion deformity. The term boutonnière deformity describes a finger with flexion of the PIP joint and hyperextension of the DIP joint (Fig. 72.3). The term swan-neck deformity describes the appearance of a finger with hyperextension of the PIP joint and flexion of the DIP joint (Fig. 72.4). A Z-shaped deformity of the thumb consists of flexion of the MCP joint and hyperextension of the IP joint (see Fig. 72.4). Telescoped
Fig. 72.4 Swan-neck deformities of the fingers and Z-shaped defor mities of the thumbs. (From Hochberg M, Silman A, editors: Rheumatology, ed 3, Philadelphia, 2003, Mosby, p 644.)
shortening of the digits, produced by partial resorption of the phalanges secondary to PsA, RA, or other destructive arthritis, is often associated with concentric wrinkling of the skin (“opera-glass hand”).
Treatment Treatment of arthritis of the wrist, MCP, PIP, or DIP joints depends on identifying the underlying cause and addressing treatment to that disorder. For example, RA should be treated with methotrexate, other disease-modifying agents,
Chapter 72—Arthritis of the Wrist and Hand
or a biologic agent. OA should be treated with pain control, physical therapy, and possibly the use of assistive devices when the hand is affected. General measures include resting of the affected joint by splinting and physical and occupational therapies. Soft tissue causes of hand and wrist pain are treated in a specific fashion, depending on type. Specific disorders are described in separate chapters. For persistent inflammatory synovitis, intra-articular corticosteroids are often helpful. The radiocarpal (wrist) joint can be injected through a dorsoradial approach.3 With the wrist slightly palmar flexed, the needle is inserted perpendicularly to a depth of 1 to 2 cm at a point distal to Lister's tubercle of the distal
radius (a bony prominence palpated along the distal radius) and just ulnar to the extensor pollicis longus tendon. The MCP, PIP, and DIP joints can be readily entered through a dorsoradial or a dorsoulnar approach using a 28-gauge needle.3 It is sometimes necessary to tease the needle tip into the joint space while the operator applies slight traction to the finger, to pull the articulating surfaces apart. A correctly placed intra-articular injection produces fluid distention of the joint on all sides.
References Full references for this chapter can be found on www.expertconsult.com.
619
IV
Chapter
73
Carpal Tunnel Syndrome Richard M. Keating
CHAPTER OUTLINE Etiology 620 Clinical Features and Physical Examination 620
The carpal tunnel is an anatomic region in the wrist and the site of the body's most common entrapment neuropathy. The true carpal tunnel is bounded on its dorsal and lateral aspects by the carpal bones and the intercarpal joints and on its volar aspect by the transverse carpal ligament (flexor retinacu lum).1 Passing through this canal are nine flexor tendons that include the flexor digitorum profundus, flexor digitorum sub limis, and flexor pollicis longus, along with the median nerve. In 1854, James Paget first reported what is now considered carpal tunnel syndrome (CTS).2
Etiology Any process that can result in swelling of the flexor tendons or in infiltration of the carpal tunnel space can cause the symp toms of CTS by pressure on the median nerve. Most often, nonspecific tenosynovitis in an otherwise healthy person is thought to be the cause of CTS.3 Synovitis from rheumatoid arthritis, inflammation from a gout attack or tophi deposition, inflammation from systemic lupus erythematosus, a pseudo gout attack, or any other inflammatory process can also result in CTS. In addition, infiltrative diseases such as amyloid can cause CTS. Obesity, hypothyroidism, acromegaly, diabetes, and pregnancy are all recognized risk factors for CTS. More commonly, however, CTS is idiopathic and is believed to be caused by repetitive motion, whether occupational or recreational. On rare occasion, CTS may be attributable to a space-occupying lesion in the carpal tunnel such as a ganglion, lipoma, or even a fracture callus.
Clinical Features and Physical Examination The typical CTS sufferer is a woman between 40 and 60 years old.4 The usual symptoms include burning pain, paresthe sias, numbness, or even sensory loss along the median nerve distribution: fingers 1, 2,3, and the radial aspect of finger 4 (the thumb, first two fingers, and the radial half of the ring finger). Nocturnal awakening with symptom exacerbation is a charac teristic and frequent complaint, and the presence of symptoms on first awakening is also common. Many patients awaken to 620
Diagnostic Studies 621 Treatment 621
find themselves shaking their hand or forearm to alleviate the symptoms. Some patients experience pain or paresthesia radi ation more proximally up the forearm, to the elbow region or even toward the shoulder. Repetitive flexion and extension at the wrist worsen the symptom complex. Physical examination findings, especially early in the course of CTS, are entirely normal. With a longer duration of symp toms, one can see flattening of the thenar eminence from muscle loss.5 Provocative maneuvers employed by the clini cian to reproduce symptoms and to help make the diagnosis of CTS include Tinel's sign. The volar aspect of the wrist, at the level of the carpal tunnel, is percussed in a tapping man ner. The proper site for percussion is at the flexor retinacu lum, just radial to the palmaris longus tendon at the distal wrist crease. This maneuver is performed with the patient's wrist in slight extension. A positive test result is characterized by reproduction of paresthesia in the median nerve distribu tion (along fingers 1, 2, 3, and the radial aspect of finger 4)4 (Fig. 73.1). Another provocative test is the Phalen maneuver. The wrist is flexed for 30 to 60 seconds; this maneuver may well reproduce finger paresthesias (Fig. 73.2). Wrist extension narrows the carpal tunnel, increases pressure within the canal, and thereby reproduces the symptoms. This test is termed the reverse Phalen maneuver. Simply elevating the affected hand for 1 or 2 minutes may also reproduce the patient's symp toms. A good sensory examination may demonstrate dimin ished touch, two-point discrimination, or vibratory sense in the median nerve distribution. Chronic symptoms may result in loss of thenar muscle bulk, with resultant weakness in the abductor pollicis brevis (weakness of resisted palmar abduc tion of the thumb) and opponens pollicis muscles (inability to maintain a pinch between tip of thumb and tip of little finger against resistance).4 The reported sensitivity and specificity of these maneuvers varies widely, and the diagnosis should always still be considered if the history is consistent with CTS but no particular maneuver reproduces the pain or paresthesias. Median nerve entrapment at the elbow, known as pronator teres syndrome, can cause weakness of the intrinsic muscles in the second and third fingers with hyperextension at the MCP joints and can sometimes be confused with CTS. Pronator teres syndrome can be distinguished from CTS by a positive © 2011 Elsevier Inc. All rights reserved.
Chapter 73—Carpal Tunnel Syndrome
621
Fig. 73.3 Injection for carpal tunnel syndrome. Fig. 73.1 Tinel's sign.
Fig. 73.2 Phalen's test.
Tinel sign at the elbow instead of at the wrist. Other condi tions that can be confused with CTS include diabetic neuropa thy and cervical radiculopathy.
Diagnostic Studies CTS is a clinical diagnosis. The clinician usually makes the diag nosis based on history, with possibly some support from physi cal examination maneuvers. The diagnosis can be confirmed by an electrodiagnostic study that demonstrates slowing of sensory conduction through the median nerve as it traverses the carpal tunnel, but this test is not absolutely required to make the diag nosis. CTS may also be a ssociated with prolonged distal motor latency, although sensory conduction is far more often affected than is motor conduction.3 Electrodiagnostic studies may also be useful in localizing the entrapment site. However, falsenegative results can occur in up to 10% of patients.6 Occasionally, magnetic resonance imaging or ultrasonography demonstrates swelling within the flexor tendons from tenosynovitis.
Treatment Treatment of CTS can start conservatively, with avoidance of repetitive action, volar splinting (especially at night) of the wrist in a slightly extended position, and judicious use of nonsteroi dal anti-inflammatory drugs (NSAIDs) for pain and inflamma tion.7 However, a 2003 systematic review found no significant benefit from using NSAIDs as compared with placebo.8 In the setting of CTS and concomitant first carpometacarpal joint osteoarthritis, splinting of both the wrist and the first carpo metacarpal may be preferred. The purpose of referral to a hand occupational therapist is to instruct the patient on stretching exercises for the volar carpal ligaments may be helpful. A local corticosteroid injection of the carpal tunnel may be useful if the condition is of shorter duration (four spaces
747
E–Thoracic arachnoiditis
Burning pain is indeed the characteristic manifestation on one or both lower extremities, with or without hyperalgesia and allodynia and usually accompanied by sensory disturbances including hypoesthesia, dysesthesia, and a tingling sensation. Hyperreflexia may be noted, although it depends on the presence of other lesions. Muscle spasms are common. Peculiarly enough, most patients also have autonomic nervous system manifestations, such as low-grade fever, frequent diaphoresis and nocturnal sweating, and chronic fatigue. Most patients with cauda equina nerve root involvement have considerable bladder dysfunction; incontinence and incomplete emptying are more common in women, whereas dysuria, frequency, and residual urine after micturition occur more often in men. Rectal dysfunction is more commonly manifested as constipation, with or without rectal incontinence, and it is present in both genders in approximately 40% of patients. In most clinical settings, seldom are patients asked about changes in sexual function after the onset of arachnoiditis. In this same group of patients, investigators found that loss of libido and difficulty in arousing were the most frequent dysfunctions in both men and women. Men reported impotence, penel pain at erection, and low back pain during sexual intercourse, and women reported pain during and after intercourse.38 Needless to say, considerable depression is present in most patients with arachnoiditis. Some patients also have anxiety and feelings of loss, guilt, and despair because no cure is available. These symptoms contribute to intramarital and interfamily conflicts, as well as social dysfunction, ending in separation or divorce in more than one third of the patients. Cigarette smoking is prevalent, as are isolation and disability. This perspective implies a population group with several disabling
Fig. 93.8 Quantitative scale to estimate and compare the degree of extent and severity brought by the pattern of distribution and clumping of the nerve roots. The scale lists the number of interspaces involved and includes other associated lesions.
clinical manifestations that impair the ability to remain in a functional family, preclude participation in social interactions, and make it impossible to support themselves and their families. These patients become dependent on the health care system or on their close relatives, and the result is a sense of permanent loss.39
Correlative Diagnosis In a group of patients seen from 1989 to 2008, Aldrete attempted to identify suggestive features that would indicate the apparent injurious event that produced arachnoiditis (confirmed by radiologic diagnosis). Patients who had undergone surgical procedures by far exceeded those whose arachnoiditis was caused by neuraxial anesthesia, epidural steroid injections, and other irritant substances (e.g., neurolytics, dyes, local anesthetics containing preservatives or enzymes). The numbers of cases attributed to the intrathecal injection of Pantopaque for myelograms declined. Usually, the localization of symptoms to one or both sides corresponded to the intervertebral level affected and the findings of the neurologic examination. Numerous patterns of nerve root clumping exist, and no single pattern signifies the typical representation of arachnoiditis. Nevertheless, it is important to determine the location of the clumping as well as the intervertebral levels affected.31–34,36 In cases of arachnoiditis caused by surgical interventions, in addition to finding some of the nerve roots clumped and the dural sac retracted or dilated at the level of the operated intervertebral space, these patients also had peridural scarring and fibrosis (see Fig. 93.8). Not uncommonly, distal ectasia or pseudomeningocele may be present (see Chapters 96 and 98). A scale to grade the extent of clumping, the levels included, and
748
Section IV—Regional Pain Syndromes
other related lesions has been proposed. However, because the same patient may have undergone myelographies, laminectomies, and various invasive procedures, in some cases it is not clearly evident which intervention caused the lesions unless a sudden appearance of clumped nerve roots (see Figs. 93.2 and 93.3) at MRI corresponds to the relevant clinical neurologic findings and the level at which the intervention was done.
Prevention In this disease, prevention is a primordial concern that would reduce the number of cases of arachnoiditis. Although the recommendations for prevention appear to be simple, they are crucial. In the case of suspected infections, associated symptoms or findings may be helpful to define the cause. An MRI scan confirms the diagnosis of peridural or intrathecal location. Although the use of spinal taps to sample CSF appears reasonable, a postdural puncture headache in a patient with increased CSF pressure would increase the persistence of postural cephalalgia. It is suggested that an MRI scan be obtained first, especially with the present availability of MRI. Thereafter, dural puncture may be necessary only to obtain a specimen for culture and sensitivity. The occurrence of paresthesias during an interventional procedure of the spine may be a reason for stopping the procedure and choosing a different technique, because perforation of the dura and arachnoid is implied, as well as penetration of the perineural layer of a nerve root. Furthermore, the injection of local anesthetics, even at their usual concentrations, may, under these circumstances, irritate the endoneurial structures and initiate an inflammatory response.6,22,23 Because the posterior epidural space has no nerve trunks, eliciting paresthesias implies that the tip of the needle was in the subarachnoid space. Strict aseptic technique is essential when the vertebral canal is to be invaded; currently, the injection of neuroirritant or neurolytic substances into the canal is best avoided.
Treatment Because different disease mechanisms are involved in the two phases of arachnoiditis, the therapeutic approach needs to be tailored to each of these stages. The presence of blood or serosanguineous CSF usually implies the puncture of a vessel within the intrathecal compartment. The injection of any chemical substances, including local anesthetics or dyes,1,2,28 may, under these circumstances, appear to increase the likelihood of arachnoidal inflammation. Similarly, the concomitant peridural administration of certain additives such as sodium bicarbonate, vasoconstrictors (epinephrine or phenylephrine), or therapeutic agents such as corticosteroids or blood in the presence of an incidental penetration of the dura may initiate intrathecal inflammation, even when small volumes of these substances have been administered. The decision to postpone these procedures is not easy, and it needs to be practical. If feasible, however, a delay may be considered before proceeding, in view of the added risk weighed against rescheduling the procedure for another day. As alternatives, one may consider proceeding but using an extraspinal (paravertebral) or caudal technique or a peripheral nerve block, if indicated.
Treatment of the Acute Phase of Arachnoiditis Because of the critical interval when proper diagnosis and treatment may reduce or stop the inflammatory process, treatment is urgent. If a neurologic deficit, uncontrollable severe burning pain, or loss of bladder or bowel control occurs after an invasive or surgical procedure, the following steps are recommended34,40,41: Perform a complete neurologic examination. Obtain a neurology consultation. ■ Perform an MRI scan to search for specific lesions that may need to be treated promptly (e.g., intrathecal or extradural hematoma, dural leaks). ■ ■
Once the clinical diagnosis of arachnoiditis, cauda equina syndrome, pseudomeningocele, or any other neurologic deficit is made and is confirmed by the typical appearance of enhanced nerve roots, and if the patient is considered to be in the inflammatory stage of the disease (estimated to last 8 to 10 weeks after the injurious event; see Fig. 93.4), treatment is indicated to prevent the condition from evolving into the permanent proliferative phase. The following protocol is recommended: ■ ■ ■ ■ ■
Limit physical activities. Administer steroids intravenously. Administer magnesium oxide. Use anti-inflammatory agents such as indomethacin. Use an anticonvulsant. Administer an antidepressant. Monitor improvement by repeating the neurologic examination every 3 days and the MRI scan every 3 to 4 weeks. ■ In the event that radiologic confirmation is inconclusive but the clinical manifestations are evident, treating physicians may consider proceeding with this protocol. ■ For information, consult www.arachnoiditis.com. ■ ■
Preliminary observations have indicated that the sooner this protocol is initiated, the better the chances will be for having the symptoms subside completely or partially. This study, still in progress, appears to suggest that procrastination is not helpful, whereas prompt treatment may offer the possibility of reversing the neurologic deficits and burning pain. Once the third month passes, usually the symptoms are permanent. Interventional procedures during this phase of arachnoiditis are best avoided.
Treatment of Chronic Arachnoiditis Most patients with the diagnosis of arachnoiditis have features of neurogenic pain; therefore, the concepts already described in Chapters 2 to 6, 32 to 38, and 98 apply to its mechanisms, pathophysiology, and proposed treatment. However, some special characteristics in this disease merit mention.32,40 Considering that the intensity of burning pain, hyperalgesia, and allodynia is severe and continuous, the initiation of opioid medications is not one to be undertaken lightly. Because tolerance to this group of medications and the dependency syndrome most likely will develop, it is preferable to initiate treatment with schedule III opiates.40,42 Apparent increases in pain intensity, usually accompanied by requests to increase the dosage, usually imply a reduction of the drug's efficacy,
Chapter 93—Arachnoiditis and Related Conditions
owing to tachyphylaxis rather than to progression of the disease, given that arachnoiditis tends to evolve very slowly.43 Moreover, the development of hyperalgesia with progressive doses of opioids44 has been recognized as a detractor to the indiscriminate use of these medications. Naturally, other associated conditions such as spondylolisthesis, spondylosis, recurrent herniated nucleus pulposus, and so on, must be ruled out because their symptoms may be superimposed on those of arachnoiditis. These other disorders manifest with similar symptoms but require a different type of treatment. Whenever possible and as early as feasible, an anticonvulsant medication is indicated. Gabapentin has been the most effective in taming the pain. Pregabalin, topiramate, and phenytoin are possible alternatives if side effects to gabapentin develop. Psychological counseling is usually required in most patients to help them to cope with the sense of loss and specifically the depression,39 which can become severe. Psychiatric consultation is required in patients with severe cases and to define selectively the type of antidepressant best for each of these patients, as well as to determine the need for anxiolytic medications, hypnotics, and so on. Muscle relaxants are indicated if severe muscle spasms appear. The usual physical therapy modalities may actually increase the pain; however, because it is crucial to maintain some type of fitness, it is preferred to institute a program of isometric exercises, together with hydrotherapy and a stationary bike program for cardiovascular fitness. Selectively, other treatments are designed for each patient. In cases of neurogenic bladder, patients are taught to reduce fluids at certain times (evening) to prevent sleep disturbances. If necessary, women with marked sphincter dysfunction may be taught self-catheterization, as well as how to prevent urinary tract infections. Medications indicated for erectile dysfunction may be tried, although their effectiveness is usually meager. Other measures have been proposed to help with some of the autonomic nervous system symptoms, such as anticholinergic medications to reduce the profuse diaphoresis experienced by these patients. Because of its effective relaxing action on striated muscle, magnesium oxide assists with the treatment of muscle spasms and also appears to be effective in the treatment of constipation occurring from the ingestion of opiates or rectal neurogenic malfunction. In cases of impairment of CSF ascending return from either surgical interventions resulting in dural sac ectasia or massive clumping of nerve roots, propranolol, 40 to 80 mg/day, has been shown to reduce the pressure sensation experienced by some patients in the most dependent region of the spine when the cephalic return of the CSF is impeded by the clumped nerve roots, scar tissue, or intrathecal cysts. That is why most patients with arachnoiditis have been found to have elevated CSF pressure. Therefore, the concurrent administration of acetazolamide, 250 to 500 mg/day, appears to tame the pain, presumably by changing the CSF pH. In both instances, the effects on the heart rate from the former agent and on plasma potassium concentration from the latter agent must be monitored. Acupuncture, in its various modalities, has had limited use and ambiguous results. Nevertheless, it is worth trying, although its efficacy appears to depend greatly on the experience and expertise of the practitioner.
749
Interventionism Most invasive procedures have no application in cases of arachnoiditis because most of these procedures are aimed at extradural structures. Even so, most of them have been tried. Undoubtedly, these procedures may provide partial and shortlasting pain relief because in many cases procedures such as epidural corticosteroid, facet, or sacroiliac joint injections may address concomitant disease but have little significant and longer-lasting effect on arachnoiditis. The same commentary applies to diagnostic procedures such as differential spinal procedures and diskograms, for example.
Spinal Cord Stimulation Two other modalities appear to have a more realistic indication, one of which is spinal cord stimulation, which supposedly acts by one or more of the following mechanisms: Interruption of stimuli traveling through spinothalamic fibers ■ Expand descending dorsolateral funiculus pathways ■ Supraspinal gating mechanisms ■ Alteration of spinal neurotransmitter pools by disinhibition at supraspinal sites ■
Undoubtedly, technologic advances have improved since this modality was first proposed. Although assessments of this modality reported that the efficacy was similar to that of placebo, most other publications included patients with various diagnoses, some of them subgroups of patients with arachnoiditis. Results varied, but one concept seems to have been constant: after 6 months from implantation, only 50% of the patients had 50% of pain relief; the rest had either unsatisfactory results or had left the study. Problems with infection, fibrosis around the tip of the electrode, and lead migration still plague this technique. Two different studies showed that improvement after use of this modality differs little from the effect produced by placebo.45,46 Although these latter studies included patients with chronic pain, these commentaries apply solely to the indications for arachnoiditis. Moreover, Carter45 assessed the evidence from the published articles on spinal cord stimulation by meta-analysis and found significant problems with the methodology of most studies, including patient selection, lack of comparative methods of treatment, lack of randomization, and blinding. Carter45 concluded that the absence of quality evidence in the literature prevents recommendation of this modality at present.
Nonimplantable and Implantable Pumps Although implantable and nonimplantable pumps were initially proposed for patients with terminal cancer, the application of these devices to patients with chronic nononcologic pain has become customary. Specially designed catheters that are surgically implanted are used for this pain management approach. Although these infusions temporarily reduce the pain in most patients, their effect is palliative because the drugs do nothing to improve the arachnoiditis. Patients are provided a vacation from pain, and many patients feel that it is worth it. The concern about infection and the frequent occurrence of epidural fibrosis make this location and the limited period of implantation an alternative only for shortlasting therapy.48,49
750
Section IV—Regional Pain Syndromes
Implantable infusion pumps that deliver smaller doses of opiates into the subarachnoid space appear to provide more effective pain relief. This therapeutic approach seems to be especially indicated in patients with chronic arachnoiditis. These pumps require refills every 6 to 8 weeks. Undoubtedly, they produce analgesia and allow for physical activities that otherwise would be impossible. Infusates combining morphine with baclofen, bupivacaine, clonidine, or ketamine allow for reduction in the dose of the opiate or another opioid such as hydromorphone.50 Infections are rare after the initial implantation; however, dependency develops gradually. Patients believe that their disease is advancing, whereas they are developing a tolerance that necessitates increases in the dosage.51 Larger doses of morphine produce significant sexual dysfunction in both men52 and women,53 with hyperalgesia, allodynia, and hyperreactivity that is not reversible with naloxone, possibly related to the formation of morphine-3glucuronide.34,51 Lower extremity edema has been reported in approximately 20% of the patients receiving intrathecal infusions of opiates, purportedly because of sympathetic blockade from these medications.54,55 Most patients with this problem have had varicose veins or pedal edema before implantation, and such a condition becomes a relative contraindication to this therapeutic modality. However, the main concern has been the reports of granulomas forming at the tip of the catheter. These granulomas seem to occur mostly with opiate infusions,51,56 starting within 6 months and from doses higher than 10 mg/day. As the catheter tip becomes gradually obstructed, the tendency has been to increase the dosage or the concentration, an approach that in fact accelerates granuloma formation. Multifocal accumulation of neutrophils, monocytes, macrophages, and plasma cells is characterized by high protein and normal glucose levels in the CSF.57,58 Opiates have been shown to initiate release of nitric oxide in human endothelial cells; the continued exposure of immunocytes to morphine may lead to an exaggerated response of monocytes to other proinflammatory stimuli that activate nitric oxide synthase in the arachnoid vasculature and increase local capillary permeability.59 The absence of positive stains for bacteria, the failure to obtain CSF or infusate cultures, and the finding of normal CSF glucose levels imply the presence of granuloma, which is confirmed by the finding of a soft mass with a necrotic center at surgery.59,60 Currently, the N-type blocker ziconotide, which interrupts the transmission of pain by
c losing the calcium channels, is being infused for this purpose, although its elevated cost and side effects have limited its application. Because of possible liability,61 these complications have reduced the previously wide use of these devices. In an attempt to avoid granulomas, ziconotide has been used more; however, its toxic effects in some patients61 and its high cost have discouraged some practitioners.
Nonconventional Treatment of Chronic Arachnoiditis In addition to the use of propranolol, indomethacin, and acetazolamide, it appears prudent to continue a sensible strategy that, although not specific, is tangibly applicable to this disease. Medications that have been approved by the US Food and Drug Administration have been reevaluated for different indications. When drug studies have suggested an apparent beneficial effect on one of the pathologic processes in patients with arachnoiditis, it seems logical and justified to assess the value of these drugs, as long as they are demonstrated to have minimal risk. Some of the medications include the following: probenecid,62 a drug used to treat gout that has been shown to facilitate the transfer of certain medications across the dural barrier; the cholesterol-lowering simvastatin, which has revealed itself as a notable anti-inflammatory drug; and the antioxidant lipoidic acid, already known and available in alternative medicine. This sensible approach of giving a second look to medications that may be considered “off label” has been legitimized by the use of the erythropoietin as a protector of neural tissue in stroke,63,64 diabetic neuropathy,65 and other neurologic conditions.64 Similarly, antioxidants such as N-acetylcysteine, neurotrophic peptides such as nerve growth factor, and prosaposin have been tried, without consistent effect. The tumor necrosis factor-α inhibitor etarnecept,66 injected paraspinally, has been claimed to reduce cervical disk pain and arachnoiditis.65 The neurotransmitter memantine47 is being tried in multiple sclerosis, amyotrophic lateral sclerosis, and diabetic neuropathy and is showing only some light benefit to patients with diseases that have, in the past, been considered incurable.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
94
IV
Spondylolysis and Spondylolisthesis Nikolai Bogduk
CHAPTER OUTLINE Spondylolysis 751
Spondylolisthesis 755
Pathology 752 Diagnosis 752 Relationship with Pain 754 Treatment 755
Fundamental to the stability of the lumbar spine is the architecture of the posterior elements of the lumbar vertebrae. The inferior articular processes project downward and act like hooks to engage the superior articular processes of the vertebra below (Fig. 94.1A). This arrangement provides for stability against anterior translation. If the upper vertebra in a segment attempts to translate forward (Fig. 94.1B), its inferior articular processes impact the superior articular processes of the lower vertebra and thus prevent translation. The inferior articular processes are suspended from the lamina on each side (Fig. 94.2A). The superolateral portion of the lamina can be perceived as lying between the superior articular process and the inferior articular process of the parent vertebra. Accordingly, this portion is known as the pars interarticularis: the part between the joints (see Fig. 94.2A). Defects can occur in the pars interarticularis in which the inferior articular process becomes disconnected from the rest of its parent vertebra (see Fig. 94.2B). Traditionally, this condition is known as spondylolysis because it was originally attributed to dissolution of the pars interarticularis. The perceived threat to the stability of the lumbar spine is that when a pars defect develops, the vertebra is denied the restraining function of the inferior articular processes, and it can dislocate into forward translation (Fig. 94.3). The resultant dislocation is known as spondylolisthesis: slipping of the vertebra. These abnormalities may have some relevance in the assessment of instability and deformity in children, but they have little relevance in adult pain medicine. Arcane is the belief that radiographic abnormalities of the lumbar spine constitute or provide a diagnosis of low back pain. Nonetheless, spondylolysis and spondylolisthesis are still promoted as causes of low back pain in some medical circles. They are still promoted as causes of pain in medicolegal circles. Indeed, according to the American Medical Association Guides to the Evaluation of © 2011 Elsevier Inc. All rights reserved.
Relationship with Pain 756 Treatment 756 Mechanisms of Pain 756
ermanent Impairment,1 patients are rewarded with higher P total person impairment scores if they exhibit spondylolysis. Nothing could be so undeserving. Nothing could be so dissonant with the scientific evidence.
Spondylolysis An early belief concerning spondylolysis was that it constituted a congenital defect, produced by failure of ossification centers in the lamina to fuse with those of the pedicle and vertebral body. This belief is incompatible with the embryology of the lumbar spine. No separate ossification center arises in the lamina.2 Consequently, the lamina has no ossification center that can fail to fuse with that of the pedicle body and produce a defect. The pars interarticularis develops from a single ossification center that produces the lamina, pedicle, and articular
IAP
SAP
A
B
Fig. 94.1 Structure and function of the inferior articular processes of lumbar vertebrae. A, In a lateral view, the inferior articular processes (IAP) hang down like hooks to engage the superior articular processes (SAP) of the vertebra below. B, If the upper vertebra attempts to translate forward, its inferior articular processes impact the superior articular processes of the vertebra below, whereby translation is prevented.
751
752
Section IV—Regional Pain Syndromes SAP Pars defect
Pars interarticularis IAP
Table 94.1 Prevalence of Spondylolysis in Athletes Category Contact sports Gymnasts
A
Various sports
B
Fig. 94.2 Defect in the pars interarticularis. A, An oblique view showing the superior articular process (SAP), the inferior articular process (IAP) of a lumbar vertebra, and the pars interarticularis. B, The same view showing a pars defect.
Pars defect
*
A
B
Fig. 94.3 Spondylolisthesis. A, A defect in the pars interarticularis prevents the inferior articular process from protecting the vertebra from forward translation. B, Disconnected from its posterior elements by the defect (*), the vertebral body is able to translate forward, thus leaving its inferior articular processes, laminae, and spinous processes behind.
processes on each side. The possibility of failure to fuse applies only to the midline posteriorly, where the ossification centers of each side can fail to meet (spina bifida), or to the neurocentral junction, between the pedicles and the vertebral centrum. Furthermore, investigators have shown that pars defects do not occur in infants,2 and they do not occur in individuals paralyzed from birth, who have never used their lumbar spine in weight bearing.3 Spondylolysis has also been viewed as a genetic problem, largely because it was found to have an inordinately high prevalence among Native Alaskans.4 Later studies, however, showed that this prevalence was not the result of race. Not all Native Alaskans exhibit the high prevalence. Rather, the prevalence of this condition is related to differences in lifestyle; the defect is therefore an acquired abnormality.4 In all races, the prevalence increases with age,5 and it is related to repeated activities that involve hyperextension, rotation, or flexion of the lumbar spine.5 Anatomic studies have shown that the pars interarticularis is the weakest region of bone in a lumbar vertebra.6 Ironically, however, it is subject to enormous stresses during activities of daily living. Whereas most individuals are endowed with a pars interarticularis that is thick enough to withstand the stress put on it, others have a less than adequate pars and are susceptible to acquired injuries. Biomechanical studies have shown that the pars interarticularis is susceptible to stress failure. This can occur if the vertebra is loaded in repeated torsion or repeated extension.7–10 In all these movements, impaction of the inferior articular process, as it resists movement, causes it to bend backward, like a
Prevalence (%) >20 11 >20
Reference Ichikawa et al11 Jackson et al12 Hoshina13
Football
13
McCarroll et al14
Fast bowlers in cricket
50
Foster et al15
hatchback, and this bending stresses the pars. Under repeated loading, the pars will fracture. These biomechanical data correlate with the available epidemiologic data. Pars fractures are more common in athletes, particularly, although not exclusively, in those whose sports involve twisting of the lumbar spine or forced extension (Table 94.1).11–15 Among Native Alaskans, these fractures are more common in individuals who live on ice and who use kayaks.4 However, pars fractures are not restricted to such individuals. Some 7% of the asymptomatic adult population has spondylolysis.16 The prevalence is higher (7.7%) in men than in women (4.6%), but it varies by geographic region and by the nature of work and the number of pregnancies.17
Pathology Overwhelmingly, the epidemiologic and biomechanical evidence indicates that pars defects are stress fractures. This view is consonant with pars morphology. If studied early, spondylolysis has all the features of an acute fracture: hyperemia and a jagged fracture line. When the fracture does not heal, the appearance of the defect is that of a pseudarthrosis. The bony margins are eburnated and smooth. The defect is filled with fibrous tissue, thus forming a syndesmosis.18 The fibrous tissue may contain fragments of bone,19 a finding that underscores the traumatic origin of the defect. The defect may undercut the capsules of one or both of the adjacent zygapophysial joints.18 Under those conditions, it can communicate with the cavities of those joints, as may become evident on arthrography of the joints.20 When pars fractures are bilateral, the entire lamina and its inferior articular processes are effectively disconnected from the pedicles and vertebral body. The lamina becomes flail, for which reason it has been described as the “rattler.” The multifidus muscle still acts on the spinous process of the lamina and draws it into extension. However, only the fibrous tissue of the defect resists this motion. Consequently, the flail lamina can exhibit excessive motion during normal movements of the lumbar spine.
Diagnosis The traditional means of diagnosing a pars fracture has been plain radiography. The fractures can be difficult to see on anteroposterior or lateral films, and for that reason the oblique view of the lumbar spine was introduced. In an oblique view, the posterior elements of a lumbar vertebra assume the appearance of a Scottie dog (Fig. 94.4). The pars interarticularis corresponds to the neck of the dog. In a patient with a
Chapter 94—Spondylolysis and Spondylolisthesis
Ear
SAP Lamina
753
Neck
Pedicle
Eye Snout
TP Tail
IAP
Forelimb
Hindlimb
A
B
Fig. 94.4 Radiographic appearance of the pars interarticularis. A, An oblique view with the posterior elements labeled. iap, inferior articular process; sap, superior articular process; TP, transverse process. B, How the posterior elements can be likened to the appearance of a Scottie dog.
Table 94.2 Relationship between History and Bone Scan in Patients with a Radiographically Evident Pars Defect Bone Scan History
Positive*
Negative*
Trauma within 1 year
9
4
Repeated minor trauma
9
20
Chronic back pain
5
35
No pain
0
14
*Number of patients. Data from Lowe J, Schachner E, Hirschberg E, et al: Significance of bone scintigraphy in symptomatic spondylolysis, Spine 9:654–655, 1984.
Fig. 94.5 Oblique radiograph of a pars interarticularis fracture. The fracture appears as a white line, across the neck of the “Scottie dog,” between the arrows.
pars fracture, the fracture appears as a necklace around the neck (Fig. 94.5). Radiography, however, can detect only an established fracture. A greater imperative is to detect abnormalities that precede actual fracture, so that fracture can be averted. This is possible with bone scanning. Bone scans show hyperemia, and therefore scan results are positive for stress reactions, recent fracture, or a healing fracture.3,21 Typically, scan results are not positive in chronic pars fractures, because the hyperemia has settled.
Once a pars fracture has occurred, however, the role and utility of bone scan are questionable, given that the relationship between clinical features and bone scans is imperfect (Table 94.2). Pars defects do not produce positive results on bone scan in asymptomatic individuals. Scan results may be positive in patients with chronic back pain or in patients with a history of repeated minor trauma and are more likely to be positive in patients with a history of a traumatic incident, but not reliably so.22 In athletes with back pain who are suspected of having a pars fracture, the correlations between bone scan and radiography are varied and differ from study to study (Table 94.3).23–26 Most of these patients have negative results of both investigations. Only a few have positive results of both. Some have a positive bone scan but a negative radiograph, a finding consistent with a stress reaction without actual fracture. Some have a positive radiograph but a negative bone scan, a finding consistent with an old fracture.
754
Section IV—Regional Pain Syndromes
The virtue of bone scan lies in being able to detect stress reactions before fracture occurs. Investigators have been found that athletes with positive bone scan results but negative radiographic results were able to return to their sports, and follow-up radiographs revealed no detects.25 In athletes with positive results of both tests, bone scans resolved, but radiographs revealed persisting defects. Magnetic resonance imaging (MRI) is a suitable, and perhaps preferable, alternative to bone scan. On MRI, five grades of abnormality can be detected, ranging from completely normal, through stress reactions without fracture, incipient or partial fracture, overt fracture, and fracture without reactive edema.27 In this regard, MRI has the advantage over bone scan in that it can simultaneously show bone marrow reaction and fracture. Its cost effectiveness has not been calculated, but the cost of a single MRI scan would seem competitive with that of a bone scan in addition to plain radiography. The data suggest that in individuals at risk of a stress fracture, bone scan or MRI is the investigation of choice to screen for stress reactions before fracture. However, only a few patients suspected of fracture actually have a fracture. Plain radiography has no role as the initial test. If bone scan is used, it is the critical test. Radiography is indicated only if the bone scan result is positive. If MRI is used, plain radiography becomes superfluous. These guidelines, however, apply to individuals at risk of a pars fracture. They do not apply to patients in general with
Table 94.3 Correlation Between Bone Scan and Radiography in the Detection of Pars Fractures Radiography Bone Scan
Positive*
Negative*
Reference
Positive Negative
9 9
4 16
Elliott et al23
Positive Negative
18 7
5 7
Jackson et al24,25
Positive Negative
5 22
1 38
Van den Oever et al26
*Number of patients.
back pain. In those patients, pars fractures are an uncommon and unlikely source of pain.
Relationship with Pain Most vexatious is the relationship of spondylolysis with pain. Whereas detecting stress reactions to avert fracture and to preserve the integrity of the lumbar spine has merit, this does not amount to establishing a diagnosis for the cause of pain. Detecting a pars fracture does not constitute making a diagnosis. The confounding factor is that pars fractures are very common in individuals with no pain. Moreton16 reviewed the radiographs of 32,600 asymptomatic individuals and found pars fractures in 7.2%. Consequently, pars fractures can be expected to occur as an incidental finding in 7% of patients presenting with back pain. Their pain arises from sources other than the pars defect. Other studies directly compared symptomatic and asymptomatic individuals and found no difference in the prevalence of spondylolysis (Table 94.4).28,29 Finding a pars fracture in a patient has no diagnostic validity. The positive likelihood ratio is essentially 1.0, which means the test contributes nothing to diagnosis. The data of Magora and Schwartz29 actually indicate that pars fractures are more common in asymptomatic individuals. The likelihood ratio of 0.14, less than 1.0, means that finding a pars fracture actually detracts from making a diagnosis. These conclusions have been reinforced by a systematic review.30 Multiple studies have confirmed an equivalent prevalence of spondylolysis in symptomatic and asymptomatic individuals. The odds ratios for spondylolysis as a risk factor for pain are nonsignificant. Nevertheless, it is possible for a pars fracture to become symptomatic. The fibrous tissue of the defect contains nerve endings,31 ostensibly derived from the dorsal rami that innervate the affected segment, and so has the necessary apparatus to be a source of pain. What is required is the application of a means, other than radiography, by which to incriminate the fracture as a source of pain. The definitive test is to anesthetize the defect.32 Pars blocks are the only means available by which to determine whether a radiographically evident defect is symptomatic or asymptomatic. Such a test is imperative in view of the high prevalence of defects in asymptomatic individuals. Relief of
Table 94.4 Validity of Radiography in the Diagnosis of Painful Spondylolysis Pars Fracture
Pain*
Unilateral None
2 660
Bilateral None
Sensitivity
Specificity
+Likelihood Ratio
26 910
0.03
0.97
1.08
62 600
65 871
0.09
0.93
1.3
Any None
64 598
91 845
0.10
0.90
1.0
Any
44
64
0.07
0.83
0.14
None
604
312
*Number of patients.
No Pain*
Reference Lisbon et al28
Magora and Schwartz29
Chapter 94—Spondylolysis and Spondylolisthesis
pain implies that the defect is actually the source pain and predicts surgical success.32 Patients who do not respond to blocks preoperatively are less likely to respond to fusion of the defect, even if the fusion is technically satisfactory.32 Unfortunately, no systematic population studies have been conducted to establish just how often pars fractures are responsible for back pain, either in general patients or in athletes. Too many practitioners are satisfied, despite the scientific evidence, that finding a fracture radiographically is sufficient to establish a diagnosis. Also untested is the contention that the pain could arise not from the fracture, but from the zygapophysial joints of the flail lamina. Medial branch blocks of the suspected joint would be a valid test for this contention, but no study has reported the prevalence of pain from the zygapophysial joints in patients with pars fractures.
755
Although other methods have been used to quantify the magnitude of vertebral slippage,38 the most commonly used are variants of the method of Taillard.39 Spondylolisthesis is graded according to the extent to which the affected vertebra has moved across the superior surface of the vertebra below (Fig. 94.7). Four grades are recognized (I to IV) according to whether the posterior corner of the affected vertebra lies opposite one, two, three, or four quarters of the way across the supporting vertebra. A perception is that segments affected by spondylolisthesis are unstable and that the slippage will progress. Longitudinal studies deny this as a rule. In a study of 27 children followed into adulthood, no female patient exhibited an increase in slip of greater than 10%, and only 4 male patients exhibited progression, which ranged in magnitude from 10% to 28%.5 That study concluded that slippage occurs largely at the time
Treatment The ideal opportunity for treatment is before fracture occurs. Finding a stress reaction allows the affected part to be rested. Athletes can modify their training regimens. If that is done, the prospect obtains that fracture can be avoided. Bone scan is the only means by which an early diagnosis can be established. In principle, if and once a fracture has occurred, healing and complete resolution are possible. Radiographic union can be expected in some 37% of patients, especially if the fracture is unilateral.33 In practice, most pars fractures pass unnoticed and are undetected at inception. They do not need to be detected because most remain asymptomatic and become incidental radiographic findings. If and when pars fractures become symptomatic, however, their optimal management has not been established. Bracing is recommended, supplemented by hamstring stretching, pelvic tilts, and abdominal strengthening, as the patient becomes pain free during activities of daily living,33 but this regimen has not been controlled for natural history. Local anesthetic blocks of the pars fracture may be diagnostic, but they have not been established as therapeutic. In principle, radiofrequency neurotomy of the medial branches of the lumbar dorsal rami of the affected segment should relieve the pain of a pars fracture, but this treatment has not been formally tested for this condition. For persistent pain, the mainstay of treatment has been arthrodesis of the pars fracture, by various means.34–36 For some procedures, success rates of 80% have been reported. However, the efficacy of surgery, at large, is elusive because the treatment of pars fractures has often been confounded by, or confused with, the treatment of spondylolisthesis.
Spondylolisthesis Spondylolisthesis is an obvious structural abnormality of the lumbar spine that typically affects the fifth or fourth lumbar vertebra. It is characterized by anterior displacement of the affected vertebra in relation to the one below (Fig. 94.6). The displacement implies that the vertebra has slipped forward. Formally, spondylolisthesis is classified according to etiology (Table 94.5).37 Of the various forms, isthmic, lytic spondylolisthesis is the most common and constitutes the archetypical form.
Fig. 94.6 Lateral radiograph of an L5 vertebra that exhibits spondylolisthesis. For clarity, the inferior margin of L5 and the superior margin of S1 have been traced with dots.
Table 94.5 Classification of Spondylolisthesis by Etiology Type
Etiology
Dsyplastic
Congenital abnormality of upper sacrum
Isthmic Lytic Elongated pars Acute fracture
Fatigue fracture of pars interarticularis Congenital Acute trauma
Degenerative
Loss of cartilage and/or progressive deformation of zygapophyseal joints
Traumatic
Fracture in posterior elements other than pars
Pathologic
Intrinsic bone disease
Data from Wiltse LL, Newman PH, Macnab I: Classification of spondylolysis and spondylolisthesis, Clin Orthop Relat Res 117:23–29, 1976.
756
Section IV—Regional Pain Syndromes
0.25
0.50
0.75
Although the literature celebrates the success of treatment, it is not consistently clear from that literature what was being treated. Investigators treated patients for low back pain only,47 low back pain or back pain with radiculopathy,55 low back pain with or without radiculopathy,56 low back pain and sciatica,53,58 low back pain or leg pain,59 low back pain and leg pain,52 low back pain with or without nerve root irritation,53 or radicular pain only.49 Some investigators did not specify the clinical features of their patients and so ostensibly treated patients for the lesion.43,46,48
Mechanisms of Pain
Fig. 94.7 Grading of spondylolisthesis. The grade is expressed in terms of whether the posterior corner of the affected vertebra lies opposite the first, second, third, or fourth quarter of the anteroposterior width of the supporting vertebra.
of acquisition of bilateral pars fractures. No patient exhibited disease progression after the age of 18 years. These conclusions were echoed by another study of 311 adolescents.40 Only 3% exhibited progression greater than 20%. Another study41 confirmed some but disputed others of these findings. During follow-up of 272 adolescent patients, the mean progression of slip was only 3.5%, a finding indicating that, as a rule, spondylolisthesis does not progress appreciably. However, 23% of patients exhibited progression of 10% or more. (The proportion who exhibited progression of more than 20% was not reported.) Greater amounts of disease progression occurred in patients who had larger slips at presentation. However, in all cases, the greatest amount of slipping (90%) had already occurred at the time of presentation. Subsequent progression accounted for only 10% of the final slip, on average. This calculation reinforces the rule that most of the slip occurs when the pars fracture is acquired.
Relationship with Pain Spondylolisthesis is not related to back pain. This was resoundingly established in a systematic review.30 For an association with back pain, the odds ratios range between 1 and 2 for half the studies conducted and are less than 1 for the remainder. These values preclude any diagnostic significance of finding spondylolisthesis. One study42 found that women with spondylolisthesis were more likely to report pain during the previous day, but no association was reported with pain during the previous year, previous month, or previous week. No association at all was found for men. Pain intensity was not related to the magnitude of slip.
Treatment It is somewhat ironic that a condition known not to be associated with back pain has such an abundance of literature on its treatment. Proponents of conservative therapy advocate flexion exercises, other exercises,43–45 traction,43 braces,43,46 casts,43 corsets,43 and manipulation.47,48 However, arthrodesis is the longest-established treatment, with claimed success rates of 70% to 80%.49–60 The one randomized study established that operative treatment was more effective than exercises.61
The literature on treatment fails to provide evidence on the mechanism by which spondylolisthesis may cause pain. Indeed, it seems to have paid no attention to this issue, and patients have been treated without regard to differing symptoms or their cause. The lesion, rather than the symptoms, has attracted treatment. It is credible that spondylolisthesis could cause radicular pain, by stretching nerve roots, by narrowing the intervertebral foramen, or by the flail lamina's impinging on the nerve roots. The one study that explicitly addressed the last phenomenon showed that radicular pain could be relieved simply by removing the loose lamina.49 Conversely, the mechanisms by which spondylolisthesis may cause back pain are no more than speculative. It is conceivable that the patient may have back pain stemming from the disk of the affected segment, or that the patients may have pain from the pars fracture or from the zygapophyseal joints of the flail lamina. None of these contentions, however, has been formally tested, let alone proven. The one piece of circumstantial evidence was reported in a small retrospective study. The investigators claimed that progression of spondylolisthesis was associated with the onset of marked degeneration of the disk.62 The study implied that the pain the patients suffered arose in the affected disk, but this concept was not explicitly tested and proved. An alternative interpretation, consistent with the epidemiologic evidence, is that spondylolisthesis is irrelevant to the patient's symptoms. Affected patients have back pain regardless of their spondylolisthesis. Circumstantial evidence to this effect comes from one study that showed that the clinical pattern and functional disability were similar in patients with spondylolisthesis and in patients with nonspecific low back pain.63 Furthermore, when treated in the same way, patients with spondylolisthesis and patients with nonspecific back pain responded in the same way.47 If this is the case, spondylolisthesis is immaterial to the diagnosis and immaterial to outcome. Even surgery may have a nonspecific, serendipitous effect. Surgery does not only fuse the affected segment. It involves extensive débridement of the lumbar spine, with denervation of the zygapophyseal joints, the pars fracture, or disk, depending on the technique used. These procedures may be the active components of surgical treatment, rather than the arthrodesis.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
95
IV
Sacroiliac Joint Pain and Related Disorders Steven Simon
CHAPTER OUTLINE Anatomy 757 Motion 758 Pain Generators 759 Evaluation 760 Treatment 761 Education 761 Modalities 761
The sacroiliac joint (SIJ) has been a source of pain to both sufferers of low back pain (LBP) and those who refuse to recognize its contribution to this common problem.1 Many of the frustrations experienced by patients who hurt but continually have “negative” examinations and studies can be traced to this overlooked synovial joint and its maladies. In this chapter, the anatomy, motion, pain generators, evaluation, and treatment of the SIJ and its relation to LBP are explored. Historically, Meckel described motion within the SIJ in 1816, and before Mixter and Barr recognized the contribution of herniated lumbar disks to LBP in 1934, SIJ motion was believed to be a main generator of LBP.
Anatomy The axial spine rests on the sacrum, a triangular fusion of vertebrae arranged in a kyphotic curve and ending with the attached coccyx in the upper buttock. Iliac wings (innominate bones [IBs]) attach on either side, to form a bowl with a high back and a shallow front. Three joints result from this union: the pubic symphysis in the anterior midline and the left and right SIJs on the posterior (Fig. 95.1). Multiple ligaments and fascia attach across these joint spaces, thus limiting motion and providing stability (Figs. 95.2 and 95.3).2 The hip joints are formed by the femoral heads and the acetabular sockets deep within the IBs. The hips create a direct link between the lower extremities and the spine to relay ground reaction forces from weight bearing and motion. A physiologic balance between lumbar lordosis and sacral curvature exists both at rest and in motion. Changes of pelvic tilt and lumbar lordosis occur in the anteroposterior (AP) plane and rely on attached muscles and fascia, but they do not have significant effects on the SIJs, owing to a self-bracing mechanism © 2011 Elsevier Inc. All rights reserved.
Mobilization 761 Injections 761 Radiofrequency Ablation 762 Surgery 762 Exercises 762 Strengthening Exercises 762 Posture Enhancement 762
created by friction from the ligaments. The sacrum, positioned between the IBs, functions as the keystone of an arch assembly and allows cephalocaudad (CC) and AP motion.3 Innervation is varied and quite extensive because of the overall size of the joint, which includes outflow from anterior to posterior rami of L3-S1.4 The SIJ is a synovial (diarthrodial) joint that is more mobile in youth than later in life, when the upper two thirds of the joint will become fibrotic. As the capsule thickens, sacral ossification occurs, and the distinct propeller shape of the joint becomes more pronounced (Fig. 95.4). The adult female pelvis is five times more mobile than the male pelvis, and to accommodate pregnancy and parturition, it will increase another 2.5 times because of the effects of relaxin on fascia and ligaments. Ligament and muscle attachments help to maintain stability of the pelvic ring and allow movement within limits. Further motion is also limited by the irregular shape of the joint articulation, in which ridges and grooves increase resistance friction and add to the keystone arch structure. Prolonged loading, such as standing or sitting for long periods, and alterations of the sacral base (leg asymmetry or ligamentous injury) are associated the joint hypermobility and resultant LBP.3,8,9 Multiple muscle attachments cross the SIJs and contribute to pelvic stability and force transfer.3 These include the lower trapezius, latissimus dorsi, and extensor abdomen obliques, which attach cephalad to the SIJ, thoracolumbar fascial attachments to the twelfth rib, lumbar spinous and lateral processes, and pelvic brim. Fascial and muscle attachments expand to include the erector spinae, internal obliques, serratus posterior inferior, sacrotuberous ligament, dorsal SI ligament, and iliolumbar ligaments, which attach to the posterior iliac spine, pelvic brim, and sacral crest. Major movement and stabilizing muscles also attach to the SIJ, including the gluteus maximus, 757
758
Section IV—Regional Pain Syndromes Sacrum
Ilium
Iliolumbar lig.
Sacroiliac j.
Post. sacroiliac lig.
Acetabulum Sacrospinous lig.
Coccyx Pubic symphysis Fig. 95.1 Bony pelvis.
Sacrococcygeal lig.
Sacrotuberous lig.
Fig. 95.3 Posterior ligaments of the pelvis. Iliolumbar Ant. sacroiliac lig. lig.
Ant. longitudinal lig.
A Inguinal lig. Sacrotuberous lig.
Sacrococcygeal lig.
Sacrospinous lig. Fig. 95.2 Anterior ligaments of the pelvis.
gluteus medius, latissimus dorsi, multifidus, biceps femoris, psoas, piriformis, obliquus, and transversus abdominis. Vleeming et al10 concluded that the purpose of these muscles is not for motion, but for stability, to balance the forces of walking and running, and the friction of joint surfaces allows both shock absorption and transfer of bending forces.5,11
Motion Movement of the SIJ is performed in a stable environment, governed by muscle ligaments and the joint shape and cartilage, which increase friction and limit mobility by creating a self-locking mechanism.10,12,13 Motion is allowed in three dimensions: AP, CC, and left-right (LR). The major ligaments and their actions are listed here (see Figs. 95.2 and 95.3). These ligaments can be divided into four distinct layers from superficial to deep, but they are discussed relative to their function. 1. The interosseous ligament resists joint separation and motion in the cephalad and AP direction. 2. The dorsal sacral ligament covers and assists the interosseous ligament.
B Fig. 95.4 Computed tomography scans of the traverse section of the sacroiliac joint. A, Male. B, Female. Note the thicker sacral cartilage, typical of female patients. (From Paradise LE: Sacroiliac joint blocks. In Raj PP, Lou L, Erdine S, et al, editors: Interventional pain management: imageguided procedures, ed 2, Philadelphia, 2008, Saunders.)
3. The anterior SI ligament is a thickening of the anterior inferior joint capsule and resists CC and LR motion. 4. The sacrospinous ligament resists rotational motion of the pelvis around the axial spine. 5. The iliolumbar ligaments resist motion between the distal lumbar segments and the sacrum and help to stabilize the sacral position between the IBs. 6. The sacrotuberous ligament resists flexion of the iliacs on the axial spine. 7. The pubic symphysis resists AP motion of the IBs, shear, and LR forces. Next, actual movement of the pelvis and SIJs and their integrated functions are reviewed. That ground reaction forces from weight bearing pass through the legs and pelvis to the
Chapter 95—Sacroiliac Joint Pain and Related Disorders
spine has already been established. The point in the body where these forces are in balance is termed the center of gravity and has been determined to be 2 cm below the navel. Gravity can also be considered a force line that produces different effects on the pelvic girdle as it shifts from anterior to posterior relative to the center of the acetabular fossae.14 Body posture and positioning, muscle strength, and weight distribution determine alterations in the force lines. An anterior force line (e.g., a protuberant abdomen) produces anterior (downward) rotation of the pelvis over the femoral heads and decreases tension in the sacrotuberous ligament while maintaining pressure on posterior ligaments. This situation creates an overuse strain on the spinal support muscles and a resultant painful condition. As the line of gravity moves posterior to the acetabula, the pelvis rotates posteriorly (i.e., the anterior rib tilts upward), and the sacrotuberous and posterior interosseous ligaments tighten. This is easier to visualize if one imagines a line between the femoral heads on which the pelvis rotates. The vertical distance of motion is approximately 2.5 cm in each direction at L3.15 The pelvis also rotates in relation to the spine during gait. As the legs alternately move forward, the pelvic IBs rotate forward and toward the midline, but the spine and sacrum counter-rotate, although to a lesser degree.16 The SIJ lies between these moving planes and forces, central to vertical, horizontal, and rotational activity. Hula and belly dancers have perfected rhythmic pelvic motion, much to the delight of their audiences. Dysfunction of the joint without direct trauma commonly arises from an imbalance in the anterior pelvis without adequate stabilization of posterior (sacrotuberous and interosseous) ligaments. Lifting or bending while leaning forward produces an anterior pelvic tilt that slightly separates the IBs from the sacrum and makes unilateral AP shift more likely, especially if proper ergonomic technique is not used.17,18 The net effect of such a unilateral anterior rotation on the ipsilateral side would be to raise the pelvic brim and posterior superior iliac spine (PSIS) and cause apparent leg lengthening in supine positions and shortening in long sitting. (“Apparent” means that the affected leg is not necessarily longer, but appears to be so, owing to its attachment to the hip socket, which is rotated forward, or caudad in a supine position. Long sitting in this situation positions the acetabulum posterior to the SIJ and results in apparent shortening). This provides a simple test during the physical examination to determine stability of ligament structures within the SIJ. Bilateral anterior SI rotation would not produce leg length asymmetry but would stretch the iliopsoas muscles, thus simulating tight and tender hip flexors. Posterior unilateral rotation would produce ipsilateral PSIS and brim drop, as well as a shortening of the supine leg and lengthening with long sitting.
Pain Generators The net effect of this type of sustained unilateral force is to create an imbalance of attached myofascial insertions. Pain may result from periosteal irritation or circulatory congestion on the shortened side and loss of strength and tenderness on the elongated side. The joint line becomes stressed by the combined muscle and ligament pull that resists resolution and physiologic positioning and creates a painful strain. The patient should be examined to determine the possible presence of physiologic, restricted, or excessive joint motion.
759
Fig. 95.5 Distribution of pain emanating from the sacroiliac joint.
Surgical fusions of the lumbosacral spine may present special problems in this regard, and radiographic examination must be included to determine fully whether malpositioning is a contributing factor. Other conditions that produce acute or chronic discomfort must be considered and include trauma (seat belt injury, falls with pelvic ring fractures), inflammatory conditions (ankylosing spondylitis, rheumatoid arthritis, Reiter's syndrome, psoriatic arthritis, inflammatory bowel disease), infections (bacterial or mycobacterial [tuberculosis]), metabolic imbalance (gout), neoplastic disease (prostate, bowel, pulmonary), or degenerative changes within the joint.19–21 The SIJ line is densely innervated by several levels of spinal nerves (L3-S1) that, when stimulated, may produce symptoms resembling those caused by lumbar disks.4 Muscle insertions near the area, such as gluteus maximus and hamstrings, refer pain to the hip and ischial areas, respectively, when stressed. Fortin et al1,22 examined asymptomatic and symptomatic patients to generate a pain map of SI symptoms. The most common discomfort was described as aching or hypersensitivity along the joint line to the ipsilateral hip and trochanter (Fig. 95.5).1,22 Other pains, reported less frequently, occur approximately 5 cm lateral to the umbilicus on a line between the navel and the anterior superior iliac spine or referred into the groin or testicles. Sitting may become painful when anterior rotation of the pelvis changes the relationship of the acetabulum with the femoral head. Because the ischial tuberosity cannot move while a person is seated, balanced support for the pelvic “bowl” is lost, and the effect is aggravated by the tendency to
760
Section IV—Regional Pain Syndromes
sit in a lopsided way or on the sacrum, instead of on the ischial tuberosities. The resultant forces produce AP or LR torque on the SIJ. Standing decreases this pain because the femoral heads and are repositioned and thus buttress the pelvis. Sciatic nerve stretch may also be relieved by allowing the pelvis to rotate, a maneuver that shifts weight to the opposite leg.
3.
Evaluation A thorough history must be taken to seek preexisting disease or injury or new trauma and to evaluate the patient's general health status. Bladder, bowel, or sexual dysfunction or numbness often suggests an emergency that requires immediate care. The pain history should also include the duration of the problem and previous treatments, including medications, injections, thermal or electrical modalities, bracing, or manipulations and their outcomes. Provocative and palliative positions or activity can be guides to aid in treatment planning. Functional loss is significant because it can be an indication of suffering and a measure of treatment success as the patient begins to resume normal activities. Radiographic testing is indicated to investigate fractures, osteophytes, fusion of the SIJ, or lumbosacral lesions. Inflammatory changes in the SIJ are characteristic of rheumatoid spondylitis (Marie-Strumpell spondylitis) and can be verified with blood tests for human leukocyte antigen (HLA)-B27 or rheumatoid markers. Male patients in their 20s to 30s generally present with atraumatic LBP and marked stiffness. Although x-ray films may show negative results on initial reading, and although fuzziness over the SIJ region and stiffness in the lumbar spine may be the only early signs of this progressive disease, many of the tests listed later yield positive results. Quantitative radionuclide bone scanning has also been helpful in early diagnosis.23 Because many pain physicians now have access to fluoroscopy, a comparison series of traditional tests (Patrick's maneuver, Gaenslen's test, midline sacral thrust) with diagnostic SIJ infiltration suggested that infiltration may be a more reliable indicator of pain generator and should be incorporated into the testing if possible.24 How the patient walks reveals important information on antalgic gait, weight shifting, and asymmetry of the pelvic brim or of shoulder height. Spinal examination for range of motion, scoliosis, myospasm, and ligamentous irritation will localize pain generators. Familiarity with the anatomy of this region (i.e., muscles and their insertions and actions) is essential to understanding mechanical relationships with pelvic girdle positioning and the necessity of balancing forces to cure, rather than just to palliate, an SIJ syndrome. Various tests have been developed to detect SI dysfunction, and most can be performed quickly and simply during the regular examination and then verified by provocation. 1. Fortin's finger test: The patient points to the area of pain with one finger. The result is positive if the site is within l cm of the PSIS; generally it is inferomedial to the PSIS. 2. Fabere maneuver (flexion, abduction, external rotation, and extension of the hip, also known as Patrick's test): The patient lies supine. One heel is placed on the opposite knee, and the elevated leg is guided toward the examining table. The result is positive if pain is elicited along the SIJ. (This maneuver also stresses the
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
hip joint and may result in trochanteric or groin pain from the hip.) Gaenslen's test: The patient is supine. The hip and knee are maximally flexed toward the trunk, and the opposite leg is extended. Some examiners perform this test with the patient's extended leg off the examination table, to force the SIJ through maximal range of motion. The result is positive if pain is felt across the SIJ. (This maneuver also stresses the hip and can produce trochanteric or groin pain.) Compression test: The patient lies on one side. The examiner applies pressure on one pelvic brim in the direction of the other. The results are positive if pain is felt across the SIJ. Compression test at SIJ: The patient is prone. The examiner places a palm along the SIJ or on the sacrum and makes a vertical downward thrust. The results are positive if pain is felt at the SIJ. Pubic symphysis test: The patient is supine. Pressure is applied with the examining finger at the left or right pubic bone adjacent to the symphysis pubis. The results are positive if pain is felt at the site. (Most patients are not aware of this tenderness before it is elicited. The examiner should ask permission before applying pressure and should have other staff in the room to witness the examination, to avoid the misconception of inappropriate sexual contact.) Distraction test: The patient is supine. The examiner alternately presses each anterior superior iliac spine in a posterolateral direction. The results are positive if pain is felt at the SIJ or if movement is asymmetrical. Fade test: The patient is supine. The hip is flexed and adducted to midline. The examiner applies pressure to the long axis of the femur to push the ilium in a posterior direction. The results are positive if pain is felt at the SIJ. Passive straight leg raising test: The patient is supine. The examiner grasps the patient's heel and lifts the leg vertically from the examining table with the knee extended. The patient is asked to hold the leg elevated and then slowly lower it. The result is positive if ipsilateral pain is elicited at the SIJ, a finding that suggests anterior rotation. One-legged stork test: The patient is standing. The examiner is positioned behind the patient with thumbs placed on the PSIS and the sacrum at S2. The patient then flexes the palpated hip to 90 degrees. The results are positive if the examining thumb is moved upward instead of inferomedially. Van Dursen's standing flexion test: The patient is standing. The examiner is positioned behind the patient with thumbs on the PSIS. The patient flexes the trunk forward without bending the knees. The results are positive with upward motion at the involved side. Piedallu's or seated flexion test: The patient is seated. The examiner is positioned behind with thumbs placed just inferior to the PSIS. The patient flexes the trunk in a forward position. The results are positive with asymmetrical motion, elevated on the involved side. Rectal examination: Although not specific for SIJ, a thorough rectal examination is recommended to search for referred pain from the prostate or uterus
Chapter 95—Sacroiliac Joint Pain and Related Disorders or from spasm of the rectal or pelvic floors. Piriformis muscle spasm can be identified at the 2- or 10-o'clock positions. The results are positive if pain is felt at the SIJ, and this must be differentiated from anal discomfort, associated with the examination itself.
Treatment Correct diagnosis is the first part of successful treatment because it focuses therapy toward the pain generator. Control of pain early in the treatment course encourages better patient cooperation. Structural attempts to correct for mechanical malpositioning can start and then move to education, modalities, exercises, and interventions.
Education Descriptions of pelvic anatomy and rotational motion at the pelvic brim help the patient to understand what forces are continuing to stress the SIJ and cause pain. Proper ergonomic training for gait, bending, lifting, and stretching prevents repeated injury from undermining the overall treatment program and increases the patient's interest and participation.
Modalities Deep heat is tolerated better than ice and is more likely to reach affected areas. Hot packs feel good and may relax or “soften” muscles before stretching or massage. Ultrasound along the SIJ is palliative. The addition of 10% steroid gel, which can replace electrode gel required for ultrasonography, can also be used to reduce inflammation by phonophoresis. Electricity can be curative by relaxing muscle spasm electrogalvanic stimulation, functional electrical stimulation, or electrical acupuncture, or it can be palliative by blocking the pain signal (transcutaneous electrical nerve stimulation). The pain practitioner can choose from larger office-based units that follow preset cycles of stimulation or portable units that the patient can either operate at home or wear for convenient use. Traction has not been helpful for SIJ dysfunction, but it has benefited patients with LBP from spinal causes. Braces provide a form of traction that applies direct pressure and stabilization over a movable area, which can be palliative in SIJ dysfunction. The SI belt has a pad that fits over the upper sacrum, to cover both SIJs and provide support. The belt should cross the pelvic brims, fasten in the abdominal area, and fit tightly enough to resist AP motion. Ground reaction forces, however, are very strong and eventually overcome most bracing attempts. Some investigators argue that the real purpose of bracing is to remind the patient to use proper body mechanics and limit rotational forces, but pelvic support in pregnant patients has been especially helpful when pain is present and options are limited. Whatever the source of its benefit, bracing is a patientfriendly means to provide stability and some relief when the SIJs are hypermobile.
Mobilization Mobilization is helpful for restoring anatomic SIJ alignment and sacral or coccyx position. Many osteopathic, chiropractic, and physical therapy resistance techniques are used to perform these maneuvers. The reader is directed to other texts for full mechanical descriptions. Simple office manipulations are safe, effective, and immediately palliative for SI dysfunction, but efforts may
761
be frustrated by muscle spasm along the pelvic floor or spinal attachments. One simple technique that can be performed in the office, or with a helper at home, is “leg lengthening” to correct anterior rotation shortening. To perform this maneuver in the office, the patient should lie supine on an examination table with the examiner standing at the foot of the table with thumbs on the medial malleoli to evaluate for leg length discrepancy. The patient is asked to sit up (long sitting), and leg length is observed. If one leg appears to shorten, it can grasped at the ankle by the examiner and gently pulled toward the foot of the table. Leg length is tested following this manipulation, and the procedure can be repeated until the legs are of equal length. Self-manipulation is key in allowing the patient an opportunity to correct recurrent malpositioning secondary to ligament laxity. Even proper seating can help to maintain a self-bracing system for the SIJ. A small cushion beneath the proximal thighs distributes weight directly to the ischium, and a second cushion in the lumbar lordotic curve supports the spine and allows even distribution of reaction forces.
Injections Injections may be the best option for providing quick assessment and relief of inflammation and painful SIJs.25 Typical injections contain both analgesic and corticosteroid and are placed in the lower third of the joint (the true synovial portion). Although these injections have been performed “blind” for many years, the new standard has become the use of guidance by fluoroscopy, ultrasound, or computed tomography scan. Other injections to the upper two thirds of the joint can also be very effective in relieving pain by reducing ligament irritation. Ketorolac has been substituted for steroids on repeated injections with beneficial results. Contraindications to injection are local infection, sepsis, possible fracture, coagulopathy, and allergy to medications used for procedure. Procedure for sacroiliac joint injection 1. Explain the goals and general procedure to the patient. 2. The patient is place supine, preferably over a pelvic pillow, which helps to open the SIJ. 3. Sterile technique is employed over the SIJ. 4. A wheal of analgesic is placed first at the PSIS, and then a sterile syringe containing 4 mL of 0.25% preservativefree bupivacaine and 40 mg of methylprednisolone is attached to a 3-inch 25-gauge needle under strict aseptic technique. 5. The PSIS is identified, and the needle is advanced through the wheal at a 45-degree angle toward the affected SIJ (Fig. 95.6). If bone is encountered, the needle tip is withdrawn into subcutaneous tissue and is redirected superiorly and slightly more laterally. When the needle is correctly positioned in the joint space, the contents of the syringe are gently injected. If resistance is encountered, the needle is probably in a ligament and may be advanced or withdrawn a bit to achieve better position. 6. The needle is withdrawn, and a sterile pressure dressing and ice pack are placed on the site.26 Proliferant injections Proliferant injections attempt to create inflammation in an area to allow the body's natural healing mechanisms to repair the initial mobility dysfunction. An irritant such as dextrose
762
Section IV—Regional Pain Syndromes
Exercises
Sacrum
The goals of exercise programs are to provide stretch and strength to connecting muscles, to enhance posture, and to introduce means of self-manipulation for the patient. These exercises can be done alone or with a helper.
Strengthening Exercises A “six pack” of repetitions of these isometric strengthening maneuvers are recommended: six sets of six, 6 seconds on and 6 seconds off, six times daily. Joint space
Interosseous sacroiliac lig. Ilium
Dorsal sacroiliac lig.
Fig. 95.6 Schematic picture of a cross section of a sacroiliac joint injection. Note that the needle enters at the dorsal inferior aspect of the joint. (From Paradise LE: Sacroiliac joint blocks. In Raj PP, Lou L, Erdine S, et al, editors: Interventional pain management: image-guided procedures, ed 2, Philadelphia, 2008, Saunders.)
is often injected along the entire joint line. The desired results are thickening of muscle attachments or ligaments, and the goal is to stabilize a hypermobile joint. Physicians should be familiar with the technique and complications before they attempt this procedure.27
Radiofrequency Ablation Radiofrequency ablation is a technique for creating lesions (deafferentation) along sensory afferent nerves in the L4-S2 distribution. When successful, this procedure can create a longer-lasting block to painful nerve transmissions, but occasional complications have developed including gluteal, hip, or posterior thigh pain. As a result, specialized training is recommended before this procedure is attempted by the physician.21
Surgery Surgery should be considered only when pain is intractable and disabling and all other conservative treatments have failed. Screw fixation of the ilium to the sacrum has been described to benefit some patients.28
Abdominal crunches The patient lies supine with hip and knee flexed and feet flat on the floor. A partial sit-up is performed and held according the six-pack regimen. Hip abduction, adduction, and extension The patient may be standing, sitting, or lying. Isometric exercises are performed by resisting the direction of motion, using furniture or hands to push against, according to the six-pack regimen. Pelvic tilt, anterior and posterior The patient stands with hands on hips. The pelvis is tilted anteriorly (upward) then posteriorly (downward) according to the six-pack regimen. Isometric hip extension The patient may be sitting, standing or lying. One foot is elevated and braced on a pedestal in a vertical position. The hip and knee are flexed maximally against the trunk, held in the flexed position with both hands. Isometric extension is then resisted by the arms according to the six-pack regimen. Men seem to prefer a variation of this maneuver that involves standing against the inside of a door frame with one foot against the opposite side. Resisted extension of the hip and knee from pressure against the sole of the foot produces a similar effect.
Posture Enhancement Correct trunk posture enhances force distribution by maintaining correct spinal alignment. Holding the abdomen “in” (contracting the abdominal and rectus muscles) creates an internal brace against the lower back and helps to maintain adequate pelvic tilt and lumbar lordosis. Holding shoulders and head in proper alignment also enhances spinal positioning and distribution of forces.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
96
IV
Failed Back Surgery Syndrome J. Antonio Aldrete
CHAPTER OUTLINE Historical Perspective 764 Rationalization for Laminectomy and Fusions 765 Epidemiology 765 What Has Failed in the “Failed Back” Syndrome? 766 Incidental Durotomy 766 Loose Disk Fragments 766 Intrathecal or Peridural Hematoma 766 Nerve Root Cysts 767 Epidural Fibrosis 767 Insufficient Decompression 767 Minimally Invasive Access 768 Residual, Recurrent, or Adjacent Herniated Nucleus Pulposus 768
In the 1980s, the complex diagnosis of “failed back surgery syndrome (FBSS)” entered the medical literature. This unusual nomenclature refers to an unfortunate group of patients who, having undergone surgical treatment for a back problem, usually end up in worse condition than when they first sought medical care for the disorder.1 This chapter deals with a paradoxical deviation from the expected benefit obtained from surgical care because in most cases, in spite of considerable expense and substantial attention given by competent physicians, many of these care seekers achieve not only little improvement, but also, in some instances, a hopelessly worse progression of their spinal condition. The process is disappointing. Once in pain management, after many visits to physicians' offices, undergoing various procedures at pain clinics, spending days or weeks as hospital inpatients, receiving hundreds of hours of care, and incurring great expenses, these patients end up with greater disability, with several more scars, still in considerable pain and discomfort, unable to support their families or even to sit still for half an hour, and with little chance of ever riding a bicycle, returning to their jobs, having sexual intercourse when they wish, or even playing with their children. Most of these patients have no chance of ever finding a cure for their back problem. The rationale for this nomenclature is not clear, but it seems to be related to patients who, after by virtue of having some type of (low) back pain, sought to achieve full health by consulting their physicians and then their respective specialists. For whatever reason, these patients may have been subjected © 2011 Elsevier Inc. All rights reserved.
Mechanical Instability 768 Pseudarthrosis 769 Spondylolisthesis 769 Infections 769 Spinal Stenosis 769 Pseudomeningocele 770 Surgery at the Wrong Level 770 Arachnoiditis 771 Distal Dural Sac Ectasia 772
Diagnosis 772 Prognosis 774 Treatment 774
to one or multiple operations in the spine, but their initial complaints appear to have been made worse. At that point, the possibility of continuing employment becomes an illusion. In hope, these patients apply for disability in the belief that they will be taken care of completely. After going through a humiliating process, however, these patients find out that disability is not what they thought it would be. It usually consists of a minimal income with limited follow-up care. For some patients, being disabled is like being less than a second-class citizen because they have limited rights and are considered by some to be a burden to society. Literally, this vague diagnosis implies that the patient's back failed to get better. However, it is the treatment chosen by the patient's care providers that failed to restore anatomic perfection and optimal function. The appearance of this syndrome and the progressive increase in the numbers of patients receiving this denomination defy all the predictions that technology, if properly applied, may achieve a cure for most pathologic entities. A specific diagnosis for the patient with FBSS is not listed, and a precise evaluation of the effectiveness of each procedure is not performed. Moreover, this approach does not allow a determination of the optimal operation for certain conditions, nor does it ascertain which operations should be contraindicated for any one specific spinal condition. It is not clear whether the term FBSS is included in the Medicare rule or whether it is an exemption to the Medicare rule necessary to list all the diagnoses present in the admission and discharge notes. Such omission would essentially 763
764
Section IV—Regional Pain Syndromes
fail to mention in the postoperative notes such incriminating diagnoses as the following: n n n n n n n n n
Recurrent disk herniation Dural tear Incomplete removal of disk Loose disk fragment in vertebral canal Wrong interspace Failure to explore the foramen Intradural pseudocyst Entrapped nerve root Cerebrospinal fluid (CSF) fistula
The presence of one or more of these diagnoses may reveal a failure of treatment (including spinal surgery). It seems that for lack of a better global term that would encompass every one of these diagnoses, or “by default,” FBSS has been incorporated into the medical jargon.1,2 In a way, this attribution is not fair to patients because they do not understand this negative term. Moreover, the designation casts a stigma that assumes that nothing else favorable or positive can be done to help these patients. What is worse, in the current era of paying for results, someone must decide which among the treatments given was the one that failed to provide the proper outcome. When these patients are referred to pain management, the illusion that they are going to be free of pain eventually turns into a cruel reality because this treatment “manages the pain,” but rarely eliminates it. In their search for the dream of “no pain,” these patients accept procedures that are painful, while being only sedated. Soon these patients seek refuge in drugs, prescribed but dangerous drugs that are allowed in certain amounts and in certain doses, which are sometimes not enough for pain relief lasting more than a few hours and at the cost of dependency. These drugs produce hyperalgesia, allodynia, hyperpathia,3 and the very grave conclusion, opioid dependence.4 These diagnoses were not present initially, but in the postoperative period these conditions are difficult to treat successfully. Governmental agencies have gone from developing piety to advocating the relief of pain as the fifth vital sign.5,6 They suggest that opioid-tolerant patients require at least 60 mg of morphine daily, 8 mg of hydromorphone, 30 mg of oxycodone, and so on,5,7 only to have inspectors persecute and apprehend doctors because some patients overdosed.6 What does one expect when doctors are directed by the US Food and Drug Administration not to undertreat patients6,7 in pain, are professionally obligated by the Hypocratic oath to relieve pain, and provide their patients with prescriptions for large numbers of lethal pills. Pharmacists gladly oblige and fill the prescriptions, only to denounce doctors for overprescribing, although it is the pharmacists who sell and hand the drugs to the patients. Each case varies, but they all have some common denominators. After one or more laminectomies, spinal fusion, artificial disk implantation, bone growth electrical stimulation, and other operative procedures,8 these factors may include one or more of the following diagnoses: n n n n n
Recurrent disk herniation Peridural scarring Nerve root compressed by scarring Deformity of the dural sac Herniation of adjacent disk
n n n n n n
Spinal instability Facetectomy Pseudomeningocele Arachnoid cysts Arachnoiditis Foraminal restenosis
Not uncommonly after one or two laminectomies, the spine becomes “destabilized” as portions of disks are removed and laminectomies are extended laterally, thus rendering the facet joints dysfunctional and painful.8 The sequence follows with a spinal fusion to stabilize that portion of the spine. Although spinal fusions are supposed to convert two or more vertebrae into one bony (with or without hardware) union, they may result in one or more of the following: n n n n n n n n n n n
Pseudarthrosis Malposition of screws Protrusion of screws through the vertebral body Protrusion of screws into the vertebral canal Fracture of screws Displacement of hardware (cages) Intrathecal scarring Intrathecal calcification Impingement of nerve roots Pedicular pain Paravertebral muscle dysfunction and atrophy
Historical Perspective The historical events that brought the visualization of the spinal canal are mentioned in Chapter 161. The operative resection of extruded lumbar disks was popularized in 1934 by Mixter and Barr,9 who identified herniated disks as the main cause of sciatica, demonstrated that diskectomy could be performed through a laminectomy incision, and initiated the trend for elective surgical operations of the spine. The precise diagnosis of radiculopathy was facilitated by the introduction of Pantopaque (ethyl iodophenyl undecylate), which was first administered to patients in 194410 and provided good definition and contrast of images. The use of this contrast medium established myelography as the standard test for identifying spinal disease. An oil-soluble dye, Pantopaque was used extensively in spite of evidence that it caused arachnoiditis.11,12 When disk disease reappeared at the same level or on another interspace, laminectomies were repeated. However, when surgeons found evidence of instability, spinal fusions were indicated. Initially, bone grafts were used, but after 1993, pedicular screws, bars, and rods13 were preferred, followed later by intervertebral cages. More recently, various artificial disks14 have been tried, with limited success.15 The use of water-soluble dyes made myelography safer, and both computed tomography (CT) and magnetic resonance imaging (MRI) have allowed more precise visualization of extradural and intradural disease, respectively. Minimally invasive approaches to laminectomy have become popular; these operations are attempted through a small incision, but results remain inconclusive.16 The other, less common but still frequent lesion corrected surgically is malalignment of the vertebrae or spondylolisthesis.17 These procedures may have given the impression that extensive interventions in the spine are feasible and uneventful. However, reports of these procedures indicate that these
Chapter 96—Failed Back Surgery Syndrome
rocedures are currently overused in the United States.18 p Criteria for indications are lacking, and overuse is especially common in certain age groups.19
Rationalization for Laminectomy and Fusions The removal of a compressive lesion from a tubular osseous structure containing delicate neural elements such as the spinal cord, nerve roots, dural sac, and CSF more often than not eliminates the pain and dramatically improves the affected function. However, surgical access into the spine does not occur without risks and consequences. Zeidman and Long20 defined FBSS as “the condition resulting from one or more surgical interventions, with disastrous results with persistence of back pain and exacerbation of the preexisting complaints, characterized by a constellation of symptoms, including referred pain to the lower extremities, sphincter dysfunction and psychological alterations associated to the disease of the spine.” Even though the syndrome has been clearly defined, not all surgeons accept the criterion for failure. Patients seek medical attention and request help for lower back pain. If the procedure performed for this purpose does not relieve the back pain, then the operation should be considered a failure. This fact is pertinent to laminectomies and especially to spinal fusions, even when solid arthrodesis is achieved. If the patient's pain continues, the operation has not succeeded in its primary objective of relieving that pain. According to Cherkin et al,21 based on this premise, the objectives of spinal operations need to be redefined to include only those therapeutic modalities that have proven effective in relieving the specific cause of the pain experienced by that specific patient. This lack of selectivity was evident in the early stages of some clinical trials that are reported as ongoing studies, but the final conclusions have not yet appeared in the literature.13–15
Epidemiology Considering that low back pain is one of the most prevalent diseases of middle and older age, the iatrogenic component of this entity adds a threatening dimension. If more than 300,000 spinal fusions are performed annually in the United States,18 and if 20% to 40% of these patients end up with FBSS,1,2,19,21 the outcomes of these interventions need to be reviewed and the indications revised. This is especially important given that the lifetime incidence of back pain includes approximately 80% of the general population. These numbers are also substantial in terms of cost, because by the time the diagnosis of FBSS is reached, it is estimated that more than $300,000 has already been spent on the care of each patient. By that time, these patients face the prospect of persistent pain and suffering for the remainder of their life. The frequency of surgical operations of the spine for comparative populations in industrialized countries has been estimated to be 8 to 10 times more in the United States than in the Scandinavian countries, 8 times more than in the United Kingdom, and 7 times more than in Germany.16 The reasons for these disparities are numerous, but the most relevant are as follows: Labor protection is given to workers in other countries, where lifting, pulling, and carrying are done mechanically
■
n
n
n
n
765
rather than by humans. Lifting in industry, offices, hospitals, and so on is done by pulleys that have been placed strategically to avoid back injuries.22 Back-saving education is a subject taught in middle schools and is taken seriously by students, supervisors, and workers. The financial incentive is undoubtedly an uncontrollable factor that influences excessive surgical intervention in the private practice of medicine, in contrast to conservative therapy in institutional medicine. Specific clinical guidelines are lacking on when and what operations are indicated for each specific condition that produces low back pain.23 Inadequate control is exercised by governmental agencies over new surgical procedures and the implantation of medical devices. Implementation of evidence-based medicine as necessary proof that new treatments truly benefit patients is lacking.
Most cases start with low back pain. After a variable degree of conservative therapy, patients are offered laminectomy to remove the herniated portion of a disk, supposedly because the corresponding nerve root is compressed by such herniation.24 For insurance approval of these procedures, symptoms and signs of radiculopathy must be evident, and conservative therapies must be proved to have failed. The most common access into the spinal canal is through the posterior approach, and it usually requires laminectomy or laminotomy. Even then, access to the degenerated disk is narrow and is frequently complicated by swelling of the affected nerve root that has been compressed for some time.20 This swelling may improve soon thereafter, but in some cases the distal end of the root can actually become more swollen,25 depending on the radicular vascular response to the surgical manipulation. The consequences of spinal surgery must be taken seriously. The outcomes in patients younger than 30 years old who have a single degenerated intervertebral disk are more favorable than the outcomes in middle-aged patients with two or three affected disks; outcomes are worse when patients have some degree of spondylosis or when they are smokers.26,27 The outcomes are less hopeful in older patients who have multiple levels and degrees of disk disease, facet joint arthritis, osteoporosis, and spinal stenosis. Because of work-related injuries, motor vehicle accidents, and possibly other factors such as insurance coverage, however, a greater proportion of the middle-aged group undergoes spinal surgery more often.2,18,21 In his follow-up treatise, Wilkinson28 admitted that “the conclusion that in America many failed back syndromes result from excessive surgical intervention seems difficult to avoid.” He went on to list several culprits: Incorrect diagnosis, which may include misdiagnosed neoplasms, the so-called flabby back syndrome common in affluent societies where obesity is prevalent, rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, and so on. n Unnecessary surgery, such as operations on a bulging disk without radiculopathy symptoms; slight sensory loss does not necessarily mandate operation. To perform fusions in grade I spondylolisthesis is still under debate.13 n Improper or inadequate surgery, such as disk excision performed at the wrong level or the wrong side, leaving of a loose fragment of disk, or selection of the wrong hardware to execute a fusion.13,14,20 n
766
Section IV—Regional Pain Syndromes
To these items, at least three more predisposing factors may be added: Short pedicles, lumbarization of S1, sacralization of L5, and arachnoid cysts may be present. n Inadequate imaging or inconclusive interpretation may offer a misleading diagnosis or may fail to recognize associated diseases, such as vertebral hemangiomas and scoliosis. The value of diagnostic invasive tests such as differential spinal blocks, epidurography, diskography, and others is still in doubt because most disease can be identified by MRI. For example, in diskography, 1.0 mL of dye produces little pain in normal and ruptured disks alike, but 2 mL of dye will produce pain in every disk injected, a finding that casts doubt on this procedure.29 n Cigarette smoking has been found to decrease the threshold of pain,26 increase perioperative opioid requirements,30 affect wound healing, 31 increase postoperative pulmonary morbidity,32 and add to a patient's stress response.33 Furthermore, it increases dural sac pressure during bouts of coughing and thus facilitates CSF leaks.29–34 Nevertheless, this factor is rarely considered a contraindication to surgery in patients who refuse to stop smoking. n
What Has Failed in the “Failed Back” Syndrome? The reasons are multiple, and at any given time, one or more may cause the reappearance of pain and neurologic symptoms after these operations. The following causes are not listed in order of frequency or seriousness of their occurrence.
be dislodged from the disk cavity later on, when the patient is mobilized. Pain is sharp, severe, and localized to the dermatome corresponding to the compressed nerve root that is being pressured by the 0.5- to 1.4-cm fibrocartilaginous mass.40 Confirmation is again done with MRI. This condition requires immediate surgical reintervention because patients are in severe, constant pain and may also have bladder dysfunction.41 Initially, interventions were performed with bone graft and later with hardware.
Intrathecal or Peridural Hematoma Both intrathecal hematoma and peridural hematoma are serious events. A substantial amount of blood in the subarachnoid space is manifested by severe, burning low back pain, with or without radicular symptoms, immediately on the patient's awakening from the anesthetic.42 This pain usually requires high doses of opiates to control it. More common are extradural hematomas (Fig. 96.1), which initially manifest as mild to moderate back pain but with moderate to severe paravertebral muscle spasm. Depending on the size of the hematoma and its proximity to the dural sac, back pain and neurologic symptoms may appear 2 or 3 weeks postoperatively. This delay may result from the degradation of blood elements and products and the subsequent liberation of leukotrienes and cytokines that are able to cross the dural barrier.43 After 10 days, intrathecal hemosiderin may be recognized on MRI.
Incidental Durotomy Perhaps one of the most underrated complications, incidental durotomy may occur in 6% to 8% of first-time laminectomies, in 12% to 20% of repeat laminectomies, and in 14% to 30% of spinal fusions.35 Recognition of these tears allows them to be repaired on site. Unrecognized tears not only result in CSF leak but also allow for blood accumulated at the bottom of the wound (in patients in the prone position) to enter the subarachnoid space.36,37 This usually unexpected development may have serious consequences because blood is an active irritant of nerve tissue and may initiate an arachnoiditic inflammatory response. Depending on the amount of CSF lost, postural headache and even meningismus may occur, with a bulging mass under the incision. Occasionally, serosanguineous fluid, which can be tested for glucose content with a glucose strip, may leak through the incision. Ultimate confirmation can be obtained by MRI of the lumbar spine. If CSF is contained in the retrospinal tissues, eventually a soft, thin pseudomembrane will form around it. If not initially repaired, it may give rise to a pseudomeningocele.37,38 Puncture is not recommended because CSF may leak persistently.39 Further discussion on durotomies is included in Chapter 98.
2
3 I
E
5
Loose Disk Fragments With an incidence of 2% to 7%, loose disk fragments of nucleus pulposus may be “dragged out” of the anulus fibrosus cavity by the rongeurs employed to remove the loose portions of the nucleus.40 Less commonly, loose fragments can also
Fig. 96.1 Sagittal view of a magnetic resonance imaging scan of the lumbar spine 2 weeks after multiple laminectomies, with blood intrathecally (I) and extradurally (E) and a posterior and anteriorly herniated L2-3 disk. A vestigial S1-2 disk is noted (arrow).
Nerve Root Cysts Leg pain with minimal back pain may be caused by postoperative cystic outpouchings when dural tears occur in the dural cuff that accompanies the emerging nerve roots (Fig. 96-2) during their intraspinal canal passage. These cysts should be differentiated from the congenital Tarlov or arachnoid cysts that occur at the same location, but these are located along the nerve root dural cuffs. At myelography, these cysts fill immediately. Postoperative arachnoidal cysts are formed at the time of surgery when a small dural tear occurs in this same sheath location. If the tear is not repaired, the arachnoid may herniate through this dural tear to form a primary cyst, which is usually reinforced by an outer wall of fibrous tissue.44 These cysts may be identified by fluid pulsations. In any case, at surgery the ostium or opening communicating with the subarachnoid space is very small and difficult to find.
Epidural Fibrosis Epidural fibrosis is perhaps the most dreaded complication of spinal surgery and the most frequent cause of FBSS.45 Most laminectomies are usually followed by a short period (3 to 6 months) of improvement because excision of the herniated portion of the disk and removal of a portion of the lamina and the ligamentum flavum provide relief from the stenotic compression, with a satisfactory result as the patient's symptoms subside or are markedly improved.46 All along, as the wound heals, an inflammatory response is occurring around the dural sac and the paravertebral muscles (Fig. 96.3). Eventually, the cellular infiltrate gives way to collagen deposition that proliferates for months, and the incision heals, as all tissues in every organ do, with scar tissue. The operated intervertebral space heals with collagen and fibrous tissue that lead to scarring in the peridural
Chapter 96—Failed Back Surgery Syndrome
767
space and fibrous adhesions to dura, nerve roots, bone, muscles, and fascia where the operation took place.47 Guizar-Sahagun et al48 demonstrated that the administration of steroids before spinal cord injury not only did not help to prevent the inflammatory changes but also actually exacerbated them. In some cases, this proliferation of fibrotic tissue and adhesions is exaggerated, and eventually it may indent or compress the dural sac and even encircle a nerve root. If foreign bodies (e.g., Surgicel, Gelfoam,49 cotton pads),50 glues, sealants51 (e.g., ADPL), or natural materials51 are left in the wound or if access was difficult or traumatic or a large extradural hematoma was present, this reaction may be accelerated. Fatal anaphylaxis has occurred after fibrin glue application.44 Symptoms of radiculopathy may appear and depend on the nerve root affected. However, not uncommonly, all these materials may provoke more inflammation, with resulting greater fibrosis and scarring. In this regard, meticulous surgical technique makes a difference. The gradual surrounding of a nerve root by scar tissue produces radicular pain and sensory disturbances as it elicits traction and a compressive effect on the root.52 At that point, it becomes difficult to determine whether the radiculopathy is caused by a recurrent herniated disk or by peridural fibrosis. In this case, the nerve root is displaced. Nerve root involvement may be defined by electrodiagnostic studies and by MRI with gadolinium that enhances the scar tissue by transfer of the dye from the intravascular to the interstitial compartment, as would occur from inflammation or scarring.53 Conversely, disks usually do not enhance.54 Caution in the interpretation is advised because high doses of contrast agent (0.3 mmol/kg) have been demonstrated to increase the conspicuity of the disk.54 Repeated attempts to prevent peridural scarring have not been successful.55–57
Insufficient Decompression Insufficient decompression may be lateral when it occurs after a decompressive attempt within the lateral foramina that may have compressed the nerve root by an osteophyte within the
Fig. 96.2 Lateral view of lumbar spine showing previously injected residual pantopaque lodged in nerve root cuffs (arrows).
Fig. 96.3 Computed tomography scan of the lumbar spine depicting intrathecal fibrosis (if) on the left inside of the dural sac wall. Peridural scarring and fibrosis (ps) adhering to the right lamina are abundant. The epidural space (E) is preserved. A broad protruding disk (pd) mostly to the left, narrows the lateral foramen, and bilateral facet joint hypertrophy is present.
768
Section IV—Regional Pain Syndromes
lumen, soft tissue, or even bone residues from bony spurs. Within the spinal canal, central stenosis may result from a hypertrophic ligamentum flavum, short pedicles, a loose disk fragment, or a herniated disk, in which case wider decompression, such as obtained from bilateral laminotomy or lateral foraminectomy, may be necessary to gain ample access to the lesion that is generating the pain.46,48,51
Therefore, adjacent disks continue to degenerate in an accelerated process, and soon another disk is fully ruptured, thereby producing radiculopathy.54 Depending on its extent (>4 mm) or whether its location is lateral (Fig. 96.5) or broad based, the nerve root is more likely to be compressed against a hypertrophic facet joint; this finding suggests an apparent need for another laminectomy, in sort of a domino effect.56
Minimally Invasive Access
Mechanical Instability
In more recent and popular access, procedures are performed through a 3-cm skin incision with the use of a tubular amplifier that provides limited exposure. Guided by fluoroscopy, procedures such as limited minimal laminectomy, diskectomy, removal of osteophytes, and other operations are performed.58 Although these procedures are feasible to perform, the success of these operations is difficult to confirm in subsequent MRI studies. A definite objection to this approach is the practice of these procedures by nonsurgeons and in outpatient facilities. Moreover, the recurrence of disk herniation usually occurs 2 years later, as opposed to 12 years later when ample and multiple laminectomies are performed (Fig. 96.4).
An incompletely removed herniation may be extruded again because the anulus fibrosus is usually left open, thus liberating a free fragment in the vertebral canal.44 A single herniated nucleus pulposus is more frequent in young patients (see Fig. 96.4), whereas in middle-aged and older patients, several lumbar disks may have various degrees of degeneration. Thus, when a herniated portion of the most severely degenerated disk is removed, the protruding31,33,38,52 or slightly herniated disks may not be able to tolerate the new undue pressures applied while in the erect position or during flexion.
Certain preexisting abnormalities predispose patients to lumbosacral spine instability. Among them are sacralization of L5 or lumbarization of S1 and scoliosis from 5 to 15 degrees, which, if present, may render that portion of the spine unstable. Usually, these congenital variances can be recognized in sagittal MRI views.57 Prior facetectomies, extensive bilateral laminotomies, and severe unilateral spondylosis destabilize the adjacent segments of the spine. Malalignment of adjacent vertebrae may occur after extensive diskectomy, thus leading to spondylolisthesis. Alteration of the usually even axial surface of each vertebra, whether by scoliosis, a degenerated disk, an osteophyte, or one-sided spondylosis, may change the individual support given by each segment. In addition, an unstable spinal segment prevents the normal dissipation of the load sharing and thus changes the distribution of stress forces throughout the axial topography of each vertebra.51,53 Depending on which lesion predominates, spinal stenosis, spondylolisthesis, or ligament stretching may result, reducing and morphologically changing the transverse diameter of the vertebral canal or the neural foramen. During the aging process, these changes occur gradually. In severe trauma, some of these changes may appear suddenly. Diskectomies, as helpful as they may be in reducing the compression of neural elements under certain circumstances, may affect the stability of the spine sufficiently to precipitate the need for a stabilizing fusion.57
Fig. 96.4 Axial magnetic resonance image of the lumbar spine (L3-4 level) demonstrating a centrally located herniated nucleus pulposus (arrow) compressing the dural sac (darker semilunar structure). The posterior epidural space is shown to be accessible.
Fig. 96.5 Axial magnetic resonance image of the lumbar spine showing a paracentral L4-5 herniated disk, toward the left, narrowing the lateral foramen. Impingement of the dural sac is present, with reduction in size of the posterior epidural space.
Residual, Recurrent, or Adjacent Herniated Nucleus Pulposus
Pseudarthrosis After spinal fusions, it is essential to monitor the stability of the fused unit; however, the usual plain films on flexion and extension show only extreme causes of instability.58 To determine whether bone growth is taking place between vertebrae, either CT or MRI59 is required to detect the presence of any vacuum phenomena or spaces (Fig. 96.6) in between where new bone growth should be.60 In all fairness, a maximum of 2 years is suggested as a waiting period for fusion to be successful. If no bone pockets persist, most likely the pseudarthrosis is permanent. If hardware was applied, then as long as the screws and plates are in place and are not causing side effects, they can be left in place. However, if pain persists and the screw head sites are tender, or if the screws are bending or fractured, the screws may have to be removed. This may leave an unstable spine that is sometimes worse than it was before because the disks usually have been removed.53 Occasionally, when bone fragments are placed in between the vertebral bodies, close to the posterior edge, growing graft bone eventually may protrude into the vertebral canal and acting as an osteophyte and impinge on the dural sac. Repeat fusion procedures are usually less likely to succeed than is the first attempt.61–63
Spondylolisthesis The overriding of a vertebra over the posterior plate of the one below results in undue compression of the posterior end of the intervertebral disk, narrowing of the lateral foramen, and possible impingement of the corresponding nerve root. This condition produces moderate constant pain that is exacerbated by standing and walking.53,59 According to the degree of disparity of the alignment of the two vertebrae involved, spondylolisthesis is given one of four grades (I to IV) (Fig. 96.7).55 Grade I may be treated with conservative measures; a higher level of deviation usually requires surgical stability (Fig. 96.8). It is desirable not only to stabilize the two adjacent vertebrae but also to attempt to correct the misalignment and relieve the pain.56,61 However, patients may need to be informed that with
Fig. 96.6 Lumbar spine computed tomography scan at the L4-5 level showing areas of nonsolidification implying pseudarthrosis (open arrow). In addition, a dilated dural sac with a cluster of nerve roots adhering to the left wall of the dural sac (black arrow) is present, indicative of arachnoiditis. Bilateral spondylosis (open diamonds) and evidence of a left laminectomy are visible.
Chapter 96—Failed Back Surgery Syndrome
769
the fusion, the “slip vertebra” will be prevented from mobilizing any further, but usually it is not possible to return it to its previous aligned position.
Infections Infections can occur in the soft tissue as cellulitis, fasciitis, epidural abscess (Fig. 96.9), or meningitis, with delayed clinical manifestations for up to 1 month.64 Diskitis may also be present and produce localized pain, low-grade fever, and malaise for months.63 Ultrasound or radiologic imaging64 usually identifies the location of the infections.65 Most of these infections can be treated conservatively,66 but if a neurologic deficit persists, surgical drainage and evacuation may be necessary.62 Infections with methicillin-resistant Staphylococcus aureus (MRSA) have become more common after laminectomy. These infections are characterized by a prolonged period of purulent discharge through the surgical incision, and they require an infectious disease consultation and intravenous antibiotic therapy for months. Needless to say, if this complication occurs in a patient with spinal fusion with metal hardware, the hardware may need to be removed prematurely, and this situation presents a disastrous dilemma.
Spinal Stenosis Repeated operations may produce both axial and radicular pain that may be caused by a herniated disk, hypertrophy of the facet joints (Fig. 96.10), progression or overgrowth of a previous spinal fusion, or hypertropic osteophyte, which may coexist with peridural scarring that significantly compressed the dural elements.67 Although bony and ligamentum compression may be mechanically reduced, pain relief may be minimal.
Fig. 96.7 Lateral view of plain film of the lumbar spine showing mild spondylolisthesis of L5 on S1 with reduction of the lateral foramen (x). Residual Pantopaque is shown at the end of the dural sac (white arrow) and at the L4 and L5 levels.
770
Section IV—Regional Pain Syndromes
b
D
5
2
Fig. 96.8 Sagittal magnetic resonance image of the lumbar spine showing a IV grade spondylolisthesis of L5 on S1 with expansion of the dural sac cephalad. From L2 down, the lumbar nerve roots appear to be tethered posteriorly. The S1-2 vestigial disk is well developed, allowing for considerable instability of the L4-5-S1-2 segment of the spine.
Fig. 96.10 Computed tomography scan of the lumbar spine depicting spinal canal stenosis as result of hypertrophy of the ligamentum flavum (black arrowhead); also, the epidural space (black arrow) has become rather narrowed by it. D, Dural sac.
Fig. 96.11 Six days after laminectomy, an axial magnetic resonance image of the lumbosacral spine depicts an infiltration of the paravertebral muscles probably with cerebrospinal fluid, also present in the subcutaneous tissue (O). Within the dural sac (d), the nerve roots are enhanced and located in the anterior half of the sac with an asymmetrical distribution. The posterior epidural space (white arrow) also contains fluid.
A
B
Fig. 96.9 Sagittal (A and B) T2W MR images of diskitis at the L5-S1 disk level showing high-S1 fluid within the disk. There are high-S1 fluid collections (white arrows) in the epidural space consistent with abscesses.
Pseudomeningocele Pseudomeningoceles and other postoperative dilatations of the dural sac are discussed in detail in Chapter 98. One early typical CSF leak after minimally invasive surgery is shown in Figure 96.11.
Surgery at the Wrong Level Indeed, the surgeon's nightmare can occur because sometimes the S1-2 space is mobile or the L5-S1 space is immobile, thus misleading the surgical team.35 The only way to avoid operating in the wrong space is to follow the routine that the whole operating team must “wait 1 minute” before starting the operation. In addition, once the lumbar fascia is reached, the level at which the operation is to be conducted must be verified by placing a metal object (hemostat) in the intended space and then taking a lateral radiograph or, best
Chapter 96—Failed Back Surgery Syndrome
771
Fig. 96.12 Sagittal magnetic resonance image of the lumbo sacral spine with extensive scarring on the anterior epidural space from the L4-5 disk caudad, 7 months after laminectomies, at L4-5 and L5-S1 (open arrow). Thickened nerve roots are noted displaced anteriorly in the dural sac (white arrow), a finding suggestive of arachnoiditis.
O O
Fig. 96.13 Postmyelogram computed tomography scan of L3 illustrating clumped nerve roots, suggestive of arachnoiditis in the chronic phase. Evidence of asymmetrically placed vertical bars (O) is present.
practice, two fluoroscopic views (anteroposterior and lateral).67 This error may be more likely to occur when microdiskectomies are performed when exposure is marginal and when fluoroscopy guidance depends on the interpretation of the operator.
Arachnoiditis Arachnoiditis is recognized as one of the most common and serious complications of spinal operations. Only the postoperative aspects of this disease are discussed here. A complete description of arachnoiditis from other causes is contained in Chapter 93. A definite incidence has not been determined, but isolated series have indicated that arachnoiditis occurs
in 5% to 22% of patients who undergo lumbar laminectomies and in 8% to 24% of patients who undergo spinal fusions.19,28,62 One of the most revealing studies was conducted by Matsui et al,68 who performed lumbar spine MRI on the third, seventh, twenty-first, and forty-second days in 10 patients (7 with herniated nucleus pulposus and 3 with spinal stenosis) who underwent spinal surgery by a posterior approach. In axial views, intrathecal adhesions to the cauda equina were prevalent at the “laminectomized” levels in all patients. Partial adhesions were found at 9 levels 6 weeks after the surgical procedures. Most of these adhesions had resolved by the forty-second day, but in 5 of 14 spaces exposed, partial nerve root adhesions were still present. An initial shrinking or indentation of the dural sac returned to nearly normal levels at the end of the observation period. This study showed that although some of these changes are transitory, intradural lesions (enhanced or clumped nerve roots) may occur, even when only extradural surgery is performed (Figs. 96.12 and 96.13). The possible mechanisms for these events are described in the section on intrathecal hematoma and extradural hematoma (see Fig. 96.1).43 Nakano et al69 reported that laminectomy in rats consistently induced an increase in vascular permeability in the cauda equina, as well as an increase in the vesicular transport of the endothelial cells with opening of the “tight junction.” This finding suggests a breakdown of the blood-nerve barrier that facilitates the formation of adhesions. Furthermore, the same group70 was able to show that the administration of the anti-inflammatory agents indomethacin and methylprednisolone, 24 hours after laminectomy, suppressed the formation of such adhesions and the leakage from the nutrient vessels. Moreover, as shown by Guizar et al,48 the same steroid medication, when given to rats preoperatively, exerted no protective effect, but the formation of adhesions was considerably reduced when these drugs were given 3 or 6 weeks after laminectomy.
772
Section IV—Regional Pain Syndromes
Conducting serial neurologic examinations and obtaining imaging studies (preferably an MRI with contrast) of the operated region are crucial in patients who develop severe pain and neurologic deficits after laminectomy. This premise also applies to cases of arachnoiditis in patients who had a fusion with bone or titanium hardware. When the devices are made of other metals, a myelogram, followed by CT, is necessary to visualize the intrathecal structures. Early manifestations are swollen, enhanced nerve roots that may be located in their normal position or in the anterior half of the sac (Fig. 96.14).72 Depending on the extent and intensity of the inflammatory reaction, clumping of nerve roots is not seen clearly until 2 or 3 months after the adverse event (Fig. 96.15; see also Fig. 96.13). Thereafter, the swelling gradually subsides, and the nerve roots remain adhered to each other in clumps or to the interior wall of the dural sac.73,74 This condition is permanent. Although arachnoiditis is not present in every case of FBSS, it nevertheless complicates the clinical features of FBSS and makes the differential diagnosis difficult, especially if metal hardware has been implanted,75 as shown in Figure 96.16.
work accidents, as trivial as they may appear, may give clues to the patient's actual complaints. Monitoring spinal evoked potentials in the perioperative period may prevent permanent injury.80 Specific tracking81 of the time of appearance of symptoms in relation to one of the operations performed not only may help to determine the cause of the FBSS but also may assist in considering certain therapeutic modalities that have not been of benefit in the past (Fig. 96.17). Repeated operations may produce both axial and radicular pain that may be caused by progression or overgrowth of a previous spinal fusion or hypertrophic osteophyte that may coexist with peridural scarring, thus significantly compressing the dural contents.60,61 Although bony and ligamentum compression may be mechanically reduced, pain relief would likely be minimal.
Distal Dural Sac Ectasia This complication is discussed in Chapter 98.
Diagnosis Practitioners need to have a precise understanding of FBSS because it usually includes numerous diagnoses that have been globalized in the definition. Because adequate noninvasive procedures are available, to subject these patients to invasive tests such as differential spinal or epidural blocks, diskograms, and neuroplasty is not only futile and wasteful but also hazardous.76–79 A complete, detailed history, including diagnostic tests, adverse events, and attempted therapeutic modalities, described chronologically, is desirable. Minor injuries and
D
Fig. 96.14 Postmyelogram computed tomography scan of the lumbar spine showing enhanced (edematous) nerve roots located in the dural sac (D), at the level of the L3 vertebra, a finding suggesting arachnoiditis in the early inflammatory phase.
Fig. 96.15 Postmyelogram computed tomography scan at the L4 vertebra with pedicular screws, bilaterally. The right screw is misplaced, invading the vertebral canal and impinging on the dural sac. The nerve roots are mostly clustered in two clumps, indicative of arachnoiditis in the chronic proliferative phase.
d
Fig. 96.16 Post myelogram computed tomography scan of the L4 vertebra showing a right laminectomy and evidence of an attempted fusion by replacing the intervertebral disk with one cage (white arrowhead) and vertical bars (black squares) asymmetrically placed. The dural sac (d) is deformed and contains enhanced nerve roots. The posterior epidural space has been replaced by fibrosis.
Chapter 96—Failed Back Surgery Syndrome Symptoms may be classified as follows:
Mechanical, noted as increased back pain when standing, walking, or sitting n Related, including referred pain, muscle spasms, pain in the hips or sacroiliac joints, and bone friction, as in pseudarthrosis n Neurologic, including headaches, electrical shock–like pain, burning, lacerating pain from stretching of the dural sac or the nerve roots, numbness, and weakness not following a dermatome path; symptoms indicate alterations of proprioception such as dizziness, tinnitus, a positive Romberg sign, and loss of balance n Functional, implying dysfunction of bladder, bowel, sexual activities, and autonomic dysfunction (e.g., excessive sweating, heat intolerance, hypertension)
Radicular Pain
Laminectomy
Loose fragment or bleeding
Reexploration
Relief 6 months
Same pain
Radicular pain
Lesion missed
Recurrent disc herniation
Peridural root scarring
Relief of pain with numbness, drop foot
Surgical injury to root
Fusion
Fig. 96.17 Algorithm complications.
for
the
diagnosis
Aggregated, caused by other related illnesses such as diabetic neuropathy, rheumatoid arthritis, and lupus erythematosus n Psychogenic, such as fears, depression, anxiety, hopelessness, insomnia, and suicidal ideation n Radicular, including pain and sensory alteration (e.g., numbness, tingling, formication) and weakness along a specific dermatome, usually resulting from extradural compression of a nerve root n
n
Immediate severe radicular pain Neurologic deficit
773
of
postlaminectomy
Patients usually have several of these clinical manifestations requiring early consultation, understanding, and guidance. A detrimental trend has been the globalization of the radiologic findings referred to by radiologists as “surgical changes” or “peridural enhancement.” These statements are difficult to understand and to interpret by nonradiologists. It is imperative to have a detailed and precise description of all the abnormal findings, even if they have been described before, level by level, in the narrative and a complete listing of the various diagnoses with opinions regarding their possible occurrence, at the end of the report. A retrospective review was conducted of the medical records of 684 patients diagnosed with FBSS.76 After a history was obtained and a physical examination was performed, followed by a review of imaging studies, specific possible pain generators were identified. By correlating these possible pain generators with the location, extent, and side of the clinical symptoms, their frequency in these patients was noted (Table 96.1). Because some of these pain generators are not surgically correctable, patients with FBSS need to be informed that the presenting symptom, pain, will likely continue after any subsequent operation. A list of specific diagnoses is preferable, to avoid the generalized and imprecise diagnosis of FBSS. Because of the current availability of objective radiologic findings as evidence, the “Waddell signs evaluation” may be discarded, given that it was based on nonorganic, attitudinal, and preconceived notions.82 Earlier, Waddell and Richardson83 had already cast certain doubts regarding the reliability of this evaluation. These doubts were reinforced by the report of Polatin et al,84 who conducted a prospective study in patients with low back pain and noted inconsistencies in the evaluation processes performed by the participating physicians.
Table 96.1 Guide to Diagnosis and Therapy for Failed Back Surgery Syndrome Presumptive Diagnosis
Diagnostic Tests
Initial Therapy
Extended Therapy
Retained disk fragment
H&P, MRI
Reexploration
Analgesics, protocol
Foreign body fragment
CT, MRI
Removal
Repeat CT or MRI
Periradicular fibrosis
H&P, electrodiagnostics, MRI
IV protocol
Protocol, muscle relaxants
Pseudomeningocele
H&P, MRI
Bed rest, binder
Propranolol, acetazolamide
Nerve root cyst
H&P, MRI, myelogram
Analgesics, binder
Surgical resection, disk plication
Spinal stenosis
H&P, radiographs, MRI, or CT
Analgesics, MgO2, muscle relaxants
Peridural steroid, bilateral laminotomy
Arachnoiditis
H&P, MRI
IV protocol
Analgesics, oral steroids for flare-ups, protocol
CT, computed tomography; ESI, epidural steroid injection; H&P, history and physical examination; IV, intravenous; MgO2, magnesium peroxide; MRI, magnetic resonance imaging
774
Section IV—Regional Pain Syndromes
Prognosis This prediction relates only to patients who have already been assigned the diagnosis of FBSS. Unfortunately, the prognosis is not hopeful because, by definition, the label implies a hopeless condition, essentially condemning these patients to severe chronic pain, dysfunction, and disability. Attempts to identify the factors with a greater effect on the eventual symptoms noted after herniated nucleus pulposus resection showed that men usually had more spinal canal compromise than women,22,84 as well as more positive sciatic nerve tension,85–87 both of which correlated with larger disk herniations. In nonoperated groups, a shorter duration of sciatica symptoms predicted good outcomes.88 Moreover, younger patients with symptoms that lasted less than 6 months and had no litigation also had better outcomes. In contrast, larger disks in relation to the vertebral canal diameter, cigarette smoking, involvement in litigation, and age were predictors of a poor outcome. In the operated groups, larger anteroposterior diameter and smaller central and paracentral herniations indicated better outcomes, whereas concurrent and preexistent diseases, cigarette smoking, spondylosis, worker's compensation claims, middle age, and female gender led to the worst outcomes.18,89 These findings confirm that morphometric features of disk herniation as they relate to the dimensions of the spinal canal, examined by MRI, appear to be the most reliable predictors of prognosis.13,84,90 The volume of complex operations performed by one specific surgeon in one specific hospital has been shown to affect the outcomes of most operations.13–15 In addition, patients with obesity, patients who smoke tobacco products, patients with osteoporosis, or patients with certain congenital anatomic variances (e.g., short vertebral pedicles, spondylosis, the presence of a rudimentary disk at S1-2, lateral recess stenosis, or mild scoliosis of the lumbar region) have a greater predisposition to postlaminectomy complications ending in FBSS.19,63,91
Treatment Prevention is the best treatment, although a constellation of therapeutic modalities has been used in efforts to relieve pain, which is the most significant manifestation of this disease. Most of these techniques, however, have proven not only to be merely palliative but also to have been inadequately evaluated
according to determinations of evidence-based effectiveness.13 In most cases, therapeutic approaches have been less than satisfactory, including intrathecal92 or epidural infusions of opiates,93 spinal cord stimulation,94,95 sympathetic blocks,96 epidural injections of corticosteroids,97 and anti-inflammatory drugs.98 Other forms of therapy using neurolytic substances78,99 are associated with a high risk of injury and have a low benefit ratio.79,100–102 Further surgical interventions are indicated only when precisely necessary, such as in the case of a loose disk fragment compressing a nerve root, a sudden sensory or motor deficit, or a severe infection. A guideline for treatment based on clinical diagnosis is depicted in Table 96.1. When fusions include implanted hardware, a screw may be pressing on a nerve root. Moreover, if a screw is malpositioned or if a screw is fractured, screw removal may be indicated. If screws protruding through the S1 vertebral body produce pelvic pain, they may have to be removed or replaced. Because fusions have not been proven to be cost effective and given their high incidence of complications and failure to relieve the patient's chief complaint of pain, Deyo et al13,94 emphasized that research should address who should undergo fusion rather than how to perform another fusion.103 Destructive or neuroablative procedures are not recommended because they may result in added morbidity and neural deficit.95 The treating physician must determine whether the pain originates in the fusion elements (e.g., protruding or loose screws, compressed nerve root) or intrathecally (e.g., arachnoiditis, pseudocyst, syringomyelia). Then specific treatment may be directed to the source of the pain. For further information, readers are directed to Chapters 93 and 98 for in-depth details on these therapeutic modalities. The selection of patient candidates for spinal surgery is crucial, to avoid further increasing the population of patients with FBSS. The aims of the operation should be reevaluated, and the surgeon should focus on the elimination of pain, rather than on the technical success of the operation.103 Implantation of hardware and spinal interventions must be proven beneficial for at least 2 years in 400 patients before the application of these techniques can be generalized to a larger population.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
97
IV
Pelvic Girdle and Low Back Pain in Pregnancy Colleen M. Fitzgerald and Cynthia A. Wong
CHAPTER OUTLINE Epidemiology and Definitions 775 Musculoskeletal Changes During Pregnancy 775 Differential Diagnosis of Low Back and Pelvic Pain 776 Clinical History 776 Physical Examination 777 Patrick's Fabere Test 777 Posterior Pelvic Pain Provocation Test (or Thigh Thrust) 777 Long Dorsal Sacroiliac Ligament Palpation 777 Pubic Symphysis Palpation 777 Modified Trendelenburg's Test 777
Epidemiology and Definitions Low back pain is a common complaint in pregnancy. Up to 76% of women experience low back pain during pregnancy,1 and as many as 50% of these women take time off from work or have reduced social interactions as a result of their pain. In one cohort study, 37% of women with back pain in pregnancy continued to report back pain at 18 months post partum.2 A population survey study found that 68% of women with moderate to severe pain continued to have pain after pregnancy.3 In a follow-up study of women prospectively identified with severe low back pain during pregnancy, 19% stated that they had refrained from another pregnancy because of fear of recurrent low back pain.4 Variations in reported prevalence and incidence rates of low back pain during pregnancy likely reflect variable definitions of low back pain. Pelvic girdle pain is a specific form of low back pain. It may occur separately or in conjunction with low back pain.5 Some studies include lumbar and pelvic pain in the same group. Other studies suggest that pelvic girdle pain in pregnancy is a distinct diagnosis. Pelvic girdle pain is defined as pain experienced between the posterior iliac crest and the gluteal fold, particularly in the region of the sacroiliac (SI) joint. The pain may radiate to the posterior thigh and may also occur in conjunction with or separately in the symphysis. Endurance capacity for standing, walking, and sitting is diminished. Most commonly, the pain arises in relation to pregnancy, trauma, or reactive arthritis. Pelvic girdle pain is a diagnosis of exclusion after ruling out lumbar causes of pain. © 2011 Elsevier Inc. All rights reserved.
Gaenslen's Test 777 Active Straight Leg Raise Test (for Assessing Lumbopelvic Stability) 777
Imaging 778 Treatment 779 Physical Therapy 779 Medical Therapy 779 Interventional Injections 780
Labor and Delivery 780 Postpartum Pelvic Girdle Pain and Low Back Pain and Prognosis 780
The pain or functional disturbances should be reproducible by specific clinical tests.5 The single greatest risk factor for developing pelvic girdle pain during pregnancy is a history of low back pain.5 Pelvic trauma may predispose a patient to pelvic girdle pain in pregnancy. A history of oral contraceptive use, time interval since last pregnancy, height, weight, smoking, and age are not risk factors.5 Elite athletes were not protected against low back and pelvic girdle pain compared with controls.6 In a Danish cohort study of 1789 consecutive women whose pregnancies were at 33 weeks' gestational age, 24% of these women had daily pelvic girdle pain diagnosed by history and an objective clinical examination.7 The investigators classified pelvic girdle pain into four distinct groups—double-sided SI syndrome (6.3%), pelvic girdle syndrome defined as daily pain in both SI joints and the pubic symphysis (6%), one-sided SI syndrome (5.5%), symphysiolysis (2.3%)—and a fifth miscellaneous group characterized by a daily report of pelvic joint pain with inconsistent objective findings (1.6%). The investigators also found that women with pelvic girdle syndrome during pregnancy had a markedly worse postpartum prognosis for long-term pain than did women with single joint pain.7
Musculoskeletal Changes During Pregnancy A woman's body goes through tremendous changes that affect all organ systems during pregnancy, and the musculoskeletal system is no exception. Overall weight gain averages 9 to 18 kg. 775
776
Section IV—Regional Pain Syndromes
A 20% weight gain may double the force on joints.8–11 The center of gravity shifts to a more upward and forward position.12,13 Hyperlordosis, rotation of the pelvis on the femur, an increase in the anterior flexion of the cervical spine, and adduction of the shoulders also occur.14 The abdominal muscles stretch as the gravid uterus grows while the muscles of the low back work harder to maintain upright posture. The muscles of the pelvic floor bear the weight of the growing uterus and eventually allow passage of the fetus. This process creates a natural disruption of the “core” musculature. Inherent pelvic asymmetry associated with pregnancy may have effects on muscle length that lead to suboptimal biomechanical alterations. These changes may cause the pelvic floor muscles to have a less protective effect on the pelvic joints they surround. The hormone relaxin has been identified as the major contributor to joint laxity during pregnancy.15 Evidence showing that elevated serum relaxin levels correlate with pain is inconsistent.16–21 Relaxin levels increase during the first trimester, decline early in the second trimester to a level that remains stable throughout the pregnancy, and then decline sharply after delivery. Widening of the symphysis pubis and increased mobility of the SI synchondroses begin as early as the 10th through the 12th week of pregnancy as a result of relaxin.8 The strong SI ligament, which normally resists forward flexion of the sacral ala, becomes lax in response to the effects of relaxin.8 Studies using an animal model showed that relaxin has a potent effect on the amount of collagen in the nonpregnant rat pubic symphysis.22 A clear relationship exists between asymmetric laxity of the SI joints and pregnancy-related pelvic pain.23 Asymmetric laxity of the SI joints in pregnancy is believed to increase the presence of postpartum pelvic pain by as much as threefold.24
Differential Diagnosis of Low Back and Pelvic Pain Many potential pathoanatomic pain generators may lead to low back pain or pelvic girdle pain in pregnant women. The cause may be musculoskeletal (joint, ligament, muscle, bone), hormonal (ligamentous laxity), inflammatory, neural (peripheral or central), or related to changes in tissue composition (collagen).25 Any cause of musculoskeletal pain in the nonpregnant state may also occur in pregnancy. The SI joint is thought to be the most common source of pelvic girdle pain in pregnancy because most patients present with posterior pain.26 Myofascial pain of the low back, pelvis, hip, or lower extremities may be seen in conjunction with other musculoskeletal diagnoses. Weakness and deconditioning of one muscle group may lead to pain and dysfunction in another. Up to 52% of pregnant women with low back and pelvic pain have been found to have pelvic floor dysfunction.27 SI joint pain is often mistaken for sciatica. Lumbar disk herniation, an unusual cause of low back pain in pregnancy, occurs in only 1 of 10,000 pregnant women.28 True sciatica in pregnancy is rare.13 The differential diagnosis of musculoskeletal causes of low back and pelvic girdle pain is listed in Table 97.1.
Clinical History The onset of low back pain or pelvic girdle pain in pregnancy typically occurs between 18 and 36 weeks' gestation. Patients may complain of low back pain or buttock,
tailbone, hip, or groin pain of varying characteristics and intensity. Many women say the pain began in pregnancy and that they never experienced anything like this in the past. The pain often radiates from the low back into the buttock and posterior thigh past the knee and occasionally into the calf. It is typically better at rest or in sitting and worse with changing positions such us moving from a sit to a stand or turning in bed. It may also worsen with increasing the speed of walking or with stair climbing. Patients may complain of pain at night or difficulty lying on their side. Some patients describe numbness or tingling or giveaway weakness of the lower extremities. Pain may vary from mild to disabling. Disabling pain not only limits mobility but also may interfere with job performance, child care, and attempts at exercise. Pregnant women may also complain of urinary urgency and frequency, as well as constipation. Some women experience urinary incontinence particularly with coughing, laughing, or sneezing. The patient's signs and symptoms are often nonspecific, and it may be difficult to differentiate between SI joint pain and true radiculopathy related to lumbar disease. The onset of sudden urinary retention, fecal incontinence, or numbness in the perineal area should prompt the physician to consider cauda equina syndrome. Physical examination can help differentiate these potential diagnoses.
Table 97.1 Differential Diagnosis of Low Back Pain and Pelvic Girdle Pain in Pregnancy Category
Diagnoses
Pelvic (skeletal/joint)
Sacroiliac joint dysfunction, sacroiliitis Pelvic obliquity or derangement, pelvic asymmetry Pubic symphysitis, osteitis pubis, pubic symphysis separation Coccydynia Pelvic insufficiency, stress fracture Bony metastasis
Lumbar
Lumbar degenerative disk disease, spondylosis, or spondylolisthesis (with referral to posterior pelvis: L4/L5/S1)
Hip
Hip osteoarthritis Hip fracture Acetabular labral tears Chondrosis Developmental hip dysplasia Femoral acetabular impingement Avascular necrosis of the femoral head
Muscular/fascial
Pelvic floor myofascial pain Levator ani syndrome Tension myalgia Myofascial pain syndromes of associated extrinsic muscles (iliopsoas, adductor, piriformis) Dyssynergia of the pelvic floor muscles Vaginismus, dyspareunia
Neurologic
Radiculopathy Plexopathy Peripheral neuropathy (pudendal neuropathy)
Chapter 97—Pelvic Girdle and Low Back Pain in Pregnancy
Physical Examination A directed examination of the pregnant patient is an important part of the workup of low back and pelvic pain in pregnancy, especially because diagnostic tests are limited. A detailed neurologic examination, a lumbar examination including range of motion, and hip range of motion testing are the initial steps. Abdominal examination, particularly of the rectus abdominis musculature to assess for diastasis, and an internal pelvic floor muscle examination to assess for pelvic floor myofascial pain or dysfunction may also be appropriate. Certain provocation tests for pelvic instability have been investigated; in general, the tests have high specificity (80% to 100%) and variable sensitivity (40% to 90%).5 These tests are designed to provoke a painful response in an affected pelvic joint region (SI joint or pubic symphysis), although they do not definitively identify the anatomic pain generator (bone, joint, ligament, tendon, muscle).
Patrick's Fabere Test The patient is placed supine, with one leg flexed, abducted and externally rotated so that the heel rests on the opposite kneecap. This test result is positive with production of pain anywhere in the pelvic girdle (Fig. 97.1).
Posterior Pelvic Pain Provocation Test (or Thigh Thrust) The patient is placed supine, the femur is flexed so that it is perpendicular to the table and the knee is flexed at 90 degrees. A gentle force is applied to the femur in the direction of the exa mination table. The test result is positive when the patient expe riences pain in the gluteal region or ipsilateral leg (Fig. 97.2).
777
5 seconds after removal of the examiner's hand, it is recorded as pain. If the pain disappears within 5 seconds, it is recorded as tenderness. When the identical pain is felt directly in the vicinity, but outside the borders of the ligament, the test result is not deemed positive.
Pubic Symphysis Palpation The examiner palpates the subject's pubic symphysis joint and checks for tenderness while the patient is lying supine. If palpation causes pain that persists 5 seconds after removal of the examiner's hand, it is recorded as pain. If the pain disappears within 5 seconds, it is recorded as tenderness.
Modified Trendelenburg's Test The standing woman turns her back to the examiner and, standing on one leg, flexes the other leg at 90 degrees (hip and knee). The test result is considered positive if pain is experienced in the symphysis (Fig. 97.3).
Gaenslen's Test The patient lies on her side with the upper leg (test leg) hyperextended at the hip. The patient holds the lower leg flexed against the chest, and the examiner stabilizes the patient's pelvis while extending the hip of the test leg. A positive test result is pain provoked in the ipsilateral (upper) pelvic girdle.
Active Straight Leg Raise Test (for Assessing Lumbopelvic Stability)
The patient lies on her side with slight flexion in both hip and knee joints. The areas above both SI joints are palpated. Specifically, the long dorsal SI ligament is palpated directly caudomedially from the posterior iliac spine to the lateral dorsal border of the sacrum. If palpation causes pain that persists
The test is performed with the patient supine with straight legs extended on the table, feet 20 cm apart. The patient raises the each leg one at a time 30 degrees above the table without bending the knee. The test result is positive when the patient describes a heaviness or difficulty in performing the task. In the second part of the maneuver, posterior compression is applied at the iliac crests in a lateral to medial direction, and the patient is then asked to perform a straight leg raise actively. The test result is considered positive if ease of motion is greater (Fig. 97.4).
Fig. 97.1 Patrick's Fabere test. The patient is supine, with one leg flexed, abducted and externally rotated so that the heel rests on the opposite kneecap. The test result is positive with production of pain anywhere in the pelvic girdle.
Fig. 97.2 Posterior pelvic pain provocation test. The patient is supine, the femur is flexed so that it is perpendicular to the table, and the knee is flexed at 90 degrees. Gentle force is applied to the femur in the direction of the examination table. The test result is positive when the patient experiences pain in the gluteal region of the ipsilateral leg.
Long Dorsal Sacroiliac Ligament Palpation
778
Section IV—Regional Pain Syndromes
Fig. 97.3 Modified Trendelenburg's test. The standing woman turns her back to the examiner and, standing on one leg, flexes the other leg at 90 degrees (hip and knee). The test result is considered positive if pain is experienced in the symphysis.
Fig. 97.4 Active straight leg raise test. The patient is supine with straight legs extended on the table, feet 20 cm apart. The patient raises the each leg one at a time 30 degrees above the table without bending the knee. The test result is positive when the patient describes a heaviness or difficulty in performing the task. In the second part of the test, posterior compression is applied at the iliac crests in a lateral to medial direction, and the patient is then asked to perform a straight leg raise actively. The test result is positive if the ease of motion is greater.
Imaging Imaging in pregnancy may be limited because of the potential for radiation exposure of the fetus. However, most single diagnostic radiologic procedures are associated with little, if any,
known fetal risk.29 In deciding whether to perform an imaging procedure on a pregnant woman, the risk to the fetus must be weighed against the risk to the mother of making the wrong or delayed diagnosis by avoiding imaging. Ultrasonography and magnetic resonance imaging (MRI), which do not use ionizing radiation, are the imaging modalities of choice during pregnancy.29 No adverse effects of diagnostic ultrasound on the fetus, including duplex Doppler imaging, have been documented, although concern exists that tissue temperature elevation (a function of the intensity, frequency, beam width, exposure time, and tissue composition) could have adverse effects.29–31 The United States Food and Drug Administration (FDA) has set an upper limit of 94 mW/cm2 for the spatialpeak temporal average intensity of the ultrasound beam used for obstetric imaging.31 No evidence indicates harmful effects to the fetus from MRI, although current data are derived from studies using 1.5 T or lower magnetic field strength.30 Some investigators have raised concern about potential fetal harm resulting from the heating effects of radiofrequency pulses and the acoustic effects of noise.32 The American College of Radiologists stated that MRI may be used in pregnant women at any gestational age if the test is considered necessary by referring physicians.33 Written informed consent is recommended. Animal studies of gadolinium showed potential fetal toxic effects, although demonstration of fetal harm in humans is lacking (FDA category C drug).30 After maternal administration, gadolinium rapidly crosses the placenta, appears in the fetal bladder, and then moves into the amniotic fluid, from which it is potentially swallowed by the fetus and absorbed through the gastrointestinal tract.34 The fetal half-life of gadolinium is not known, but it is potentially prolonged. The American College of Radiologists recommended a “well documented and thoughtful risk-benefit analysis” before using gadolinium in pregnancy.33 Fortunately, gadolinium is not necessary for most pelvic imaging.34 Fetal exposure to ionizing radiation may result in (1) cell death and teratogenic effects, (2) carcinogenesis, and (3) mutations in germ cells. High-dose radiation exposure (much greater than that of a normal diagnostic procedure) before embryo implantation will likely result in embryo death. Strong evidence indicates that in utero radiation exposure increases the risk of childhood cancers, particularly leukemia, although the extent of the risk of controversial.30 The most common human teratogenic effects of ionizing radiation are growth restriction, mental retardation, and microcephaly.30 The risk appears greatest for exposures between 8 and 15 weeks' gestation. Data based on animal studies and epidemiologic studies of atomic bomb victims suggested that the risk to intelligence is linear based on dose, although the threshold for risk of severe mental retardation has been estimated at 60 to 310 mGy.30 Natural background radiation dose to the fetus during pregnancy is approximately 1 mGy. Computed tomography (CT) outside the pelvis or abdomen is associated with minimal fetal exposure, and CT scans may be safely performed at any gestational age, provided the pelvis is shielded. The estimated mean fetal absorbed dose of an abdominal or pelvic CT scan is 30 mGy, although this dose can be reduced by altering parameters such as the slice thickness and pitch. In the 2008 European guidelines for diagnosis and treatment of pelvic girdle pain, MRI was recommended for use in discriminating changes in and around the SI joint and for
Chapter 97—Pelvic Girdle and Low Back Pain in Pregnancy
excluding ankylosing spondylitis and traumatic injuries (post partum) or tumor.5 The guidelines stated that conventional radiography, CT, or scintigraphy (bone scan) had no role in the diagnosis of pelvic girdle pain.
Treatment Physical Therapy Treatment options for low back pain and pelvic girdle pain during pregnancy include physical therapy, bracing, other treatment modalities (e.g., cold, transcutaneous electrical nerve stimulation), oral medications, and injection therapy. Surgery is reserved for patients with progressive neurologic disease such as cauda equine syndrome related to acute disk herniation and is rarely necessary. After activity modification, physical therapy may offer significant relief to patients with low back pain. A 2007 systematic review of treatment options for back and pelvic pain in pregnancy suggested that pregnancy-specific exercises, physical therapy programs, acupuncture, and the use of special pillows resulted in better outcomes than did usual care.35 Adverse effects appeared minor or transient. However, the investigators emphasized that most studies had moderate to high potential for bias and that further study was required. No studies have addressed the prevention of back and pelvic pain. In general, studies show that women with low back pain who receive education and physical therapy report lower pain intensities and disability, better quality of life, and improved results of physical tests. Physical therapy focuses on postural modifications, stretching, manual therapy, self-mobilization techniques, awareness of symmetrical body mechanics, functional rehabilitation, and core strengthening. Core strengthening involves strengthening of the muscles around the lumbar spine to maintain functional stability.36 These core muscles include the diaphragm and the transversus abdominis, multifidus, and gluteal and pelvic floor muscles. Transversus abdominis contraction decreases SI joint laxity to a greater degree than does general abdominal exercise,37 and strengthening the pelvic floor musculature increases the stiffness and stability of the pelvic ring.38 Pelvic floor muscle training in pregnancy not only encompasses Kegel exercises but also includes endurance muscle training, relaxation and biofeedback, and functional retraining. In the postpartum period, pelvic floor muscle training may broaden to include electrical stimulation, weighted cones, and pressure biofeedback. A multicenter Swedish study of 386 pregnant women with pelvic girdle pain compared standard therapy (education and home exercise) with stabilizing exercises, with and without acupuncture.39 Women who received stabilizing exercises in addition to standard therapy had less pain, and the addition of acupuncture to standard therapy and stabilizing exercises resulted in even further reduction in pain.39 Acupuncture is generally considered safe during pregnancy, although certain acupuncture points that stimulate the cervix and uterus should be avoided. Other modalities to treat back and pelvic pain have not been well studied in the setting of pregnancy. Deep heat is contraindicated in pregnancy (hyperthermia is teratogenic); therefore, cold modalities are preferred. Transcutaneous electrical nerve stimulation has not been studied in pregnancy. Bracing in the form of a SI joint belt may be used for SI joint
779
or pubic symphysis pain during pregnancy and post partum. The belt facilitates motor control of core stabilizing muscles and provides a sense of stability through joint approximation. Placement of the belt just caudal to the anterior superior iliac spines decreases SI joint laxity to a greater degree than when the belt is placed lower at the level of the pubic symphysis.40 Studies showed that the combination of a pelvic belt with muscle training improved pelvic stability; the belt decreased sagittal rotation in the SI joints by 19%.41 Physical therapy may also be of benefit post partum. In a randomized controlled trial in postpartum women with pelvic girdle pain, women randomized to receive pelvic stabilizing exercises in additional to routine physical therapy had less disability 2 years after delivery than did women who received physical therapy alone.42
Medical Therapy Almost all drugs cross the placenta from the maternal to the fetal circulation. The medical management of pain during pregnancy is complicated by the need to limit the transfer of drugs across the placenta, particularly during the first trimester. Unfortunately, placental transfer of drugs and drug effects on the fetus are difficult to measure. Drug teratogenicity is species specific and depends on timing of exposure, dose and duration of exposure, maternal physiology, embryology, and genetics. The classic period of structural teratogenicity coincides with the period of organogenesis, between 31 and 71 days' gestation (starting the first day of the last menstrual period), although the central nervous system continues to develop throughout gestation and indeed during the first several years of life. Therefore, behavioral teratogenicity is a possible consequence of drug exposure at any gestational age. The FDA uses a five-category pregnancy drug classification system (categories A, B, C, D, X); however, this classification has some major limitations. There are very few controlled studies in humans in which lack of fetal harm has been demonstrated. All new drugs are classified as category C (either animal studies have revealed adverse effects, but no controlled studies in women have been reported, or studies in women and animals are not available). Unfortunately, this situation does not help the practitioner or patient assess the drug's safety during pregnancy. Several Internet databases offer information on drug use during pregnancy and lactation, as does a well-known reference book.43 Some drug companies maintain pregnancy registries for specific drugs. No studies of drug use for the treatment of back and pelvic girdle pain during pregnancy have been reported. Acetaminophen is the first-line analgesic drug of choice for the treatment of mild pain during pregnancy, although it has no anti-inflammatory effect and therefore is unlikely to be effective for low back and pelvic girdle pain. Low-dose aspirin is considered safe; however, higher doses should be avoided because they may be associated with an increased risk for placental abruption and other bleeding problems, as well as fetal gastroschisis.43,44 Nonsteroidal anti-inflammatory drugs (NSAIDs) may cause constriction of the ductus arteriosus and may have adverse effects on fetal renal function, leading to oligohydramnios. These drugs are not recommended for use for more than 2 days beyond the first trimester.44 Opioids are considered safe during pregnancy, although the potential exists for neonatal abstinence syndrome after delivery.
780
Section IV—Regional Pain Syndromes
Cyclobenzaprine, a muscle relaxant, is a class B drug. Data are inconsistent on whether benzodiazepines are associated with increased risk of cleft lip and palate and other congenital defects, and most practitioners try to avoid long-term benzodiazepine use during pregnancy. Diazepam is a class D drug. Lidocaine patches (class B) are presumably safe. Prednisone and prednisolone are inactivated by the placenta, and only a small amount crosses the placenta. Use in early pregnancy may be associated with an increased risk of orofacial clefts, and treatment of asthmatic patients with oral steroids during pregnancy is associated with an increased risk of preeclampsia and prematurity.45 The safety of a low dose of tapering steroids is uncertain.
Interventional Injections Interventional injections have gained popularity in the treatment of low back and pelvic girdle pain. No studies have addressed their efficacy in pregnancy. Fluoroscopy-guided injections require exposure to ionizing radiation. Alternatives include blind injections, MRI-guided injections, and ultrasound-guided injections. Clinically guided blind SI joint injections are usually not successful; in one study, only 22% of blind injections were placed intra-articularly.46 MRI-guided SI joint injection is safe and effective.47 Ultrasound-guided caudal epidural injections had 100% accuracy in one study.48 Ultrasound-guided SI joint injection may require more technical skill, however. In a study in nonpregnant patients, the percentage of successful injections increased with greater experience.49 Local anesthetics appear to be safe for joint injection; the safety of glucocorticoid injection during pregnancy has not been established. For radicular pain, ultrasound-guided selective nerve root block is preferable to a caudal approach, and if ultrasound is not available, a blind interlaminar or caudal approach may be used. For axial back pain, an ultrasoundguided caudal or interlaminar approach is recommended.
Labor and Delivery No data suggest that a history of low back pain or pelvic girdle pain will have a positive or negative effect on labor or delivery. Patients are advised to assume positions during childbirth that are most comfortable for them. Patients with a history of herniated disk are advised not to assume a flexed position while pushing because this position contributes to further disk herniation.
Neuraxial analgesia may effectively block low back and pelvic pain, and women with effective analgesia should not assume positions that cause pain in the absence of neural blockade.
Postpartum Pelvic Girdle Pain and Low Back Pain and Prognosis Pelvic girdle pain is usually self-limiting and resolves within several weeks to months after delivery; however, 8% to 10% of women may continue to have pain for 1 or more years.7,50,51 The process of childbirth adds to disruption of core musculature; abdominal muscles are disrupted by cesarean delivery, and pelvic floor muscles are disrupted by vaginal delivery. In an MRI study of 80 nulliparous and 160 primiparous women, none of the nulliparous and 20% of the primiparous women exhibited damage to the levator ani muscles.52 Although not well studied, trauma to the pelvic floor during childbirth likely has an impact on the persistence of postpartum pelvic girdle pain or the new onset of pelvic girdle pain, particularly in the setting of an instrumental delivery. Clearly, musculoskeletal changes persist post partum, including pelvic floor muscle defects, rectus abdominis diastasis, pelvic asymmetry or obliquity, and impaired load transfer with overall decreased core strength. Additionally, scar tissue (perineal or abdominal) may interfere with fascial support. Breast-feeding causes notable thoracic kyphosis and poor posture. Risk factors for persistent pelvic girdle pain include prepregnancy back pain, prolonged duration of labor,51 a high number of positive pain provocation test results, a low mobility index,7 the onset of pain in early gestation, and the inability to lose weight after delivery.50 Emotional well-being may also play a role in recovery from pelvic girdle pain.53,54 Low back pain may also persist after delivery. In several studies, the incidence of persistent back pain ranged from 21% to almost 50%.54–56 Risk factors for postpartum back pain included prepregnancy back pain and an inability to lose weight after delivery.54 Treatment options for postpartum low back and pelvic pain do not differ from the options available to pregnant patients but now include oral NSAIDs and fluoroscopically guided injections.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
98
IV
Postoperative Deformities of the Dural Sac J. Antonio Aldrete
CHAPTER OUTLINE Pseudomeningoceles 781 Dural Sac Ectasia 782 Distal Dural Sac Dilatation 783 Arachnoid Webs 783
The dural sac has an important role in the protection of the central nervous system. This delicate wrap not only involves and surrounds these vital organs, but also contains the cerebrospinal fluid (CSF). The CSF lubricates these organs and their constituents and also acts as a transporter. Circulation of the CSF starts from the brain; the CSF then descends behind the spinal cord toward the distal end of the dural sac and finally ascends anterior to the dural sac. In essence, the CSF communicates with all organs as it lubricates their surface and transports enzymes, drugs, neurotransmitters, proteins, glucose, and other ingredients.1 The CSF also reaches adjacent structures such as the eyes, through the canaliculus present within the optic nerve, and the inner ear, by way of the labyrinth. While being eliminated, the CSF passes not only through the arachnoid villi into the venous system but also through the lymphatic system of the neck and even into the retroperitoneal space (Fig. 98.1). Not uncommonly, after undergoing spinal surgery, patients continue to experience symptoms, either similar to or different from those present preoperatively. Commonly, these patients are referred to pain management specialists for evaluation and treatment. However, not infrequently, the cause of the postoperative symptoms has not been precisely determined. In this chapter, some of the possible postoperative complications affecting the dural sac, its surroundings, and its contents are discussed. This discussion is a warning to pain practitioners not to assume the diagnosis, but rather to attempt to define the cause of the new clinical manifestations. This issue may also have considerable medicolegal importance.
Pseudomeningoceles The dural sac deformity known as pseudomeningocele usually originates as an intraoperative complication following an incidental dural tear that may or may not have been recognized intraoperatively.2 When the tear is observed intraoperatively, © 2011 Elsevier Inc. All rights reserved.
Dural Cuff Diverticula 783 Diagnosis 784 Treatment 785
an attempt to repair it is usually conducted while the surgeon has complete exposure of the surgical field. Such repair is usually difficult because the delicate dura may be torn, even by the passage of a fine needle; thus, the dural repair may need to be reinforced with tissue (muscle or fascia) or by a patch of synthetic material.3–5 If the tear is not repaired or if the repair ruptures in the first postoperative days, leakage of CSF may be abundant, and CSF may permeate the soft tissues posterior to the spine (Fig. 98.2). Patients who have a continuous CSF leak tend to remain recumbent because the postural headache can be severe.2,3 Such leakage may exit through a wound that has not yet healed. If the skin incision has healed, then the fluid will accumulate posteriorly in a single pseudosac (Fig. 98.3). Occasionally, however, patients may have two or more communicating sacs that are evident only on magnetic resonance imaging (MRI) or computed tomography (CT) postmyelographic studies (Fig. 98.4). Wound healing is usually delayed, but in most instances, it eventually takes place, although the sac remains as a pseudomeningocele. If the communicating ostium is large, occasionally a nerve root of the cauda equina may be trapped.6 In addition to conducting the usual history, a comparison of the patient's current complaints with those present preoperatively is helpful. The appearance of clear or serosanguineous fluid in the wound dressing may suggest possible leakage of CSF, which, in turn, implies a dural rent that has continued to leak after the wound was apparently closed. This complication may be confirmed by the presence of a posturedependent headache occurring in the first postoperative days. Once the wound has closed, a moderately tender and fluctuating “bulge” may be evident. This bulge may increase in size when the patient remains standing for a while. Removal of the posterior bone support of the vertebral canal (laminae and spinous processes) may allow the dural sac to bulge through the canal, as seen after extensive laminectomies, bilateral laminotomies, and facetectomies 781
782
Section IV—Regional Pain Syndromes
Fig. 98.1 Scintillogram of the lumbosacral dural sac depicting two partial obstructions (thin white arrows). Dye is seen leaving through the retroperitoneal lymphatic system (thick white arrow).
3
P
4
Fig. 98.3 Sagittal magnetic resonance view showing a single pseudomeningocele (P) posterior and communicating with the dural sac. Evidence of diskitis is noted at the L3-4 intervertebral disk (white arrowhead). d
Fig. 98.2 Axial magnetic resonance view of the L5 vertebra showing a left laminectomy (white arrow), the dural sac (d) containing clumped nerve roots, and free cerebrospinal fluid in the paravertebral muscles (O) and in the subcutaneous tissue (black arrowheads).
(Fig. 98.5). Pseudomeningoceles are thought to be related to dural injuries, but they have also been attributed to a spontaneous burst of the dural wall during early postoperative ambulation, strenuous physical therapy, or vigorous and repeated coughing, chiefly in smokers.7 Moreover, glues, hemostatic powders, or synthetic materials containing chemical solvents have also been suspected.8 However, this assumption remains to be proven.
Dural Sac Ectasia Dural sac ectasia is an isolated dilatation of the dural sac that may occur several months after single disk excision through a laminectomy. This procedure tends to elicit considerable fibrosis at the most cephalad and the most caudad
F
*
*
Fig. 98.4 Axial magnetic resonance view of the lumbar spine showing tracts of pedicular screws in the body of the vertebra with a deformed and dilated dural sac (white arrowhead) containing enhanced nerve roots (white dots), some of them clumped and adherent to the dural sac wall; inflammation and fibrosis are noted (F) posterior to it. A bilateral laminotomy has been performed. Two pseudomeningoceles (white asterisks) are visible.
points of the operative procedure and creates an isolated, but well-circumscribed widening of the dural sac with fibrotic rings just above and below the site of the operation (Fig. 98.6). Usually, the rest of the dural sac appears to be normal, but the CSF dynamics may be mildly affected.9 Attempts to liberate
Chapter 98—Postoperative Deformities of the Dural Sac
783
Fig. 98.5 Postmyelogram computed tomography scan at the L5 vertebra level showing a bilateral laminotomy and facetectomy, with posterior extrusion of the dural sac that contains enhanced and clumped nerve roots.
F Fig. 98.7 Sagittal magnetic resonance view of the lumbar spine depicting distal dural sac dilatation following L3-4, L4-5, and L5-S1 bilateral laminectomies. The nerve roots appear adherent to the posterior wall of the dural sac.
postoperatively, are weakness, alterations of sensibility in the lower extremities but not necessarily with a radicular distribution, and the sensation of pressure in the lower back, usually including the sacral region. Radiologic imagines delineate the extent of the dilatation, as well as nerve roots within the cavity that may be subjected to undue pressure (Fig. 98.7).
Arachnoid Webs
Fig. 98.6 Postoperative lumbar spine myelogram showing a dural sac ectasia at the L5 level, after diskectomies at L4-5 and L5-S1.
the sac from the surrounding fibrotic rings may be hazardous because the wall of the sac, at these points, is usually hardened, but friable, and easy to damage by traction or pressure. These lesions are best left alone, unless the fibrosis surrounding the sac produces enough constriction to produce a serious impediment to the normal circulation of the CSF.
Distal Dural Sac Dilatation Distal dural sac dilatation usually appears after operations (laminectomies, laminotomies, or fusions) performed at the L4-5 or the L5-S1 levels that leave a substantial constricting ring above the upper point where the surgical procedure was performed. Symptoms, which begin to appear 5 or 6 months
Also labeled “focal arachnoiditis,” arachnoid webs are membranous extensions of the subdural arachnoid. These webs extend toward the pia and may resemble intradural arachnoid cysts with an inward retracting point at the internal wall of the dural sac and a protrusion of the external dural wall just above it (Fig. 98.8). This specific point of localized inflammation is usually caused by traumatic needle puncture or suture or by the application of chemical glues, sealants,10,11 or hemostatic pads12 placed at the site of a repaired dural tear. Intrathecally, these webs may form a septum-like partial barrier to the normal flow of CSF that may give the radiographic impression of a pseudocyst.13,14 These apparent barriers are truly welldefined septa, as described in the sagittal plane by Roche and Vignanendra,15 who believed that these webs split the subarachnoid space without being in continuity with the peridural fibrosis and without involving the spinal cord.
Dural Cuff Diverticula Dural cuff diverticula are usually expansions of one or more localized dural cuffs of the nerve roots as they pass through the lateral foramen. Generally, these diverticula are caused by
784
Section IV—Regional Pain Syndromes
Fig. 98.8 Sagittal magnetic resonance view of the lumbar spine with arachnoid webs and buckling the posterior wall of the dural sac, typical of “focal” arachnoiditis.
Fig. 98.9 Coronal magnetic resonance view of the lumbar spine depicting a dilated, right dural cuff and a distal dural sac diverticula (white arrows) after an L5-S1 laminectomy and diskectomy.
postoperative fibrosis around the dural cuff within the lateral foramen and often are present during surgical exploration, after the removal of an osteophyte in the foramen, or during facetectomies (Fig. 98.9). Occasionally, dilatation of multiple dural cuffs may be noted, distal to the application of Harrington rods or other similar devices that tend to partial compression of the dural sac with the hooklike attachments usually placed under the transverse processes or the ribs (Fig. 98.10). In both cases, symptoms may resemble those of radiculopathy and localized tenderness. Removal of the osteophyte or fibrosis inside the foramen is usually difficult; besides, these diverticula are prone to recur, and traction placed on adjacent tissues may further damage the dura. The transforaminal approach16 for the injection of steroid and other medications may lead to puncture of the nerve root, the radicular artery, and even the intraforaminal dural cuff.
Diagnosis Pain on and around the healed incision is common. Patients occasionally note a bulge that fluctuates on palpation that is slightly tender but shows no signs of an abscess. In any of these postoperative complications, spasms of the lower extremity muscles, paresthesias, photophobia, phonophobia, headache, loss of balance, altered gait, tinnitus, and muscle weakness may also be present. These findings suggest alteration of proprioception. These lesions may be easily identified (see Figs. 98.2 to 98.4) by MRI. However, if hardware has been used, unless it is made of titanium, the only approach possible is myelography
Fig. 98.10 Myelogram of the thoracolumbar spine showing dilatation of distal dural cuffs after bilateral Harrington rod implantation.
Chapter 98—Postoperative Deformities of the Dural Sac
f ollowed by CT, which may not be desirable in the early postoperative period. As an alternative, ultrasound may be used to identify the presence of any of these lesions.3 For complicated cases and when several lesions are suspected, a scintillogram (see Fig. 98.1) can define the precise morphology of the dural sac, the presence of CSF leaks, stenosis, and morphologic deviations.
Treatment Unless a major defect is present and even though dural leaks secondary to surgical interventions may initially diffuse into the posterior soft tissues (see Fig. 98.2), approximately 50% of these dural leaks gradually coalesce into a cystlike, rounded structure (see Fig. 98.3) adherent to and in communication with the dural sac at the level where the intervention took place. An elastic low thoracoabdominal corset may be helpful in reducing the size of the extra sac.15 In persistent cases, decompression may be achieved by continuous drainage of CSF through a catheter inserted above the pseudomeningocele for 8 to 10 days. This temporary catheter implantation requires that the patient remain in bed for this period because it is essential to reduce the internal pressure within the sac, to allow its closure.16 Reoperation to close the pseudomeningocele is not easy because the ostium that connects the pseudomeningocele to the main dural sac is difficult to locate. Attempts to find the ostium by injection of colorant dyes (methylene blue or indigo red) may result in severe inflammatory reaction with intradural cyst and pseudocyst formation and arachnoiditis. Pseudomeningocele after spinal surgery at any level remains a serious and common liability from these interventions.5,8,9,17
785
Small pseudomeningoceles, dural sac ectasias, and distal dilatations may be treated conservatively with an elastic low back support,18 in addition to acetazolamide, 500 mg twice daily, and propranolol, 1 mg once daily.17 These drugs are reported to reduce the volume of CSF,18,19 and they can be used if no medical contraindications to these medications are present. Insertion of a spinal or epidural needle near or into the scar of a previous spinal operation should be done only after a clinical examination has been conducted and imaging studies have been carefully examined.20 These scars usually have considerable fibrosis, and the posterior epidural space is absent. Moreover, the posterior surgical entry into the spine usually abolishes the posterior epidural space (see Figs. 98.1 to 98.8), and the dural sac may be closer to the skin than under normal circumstances (see Figs. 98.3 and 98.8). Further, the nerve roots and the spinal cord may be tethered to the posterior wall of the sac (see Fig. 98.9) and may thus be at risk of direct injury.20 Excessive intradural pressure for a prolonged period may exacerbate the existing neural injury.21,22 As an alternative, a one-way valve may be implanted to prevent the buildup of intradural pressure; however, these devices need frequent revisions and replacement. Attempting any interventional procedures that may incidentally puncture any of the dural sac defects mentioned in this discussion is ill advised, not only because CSF leakage may be reinitiated, but also because gravity promotes the persistence of this leakage, given that these defects are usually at the distal end of the spinal canal.13.14
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
99
Osteitis Pubis Steven D. Waldman
CHAPTER OUTLINE Signs and Symptoms 788 Testing 788 Differential Diagnosis 788
Treatment 788 Conclusion 789
A common cause of anterior pelvic pain, osteitis pubis is relatively straightforward to diagnose if the clinician thinks of it. This disease of the second through fourth decades affects female patients more frequently than male patients.1 Osteitis pubis is a constellation of symptoms consisting of localized tenderness over the symphysis pubis, pain radiating into the inner thigh, and a waddling gait.2,3 The characteristic radiographic changes of erosion, sclerosis, and widening of the symphysis pubis are pathognomonic for osteitis pubis4 (Figs. 99.1 and 99.2). Osteitis pubis occurs most commonly following bladder, inguinal, or prostate surgery and pregnancy and is thought to result from hematogenous spread of infection to the relatively avascular symphysis pubis.5–7 This condition is often seen in athletes involved in kicking sports because of the stresses placed on the pubic symphysis8–10 (Fig. 99.3). Osteitis pubis can appear without an obvious inciting factor or infection.1,8
of the pelvis is indicated if an occult mass or tumor is suspected. Radionuclide bone scanning may be useful to rule out stress fractures not seen on plain radiographs4 (Fig. 99.4). The injection technique described subsequently serves as both a diagnostic and a therapeutic maneuver.
Signs and Symptoms
Treatment
On physical examination, the patient exhibits point tenderness over the symphysis pubis. The patient may be tender over the anterior pelvis and may note that the pain radiates into the inner thigh with palpation of the symphysis pubis.1,2 Patients may adopt a waddling gait to avoid movement of the symphysis pubis.3 This dysfunctional gait may result in lower extremity bursitis and tendinitis, which may confuse the clinical picture and further increase the patient's pain and disability.
Initial treatment of the pain and functional disability associated with osteitis pubis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 inhibitors and physical therapy. The local application of heat and cold may also be beneficial. For patients who do not respond to these treatment modalities, the following injection technique with local anesthetic and steroid may be a reasonable next step.11 Injection for osteitis pubis is carried out by placing the patient in the supine position. The midpoint of the pubic bones and the symphysis pubis is identified by palpation. Proper preparation with antiseptic solution of the skin overlying this point is then performed. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 3½-inch, 25-gauge needle. The needle is then carefully advanced through the previously identified point at a right angle to the skin directly toward the center of the pubic symphysis. The needle is advanced very slowly until it impinges on the fibroelastic cartilage of the joint
Testing Plain radiographs are indicated in all patients who present with pain thought to be emanating from the symphysis pubis, to rule out occult bony disease and tumor. Based on the patient's clinical presentation, additional testing including complete blood count, prostate specific antigen, sedimentation rate, serum protein electrophoresis, and antinuclear antibody testing may be indicated.1,2 Magnetic resonance imaging 788
Differential Diagnosis A pain syndrome clinically similar to osteitis pubis can be seen in patients suffering from rheumatoid arthritis and ankylosing spondylitis. However, these patients lack the characteristic radiographic changes of osteitis pubis. Multiple myeloma and metastatic tumors may also mimic the pain and radiographic changes of osteitis pubis. Insufficiency fractures of the pubic rami should also be considered if generalized osteoporosis is present.
© 2011 Elsevier Inc. All rights reserved.
Chapter 99—Osteitis Pubis
789
Fig. 99.1 In this 61-year-old woman, local pain and tenderness about the symphysis pubis were the major clinical abnormalities. The radiograph (A) reveals considerable bone sclerosis on both sides of the symphysis with narrowing of the joint space. Marked increased accumulation of the bone-seeking radiopharmaceutical agent (B) is observed. In this 34-year-old woman, a routine radiograph (C) shows unilateral osteitis pubis. A coronal T1-weighted (TR/TE, 633/17) spin-echo magnetic resonance image (D) shows low signal intensity in the involved bone. (A and B, Courtesy of M. Austin, MD, Newport Beach, Calif. C and D, Courtesy of S. Eilenberg, MD, San Diego, Calif. From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 2132.)
(Fig. 99.5). The needle is then withdrawn slightly back out of the joint, and, after careful aspiration for blood and if no paresthesia is present, the contents of the syringe are then gently injected. Resistance to injection should be minimal. The proximity to the pelvic contents makes it imperative that this procedure be carried out only by clinicians well versed in the regional anatomy and experienced in performing injection techniques. Many patients also complain of a transient increase in pain following the aforementioned injection technique. Reactivation of latent infection, although rare, can occur, and careful attention to sterile technique is mandatory. In rare patients, surgical wedge resection of the demineralized portion of the pubic symphysis with internal fixation is required for relief of symptoms.12
Conclusion Osteitis pubis should be suspected in patients presenting with pain over the pubic symphysis in the absence of trauma. The foregoing injection technique is extremely effective in the treatment of osteitis pubis. This technique is a safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection and universal precautions to avoid risk to the operator. Most side effects of this injection technique are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately following injection.
790
Section IV—Regional Pain Syndromes
Fig. 99.2 Anteroposterior pelvis radiograph showing classic findings of osteitis pubis. (From Mandelbaum B, Mora S: Osteitis pubis, Oper Tech Sports Med 13:62, 2005.)
Fig. 99.4 Isotope bone scan shows concentration of radiotracer activity at the symphysis pubis in a patient with increased marginal osteoblastic activity in a 27-year-old soccer player with osteitis pubis (arrows). (MacMahon PJ, Hogan BA, Shelly MJ, et al: Imaging of groin pain, Magn Reson Imaging Clin N Am 17:655, 2009.)
Osteitis pubis
Fig. 99.5 Injection technique for osteitis pubis. (Waldman SD: Osteitis pubis. In Waldman SD, editor: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 401.)
The use of physical modalities including local heat and gentle stretching exercises should be introduced several days after the patient undergoes this injection technique. Vigorous exercises should be avoided because they will exacerbate the patient's symptoms. Simple analgesics, NSAIDs, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique. Fig. 99.3 Patients with osteitis pubis often develop a waddling gait. (From Waldman SD: Osteitis pubis. In Waldman SD, editor: Atlas of common pain syndromes, Philadelphia, 2002, Saunders.)
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
100
IV
Piriformis Syndrome Lowell W. Reynolds and Thomas F. Schrattenholzer
CHAPTER OUTLINE Historical Considerations 791 Clinically Relevant Anatomy 791 Etiology 791 Differential Diagnosis 791 Clinical Presentation 791
Historical Considerations Initially described in 1928, piriformis syndrome is thought to be responsible for as much as 6% of sciatica.1,2 Piriformis syndrome may be even more common, because it is often underdiagnosed and undertreated.3–5 Misdiagnosis frequently occurs because piriformis syndrome can resemble more common pain syndromes such as lumbar radiculopathy, sacroiliac joint dysfunction, and greater trochanteric bursitis.4,5 It is usually caused by compression or irritation of the proximal sciatic nerve by the piriformis muscle.6
Clinically Relevant Anatomy The piriformis is a flat, pyramid-shaped muscle. It originates anterior to the S2-4 vertebrae, near the sacroiliac capsule and the upper margin of the greater sciatic foramen. This muscle passes through the greater sciatic notch and inserts on the superior surface of the greater trochanter of the femur. As the piriformis courses through the sciatic notch, it comes in close proximity to the sciatic nerve (Fig. 100.1). With the hip extended, the piriformis muscle is primarily an external rotator. When the hip is flexed, however, this muscle helps to abduct the hip. The muscle is innervated by branches of the L5, S1, and S2 nerve roots. Lower lumbar radiculopathy can also cause secondary irritation of the piriformis muscle.7,8 Many developmental variations exist between the sciatic nerve and the piriformis muscle. In approximately 20% of the population, the muscle belly is split by the sciatic nerve. In 10% of the population, the tibial and peroneal divisions are not enclosed in a common sheath. The peroneal portion splits the piriformis muscle belly, whereas the tibial division rarely splits the muscle belly.9–11
Etiology Approximately 50% of patients with piriformis syndrome have a history of direct trauma to the buttock, hip, or lower back.2 Blunt injury causes hematoma formation and subsequent scarring © 2011 Elsevier Inc. All rights reserved.
Treatment 792 Physical Therapy 792 Acupuncture 792 Injections 792 Surgery 792
Conclusion 792
between the sciatic nerve and the piriformis muscle. Sciatic nerve injury can also occur with prolonged pressure on the nerve. Other causes of spontaneous piriformis syndrome are the following12,13 Pseudoaneurysms of the inferior gluteal artery adjacent to the piriformis muscle n Bilateral piriformis syndrome resulting from prolonged sitting during an extended neurosurgical procedure n Cerebral palsy n Total hip arthroplasty n Myositis ossificans n Vigorous physical activity n
Differential Diagnosis The differential diagnosis includes the following: n n n n n n n
Lumbosacral radiculopathy Lumbar degenerative disk disease Lumbar facet arthropathy Lumbar spondylolysis and spondylolisthesis Myofascial pain Trochanteric bursitis Ischial tuberosity bursitis
Clinical Presentation When the piriformis muscle spasms or becomes inflamed, the condition may mimic sacroiliac joint dysfunction, greater trochanteric bursitis, or lumbar radiculopathy. Generally, the patient complains of low back, buttock, and hip pain that radiates down the ipsilateral leg.4 Physical examination shows tenderness over the sacroiliac joint region and the superior aspect of the greater trochanter of the femur.6 Palpation of the muscle belly is difficult because of the overlying gluteal muscles. A more reliable way of palpating the piriformis muscle is during a rectal examination. A sausage-shaped mass may be felt laterally that can reproduce the patient's pain.14 791
792
Section IV—Regional Pain Syndromes
Acupuncture
Ilium
Acupuncture has been used for centuries to reduce muscle spasm and to promote healing. Several techniques can be used such as needling, cupping, and electrical stimulation of inserted needles. Improving blood flow to the affected region seems to be an important component.17 Sacrum
Injections
Piriformis m.
Acetabulum Greater trochanter
Sciatic notch
Sacrospinous lig.
Ischial tuberosity
Sciatic n. Femur
Fig. 100.1 Clinically relevant anatomy for piriformis syndrome.
Other findings on examination may include the following: The Pace test reproduces pain with weakness to resisted abduction and external rotation.2 n The Freiberg test elicits pain on forced internal rotation of the extended thigh.15 n Shortening of the involved lower extremity may be observed.16 n
Treatment A trial of nonsteroidal anti-inflammatory and muscle relaxant medications should be given to reduce inflammation and spasm of the piriformis muscle. Patients should be educated about the possible causes of piriformis syndrome and ways in which to prevent further injury. Measures may include avoiding or reducing aggravating physical activity until the current flare-up has subsided. Applying heat, massage, and stretching to the muscle in spasm may also significantly reduce the patient's discomfort.
Physical Therapy Patients with piriformis syndrome often respond to a trial of physical therapy. Stretching exercises are intended to lengthen the contracted piriformis muscle. The most common stretching exercise is to have the patient lie supine with the affected knee bent and pulled into the chest and toward the midline. This position should be held for 30 seconds and should be repeated several times a day. A similar stretch can be performed in the standing position.5 Care should be taken not to pull the affected knee toward the contralateral chest, because this maneuver may cause stretching at the sacroiliac joint. Ultrasound, electric stimulation, and the use of vapor-coolant spray over the area in combination with stretching have produced good results.
Various injection techniques and injectates may be used for treating piriformis syndrome. Traditionally, injection procedures have been done using a blind technique. With the patient in a lateral decubitus position with the affected side upward, the patient's ipsilateral leg is flexed until the knee rests on the treatment table. A line is then drawn from the greater trochanter to the posterior superior iliac crest. The injection site is then located approximately 5 cm below the midpoint of this line. A 22-gauge spinal needle is then inserted slowly until paresthesias are identified. After negative aspiration, 40 mg methylprednisolone and 10 mL 0.25% bupivacaine may be injected. Care must be taken not to inject into the sciatic nerve.18 Alternative techniques such those using fluoroscopy,19 electromyographically assisted fluoroscopy,20 ultrasound guidance,21 computed tomography guidance,22 or magnetic resonance imaging guidance may be used.23 These techniques may improve the reliability of proper needle placement and may allow definitive diagnosis and treatment. Botulinum toxin (Botox) is an alternative to the local anesthetic and corticosteroid injectate therapy just described. Botulinum toxin can prolong the relaxation of the piriformis muscle and reduce the associated radicular symptoms.24,25 Dry needling, synonymous with acupuncture, may also have a role in the treatment of piriformis syndrome. Unlike with trigger points, however, the efficacy of this technique has not been adequately studied.
Surgery If more conservative treatments prove ineffective, persistent piriformis syndrome may be treated by surgical intervention. Patients who have objective pathologic changes or dysfunction tend to be more responsive to surgical intervention. The procedure involves dissecting the piriformis muscle and the sciatic nerve. The section of the piriformis muscle overlying the sciatic nerve is often removed. Most patients ambulate 1 day after surgery and progress to weight bearing within a week. Although patients often have persistent paresthesias in the distribution of the sciatic nerve for several weeks postoperatively, many patients report immediate relief of their sciatic pain.26,27
Conclusion Piriformis syndrome often masquerades as lumbar radiculopathy, sacroiliac joint dysfunction, or greater trochanteric bursitis. Performing a careful history and physical examination is imperative for differentiating this disorder from other common ailments. Correct diagnosis significantly improves the patient's chances of responding to appropriate therapies.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
101
IV
Orchialgia Lowell W. Reynolds and Shawn M. Sills
CHAPTER OUTLINE Historical Considerations 793 Pathophysiology 793 Differential Diagnosis 794 Diagnosis 795
Historical Considerations One of the most frustrating clinical situations for the physician and for the patient is the management of orchialgia, or testicular pain. Also known as orchiodynia or orchidalgia, this syndrome frequently has no obvious identifiable, causative factors.1 In addition, the male psyche, strongly influenced by the genitalia, brings a strong psychological dimension to the management of this problem.2 Orchialgia can be classified in various ways. These include time course (acute or chronic), age at onset (pediatric or adult), anatomic site (referred or nonreferred), pathology (mechanical or infectious), severity (severe or mild), treatment (surgical or supportive), mechanism (traumatic or nontraumatic), whether it is medication induced, whether it is physical versus psychiatric (pain disorder resulting from a general medical condition or pain disorder associated with psychological factors), or whether it is reality based (malingering or real).3 Chronic orchialgia is defined as intermittent or constant, unilateral or bilateral testicular pain lasting 3 months or longer that interferes with the daily activities of a patient sufficiently to prompt him to seek medical intervention.4 This chapter provides an explanation of the nerve supply and innervation of the testis, develops a differential diagnosis for orchialgia, highlights the key components of the history and physical examination, and discusses the common therapeutic approaches.
Pathophysiology The innervation of the testis is poorly understood (Fig. 101.1).5 However, the autonomic supply to the testes and epididymis is mostly sympathetic and originates from the T10-L1 segments.6 Approximately 10% of the autonomic supply is parasympathetic and originates from the S24 segments.7 The term spermatic plexus describes the group of autonomic fibers that accompany the internal spermatic vessels (the testicular artery and vein) and vas deferens to the epididymis and the testis.6 © 2011 Elsevier Inc. All rights reserved.
Conservative Management 796 Surgical Treatment 797 Conclusion 797
Three nerve groups contribute to this plexus: (1) the superior spermatic nerves, (2) the middle spermatic nerves, and (3) the inferior spermatic nerves.8,9 The superior spermatic nerves, composed of fibers from the intermesenteric and renal plexuses, run toward the testicular artery and follow its course to the testis. This association between the intestinal and testicular nerves may account for the visceral symptoms of a “sick stomach” associated with testicular trauma. The middle spermatic nerves arise from fibers of the superior hypogastric plexus. The middle spermatic nerves pass to the midureter and then travel inferiorly and laterally along the vas deferens to the internal abdominal ring, where they join the spermatic cord and plexus.10 The inferior spermatic nerves originate from the pelvic plexus, or inferior hypogastric plexus, and may provide the predominant sympathetic input to the testis.7 Hypogastric nerves entering the plexus from the superior hypogastric plexus are joined by pelvic and sacral splanchnic nerves at the prostatovesical junction anterior to the rectum. The inferior spermatic nerves then join the vas deferens to exit the internal abdominal ring. Some afferent and efferent fibers cross over to the contralateral pelvic plexus.11 This neural crosscommunication may explain how pathologic processes in one testis affect the function of the contralateral testis. The somatic supply to the testes and scrotum originates from the L1 and L2 nerve roots through the iliohypogastric, ilioinguinal, and genitofemoral nerves.12 The iliohypogastric nerve is a branch of the L1 nerve root, with a contribution from T12 in some patients.13 It follows a curvilinear course along the ilium until it perforates the transversus abdominis muscle to lie between it and the external oblique muscle. The anterior branch goes on to provide cutaneous sensory innervation to the abdominal skin above the pubis. The nerve may interconnect with the ilioinguinal nerve along its course, and this feature results in the variable sensory distribution of these nerves. The ilioinguinal nerve is a branch of the L1 nerve root, with a contribution from T12 in some patients.14 It follows a curvilinear course along the ilium, until it perforates the transversus abdominis muscle at the level of the anterior 793
794
Section IV—Regional Pain Syndromes
AUTONOMIC
SOMATIC
Superior spermatic nerves Renal and intermesenteric plexus Iliohypogastric n.
Ilioinguinal n.
Genitofemoral n. Middle spermatic nerves Superior hypogastric plexus
Genital br.
S2 S3 S4
Inferior spermatic nerves Pelvic plexus (inferior hypogastric plexus)
Femoral br.
Pudendal n.
Fig. 101.1 Innervation of the testis.
superior iliac spine. In general, this nerve supplies sensory innervation to the upper portion of the skin of the inner thigh, the root of the penis, and the upper scrotum. The genitofemoral nerve arises from fibers of the L1 and L2 nerve roots.15 This nerve passes through the psoas muscle, where it divides into a genital and a femoral branch. The femoral branch passes beneath the inguinal ligament along with the femoral artery and provides sensory innervation to a small area of skin on the inside of the thigh. The genital branch passes through the inguinal canal and travels with the spermatic cord to provide innervation to the cremaster muscle, as well as the parietal and visceral tunica vaginalis. The S2-4 nerve roots provide innervation to the posterior and inferior scrotum through the pudendal nerve.16 Damage to the testes or epididymis or to the nerve supply of these structures results in orchialgia. In addition, lesions affecting somatic structures in the same segmental nerve supply as the testes, namely, L1 and L2, may refer pain to this area. As in other neuropathic pain syndromes, sympathetically
maintained and mediated pain may occur after injury to these structures. Thus, patients who do not respond to inguinal denervation or subcutaneous blockade may respond to application of local anesthetics to the pelvic plexus.17
Differential Diagnosis Orchialgia may result from a host of processes that have nothing to do with intrascrotal disease (Table 101.1).3 Somatic structures in the same segmental nerve supply as the testis (L1, L2) may refer pain to this area. Radiculitis is the most likely cause of referred orchialgia.18 Degenerative lesions of the lower thoracic and upper lumbar spine refer an “aching” pain to the groin and testis.19 Nephrolithiasis masquerades as orchialgia when a midureteric stone is present. This occurs by two mechanisms. First, the ureteric autonomic afferents arising from the same somatic segment at L1 and L2 cross over to the testis afferents in the autonomic ganglia. Second, the
Chapter 101—Orchialgia
795
Table 101.1 Differential Diagnosis of Orchialgia
Table 101.2 Diagnostic Workup for Orchialgia
Referred Pain
Past medical history: nephrolithiasis, low back pain, hernia
Radiculitis
Past surgical history: herniorrhaphy, scrotal surgery
Nephrolithiasis
Laboratory Tests
Ilioinguinal, genitofemoral neuralgia
Complete blood cell count with differential
Inguinal hernia
Urinalysis with culture and sensitivity
Tendinitis of the inguinal ligament
Other Tests
Abdominal aortic aneurysm
Testicular ultrasonography
Appendicitis
Color flow Doppler imaging
Epilepsy
Radionuclide scans
Causative Factors
Magnetic resonance imaging of testes or low back
Testicular torsion
Electromyography
History and Physical Examination
Torsion of the testicular appendage Infection: scrotitis, epididymitis Trauma Surgery (herniorrhaphy, vasectomy) Inguinal hernia Tumor Vasculitis, Henoch-Schönlein purpura Idiopathic scrotal edema “Blue balls” (sexual frustration) Self-palpation orchitis Hydrocele Varicocele Spermatocele
genitofemoral nerve lying in contact with the ureter at the L4 vertebral level can become irritated and refer pain along its distribution.20 Ilioinguinal neuralgia and genitofemoral neuralgia not uncommonly follow inguinal herniorrhaphy.21 These complications are usually caused by the entrapment of neural tissue by suture placement, surgical clips, fibrous adhesions, or a cicatricial neuroma.18 A small indirect inguinal hernia may irritate the genital branch of the genitofemoral nerve.19 Tendinitis at the insertion of the inguinal ligament into the pubic tubercle may cause testicular pain,4 as can pelvic floor dysfunction.22 Even acute abdominal aortic aneurysm rupture or leakage may produce testicular pain,23 as may aneurysm of the common iliac artery.24 Causative factors for orchialgia include torsion, ischemia, infection, trauma, tumor, inguinal hernia, hydrocele, spermatocele, varicocele, vasculitis, polyarteritis nodosa,25 edema, and previous surgery (e.g., herniorrhaphy, vasectomy, or other scrotal procedures).26,27 In the acute setting, and especially in the pediatric population, acute testicular pain should be considered testicular torsion until proven otherwise.28 The prognosis of testicular torsion is poor; up to 55% of affected boys will lose a testis, even with immediate surgical exploration.29 Typically, this poor outcome is the result of the slow response of the patient or the patient's parents to present to a physician. Torsion of the testicular appendage may also occur and is sometimes associated
with the “blue dot” sign, which is a blue discoloration beneath the skin of the scrotum.30 Intermittent torsion may manifest with recurrent severe pain. These patients usually have a “bellclapper” deformity that puts them at risk for torsion.31 Any man with a history of recurrent pain and a horizontal testicular lie, even in the absence of pain at the time of physical examination, should have exploration and bilateral testicular fixation.32 Autoimmune testicular vasculitis, with involvement of medium-sized arteries, may manifest in the absence of any systemic symptoms.33 Acute scrotitis, which is usually bacterial, may also cause acute orchialgia and should especially be considered in the diabetic patient or otherwise immunocompromised patient. When bacterial infection becomes fulminant, gangrene can set in (Fournier's gangrene).27 Epididymitis or orchitis often occurs secondary to chlamydial or Ureaplasma infection.26 Trauma is a leading cause of acute testicular pain and may lead to hematocele, ruptured testes, or sperm granuloma.34,35 Self-palpation orchitis, caused by frequent squeezing of the testis by a neurotic man overly concerned about developing testis cancer, may manifest as orchialgia.36 Malignant disease may manifest as persistent scrotal pain. If malignant disease is suspected, this possibility should be investigated with magnetic resonance imaging (MRI) or scrotal ultrasonography.37 Hydrocele, spermatocele, and varicocele are amenable to surgical management, which may be highly effective.38 However, these lesions may be incidental findings, and surgical intervention may exacerbate the pain.39 Indeed, surgery is often the cause of orchialgia.4 During herniorrhaphy, if the vascular supply is compromised, acute ischemic orchitis and testicular atrophy may follow.40 Vasectomy with distention of the epididymis is commonly associated with orchialgia.41,42 However, the cause of orchialgia may never be identified. Up to 25% of patients with chronic orchialgia have no obvious cause of the pain.4 A strong clinical depressive abnormality is often evident on psychological tests.43
Diagnosis A complete history and physical examination performed with careful attention to the scrotal region comprise the cornerstone of proper evaluation (Table 101.2).44 The history should
796
Section IV—Regional Pain Syndromes
include the typical questions regarding onset, duration, exacerbating and alleviating factors, associated symptoms, and so on, but it should also include a sexual history with questions about sexual dysfunction, sexually transmitted disease risk factors, and history of sexual abuse.3 The past medical history is vital and often suggests a potential cause, such as a history of nephrolithiasis, lumbar disk disease, or hernia. The past surgical history may reveal prior inguinal surgery, such as herniorrhaphy, or other urologic procedures. The patient's complaint is usually of a squeezing, deep ache in the testis, often bilateral or alternating from one side to the other, that is intermittent and commonly associated with low back pain.43 Sometimes the patient reports that it feels as though the testis is pinched in the underwear but that trouser readjustment does not help. The onset of pain is commonly related to particular activities (e.g., long automobile journeys or unsupported seating posture).43 Occasionally, a physical examination may reveal an obvious source of pain, but usually the patient has no abnormality on physical examination. A thorough physical examination should be done to help rule out causes of radicular pain. Palpation of the testes while the patient is standing should be performed as part of the routine examination. Palpation may reveal a varicocele that classically resembles a “bag of worms.” These patients may benefit from semen analysis, because as many as 40% of patients seen in infertility clinics have an associated varicocele.3 A hydrocele may be diagnosed by transillumination of the testes. Simple laboratory tests include a complete blood cell count with differential, urinalysis, and cultures. If pyuria or hematuria is detected, these conditions are investigated in the same way as they would be in the absence of pain. If results of these laboratory studies are normal, a good next step would be scrotal ultrasound. An obvious abnormality would prompt surgical consultation and intervention. If a tumor is suspected, tumor markers, such fetoprotein, human chorionic gonadotropin, and lactate dehydrogenase, should be obtained. Other potentially useful tests are color flow Doppler imaging, radionuclide (technetium-99m pertechnetate) scans, MRI, and needle aspiration.45–49 Electromyography may be useful to distinguish ilioinguinal nerve entrapment from lumbar plexopathy, lumbar radiculopathy, and diabetic polyneuropathy.50 MRI of the thoracic and lumbar spines should be considered if radiculitis is suspected.
Conservative Management Initial relief may be obtained by implementation of modified exertional and postural habits, use of a scrotal suspension sling or jock strap, heat and cold therapy, and a trial of anti-inflammatory agents and oral antibiotics (Fig. 101.2). A minimum 1-month trial of at least two nonsteroidal antiinflammatory agents is recommended.4 Even in the presence of normal laboratory findings, a course of oral antibiotics (either from the tetracycline or the quinolone group) is indicated to treat possible chlamydial or Ureaplasma infection.26 If this management regimen fails, a multidisciplinary approach, as used in other chronic pain syndromes, is best.39 This may include the addition of a low-dose antidepressant, such as doxepin or amitriptyline of the tricyclic antidepressant class. It is important to start with a low dose at bedtime and to titrate the dose to the patient's response. This approach helps to decrease the side effects of sedation and disorientation,
MANAGEMENT OF ORCHIALGIA Behavioral modification Scrotal support sling Ice and heat therapy NSAIDs Oral antibiotics (tetracycline/quinolones)
Transcutaneous Electrical nerve stimulation Spermatic cord block Ilioinguinal/genitofemoral blocks Tricyclic antidepressants Anti-epileptic drugs Opiates Acupuncture Neuropsychology
Repeat spermatic cord block Transrectal ultrasound-guided pelvic plexus block Superior hypogastric plexus T10-L1 sympathetic chain block Pulsed radiofrequency
Neuromodulation Microscopic testicular denervation Epididymectomy Inguinal orchiectomy Fig. 101.2 Algorithm for the management of orchialgia. NSAIDs, nonsteroidal anti-inflammatory drugs.
factors that cause many patients to stop taking the medication before any therapeutic effect is achieved. Long-term opiate therapy may also be indicated. Antiepileptic drugs, such as gabapentin, may be beneficial.51,52 Transcutaneous electrical nerve stimulation (TENS) has been useful in many patients with chronic scrotal pain. A trial of TENS for 1 to 3 months is safe and may be beneficial.39 Biofeedback, acupuncture, and psychotherapy are other adjunctive therapies. Should pain continue, consultation should be sought with an interventional pain specialist for a selective nerve block. Access to a pain management clinic is a strong asset. A spermatic cord block can be tried by using a mixture of epinephrine-free local anesthetic and corticosteroid. Patients who obtain temporary pain relief may be considered for repeated spermatic cord blocks.4 Patients with ilioinguinal or genitofemoral neuralgia may be treated with similar blocks to these nerves. Pulsed radiofrequency has been used successfully for chronic groin pain or orchialgia originating from these nerves.53 For patients unresponsive to spermatic cord blockade, local anesthetic and corticosteroid applied to the pelvic plexus may be beneficial.17,54 The pelvic plexus lies anterior to the rectum at the prostatovesical junction. These periprostatic nerves are localized under transrectal ultrasound guidance. The location of these nerves may explain the association of testicular pain with prostatic inflammation or postsurgical status. As shown by the success of this block, the
pelvic plexus may provide the predominant sympathetic and parasympathetic efferent input to the testis. Alternatively, the superior hypogastric plexus may be blocked. In the case of testicular cancer, neurolysis of this plexus using 8 to 10 mL of 10% aqueous phenol or 50% alcohol may produce longlasting pain relief.55 A lumbar sympathetic chain block at the T10-L1 level is a third approach. Occasionally, tendinitis caused by insertion of the inguinal ligament into the pubic tubercle may masquerade as testicular pain. This condition usually responds well to injection of the tubercle and ligament with a mixture of local anesthetics and corticosteroid.1
Surgical Treatment Surgical treatment may ultimately be necessary if medical management proves unsuccessful. Orchidectomy, with the inguinal approach favored over the scrotal approach, is usually a last resort. The response to this procedure is unpredictable, and the impact on the male psyche may be profound. Consequently, other testissparing procedures have been advocated. Neuromodulation, such as spinal cord stimulation, has proven effective in treating groin and testicular pain. This approach may be indicated in select patients. Many urologists prefer epididymectomy as the initial surgical treatment, especially when the pain seems to be localized to the epididymis.4 Alternatively, microscopic testicular denervation or laparoscopic testicular denervation may offer
Chapter 101—Orchialgia
797
patients a significant reduction in pain with a technique that is minimally invasive and causes minimal morbidity.56–60 In these procedures, the spermatic plexus and adventitia are stripped away from the vas deferens and vessels and are divided, or the vessels with nerves themselves are simply divided. Spermatic cord block should be performed before these procedures and is a prognostic indicator of surgical success.
Conclusion Chronic orchialgia is a difficult problem to manage. The clinician should be aware of the unique relationship of the genitalia and the male psyche. Behavioral and psychological issues should be addressed concurrently with medical therapy. Despite the often unclear cause of orchialgia, the possibility of testicular cancer remains ever present and should be carefully sought in all patients suffering from orchialgia. The ultimate goal of therapy is the patient's return to gainful activity, with minimal loss of function and sparing of the testes. Improved interventional techniques, such as transrectal ultrasound–guided pelvic plexus blockade and microsurgical denervation of the spermatic cord, are helping in achieving this goal.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
102
Vulvodynia Lowell W. Reynolds and Brett T. Quave
CHAPTER OUTLINE Historical Considerations 798 Clinically Relevant Anatomy 798 Clinical Presentation 798 Diagnosis 798 Treatment 799
Pharmacology 799 Injections 799 Psychology 800 Surgery 800
Conclusion 800
Education 799
Historical Considerations Vulvodynia is a complex syndrome of vulvar pain, sexual dysfunction, and psychological distress. Multiple attempts have been made to categorize varying types of vulvodynia. Some of these classifications include primary vulvodynia, secondary vulvodynia, vulvar pain syndrome, essential vulvodynia, vulval vestibulitis, dysesthetic vulvodynia, and cyclic vulvitis.
Clinically Relevant Anatomy When addressing a patient with vulvodynia, the clinician must remember to educate the patient. This includes using the appropriate anatomic vocabulary with the patient and even giving her an illustration of relevant anatomy to take home and study (Fig. 102.1). Not only does this approach improve the physician's ability to outline a treatment plan with the patient, but it also allows the patient to communicate more comfortably with the physician. Having said this, the vulva consists of the mons pubis, the labia majora, the labia minora, the vestibule of the vagina, the clitoris, the bulb of the vestibule, and the greater vestibular glands.1 The ilioinguinal and genitofemoral nerves supply the mons pubis, labia majora, and labia minora.1,2 Any of these structures may be involved in a chronic pain condition. However, the vestibule, vestibular glands, and labia are frequently involved in vulvodynia.
Clinical Presentation As noted earlier, this painful condition has many differing terms. Vulvodynia is either primary (or essential) or secondary. Primary or essential vulvodynia is idiopathic. Secondary vulvodynia results from an infection or other known cause. Regardless of the primary or secondary classification, vulvodynia typically is described as a burning or aching sensation that is painful to the touch.3 Patients frequently scratch and wash the affected area, thus leading to excoriations and extensive drying. 798
Vulvar vestibulitis is a painful condition that occurs when something is inserted into the opening of the vagina. This may occur with insertion of a tampon or during sexual activity. Dysesthetic vulvodynia is a painful condition that persists even in the absence of touch or pressure. These burning and aching sensations can be constant, or they can be caused by light, normally nonpainful touch. These findings are similar to complex regional pain syndrome, which is known for such conditions as allodynia and hyperalgesia.4 Pain that occurs with contact seems to lessen with age, but the overall prevalence of vulvodynia remains fairly consistent at approximately 16% of the female population regardless of age. Hispanic women tend to have an 80% higher likelihood of having chronic vulvar pain than do African American or white women.5 Some women experience worsening symptoms before menses or after sexual intercourse, a disorder referred to as cyclic vulvitis. This condition may have an infectious origin, or it may simply reflect an increased sensitivity to hormone replacement therapy. These patients may be completely pain free at other times of the month. Depression frequently is found in conjunction with vulvodynia but is rarely the cause. The opposite, in fact, is true. Usually, the chronic pain of vulvodynia leads to depression. This depression may manifest as depressed mood and loss of interest in work, recreation, and sexual activity. Sleep disturbances are also common with depression and lead to further reduced function and worsening pain.6
Diagnosis A thorough history and physical examination are essential in making a diagnosis of vulvodynia (Table 102.1). Various sensory and pain testing modalities can be used to make the diagnosis and to assess for severity.7,8 Biopsy results consistently reveal a low-grade chronic inflammatory process that is not pathognomonic. Histologic studies may illustrate neural hyperplasia. Infection should be excluded as the cause of vulvodynia. This is frequently difficult, especially if a fungus is the © 2011 Elsevier Inc. All rights reserved.
Chapter 102—Vulvodynia Mons pubis
799
Clitoris
Labium minus
Urethra
Labium majus
Vestibule of vagina
Vaginal orifice
Greater vestibular glands Anus
Fig. 102.1 Female external genitalia.
Table 102.1 Diagnosis of Vulvodynia History: illnesses, hygiene, pain, depression Physical examination: vulva, vagina, pelvis Biopsy lesions Microscopic examination Culture
infective agent. Two of the more common causes of secondary vulvodynia are Candida albicans and group B Streptococcus. Cultures can be performed to help make this diagnosis. Once infections have been ruled out or treated, neuropathic vulvodynia can be addressed.4,9
Treatment Education Educating the patient about her condition is imperative. This education may involve discussing the condition with the patient, giving her handouts, and referring her to support groups. Avoiding harmful habits, such as scratching and overcleansing the vulva, should be stressed. Most importantly, ways to maintain a normal sex life, exercise regimen, and work routine should also be discussed.10,11
Pharmacology Agents to fight C. albicans or other types of infections should be administered if vulvodynia secondary to infection is suspected. The avoidance of estrogen and progesterone used in hormone replacement therapies should be considered because these agents have been implicated in vulvodynia. Other irritants should also be avoided, such as abrasive wash cloths and irritating cleansers. If these agents are thought to be the cause, they should be removed from the patient's daily regimen. Topical lidocaine,
benzocaine, doxepin, amitriptyline, baclofen, capsaicin, atropine, or nitroglycerin cream may be applied at bedtime.12 Amitriptyline and other antidepressants should be used as first-line therapy for primary vulvodynia. Typically, this approach involves slowly escalating the dose until the patient achieves pain relief or must stop because of side effects of the medication. The dose of amitriptyline may be as high as 300 mg at bedtime. Night-time dosing is preferred because amitriptyline can be very sedating. Thus, this drug not only serves as a simple analgesic but also may improve the sleep pattern of the patient. This improvement in the sleep-wake cycle may be one reason that vulvodynia sufferers, like other patients with chronic pain, respond well to tricyclic antidepressants. Other tricyclic antidepressants have also been used successfully to treat vulvodynia, but selective serotonin reuptake inhibitors generally do not seem to offer the same analgesic qualities. However, all antidepressants may reduce the depressive component of the patient's suffering.12,13 Antiepileptic medications have been used for years to treat various neuropathic pain syndromes. For instance, medications such as phenytoin, carbamazepine, and valproic acid have all been used with varying success and side effects. Some newer medications arguably work equally well and have fewer side effects. Gabapentin has been used successfully in treating postherpetic neuralgia, complex regional pain syndrome, and vulvodynia. Like most antiseizure medications, gabapentin is slowly titrated upward to find a balance of the lowest effective dose for the patient and the fewest side effects. Frequently, the dose of gabapentin may be as high as 1200 mg three times a day. Common side effects include dizziness, nausea, and sedation.14 Other antiepileptic medications such as topiramate, oxcarbazepine, lamotrigine, and pregabalin may also be effective in cases of vulvodynia caused by a neuropathic process.12,15,16
Injections The ilioinguinal and genitofemoral nerves supply the external genitalia. In the setting of vulvodynia, blocking these nerves may prove diagnostic or even therapeutic. For pain of the mons pubis
800
Section IV—Regional Pain Syndromes Umbilicus
Umbilicus
Ant. sup. iliac spine
Pubic bone
Fig. 102.2 Anterior view shows important anatomic landmarks for ilioinguinal iliohypogastric-genitofemoral nerve blocks. ASIS, anterior superior iliac spine.
or labium majora, the ilioinguinal nerve can be blocked with the patient lying supine. A mark is made on the skin 2 cm medial and 2 cm cephalad to the anterior superior iliac spine. After the skin is sterilely prepared, a 1.5-inch 25-gauge needle connected to a syringe is advanced perpendicular to the skin. When the tip of the needle reaches the fascia of the external oblique muscle, 2.5 mL of 0.25% bupivacaine and 20 to 40 mg of methylprednisolone are injected. An equal amount of solution is then injected in a fanlike manner in the surrounding area2 (Figs. 102.2 and 102.3). Blocking the genital branch of the genitofemoral nerve may reduce pain of the labia majora and labia minora. This procedure is done by placing the patient in a supine position. The pubic tubercle is then palpated. After sterile preparation, a 1.5inch, 25-gauge needle is advanced perpendicular to the skin, just lateral to the pubic tubercle below the inguinal ligament. Infiltration of 5 mL of 0.25% bupivacaine and 20 to 40 mg of methylprednisolone is used for the nerve block2 (Fig. 102.4). Other procedures may prove effective and should be considered in treating vulvodynia. Two of these include hypogastric plexus blockade and spinal cord stimulation.17,18 A discussion of these procedures is beyond the scope of this chapter.
Psychology Depression and anxiety are very common in patients suffering from vulvodynia. These patients should have their psychological issues addressed while they are receiving ongoing treatment for the primary physiologic disease.19 A referral to a psychologist or psychiatrist should be made early in the diagnosis and treatment phase. These referrals should not be made only when an organic cause for a patient's illness is excluded. This either-or mentality should be avoided, so as not to give the patient the impression that she is being written off as a “mental case.” Patients should be informed about the power of a cognitive-behavioral approach to chronic pain. Through biofeedback, visual imagery, and other powerful psychological tools, the patient can be expected to improve her pain management and coping skills.12,20 Medications prescribed by the psychiatrist not only may lessen depression and anxiety, but also, as mentioned earlier, may directly reduce pain as adjuvant analgesics.
Ant. sup. iliac spine Fig. 102.3 Technique of ilioinguinal-iliohypogastric nerve block.
Umbilicus
Pubic bone Fig. 102.4 Technique of genitofemoral nerve block (genital branch).
Surgery Various surgical approaches have been employed after nonoperative treatments have failed. Pudendal nerve decompression has been shown to be very effective for suspected pudendal canal syndrome, as supported by temporary pain relief after pudendal nerve block.21 Procedures involving resection of the hymen and vestibule with mobilization of the lower vagina to cover the resulting defect have been helpful in cases of intractable vulvar vestibulitis.22
Conclusion Understanding and treating vulvodynia are only the first steps in reducing the patient's pain. A return to a normal, active lifestyle and a reduction in depression and anxiety should also be treatment goals. These objectives can be met most easily by using a stepwise approach to diagnosis, treatment, and adjunctive psychological therapy.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
103
IV
Coccydynia Steven D. Waldman
CHAPTER OUTLINE Clinical Presentation 801 Diagnosis 801 Differential Diagnosis 801
Coccydynia is a common pain syndrome characterized by pain localized to the tailbone that radiates into the lower sacrum and perineum.1,2 It affects female patients more frequently than male patients. Coccydynia occurs most commonly after direct trauma to the coccyx from a kick or a fall directly onto the coccyx (Fig. 103.1). It can also occur after difficult vaginal delivery.2,3 The pain of coccydynia is thought to result from strain of the sacrococcygeal ligament or occasionally from fracture of the coccyx.2,3,4 Less commonly, arthritis of the sacrococcygeal joint can result in coccydynia, as can tumors affecting the coccyx and adjacent soft tissue.3,5
Clinical Presentation On physical examination, the patient exhibits point tenderness over the coccyx; the pain increases during movement of the coccyx.1,2,3 Movement of the coccyx may also cause sharp paresthesias into the rectum, which can be quite distressing to the patient. On rectal examination, the levator ani, piriformis, and coccygeus muscles may feel indurated, and palpation of these muscles may induce severe spasm.2 Sitting may exacerbate the pain of coccydynia, and the patient may attempt to sit on one buttock to avoid pressure on the coccyx (Fig. 103.2).
Diagnosis Plain radiographs are indicated in all patients who present with pain thought to be emanating from the coccyx, to rule out occult bony disease and tumor.5 Based on the patient's clinical presentation, additional testing including complete blood cell count, prostate-specific antigen, sedimentation rate, and antinuclear antibody testing may be indicated. Magnetic resonance imaging of the pelvis is indicated if an occult mass or tumor is suggested (Fig. 103.3). Radionuclide bone scanning may be useful to rule out stress fractures not seen on plain radiographs. The injection technique presented later serves as both a diagnostic test and a therapeutic maneuver.
© 2011 Elsevier Inc. All rights reserved.
Treatment 801 Conclusion 803
Differential Diagnosis Primary disease of the rectum and anus may occasionally be confused with the pain of coccydynia. Primary tumors or metastatic lesions of the sacrum or coccyx may also manifest as coccydynia.3,5 Proctalgia fugax may mimic the pain of coccydynia, but in proctalgia fugax, movement of the coccyx does not reproduce the pain.6 Insufficiency fractures of the pelvis and sacrum may, on occasion, also mimic coccydynia, as can disorders of the sacroiliac joints.
Treatment A short course of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory agents or cyclooxygenase-2 inhibitors, and use of a foam donut to prevent further irritation to the sacrococcygeal ligament is a reasonable first step in the treatment of patients suffering from coccydynia. If the patient does not experience rapid improvement, the following injection technique is a reasonable next step.7 To treat the pain of coccydynia, the patient is placed in the prone position. The legs and heels are abducted to prevent tightening of the gluteal muscles, which can make identification of the sacrococcygeal joint more difficult. Preparation of a wide area of skin with antiseptic solution is then carried out so that all the landmarks can be palpated aseptically. A fenestrated sterile drape is placed to avoid contamination of the palpating finger. The middle finger of the operator's nondominant hand is placed over the sterile drape into the natal cleft with the fingertip palpating the sacrococcygeal joint at the base of the sacrum. After the sacrococcygeal joint is located, a 1.5-inch, 25-gauge needle is inserted through the skin at a 45-degree angle into the region of the sacrococcygeal joint and ligament (Fig. 103.4). If the sacrococcygeal ligament is penetrated, a “pop” will be felt, and the needle should be withdrawn back through the ligament. If contact with the bony wall of the sacrum occurs, the needle should be withdrawn slightly. This maneuver
801
802
Section IV—Regional Pain Syndromes
A
B Fig. 103.1 Radiographic (A) and magnetic resonance imaging (MRI) (B) views of anterior luxation of the coccyx with accompanying L4-5 disk bulging (bulging is seen in the sagittal plane on MRI). (From Cebesoy O, Guclu B, Kose KC, et al: Coccygectomy for coccygodynia: do we really have to wait? Injury 38:1183, 2007.)
Fig. 103.2 The pain of coccydynia is localized to the coccyx and is made worse by sitting. (From Waldman SD: Atlas of common pain syndromes, Philadelphia, 2002, Saunders, p 227.)
A
B
Fig. 103.3 Chordoma: magnetic resonance imaging (MRI) abnor malities. Sagittal T1-weighted (TR/TE, 470/10) spin-echo (A) and T2-weighted (TR/TE, 5000/136) fast spin-echo (B) MRI scans document a sacrococcygeal tumor with a large soft tissue mass. (Courtesy of Y. Kakitsubata, MD, Miyazaki, Japan; in Resnick D: Tumors and tumor like lesions of bone: imaging and pathology of specific lesions. In Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 4017.)
Fig. 103.4 Injection technique for relieving pain in coccydynia. (From Waldman SD: Coccydynia syndrome. In Atlas of pain management injection techniques, Philadelphia, 2000, Saunders, p 244.)
Chapter 103—Coccydynia
Sympathetic trunks
803
Lumbar ganglia
Sacral splanchnic n.
Sacral ganglia Ganglion impar
A
Fig. 103.5 Anatomic location of the ganglion impar. A, Ganglion impar represents the termination of the paravertebral sympathetic chains, converging at the sacrococcygeal level. B, Sagittal, T2-weighted magnetic resonance imaging shows the ganglion impar as a small, isointense signal structure anterior to the sacrococcygeal level (white arrow). C, Contrast medium outlines the ganglion impar, seen as a filling defect (black arrow) in the pool of contrast. (From Datir DC:
B
CT-guided injection for ganglion impar blockade: a radiological approach to the management of coccydynia, Clin Radiol 65: 21A, 2010.)
C
disengages the needle tip from the periosteum. When the needle is satisfactorily positioned, a syringe containing 5 mL of 1.0% preservative-free lidocaine and 40 mg of methylprednisolone is attached to the needle. Gentle aspiration is carried out to identify cerebrospinal fluid or blood. If the aspiration test result is negative, the contents of the syringe are slowly injected. Resistance to injection should be minimal. Any significant pain or sudden increase in resistance during injection suggests incorrect needle placement, and the clinician should stop injecting immediately and reassess the position of the needle. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. Occasionally, a ganglion impar block (Fig.103.5) may be used in patients who fail to respond to the foregoing
injection technique.8 In rare patients, surgical coccygectomy may be required to provide long-lasting pain relief.9
Conclusion Coccydynia should be considered a diagnosis of exclusion in the absence of trauma to the coccyx and its ligaments. Failure to diagnose an underlying tumor can have disastrous consequences. As with all pelvic pain syndromes, careful evaluation of behavioral abnormalities that may be contributing to the patient's pain and functional disability should be considered.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
104
Proctalgia Fugax Steven D. Waldman and Jennifer E. Waldman
CHAPTER OUTLINE Clinical Presentation 804 Diagnosis 804
Proctalgia fugax is a nonmalignant pain syndrome of unknown origin that is characterized by paroxysms of rectal pain with pain-free periods between attacks.1 The pain-free periods between attacks can last seconds to minutes.2 As in cluster headache, spontaneous remissions of the disease occur and may last from weeks to years. The pain of proctalgia fugax is localized to the anus and lower rectum.3 Studies attempting to elucidate the pathologic mechanism responsible for the pain of proctalgia fugax implicated spasm of the levator ani muscles, anal sphincter, and sigmoid colon. Proctalgia fugax is more common in female patients, as well as in patients suffering from irritable bowel syndrome. The symptoms of proctalgia fugax are not typically present before puberty. The pain of proctalgia fugax is sharp or gripping and is severe. As in other urogenital focal pain syndromes such as vulvodynia and prostadynia, the causes remain obscure.1–3 Stressful life events often increase the frequency and intensity of attacks of proctalgia fugax, as does sitting for prolonged periods. However, a specific factor or activity does not typically trigger the exact onset of pain. Patients often feel an urge to defecate with the onset of the paroxysms of pain (Fig. 104.1). Depression frequently accompanies the pain of proctalgia fugax but is not thought to be the primary cause. The symptoms of proctalgia fugax can be severe enough to limit the patient's ability to carry out activities of daily living.
Clinical Presentation Results of the physical examination of the patient suffering from proctalgia fugax are usually normal. The patient may be depressed or may appear anxious. Patients suffering from proctalgia fugax often exhibit perfectionistic, neurotic, and hypochondrial personality traits. Results of rectal examination are normal, although deep palpation of the surrounding musculature may trigger paroxysms of pain. Patients suffering from proctalgia fugax often report that they can abort the attack of pain by placing a finger in the rectum. Rectal suppositories may also interrupt the attacks. 804
Differential Diagnosis 804 Treatment 804
Diagnosis As with the physical examination, results of diagnostic tests in patients suffering from proctalgia fugax are usually within normal limits. Because of the risk of overlooking rectal malignant disease that may be responsible for pain that could be attributed to a benign cause, by necessity proctalgia fugax must be a diagnosis of exclusion4,5 (Fig. 104.2). Rectal examination is mandatory in all patients thought to be suffering from proctalgia fugax. Sigmoidoscopy or colonoscopy is also strongly recommended in such patients. Hereditary forms of proctalgia fugax have been described and are associated with hypertrophy and hypertonia of the internal anal sphincter.6 Testing of the stool for occult blood is also indicated. Screening laboratory tests consisting of a complete blood cell count, automated blood chemistry studies, and erythrocyte sedimentation rate should also be performed. Magnetic resonance imaging or computed tomography of the pelvis should also be considered if the diagnosis is in doubt. If psychological problems are suspected, or if the patient has a history of sexual abuse, psychiatric evaluation should be included with laboratory and radiographic testing.3
Differential Diagnosis As mentioned earlier, because of the risk of overlooking serious disease of the anus and rectum, proctalgia fugax must be a diagnosis of exclusion. First and foremost, the clinician must rule out rectal cancer, to avoid disaster. Proctitis can mimic the pain of proctalgia fugax and can be diagnosed on sigmoidoscopy or colonoscopy. Hemorrhoids usually manifest with bleeding associated with pain and can be distinguished from proctalgia fugax on physical examination. Prostadynia may sometimes be confused with proctalgia fugax, but the pain is more constant and is duller and aching.
Treatment Several simple methods have proven effective for aborting the pain after the onset of a proctalgia fugax attack. For many patients, ingesting food or drink at the immediate onset of the © 2011 Elsevier Inc. All rights reserved.
Chapter 104—Proctalgia Fugax
805
Rectum
Anal canal
Fig. 104.1 The onset of pain of proctalgia fugax often causes the patient to feel an urge to defecate. (From Waldman SD: Atlas of common pain syndromes, Philadelphia, 2002, Saunders, p 177.)
attack helps to stop the pain.7 In addition, dilatation of the rectum either digitally or by inserting an enema or rectal suppository also aborts the pain. Patients may also find relief by attempting a bowel movement or by applying direct pressure to the perineum. Initial treatment of proctalgia fugax should include a combination of simple analgesics and nonsteroidal antiinflammatory agents or cyclooxygenase-2 inhibitors. If these medications do not adequately control the patient's symptoms, a tricyclic antidepressant or gabapentin should be added. Traditionally, the tricyclic antidepressants have been a mainstay in the palliation of pain secondary to proctalgia fugax. Controlled studies have demonstrated the efficacy of amitriptyline for this indication. Other tricyclic antidepressants including nortriptyline and desipramine have also shown to be clinically useful. Unfortunately, this class of drugs is associated with significant anticholinergic side effects, including dry mouth, constipation, sedation, and urinary retention. These drugs should be used with caution in patients suffering from glaucoma, cardiac arrhythmia, and prostatism. To minimize side effects and to encourage compliance, the primary care physician should start amitriptyline or nortriptyline at a 10-mg dose at bedtime. The dose can be then titrated upward to 25 mg at bedtime as side effects allow. Upward titration of dosage in 25-mg increments can be carried out each week as side effects allow. Even at lower doses, patients generally report
rapid improvement in sleep disturbance and begin to experience some pain relief in 10 to 14 days. The selective serotonin reuptake inhibitors such as fluoxetine have also been used to treat the pain of diabetic neuropathy. Although the selective serotonin reuptake inhibitors are better tolerated than the tricyclic antidepressants, they appear to be less efficacious for treatment of proctalgia fugax. If the patient does not experience any improvement in pain as the dose is increased, the addition of gabapentin alone or in combination with pudendal nerve blocks using local anesthetics or corticosteroid is recommended. If the antidepressant compounds are ineffective or are contraindicated, gabapentin represents a reasonable alternative. Gabapentin should be started with a 300-mg dose at bedtime for 2 nights. The patient should be cautioned about potential side effects, including dizziness, sedation, confusion, and rash. The drug is then increased in 300-mg increments, given in equally divided doses over 2 days, as side effects allow, until pain relief is obtained or a total dose of 2400 mg daily is reached. At this point, if the patient has experienced partial relief of pain, blood values are measured, and the drug dose is carefully titrated upward using 100-mg tablets. Rarely is a dose larger than 3600 mg daily required. The local application of heat and cold may be beneficial to provide symptomatic relief of the pain of proctalgia fugax. The use of bland rectal suppositories may also help to relieve symptoms. For patients who do not respond to these treatment
806
Section IV—Regional Pain Syndromes
A
B
Fig. 104.2 A, This 19-year-old man with a 2-month history of lower abdominal pain and a 10-kg weight loss during the past year presented with difficulty in passing stool and blood in his stool for 2 days. Computed tomography of abdomen and pelvis, with and without contrast medium, showed a nonenhancing mass in the rectum, compatible with fecal impaction. B, A colonoscopy revealed a large, intraluminal, polypoid hard mass starting about 5 cm above the anal verge and extending upward about 12 cm. C, A biopsy taken of the mass showed a neoplastic rectal tumor. Histopathologic examination revealed infiltrative sheets of bizarre cells ulcerating the rectal mucosa. The tumor cells had epithelioid, oval, and spindled shapes, with pleomorphic nuclei, clumped chromatin, prominent nucleoli, and abnormal mitotic figures, admixed with a moderate inflammatory component (hematoxylin-eosin stain, original magnification ×400).
modalities, injection of the peroneal nerves or caudal epidural nerve block using local anesthetic and corticosteroid may be a reasonable next step.7 The clinician should be aware that anecdotal reports have noted that the calcium channel blockers, topical nitroglycerin, and inhalation of albuterol will provide symptomatic relief of the pain of proctalgia fugax. The major problem in the care of patients thought to suffer from proctalgia fugax is the failure to identify potentially serious disease of the anus or rectum related to primary tumor or invasion of these structures by pelvic tumor.3,7 Although uncommon, occult rectal infection remains a possibility, especially in the immunocompromised patient with cancer (see Fig. 104.2). Early detection of infection is crucial to avoid potentially life-threatening sequelae. Given the psychological
C
implications of pain involving the genitalia and rectum, the clinician should not overlook the possibility of psychological abnormality in patients with pain in the rectum. Both behavior modification and biofeedback can be used to treat proctalgia fugax related to a psychological abnormality. In patients whose symptoms occur infrequently, prevention of the attacks is difficult, if not impossible. For such patients, an understanding of the condition and reassurance by the physician can be very important.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
105
Gluteal and Ischiogluteal Bursitis Steven D. Waldman
CHAPTER OUTLINE Gluteal Bursitis 808 Clinical Presentation 808 Differential Diagnosis 808 Diagnosis 809 Treatment 809
Ischiogluteal Bursitis 810 Clinical Presentation 810 Diagnosis 811 Differential Diagnosis 811 Treatment 811
Conclusion 811
Gluteal bursitis and ischiogluteal bursitis are among the myriad causes of buttock pain that are frequently misdiagnosed as primary hip disease. Frequently coexisting with tendinitis and sacroiliac joint pain, these painful types of bursitis require not only treatment of the acute symptom of pain and the decreased range of motion but also correction of the functional abnormalities that perpetuate the patient's symptoms.
Gluteal Bursitis A patient suffering from gluteal bursitis frequently complains of pain at the upper outer quadrant of the buttock and with resisted abduction and extension of the lower extremity. The pain of gluteal bursitis, also known as weaver's bottom, is localized to the area over the upper outer quadrant of the buttock, with referred pain noted into the sciatic notch.1 Often, the patient is unable to sleep on the affected hip and may complain of a sharp, catching sensation when extending and abducting the hip, especially on first awakening. The gluteal bursae lie between the gluteus maximus and medius and minimus muscles as well as between these muscles and the underlying bone (Fig. 105.1). These bursae may exist as a single bursal sac or in some patients as a multisegmented series of sacs that may be loculated. The gluteal bursae are vulnerable to injury from both acute trauma and repeated microtrauma. The action of the gluteus maximus muscle includes the flexion of trunk on thigh when maintaining a sitting position, such as when riding a horse (Fig. 105.2). This action can irritate the gluteal bursae and can result in pain and inflammation. Acute injuries frequently take the form of direct trauma to the bursa from falls directly onto the buttocks or from repeated intramuscular injections, as well as from overuse such as running for long distances, especially on soft or uneven surfaces. If inflammation of the gluteal bursae becomes chronic, calcification of the bursae may occur. 808
Clinical Presentation Physical examination of patients suffering from gluteal bursitis may reveal point tenderness in the upper outer quadrant of the buttocks. Passive flexion and adduction, as well as active resisted extension and abduction of the affected lower extremity, reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain. Results of examination of the hip and the sacroiliac joint are within normal limits. Careful neurologic examination of the affected lower extremity should reveal no neurologic deficits. If neurologic deficits are present, evaluation for plexopathy, radiculopathy, or entrapment neuropathy should be undertaken.2 These neurologic symptoms can coexist with gluteal bursitis and can thus confuse the clinical diagnosis.
Differential Diagnosis Gluteal bursitis is often misdiagnosed as sciatica or is attributed to primary hip disease. Radiography of the hip and electromyography help to distinguish gluteal bursitis from radiculopathy emanating from the hip. Most patients suffering from lumbar radiculopathy have back pain associated with reflex, motor, and sensory changes associated with back pain, whereas patients with gluteal bursitis have only secondary back pain and no neurologic changes. Piriformis syndrome may sometimes be confused with gluteal bursitis but can be distinguished by the presence of motor and sensory changes involving the sciatic nerve.3 These motor and sensory changes are limited to the distribution of the sciatic nerve below the sciatic notch. Lumbar radiculopathy and sciatic nerve entrapment may coexist as the double-crush syndrome. The pain of gluteal bursitis may cause alteration of gait that may result in secondary back and radicular symptoms and may coexist with this entrapment neuropathy. © 2011 Elsevier Inc. All rights reserved.
Chapter 105—Gluteal and Ischiogluteal Bursitis
••
Piriformis m.
••
••
Psoas m.
Sciatic n.
•• Obturator internus m.
••
Inf. gluteal a.
••
Sup gemellus m. Obturator internus m.
••
••
Inf. gemellus m.
•
••
•• ••
••
Adductor brevis m.
••
•
Adductor magnus m.
••
Adductor longus m.
Gluteus maximus m. Ischium, spine
••
Obturator n., ant. branch Obturator externus m. Pectineus m.
••
••
Pubis
809
••
Ischium, tuberosity Quadratus femoris m.
••
Semimembranosus t.
Fig. 105.1 The regional anatomy of the gluteal bursae. (From Kang HS, Ahn JM, Resnick D, editors: MRI of the extremities, ed 2, Philadelphia, 2002, Saunders.)
mass or tumor of the hip is suspected. Electromyography should be performed in patients with neurologic findings, to rule out plexopathy, radiculopathy, or nerve entrapment syndromes of the gluteal nerve or of the lower extremity nerves (Fig. 105.3). Based on the patient's clinical presentation, additional testing including complete blood cell count, human leukocyte antigen-B27 (HLA-B27) testing, automated serum chemistry studies including uric acid, sedimentation rate, and antinuclear antibody testing may be indicated. The injection technique described later serves as both a diagnostic test and a therapeutic maneuver for patients suffering from gluteal bursitis.4
Treatment Fig. 105.2 The action of the gluteus maximus muscle includes the flexion of trunk on thigh when maintaining a sitting position, such as while riding a horse. This action can irritate the gluteal bursae and result in pain and inflammation. (From Waldman SD: Gluteal bursitis. In Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 231.)
Diagnosis Plain radiographs of the hip may reveal calcification of the bursa and associated structures consistent with chronic inflammation. Magnetic resonance imaging (MRI) is indicated if occult
Initial treatment of the pain and functional disability associated with gluteal bursitis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. The local application of heat and cold may also be beneficial. Repetitive movements that incite the syndrome should be avoided. For patients who do not respond to these treatment modalities, injection of the gluteal bursa with local anesthetic and corticosteroid may be a reasonable next step. To inject the gluteal bursae, the patient is placed in the lateral position with the affected side upward and the affected leg flexed at the knee. Proper preparation with antiseptic solution of the skin overlying the upper outer quadrant of
810
Section IV—Regional Pain Syndromes
the buttocks is then performed. A syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch, 25-gauge needle. The point of maximal tenderness within the upper outer quadrant of the buttocks is then identified with a sterile-gloved finger. Before needle placement, the patient should be advised to say “there” immediately if he or she feels paresthesia into the lower extremity; this symptom indicates that the needle has impinged on the sciatic nerve. Should paresthesia occur, the needle should be immediately withdrawn and repositioned more medially. The needle is then carefully advanced perpendicular to the skin at the previously identified point until it impinges on the wing of the ilium (Fig. 105.4). Care must be taken to keep the needle in a medial position and not to advance it laterally, to avoid impinging on the sciatic nerve. After careful aspiration and if no paresthesia is present, the contents of the syringe are then gently injected into the bursa. Resistance to injection should be minimal.
Ischiogluteal Bursitis The ischial bursa lies between the gluteus maximus muscle and the bone of the ischial tuberosity. This bursa may exist as a single bursal sac or in some patients may be a multisegmented series of sacs that may be loculated. The ischial bursa is vulnerable to injury from both acute trauma and repeated microtrauma. Acute injuries frequently take the form of direct trauma to the bursa from direct falls onto the buttocks and from overuse such as prolonged riding of horses or bicycles. Running on uneven or soft surfaces such as sand may also cause ischial bursitis (Fig. 105.5). If inflammation of the ischial bursa becomes chronic, bursal calcification may occur.
Clinical Presentation A patient suffering from ischial bursitis frequently complains of pain at the base of the buttock during resisted extension of the lower extremity. The pain is localized to the area over the ischial tuberosity, with referred pain noted into the hamstring
Fig. 105.3 Possible entrapment of the superior gluteal nerve. Note the denervation hypertrophy of the tensor fasciae latae muscle (arrow), as shown on a transverse T1-weighted (TR/TE, 416/14) spin-echo magnetic resonance imaging (MRI) scan (A.), and similar hypertrophy of and high signal intensity in this muscle (arrow) on a transverse fat-suppressed T1weighted (TR/TE 500/14) spin-echo MRI scan obtained after intravenous administration of gadolinium (B). (From Resnick D: Neuromuscular disorders. In Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 3351.)
A
B
Inflamed bursa
Gluteus maximus m.
Sciatic n.
Fig. 105.4 Injection technique for relieving the pain of gluteal bursitis. (From Waldman SD: Gluteal bursitis pain. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 351.)
muscle, which may also develop coexistent tendinitis.5 Often, the patient is unable to sleep on the affected hip and may complain of a sharp, catching sensation when extending and flexing the hip, especially on first awakening. Physical examination may reveal point tenderness over the ischial tuberosity. Passive straight-leg raising and active resisted extension of the affected lower extremity reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain.
Diagnosis Plain radiographs of the hip may reveal calcification of the bursa and associated structures consistent with chronic inflammation. MRI is indicated if disruption of the hamstring musculotendinous unit is suspected. The injection technique described later serves as both a diagnostic test and a therapeutic maneuver and also treats hamstring tendinitis. Screening laboratory tests consisting of a complete blood cell count, erythrocyte sedimentation rate, and antinuclear antibody level are indicated if collagen vascular disease is suspected. Plain radiographs and radionuclide bone scanning are indicated in the presence of trauma or if tumor is a possibility.
Differential Diagnosis Although the diagnosis of ischiogluteal bursitis is usually straightforward, this painful condition can occasionally be confused with sciatica, primary hip disease, insufficiency fractures of the pelvis, and tendinitis of the hamstrings. Tumors of the hip and pelvis may be overlooked and should be considered in the differential diagnosis of ischiogluteal bursitis.
Chapter 105—Gluteal and Ischiogluteal Bursitis
811
Treatment Initial treatment of the pain and functional disability associated with ischiogluteal bursitis should include a combination of NSAIDs or COX-2 inhibitors and physical therapy. The local application of heat and cold may also be beneficial. Any repetitive activity that may exacerbate the patient's symptoms should be avoided. For patients who do not respond to these treatment modalities, the following injection technique may be a reasonable next step.6 To inject the ischiogluteal bursa, the patient is placed in the lateral position with the affected side upward and the affected leg flexed at the knee. Proper preparation with antiseptic solution of the skin overlying the ischial tuberosity is then performed. A syringe containing 4.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch 25-gauge needle. The ischial tuberosity is then identified with a sterile-gloved finger. Before needle placement, the patient should be advised to say “there” immediately if he or she feels paresthesia into the lower extremity; this symptom indicates that the needle has impinged on the sciatic nerve. Should paresthesia occur, the needle should be immediately withdrawn and repositioned more medially. The needle is then carefully advanced at that point through the skin, subcutaneous tissues, muscle, and tendon until it impinges on the bone of the ischial tuberosity (Fig. 105.6). Care must be taken to keep the needle in the midline and not to advance it laterally, to avoid impinging on the sciatic nerve. After careful aspiration and if no paresthesia is present, the contents of the syringe are then gently injected into the bursa. The proximity to the sciatic nerve makes it imperative that the injection procedure be carried out only by clinicians well versed in the regional anatomy and experienced in performing injection techniques. Many patients complain of a transient increase in pain after injection of the bursa and tendons. Patients should be warned that improvement will be limited if they continue the repetitive activities responsible for the e volution of the ischiogluteal bursitis.
Conclusion
Fig. 105.5 Ischiogluteal bursitis is often perpetuated by running on soft, uneven surfaces, such as sand. (From Waldman SD: Ischiogluteal bursitis. In Atlas of common pain syndromes, ed 2, Philadelphia, 2007, Saunders, p 258.)
Gluteal bursitis and ischiogluteal bursitis are among the myriad causes of buttock pain that are encountered in clinical practice. Frequently coexisting with tendinitis and sacroiliac joint pain, these painful types of bursitis require not only treatment of the acute symptoms of pain and the decreased range of motion but also correction of the functional abnormalities that perpetuate the patient's symptoms. The clinician should be sure to consider occult tumors of the hip joint, pelvis, and surrounding soft tissues when evaluating the patient with pain thought to have gluteal or ischiogluteal bursitis. Although the treatment is the same, ischial bursitis can be distinguished from hamstring tendinitis by the following: ischial bursitis manifests with point tenderness over the ischial bursa, whereas the tenderness of hamstring bursitis is more diffuse over the upper muscle and tendons of the hamstring. The foregoing injection technique is extremely effective in the treatment of ischial bursitis
812
Section IV—Regional Pain Syndromes
Sciatic n. Inflamed bursa and t.
Biceps femoris m. Semitendinosus m.
Fig. 105.6 Injection technique for relieving the pain of ischial bursitis. (From Waldman SD: Ischial bursitis pain. In Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 247.)
and hamstring tendinitis. This procedure is safe if careful attention is paid to the clinically relevant anatomy of the areas to be injected. The use of physical modalities including local heat and gentle stretching exercises should be introduced several days after the patient undergoes this injection technique. Vigorous exercises should be avoided because they will exacerbate the
patient's symptoms. Simple analgesics, NSAIDs, and antimyotonic agents such as tizanidine may be used concurrently with this injection technique.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
106
IV
Trochanteric Bursitis H. Michael Guo and Martin K. Childers
CHAPTER OUTLINE Historical Considerations 813 Etiology 813 Clinical Presentation 814 Diagnosis 814
Differential Diagnosis 815 Treatment 815 Complications and Pitfalls 816 Conclusion 816
Physical Examination 814 Testing 814
Trochanteric bursitis is a common painful condition caused by the irritation or inflammation of the trochanteric bursa. It is also known as the greater trochanteric pain syndrome (GTPS). This type of bursitis is mostly associated with repetitive microinjuries in the soft tissue and bursae around the greater trochanter (e.g., iliotibial band friction), but trauma (e.g., fall to the lateral hip) has also been implicated.1 The incidence of trochanteric bursitis peaks between the fourth and sixth decades of life and has a female-to-male ratio of 4:1.2,3 The difference is thought to result from female and male biomechanics.4 The prevalence of patients with trochanteric bursitis referred to an orthopedic spine clinic was reported to be 20.2%, and the mean age was 54 years.5 In the same study, 20% of patients referred for low back pain were found to have trochanteric bursitis, with higher incidences reported elsewhere.2,6 Thus, trochanteric bursitis appears to be a relatively common condition among middle-aged or older women who are evaluated by specialists for the treatment of hip or low back pain.
Historical Considerations Calcifications of the gluteal tendons associated with the trochanteric bursae were reported as early as 1930 by Nilsonne7 and were generally considered to be caused by tuberculosis.8 The condition was also thought to be acute rather than chronic until 1952, when Spear and Lipscomb9 published a case series of 64 patients. In the late 1950s and early 1960s, several journal articles8,10–13 challenged the traditional notion that trochanteric bursitis was an acute, rare condition14 and instead indicated that the condition was a discrete, and often chronic, clinical entity. However, as Anderson pointed out in 1957,8 trochanteric bursitis is a complex diagnosis usually associated with other disorders.
© 2011 Elsevier Inc. All rights reserved.
Etiology Historically, the general assumption regarding the origin of trochanteric bursitis involves one or more of three relatively constant bursae associated with the greater trochanter: two major bursae (subgluteus maximus and subgluteus medius) and one minor bursa (gluteus minimus) (Fig. 106.1).2,15 Whether disease of one or more trochanteric bursae directly results in trochanteric bursitis is not entirely clear. During hip replacement surgery in a patient with hip pain and osteoarthritis, the trochanteric bursa was reported to be enlarged and contained calcium pyrophosphate dihydrate (CPPD) crystals.16 However, prospective data from magnetic resonance imaging (MRI) and physical findings in patients with chronic lateral hip pain indicate that fluid distention of the trochanteric bursae is uncommon,17 whereas gluteus medius tendon disease appears to be much more common. Nevertheless, tendon disease and bursae distention are not mutually exclusive because one report18 noted that both tendinopathy and partial tears of the gluteus medius occurred in the presence of bursae fluid distention. In a series of 250 MRI studies of the hip, Kingzett-Taylor et al19 reported that 14 of 35 patients with gluteal tendon disease also had discrete fluid collections within the trochanteric bursae. Indeed, in 1961, Gordon11 proposed that the primary lesion in trochanteric bursitis was injury to the gluteal tendons at their insertion onto the greater trochanter and that the adjacent bursae were damaged as a consequence. Thus, trochanteric bursitis is probably caused by gluteal tendinitis in a manner analogous to that of shoulder joint bursitis and rotator cuff tendinitis. Accordingly, Walsh and Archibald18 have urged prompt review of the tendon insertions for signs of tendinopathy and tears when MRI findings demonstrate gluteus medius and minimus atrophy and fatty replacement in patients with chronic lateral hip pain.
813
814
Section IV—Regional Pain Syndromes Gluteus medius Gluteus minimus
Tensor fascia lata
Piriformis Subgluteus minimus bursa
Subgluteus medius bursa Subgluteus maximus bursa Greater trochanter
Lesser trochanter Femur
Fig. 106.1 The bursae associated with the greater trochanter.
Clinical Presentation Patients with trochanteric bursitis generally present with chronic intermittent aching pain over the lateral aspect of the affected hip.5,8,10 Pain is worsened by hip abduction or external rotation, prolonged lower extremity weight bearing, sitting in a deep chair or car seat,20 bicycling, golfing, climbing stairs,17 or lying on the affected side.21 The condition also occurs as a result of a running injury, most commonly in female athletes with a wide pelvis22 or a cavus foot.23 In contrast, in patients with hip osteoarthritis, pain is usually relieved by sitting.24 Clinical criteria for trochanteric bursitis have been proposed,8,25,26 and they include the first and second and at least one of the remaining findings: (1) history of lateral aching hip pain; (2) localized tenderness over the greater trochanter; (3) radiation of pain over the lateral thigh; (4) pain of resisted hip abduction; and (5) pain at extreme ends of rotation, particularly a positive Patrick (FABER) test result. Occasionally, pain may extend from the hip to include the lateral thigh11 and may radiate down the leg to the level of the insertion of the iliotibial tract on the proximal tibia,18 with associated paresthesia6 that does not follow a dermatomal pattern. In fact, Ege and Fano25 included “pseudoradiculopathy” as an inclusion criterion for trochanteric bursitis. Groin pain was reported in 10% of patients with trochanteric bursitis who presented to a Dutch rheumatology clinic.27 Indeed, the finding that patients complain of pain in areas of the body at sites far removed from the hip is one of the more fascinating aspects of trochanteric bursitis.
Diagnosis Physical Examination The examiner should try to localize the patient's usual hip pain by performing careful palpation of the hip area followed by active and passive range-of-motion testing. Trochanteric
bursitis is one cause of hip pain that Roberts and Williams28 categorized into one of three areas: (1) anterior groin pain, (2) posterior buttock pain, or (3) lateral trochanteric pain. Anterior groin pain should alert the clinician of the likelihood of an intra-articular cause, such as a septic joint or fracture. The most consistent physical finding in patients with trochanteric bursitis is localized tenderness over the greater trochanter, usually on the posterosuperior aspect over the tendinous insertion of the gluteus medius.8,10 With the patient in the lateral decubitus position with the painful hip facing the examiner, the clinician should palpate the hip with one fingertip in a caudal to cephalad direction, from below the greater trochanteric eminence to the area of maximal tenderness.2 While the patient is still in the lateral decubitus position, the examiner can typically reproduce the patient's usual lateral hip pain by resistive active hip abduction and external rotation. The examiner should also check for hip pain on active resisted hip extension and flexion, because this maneuver should not elicit pain in patients with trochanteric bursitis but rather indicates intra-articular hip disease.2,26 On observation of gait, a “gluteal limp” is frequently present.13 Disease (tears or inflammation) of the gluteus medius tendon results in a positive Trendelenburg sign (upward movement of the pelvis on the weight-bearing side while the pelvis moves downward on the non–weight-bearing side during gait) and is a more accurate predictor of tendon disease (assessed with MRI) as compared with two other physical signs (pain elicited by resisted hip abduction or pain in response to internal rotation).17 Leg-length discrepancy may be assessed by visual inspection of the height of the iliac crests or by comparing the side-to-side difference between the distance from the anterior superior iliac spine to the medial malleolus. However, standing plain radiographs of the pelvis to determine differences in leg length are considered more accurate than clinical measurements.28
Testing The diagnosis of trochanteric bursitis is based on clinical evidence. No radiographic findings are necessarily diagnostic, although imaging studies may help to distinguish trochanteric bursitis from an intra-articular cause of hip pain. Gordon11 reported calcifications of the tendons associated with the greater trochanter in 40% of patients with trochanteric bursitis, but these data may have reflected tuberculous involvement of the bursa, a diagnosis rarely seen today.29 Such calcifications may be identified in radiographic images of the hip as linear or small, rounded masses of varying size.2 After hip arthroplasty, some patients may develop bursitis within communicating cavities or “psuedobursae.”30 For these patients, arthrography may be useful to distinguish pain from causes other than loosening and infection. Plain radiographs may help to distinguish rare causes of trochanteric bursitis. For example, few (1% to 3%) of patients with tuberculosis have skeletal involvement.31 Moreover, patients with tuberculosis rarely present with trochanteric bursitis. Nonetheless, tuberculous involvement of the greater trochanter bursa or its associated tendons may be identified based on imaging features, with a pattern of tendon tethering suggestive of tuberculosis. For instance, in a case series of patients with tuberculous tenosynovitis and bursitis, Jaovisidha et al31 found soft tissue swelling on plain radiographs with calcification in 3 of 9 cases. When the tendon sheath was
replaced by vascular tuberculous granulation tissue, high signal intensity was observed in T2-weighted MRI scans. In 6 of 12 cases of tuberculous tenosynovitis, pulmonary tuberculosis was evident on plain chest radiographs. More advanced imaging methods, such as MRI, computed tomography, or bone scans, have characteristic features of trochanteric bursitis and have also been used to rule out other causes of lateral hip pain. MRI may demonstrate fluid distention of the trochanteric bursae and associated gluteus medius tendon disease18 represented by high signal intensity on short-echo time-inversion recovery sequences in the greater trochanteric region.2 Ultrasound also detects this type of bursa fluid distention and enlargement.32 MRI may demonstrate gluteus medius and minimus atrophy with fatty replacement. Radioisotope bone scanning may demonstrate a characteristic linear uptake29 in the lateral aspect of the greater trochanter generally seen in the early blood-pooling phase and on delayed images.2
Chapter 106—Trochanteric Bursitis
815
Table 106.1 Differential Diagnosis of Trochanteric Bursitis Iliotibial band syndrome Lumbosacral strain Osteoarthritis of the hip Lumbar radiculopathy Septic joint Hip fracture Avascular necrosis of the femur head Synovitis Lumbar facet syndrome Iliohypogastric nerve entrapment Tuberculosis with skeletal involvement Neoplasms
Differential Diagnosis Tendinopathy of the gluteal tendons is thought to be responsible for trochanteric bursitis, but the pathogenesis of trochanteric bursitis is unclear and is probably multifactorial. Numerous common musculoskeletal conditions have been reported in association with trochanteric bursitis, including leg-length discrepancy, cavus foot,23 mechanical low back pain, hip osteoarthritis,33 gluteal tendinitis, and lumbar radiculopathy,34 but a cause-and-effect relationship between any of these conditions and trochanteric bursitis has not been definitively established. Infection of the bursae can occur,35 although reports in the literature are infrequent. In a series of 100 patients with rheumatoid arthritis, 15 patients were found to have trochanteric bursitis, a finding suggesting a casual association.34 Biomechanical alteration in gait and associated forces may predispose some patients to trochanteric bursitis.19 Gordon11 postulated that a strain of the hip results in a slight tear in the relatively avascular tendon of the gluteus medius or minimus muscle with subsequent hemorrhage, local necrosis, and organization of scar tissue and tendon calcification. The cause of injury to the gluteal tendons may originate from iliotibial band friction on the tendons and their respective bursae.19 The differential diagnosis of trochanteric bursitis is listed in Table 106.1. Common conditions associated with trochanteric bursitis include degenerative processes of the hip and spine. For this reason, patients may initially present with low back pain. Symptoms of trochanteric bursitis may be confused with those of lumbosacral strain, osteoarthritis of the hip, or herniated lumbar disk.11 Because of the overlap of the iliotibial tract and the lumbar dermatomes, back and associated lower limb pain can mimic lumbar radiculopathy.5,36 Collee et al6,27 diagnosed trochanteric bursitis in 35 of 100 consecutive patients who presented to a rheumatology clinic with a primary complaint of low back pain. Distinguishing trochanteric bursitis from lumbar radiculopathy requires a careful history and physical examination, in which pain and tenderness are most often elicited in the hip rather than in the back.
Treatment Reported benefits of treatment for trochanteric bursitis are myriad, but few treatment protocols have been rigorously tested using scientific methods. A series of “deep x-ray therapy” was recommended in the 1950s,37 but it is no longer
Table 106.2 Treatment of Trochanteric Bursitis Conservative Treatment
Rest Ice or heat Nonsteroidal anti-inflammatory drugs Bisphosphonates Local corticosteroid injection Miscellaneous modalities (e.g., ultrasound, shock wave, iontophoresis) Surgery
Release of iliotibial band Removal of trochanteric osteophytes Débridement of gluteus maximus bursae
suggested. In 1959, Krout and Anderson12 reported that shortwave diathermy applied to the trochanteric and low back region was effective in 41 of 50 cases. Furia et al38 reported that shock wave therapy was an effective treatment for GTPS, and the treatment group had significant visual analog score reductions. Table 106.2 lists the routine treatment regimen consisting of rest, ice or heat, nonsteroidal anti-inflammatory drugs (NSAIDs), and local injection of a corticosteroid20 such as methylprednisolone (40 to 80 mg) or triamcinolone hexacetonide (20 to 40 mg) or mixtures of betamethasone sodium phosphate and betamethasone acetate suspension with 1% lidocaine.25,26 Ultrasound or fluoroscopic guidance may increase the precision of needle placement.14,39,40 Clinical evidence supports the use of corticosteroids in trochanteric bursitis. A favorable dose-response relationship with betamethasone was reported in a series of 75 patients with trochanteric bursitis.26 As early as 1958, Leonard13 reported that local injection of hydrocortisone acetate resulted in “complete relief of symptoms in all instances.” Gordon's 1961 description11 outlined the process of
816
Section IV—Regional Pain Syndromes
local injection for trochanteric bursitis: “The most successful method of treatment was local infiltration and needling of the bursa, selecting the point of maximum tenderness behind or above the greater trochanter as the point of entry. . . . The tip of the needle was directed against the posterosuperior point of the greater trochanter, and then the solution infiltrated in fanlike fashion adjacent to and above the trochanter.” Conservative treatment that decreases forces placed on the painful hip is generally thought to be helpful in trochanteric bursitis. Use of a cane that is held in the hand on the side opposite the painful hip reduces forces placed on the affected side equivalent to one half of the body weight.41 Correction of leg-length discrepancy with a shoe lift may similarly work to relieve pain.20 In support of this idea, Swezey36 noted an association between hip disease and leg-length discrepancies in a group of older patients with trochanteric bursitis. Swezey speculated that gait alterations resulting from back pain or prolonged bed rest could predispose patients to trochanteric bursitis. Alternatively, active exercise is considered to be the cornerstone of treatment for friction-induced bursitis in athletes. Increased flexibility and symmetrical strengthening of the muscle involved in adjacent joint motion are thought to improve faulty joint mechanics that may induce excessive tension over the greater trochanter.42 Exercises that stretch the external rotators of the hip and the iliotibial band were suggested to prevent recurrences of trochanteric bursitis in young adults.36 Alternative therapies proposed for trochanteric bursitis include identification and injections of fibrofatty nodules with corticosteroid and lidocaine.43 NSAIDs and acetaminophen have also been reported to be effective for trochanteric bursitis. Monteforte et al44 compared pain relief obtained with the use of paracetamol (known as acetaminophen in the United States) (a 500-mg oral dose twice daily for 15 days, followed by 500 mg daily for 15 days) with pain relief obtained with the bisphosphonate disodium clodronate (100-mg daily intramuscular injection for 30 days) in an open-label comparison trial of 10 patients with trochanteric bursitis who were previously unresponsive to conservative treatment. Patients treated with the bisphosphonate demonstrated better pain relief compared with those in the paracetamol-treated group, a finding suggesting that an increase in bone turnover may be implicated in the pathogenesis of trochanteric bursitis. In refractory cases, surgical release of tight fascia has been reported.11,20,45,46 In seven athletes with chronic disabling hip pain caused by a snapping iliotibial band and secondary trochanteric bursitis, partial excision of the iliotibial band with excision of the trochanteric bursa resulted in long-term pain relief and a return to athletic acitivity.44 Arthroscopy
has been used for treating refractory trochanteric bursitis, and arthroscopic procedures have included bursectomy and iliotibial band release.47,48
Complications and Pitfalls Fatal necrotizing fasciitis in a non–insulin-dependent diabetic man was reported as a complication of a single corticosteroid injection of the greater trochanteric bursa.49 Accordingly, the clinician should be wary of performing similar procedures in patients with diabetes or any other condition that could predispose them to infection from a corticosteroid injection. Because other syndromes including entrapment neuropathies, radiculopathies, and lumbar facet syndromes can mimic trochanteric bursitis, the astute clinician should carefully consider the differential diagnoses. Entrapment neuropathy of the iliohypogastric nerve can mimic the lateral thigh pain that is commonly observed in trochanteric bursitis. Perineural injection with local anesthetic over the superior margin of the ilium where the terminal branches of the iliohypogastric nerve cross the iliac crest should confirm the diagnosis.50 For patients with a presumptive diagnosis of trochanteric bursitis but who do not respond to local peritrochanteric injection of corticosteroid and local anesthetic, selective neural blockade may help to determine the underlying cause. Electromyography or transforaminal nerve root blocks may identify lumbar radiculopathy. Lumbar facet blockade may elucidate lumbar facet syndrome as the cause of lateral hip pain.
Conclusion Trochanteric bursitis, also known as GTPS, is a common cause of lateral hip pain in middle-aged or older women. This condition is readily diagnosed by finding localized tenderness over the greater trochanter, with radiation of pain over the lateral thigh and increased pain with resistive hip abduction and external rotation. The differential diagnosis includes tendinopathy of the gluteal muscles, degenerative processes of the hip and spine, lumbosacral strain, herniated lumbar disk, and, rarely, tuberculosis or infection. Treatment of this condition usually consists of rest, ice, heat, and local corticosteroid injection into the most tender area around the greater trochanter, although double-blind placebo-controlled trials have yet to demonstrate the efficacy of a particular treatment paradigm.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
107
IV
Iliopsoas Bursitis Robert Trout
CHAPTER OUTLINE Historical Considerations 817 Signs and Symptoms 817 Testing 817 Differential Diagnosis 818
Historical Considerations Although it is often overlooked in the standard evaluation of hip pain, the iliopsoas bursa is the largest in the body and measures up to 7 cm in length (Fig. 107.1).1 Also known as the iliopectineal or iliofemoral bursa, this bursa has been studied as a source of hip pain since 1834, when Fricke2 described painful bursitis in a case report. In 1917, a distended bursa was identified with arthrography by Kummer and De Senarclens,3 and for many years arthrography remained the only helpful imaging study for diagnosis until the advent of computed tomography (CT) and magnetic resonance imaging (MRI) scanning. In 1967, Melamad et al4 described the following clinical triad for iliopsoas bursitis: a mass in the inguinal region, the effects of pressure on other structures nearby, and osteoarthritis of the hip as visualized on radiographs. This triad has become less relevant because patients with only the most significant symptoms present with such findings. Along with better imaging techniques, greater emphasis has been placed on earlier conservative treatment that can help to prevent these symptoms from occurring.
Signs and Symptoms Two types of patients present with iliopsoas bursitis. First, this disorder most commonly occurs in older individuals who have some type of underlying hip disease, such as degenerative or rheumatoid arthritis. Investigators have theorized that increased intra-articular pressure causes the bursa to act as a reservoir for fluid that leaks through the anterior joint capsule, similar to the formation of Baker's cyst in the knee.5,6 Eventually, the bursa becomes distended and inflamed. Because these patients are likely to exhibit physical signs and radiographic findings of other types of articular problems, a thorough hip examination is essential to differentiate between pain from bursitis and pain related to arthritis or other bony disease. The second category of patient is younger and has completely normal radiographs. These patients are often athletes © 2011 Elsevier Inc. All rights reserved.
Treatment 819 Complications and Pitfalls 819 Conclusion 820
who perform repetitive or forceful flexion and extension of the hip. They are at risk for developing bursitis as a result of the friction of the iliopsoas tendon that overlies it because the purpose of this bursa is to reduce the friction between the tendon and the hip capsule. Thus, for a patient who presents with persistent hip pain and normal hip films, iliopsoas bursitis should remain near the top of a differential diagnosis list. Patients present with pain in the inguinal or hip regions, and this the pain often radiates to the anterior thigh. Aggravating activities include walking up stairs, putting on shoes and socks, and moving from a sitting to a standing position. Some patients may also describe abdominal pain. Although not as common, edema in the lower extremity or numbness may occur if the bursa is large enough to compress the femoral vein or nerve. Gait should be observed because a common initial finding is a shortened stride length when the patient attempts to minimize flexion and extension of the hip. A mass in the area of the inguinal ligament may be palpable and is sometimes mistaken for a hernia, a lymph node, or even an aneurysm. The mass may be pulsatile because of its proximity to the femoral artery.7 Pain can be reproduced by placing the hip in flexion, abduction, and external rotation and then moving it into extension (Fig. 107.2).8 A palpable or audible snap may occur as the bursa passes underneath the tendon; thus, this disorder is sometimes called snapping hip syndrome or iliotibial band syndrome. The Thomas test is helpful to evaluate for tight hip flexors. The patient lies supine and fully flexes one knee and hip. If the contralateral hip rises off the examination table, then a contracture is present.
Testing Initial testing with plain radiographs of the hip often demonstrates intra-articular disease such as degenerative change, effusion, or calcification. The diagnostic yield for this specific disorder is limited, however, because plain radiographs do not show an inflamed bursa unless calcification of the bursa occurs. 817
818
Section IV—Regional Pain Syndromes
Iliopsoas m.
A
Iliopsoas bursa Fig. 107.1 Iliopsoas bursa, also known as the iliopectineal or iliofemoral bursa.
B Fig. 107.3 Imaging studies for iliopsoas bursitis. A, Ultrasound. Small arrows, fluid-filled bursa; large arrows, loculations; T, inguinal ligament. B, Magnetic resonance imaging. Asterisk, fluid-filled bursa; arrows, loculations; FV, femoral vessel; T, inguinal ligament.
Fig. 107.2 Resisted hip adduction test for iliopsoas bursitis. (From Waldman SD: Physical diagnosis in pain: an atlas of signs and symptoms, Philadelphia, 2005, Saunders, p 313.)
For many years, arthrography was the only available means to diagnose a distended iliopsoas bursa, which would fill with contrast material if the bursa communicated with the hip joint. However, because of its invasiveness and its inability to visualize other nearby structures (e.g., the femoral
v essels), arthrography has become essentially obsolete for this purpose. Ultrasound is fast and noninvasive, and it has the advantage of ruling out other possible causes of a palpable inguinal mass, including hernia and aneurysm. In patients with bursitis, ultrasound studies show a well-defined mass between the anterior hip capsule and the iliopsoas muscle (Fig. 107.3A), although ultrasound has often been found to underestimate the size of the mass. CT scan also demonstrates an encapsulated mass that has a water density and, if present, a communication with the hip joint. Surrounding structures are well visualized, and displacement of the femoral vessels may be observed. MRI is the most sensitive and accurate test in evaluating the characteristics of the bursa such as its size and shape and its relation to the adjacent soft tissues and structures (see Fig. 107.3B).8 MRI is also valuable in ruling out other potential causes of hip pain such as avascular necrosis or stress fracture.
Differential Diagnosis The differential diagnosis includes both intra-articular and extra-articular causes of pain around the hip joint (Table 107.1). Differentiating bursitis from osteoarthritis of the hip may be difficult because many patients have arthritic hip changes visible on plain films. The pain of osteoarthritis
Chapter 107—Iliopsoas Bursitis
819
Table 107.1 Differential Diagnosis of Iliopsoas Bursitis Osteoarthritis Rheumatoid arthritis Avascular necrosis Femoral stress fracture Osteitis pubis Pelvic abscess or hematoma Lymphadenopathy or aneurysm Metastatic disease Radiculopathy
typically occurs during standing and weight bearing, and these patients more often demonstrate a Trendelenburg gait in which they lean toward the affected side during the stance phase. On examination, range of motion (ROM) is reduced by pain when these patients internally or externally rotate the hip. Avascular necrosis should also remain in the differential diagnosis for patients with significant hip or groin pain, particularly if they have a history of steroid use. These patients also report worsened pain with weight bearing and have a significantly antalgic gait, to avoid placing any weight on the hip joint. Avascular necrosis can be excluded by a bone scan or MRI. For athletes, primarily long-distance runners, femoral neck stress fracture causes an aching pain in the groin or thigh that is exacerbated by activity and improved with rest. ROM is reduced and painful. Radiographs may show callus formation or an actual fracture line, but early results may be negative. If such a fracture is suspected clinically, a bone scan should be performed because it is sensitive within 2 to 8 days of the injury. Osteitis pubis, or inflammation of the pubic bone, is another condition seen in athletes who perform repetitive side-to-side motions, such as in hockey or soccer. This disorder is also common in pregnant women because of the instability of the pubic symphysis. These patients report pain in the groin or thigh areas, but the pain is most tender at the pubic symphysis. Radiographs show resorption or sclerosis of the pubic bones, but results may be negative initially. A bone scan may also be needed for an early diagnosis. Radicular pain may manifest with symptoms similar to those of bursitis, with pain extending into the anterior thigh. The mass effect of an enlarged bursa on the femoral nerve may cause numbness or paresthesias. Usually, the clinician can distinguish between the two conditions by means of adequate hip and lumbar physical examinations; however, electrodiagnostic studies may be helpful if the diagnosis is unclear. For the patient who presents with a palpable inguinal mass, the other possibilities include hernia, aneurysm, and lymphadenopathy. Although these other diagnoses may also produce pain, the pain is usually not clearly related specifically to hip flexion and extension, and the patient should otherwise have a normal hip examination. Ultrasound is a good first-line test in this situation when one of these other causes is suspected.
Fig. 107.4 Injection technique for iliopsoas bursitis.
Treatment Initial treatment for most cases of iliopsoas bursitis is conservative and includes relative rest and avoidance of aggravating activities, anti-inflammatory medications, and physical therapy for localized hip flexor stretching. Johnston and Wiley9 also advocated a hip rotation strengthening program, with good results, to correct subtle muscle imbalances that may lead to the problem over time. Corticosteroid injection to the bursa is often quite helpful for rapid relief of pain symptoms. A solution of 40 mg methylprednisolone is diluted in 0.25% bupivacaine or similar equivalent in a syringe attached to a 3.5-inch, 25-gauge needle. The patient is placed in the supine position, and the femoral artery pulse is palpated. The needle is placed at a point 2.5 inches below and 3.5 inches lateral to the femoral pulse. It is then advanced superiorly at a 45-degree angle (Fig. 107.4). The patient should be advised to tell the clinician if he or she feels paresthesia into the thigh on advancement of the needle; this is a sign that the needle has impinged on the femoral nerve. If no paresthesia occurs, the needle is advanced slowly until it hits bone and then is withdrawn slightly. After initial aspiration, the medication is injected into the bursa with very little resistance.10 For patients with a significantly distended bursa or if infection is suspected, an empty syringe may be used first to aspirate the excess synovial fluid from the sac. Obviously, if the fluid appears cloudy or infected, the corticosteroid is not injected. If the clinician has difficulty in aspirating a palpable bursa, a CT scan or ultrasound-guided procedure may be performed. Although most patients respond very well to a regimen of medications, injections, and therapy, those with recalcitrant cases may still require surgical treatment. This treatment usually consists of bursectomy with possible release of the iliopsoas tendon, and it has a good outcome rate.
Complications and Pitfalls The most common pitfall of this process is a delay in making the proper diagnosis. Often, the condition is mistaken for osteoarthritis or radicular pain. Iliopsoas bursitis should always be considered in patients with persistent hip pain who have negative radiographic results and an unremarkable lumbar examination.
820
Section IV—Regional Pain Syndromes
Patients commonly experience soreness or increased pain for 1 to 2 days after an injection to the bursa, but major complications are rare with proper technique. The most serious complication is abscess or hematoma formation, and it manifests with progressively worsening hip or flank pain, guarding of hip movements, and possibly fever. Weakness occurs when the lumbosacral plexus is compressed. If these symptoms occur after injection, a pelvic CT scan should be obtained immediately. To reduce this risk, patients should be asked about clotting disorders, immune dysfunction, or use of anticoagulants before any injection.
clinically, with point tenderness in the iliopsoas tendon and reproduction of pain during flexion and extension of the hip. When further information is needed, a CT scan, ultrasound scan, or MRI scan may demonstrate the presence of a distended bursa and rule out other potential causes of hip pain. Patients typically respond well to conservative treatment and a well-placed injection, although surgery is a possible option for patients with severe or p ersistent cases.
References Full references for this chapter can be found on www.expertconsult.com.
Conclusion Iliopsoas bursitis is an often overlooked cause of hip pain that occurs in older patients with other underlying hip disease and in young athletes. The diagnosis is usually made
Chapter
108
IV
Meralgia Paresthetica Steven D. Waldman
CHAPTER OUTLINE Clinical Presentation 821 Diagnosis 821 Differential Diagnosis 821
Meralgia paresthetica is caused by compression of the lateral femoral cutaneous nerve by the inguinal ligament as it passes through or under the inguinal ligament.1,2 This entrapment neuropathy manifests as pain, numbness, and dysesthesias in the distribution of the lateral femoral cutaneous nerve.3 These symptoms often begin as a burning pain in the lateral thigh with associated cutaneous sensitivity. Patients suffering from meralgia paresthetica note that sitting, squatting, and wearing wide belts or low-rider trousers that compress the lateral femoral cutaneous nerve cause their symptoms to worsen (Figs. 108.1 to 108.3).1,4,5 Weight gain and weight loss, as well as pregnancy, have also been implicated as inciting events for meralgia paresthetica.6,7 Although traumatic lesions to the lateral femoral cutaneous nerve have been implicated in the onset of meralgia paresthetica, no obvious antecedent trauma can be identified in most patients.8–10
Clinical Presentation Physical findings include tenderness over the lateral femoral cutaneous nerve at the origin of the inguinal ligament at the anterior superior iliac spine.2 A positive Tinel sign over the lateral femoral cutaneous nerve as it passes beneath the inguinal ligament may be present11 (Fig. 108.4). Careful sensory examination of the lateral thigh reveals a sensory deficit in the distribution of the lateral femoral cutaneous nerve. A burning thigh sign may be present12 (Fig. 108.5). No motor deficit should be evident. Sitting or the wearing of tight waistbands or wide belts or low-rider trousers that compress the lateral femoral cutaneous nerve may exacerbate the symptoms of meralgia paresthetica.
Diagnosis Electromyography helps to distinguish lumbar radiculopathy and diabetic femoral neuropathy from meralgia paresthetica. Plain radiographs of the back, hip, and pelvis are indicated in all patients who present with meralgia paresthetica, to rule out occult bony disease. Based on the patient's clinical presentation, additional testing including complete blood cell count, uric acid, sedimentation rate, and antinuclear antibody © 2011 Elsevier Inc. All rights reserved.
Treatment 821 Conclusion 823
testing may be indicated. Magnetic resonance imaging (MRI) of the back is indicated if herniated disk, spinal stenosis, or a space-occupying lesion is suspected. The injection technique described later serves as both a diagnostic test and a therapeutic maneuver.
Differential Diagnosis Meralgia paresthetica is often misdiagnosed as lumbar radi culopathy or trochanteric bursitis or is attributed to primary hip disease.13,14 Radiography of the hip and electromyography help to distinguish meralgia paresthetica from radiculopathy or pain emanating from the hip. Most patients suffering from lumbar radiculopathy have back pain associated with reflex, motor, and sensory changes accompanied by neck pain, whereas patients with meralgia paresthetica have no back pain and no motor or reflex changes. The sensory changes of meralgia paresthetica are limited to the distribution of the lateral femoral cutaneous nerve and should not extend below the knee (see Fig. 108.4). Lumbar radiculopathy and lateral femoral cutaneous nerve entrapment may coexist as the double-crush syndrome. Occasionally, diabetic femoral neuropathy may produce anterior thigh pain that may confuse the diagnosis.
Treatment The patient suffering from meralgia paresthetica should be instructed in avoidance techniques to help reduce the unpleasant symptoms and pain associated with this entrapment neuropathy. A short course of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory agents, or cyclooxygenase-2 inhibitors is a reasonable first step in the treatment of patients suffering from meralgia paresthetica.1,2 If the patient does not experience rapid improvement, the following injection technique is a reasonable next step.15,16 To treat the pain of meralgia paresthetica, the patient is placed in the supine position with a pillow under the knees. Lying with the legs extended increases the patient's pain because of traction on the nerve. The anterior superior iliac spine is identified by palpation. A point 1 inch medial to the 821
822
Section IV—Regional Pain Syndromes
Ant. sup. iliac spine Ant. inf. iliac spine
Fig. 108.3 Direct compression of the lateral femoral cutaneous nerve is caused by the waistband of low-cut “taille basse” trousers. (From Moucharafieh R, Wehbe J, Maalouf G: Meralgia paresthetica: a result of tight new trendy low cut trousers [“taille basse”], Int J Surg 6:164, 2008.)
Lat. femoral cutaneous n.
Fig. 108.1 Obesity and wearing of wide belts may cause compression of the lateral femoral cutaneous nerve and result in meralgia paresthetica. (From Waldman SD: Atlas of common pain syndromes, Philadelphia, 2002, Saunders, p 235.)
Likely points of compression
Iliac m. and fascia
Inguinal lig.
Lat. femoral cutaneous n. ASIS
Post. br.
Inguinal lig.
Ant. br.
Sartorius m.
a
Fig. 108.2 Area of compression of the lateral femoral cutaneous nerve by low-cut “taille basse” trousers (danger zone) (a), site of compression within the muscle; ASIS, anterior superior iliac spine. (From Moucharafieh R, Wehbe J, Maalouf G: Meralgia paresthetica: a result of tight new trendy low cut trousers [“taille basse”], Int J Surg 6:164, 2008.)
20 Rheum 5.13
Fig. 108.4 Course of the lateral femoral cutaneous nerve. The potential for entrapment of the lateral femoral cutaneous nerve can be seen by its course just under the inguinal ligament and medial to the anterior superior iliac spine. (From Klippel JH, Dieppe PA, editors: Rheumatology, ed 2, London, 1998, Mosby.)
Chapter 108—Meralgia Paresthetica
A
823
B Fig. 108.5 A and B, Eliciting the burning lateral thigh sign for meralgia paresthetica.
Ant. sup. iliac spine
Inguinal lig. Iliopsoas m.
Iliacus
SAR Medial
Lat. femoral cutaneous n. Femoral n. Femoral a. Femoral v. Pectineus m. Sartorius m.
Fig. 108.6 Injection technique for relieving the pain of meralgia paresthetica. (From Waldman SD: Atlas of interventional pain management, ed 3, Philadelphia, 2009, Saunders, p 522.)
anterior superior iliac spine and just inferior to the inguinal ligament is then identified and is prepared with antiseptic solution (Fig. 108.6). A 1.5-inch 25-gauge needle is then advanced perpendicular to the skin slowly until the needle is felt to pop through the fascia. Paresthesia is often elicited. After careful aspiration, a total of 5 to 7 mL of 1.0% preservativefree lidocaine and 40 mg of methylprednisolone is injected in a fanlike manner as the needle pierces the fascia of the external oblique muscle. Care must be taken not to place the needle too deeply, to avoid entering the peritoneal cavity and perforating the abdominal viscera. After injection of the solution, pressure is applied to the injection site to decrease the incidence of postblock ecchymosis and hematoma formation, which can be quite dramatic, especially in the anticoagulated patient. Ultrasound guidance (Fig. 108.7) may be beneficial in patients whose anatomic landmarks are difficult to identify.17 Care must be taken to rule out other conditions that may mimic the pain of meralgia paresthetica. The main side effects of the just-described nerve block are postblock ecchymosis and
Fig. 108.7 Ultrasonographic image of the lateral femoral cutaneous nerve (solid arrows), which has already branched into smaller nerves and appears as hypoechoic structures. SAR, sartorius muscle. (From Seib RK, Peng PWH: Ultrasound-guided peripheral nerve block in chronic pain management, Tech Reg Anesth Pain Manag 13:110, 2009.)
hematoma formation. If needle placement is too deep and enters the peritoneal cavity, perforation of the colon may result in the formation of intra-abdominal abscess and fistula. Early detection of infection is crucial to avoid potentially life-threatening sequelae. If the needle is placed too medially, blockade of the femoral nerve may occur and may make ambulation difficult.
Conclusion Meralgia paresthetica is a common pain complaint encountered in clinical practice. It is often misdiagnosed as lumbar radiculopathy. If a patient presents with pain suggestive of lateral femoral cutaneous neuralgia and does not respond to lateral femoral cutaneous nerve blocks, a diagnosis of lesions more proximal in the lumbar plexus or L2-3 radiculopathy should be considered. Such patients often respond to epidural steroid blocks. Electromyography and MRI of the lumbar plexus are indicated in this patient population to help rule out other causes of lateral femoral cutaneous pain, including malignant disease invading the lumbar plexus or epidural or vertebral metastatic disease at L2-3.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
109
Femoral and Saphenous Neuropathies Bernard M. Abrams
CHAPTER OUTLINE Historical Considerations 824 Femoral Neuropathy 824 Anatomy 824 Clinical Presentation 825 Etiology 825 Iliac Hemorrhage 825 Iliac Abscess 826 Abdominal Aortic Aneurysms 826 Trauma, Stretch, or Compression 826 Idiopathic Etiology 826 Tumors, Complications of Cancer Therapy, and Other Space-Occupying Lesions 826 Diabetes Mellitus 826 Pregnancy and Delivery 826 Iatrogenic Causes 826 Hip Arthroplasty 826
Neural Blockade and Tourniquet Use 826 Abdominal Hysterectomy and Tuboplasty 826 Laparoscopy 826 Renal Transplantation 826 Lithotomy Positions 827 Inguinal and Femoral Herniorrhaphies 827 Diagnosis and Testing 827 Treatment 827 Prognosis 827
Saphenous Neuropathy 827 Anatomy 827 Etiology 828 Clinical Presentation 828 Diagnosis and Testing 828 Treatment 828
Femoral and saphenous neuropathies are uncommon painproducing conditions. Femoral neuropathy can produce pain of the anterior thigh and midcalf and is associated with weakness of the quadriceps muscle. This disorder can be caused by myriad factors.1 The saphenous nerve, a pure sensory nerve and anatomic extension of the femoral nerve, can produce medial calf pain that may be confused with medial calf claudication.2
association of the relatively uncommon femoral neuropathy with diabetes mellitus persisted when, in fact, diabetes is much more commonly associated with lumbar plexopathy. The long history of this erroneous association terminated only with the advent of modern meticulous electrodiagnostic methods and should serve as a cautionary note not to neglect the multiple possible causes of true femoral neuropathy.7
Historical Considerations
Femoral Neuropathy
In 1960, Kopell and Thompson3 described entrapment of the saphenous nerve, but undoubtedly saphenous nerve dysfunction and injury have been known for many years as a result of experience with trauma and surgery in the region of the medial thigh. Descriptions of diabetic neuropathy as early as 1890 recognized cases characterized by asymmetrical lower extremity pain and weakness.4 This concept dates back to 1798, when John Rollo mentioned neurologic disorders in his book Cases of Diabetes Mellitus, and it persisted through the eighteenth, nineteenth, and twentieth centuries until, at least, 1976.5 Then it became recognized that what had previously been termed femoral neuropathy was much more frequently lumbar plexopathy. Asbury6 clarified the issue advocating the term proximal diabetic neuropathy in view of the ambiguities associated with the earlier term diabetic amyotrophy. Unfortunately, the
The femoral nerve arises from the lumbar plexus within the psoas major muscle. It is formed from the posterior divisions of the ventral rami of the L2-4 spinal nerve roots (Fig. 109.1). After emerging from the lateral border of the psoas muscle, the femoral nerve lies in a groove between the psoas and iliacus muscles. As it approaches the external iliac artery (which is anteromedial to it), the nerve and artery descend toward the pelvis. In its descent, the nerve gives off some branches to innervate the iliacus and psoas muscles.7 The psoas is also innervated by branches of the L2 and L3 spinal nerve roots. Authorities differ on whether clinically significant innervation of the iliacus and psoas muscles arises from the beginning of the femoral nerve or from fibers of the lumbar plexus proximal to the origin of the femoral nerve. Therefore, weakness of hip
824
Anatomy
© 2011 Elsevier Inc. All rights reserved.
Chapter 109—Femoral and Saphenous Neuropathies
825
Table 109.1 Causes of Femoral Neuropathy Lat. femoral cutaneous n.
Femoral n.
Retroperitoneal and Iliacus Compartment Hemorrhage Spontaneous Associated with anticoagulants (e.g., heparin, warfarin [Coumadin]) Traumatic iliacus muscle avulsion Hemophilia and other coagulopathies Traumatic pseudoaneurysm and iliacus hematoma Iliacus abscess Abdominal aortic aneurysm and pseudoaneurysm Trauma, stretch, or compression Idiopathic Tumors, enlarged lymph nodes, complications of radiation, and chemotherapeutic injection Diabetes mellitus (usually as part of lumbar plexopathy) Pregnancy and labor
Saphenous n.
Fig. 109.1 Anatomy of the femoral nerve.
Iatrogenic Hip arthroplasty Neural blockade and tourniquet use Abdominal hysterectomy including retractor injury Renal transplants and other urologic and pelvic surgery Lithotomy position for delivery and surgery, including vaginal hysterectomy Inguinal and femoral herniorrhaphies
flexion resulting from involvement of the psoas and iliacus may or may not be included in the definition of the femoral nerve syndrome, depending on which viewpoint is espoused. The femoral nerve, the psoas muscle, the iliacus muscle, and the iliolumbar vessels, roofed over by the iliacus fascia, form a tight iliacus compartment. This compartment accounts for femoral nerve lesions resulting from space-occupying processes in this area. The femoral nerve then passes beneath the inguinal ligament, gives off a branch to the pectineus muscle, and then enters the femoral triangle lateral to the femoral artery and separated from the artery by some psoas fibers. Approximately 4 cm distal to the inguinal ligament, the artery bifurcates into an anterior division and a posterior division. The anterior division innervates the sartorius muscle and forms the medial and intermediate femoral cutaneous nerves that give sensory innervation to the skin of the medial and anterior surfaces of the knee, the medial surface of the lower leg, medial malleolus, and part of the arch of the foot and great toe. The anterior division also gives motor branches to the quadriceps muscles composed of the rectus femoris, vastus lateralis, vastus intermedius, and vastus medialis muscles. It continues as the saphenous nerve (see later).
as anticoagulation. Severe femoral nerve lesions produce weakness and eventually wasting of the quadriceps group of muscles, loss of the knee reflex (although this may also be seen in high lumbar radiculopathies [L3-4]), and sensory abnormalities over the anterior aspect of the thigh and the medial part of the lower leg. In proximal diabetic neuropathy8,9 (actually lumbar plexopathy in most cases), patients characteristically have severe pain radiating from the groin into the anterior thigh. This pain is usually worse at night and at rest (in contrast to a lumbar radiculopathy), and it subsides over several days to weeks, followed by severe painless weakness of the quadriceps group of muscles. This pain may be severe enough to require opioids for relief. During examination of a patient with suspected femoral neuropathy, the iliopsoas muscle and hip adductor strength must be evaluated to differentiate among femoral neuropathy, combined obturator and femoral neuropathy, and upper lumbar plexopathy or L2, L3 radiculopathy.10
Clinical Presentation
Numerous conditions, many of them iatrogenic, can produce femoral neuropathies. The most common causes are listed in Table 109.1.
Patients with femoral neuropathies usually complain that their lower extremity buckles at the knee and they cannot maintain their stance, especially when trying to descend stairs.8 These patients may have pain, numbness, and paresthesias in the entire femoral nerve and saphenous nerve distribution, or sensory abnormalities may be mild or even absent entirely. When pain is felt, it may be in the inguinal region or in the iliac fossa. When flank pain is severe in patients with other symptoms and signs of femoral neuropathy, hemorrhage in the iliacus compartment should be strongly suspected, especially in circumstances conducive to hemorrhage, such
Etiology
Iliac Hemorrhage A hemorrhage in the tight iliacus compartment can compress the femoral nerve. Causes range from the common hemorrhage resulting from anticoagulation to hemophilia and other coagulopathies. The characteristic clinical picture consists of femoral nerve dysfunction and severe pain and swelling. The pain is generally located in the iliac fossa and groin and is associated with a flexed posture of the leg at the hip. Ecchymoses may be present in the upper thigh.9 Hematomas
826
Section IV—Regional Pain Syndromes
within the psoas muscle characteristically cause widespread lumbar plexopathy, but occasionally patients have only femoral dysfunction. False aneurysms may form within the psoas muscle.10–30 Traumatic avulsion of the iliacus muscle may occur in otherwise healthy people, occasionally after only minor trauma.31,32,34
Iliac Abscess Iliac abscess may develop independently or may result from infection of a hematoma. With the addition of the signs of infection, the signs are the same as in hemorrhage.33
Abdominal Aortic Aneurysms Sometimes, abdominal aortic aneurysms rupture into the psoas muscle and produce false aneurysms that compress the femoral nerve. Other arteries, including the profunda femoral artery and the iliac artery, may have aneurysms or false aneurysms that compress the femoral nerve.35–42
Trauma, Stretch, or Compression Direct injury by bullet wounds, stab wounds, blunt injuries, and hip and pelvic fractures can compromise the femoral nerve. Gymnasts and dancers have been reported to incur femoral nerve injuries during hyperextension of the hip. Damage during coma and drunken stupors has also been reported, and alcoholism itself has been reported as a cause.43–49
Idiopathic Etiology One report in 197049 found that 18 of 50 patients had no demonstrable cause of their neuropathy. Given that most of these patients were men who were more than 50 years old and who had eventual resolution of the neuropathy over months, some may of these patients have had occult diabetic plexopathy.
Tumors, Complications of Cancer Therapy, and Other Space-Occupying Lesions Tumors may arise primarily from the nerve sheath, they may arise from the iliopsoas muscle or the ilium itself, or rarely they may be primary malignant neoplasms or metastases and cause femoral neuropathy.50–60 Infusions of chemotherapeutic agents into the femoral artery may also cause femoral neuropathy.5
Diabetes Mellitus Although the older literature described diabetes as the most common cause of femoral neuropathy, current electrodiagnosis has clearly identified the lumbosacral plexus as the primary pathologic site of the lesion. The femoral nerve is often the most severely affected structure involved, although other portions of the lumbosacral plexus can clearly be shown to be affected.7 An association with renal failure has been noted.61
Iatrogenic Causes Unfortunately, iatrogenic femoral neuropathy is all too frequent. It has been associated with many different surgical procedures in the abdomen, pelvic inguinal, and hip areas.69 This complication has most frequently been associated with abdominal hysterectomy and the use of self-retaining retractors that compress the femoral nerve directly or within the iliopsoas muscle and the lateral wall of the pelvis. The incidence of iatrogenic femoral neuropathy is significantly lower when these retractors are not used. Hip replacement and repair have also been reported as common causes of femoral neuropathy, although sciatic neuropathy occurs more frequently in these situations. Other circumstances in which femoral neuropathy may occur are renal transplantation, inguinal or femoral herniorrhaphy, lymph node resection in the groin, femoral artery surgery, cardiac catheterization, and angioplasty. Suturing of the femoral nerve may occur during surgery, as may extrusion of cement, adverse effects of tourniquet use, and untoward effects of neural anesthetic blockage.
Hip Arthroplasty Following hip arthroplasty, femoral neuropathy occurs much less frequently than does sciatic neuropathy (0.1% to 2.3%). When femoral neuropathy occurs, it is usually the result of retractor compression, heat from bone cement or nerve encasement in cement, laceration, and complicating iliac hematoma. The onset of the disorder may be delayed by scar formation. Iliacus hemorrhage following prophylactic anticoagulation postoperatively has also been reported.70–80
Neural Blockade and Tourniquet Use Both neural blockade in the psoas compartment and ilioinguinal block for hernia repair have been associated with transient or permanent femoral nerve damage. Use of a tourniquet has damaged both the femoral and saphenous nerves.81–83
Abdominal Hysterectomy and Tuboplasty Abdominal hysterectomy has been the operation most strongly associated with intraoperative femoral nerve palsies. Two studies in the 1980s gave statistical incidences of 11.6% and 7.5%, respectively.84,85 Based on cadaver anatomic studies and clinical experience, the lateral blade of self-retaining retractors was ascribed to be the likely cause of femoral neuropathy. The abandonment of this instrument led to a reduction in femoral neuropathies from 7.5% to 0.7%.86 Other possible situations conducive to femoral neuropathy include suturing of the nerve and attempts at tubal ligation and reanastomosis.87–100
Laparoscopy Laparoscopy and suprapubic interventions have been implicated in the development of femoral neuropathy.
Pregnancy and Delivery
Renal Transplantation
Femoral neuropathy has been reported as a result of pregnancy and delivery, even in patients with uncomplicated situations.62–68 During pregnancy and before delivery, pressure on the femoral nerve in the pelvis is presumably implicated.64
Femoral neuropathy has been reported with some frequency in renal transplants that involve retroperitoneal placement of the donated kidney. Again, self-retaining retractors have been implicated, but even without the use of these instruments, delayed femoral neuropathy resulting from compression of the
Chapter 109—Femoral and Saphenous Neuropathies
nerve by hematoma has been seen and confirmed at autopsy. In addition, surgical procedures for genitourinary malignant diseases and other pelvic urologic operations have been complicated by femoral neuropathies.101–116
Lithotomy Positions Prolonged and, rarely, even brief intervals in the lithotomy position have produced femoral neuropathies, possibly because of kinking and compression of the nerve below the inguinal ligament. Prolonged lithotomy position for obstetric delivery and for surgical procedures such as laparoscopy may produce femoral neuropathy.117–119
Inguinal and Femoral Herniorrhaphies Femoral neuropathy may complicate inguinal or femoral herniorrhaphies when suture material is cut or placed around the nerve. Delayed onset of the neuropathy may result from later development of scar tissue.120–122
Diagnosis and Testing The cause of femoral neuropathy may be obvious because of the setting in which it arose, such as immediately postoperatively following a surgical procedure well known to be associated with this complication. Renal transplants, abdominal hysterectomy, and prolonged lithotomy positions head this category. Injections, catheterizations, and hernia surgery in the groin provide clear causality on many occasions. Confusion may arise in cases of delayed onset resulting from scarring or hemorrhage, although hemorrhage is generally associated with severe pain in the iliacus fossa. Again, circumstances may clearly show the cause in patients with hemorrhagic lesions, such as patients who undergo anticoagulation or those who have hemophilia or another coagulopathy. One of the maneuvers necessary when evaluating more occult causes is strict delineation of the anatomic boundaries of the patient's deficits. Often, what appears to be pure femoral neuropathy clinically may actually be part of a radiculoplexopathy. In patients with radiculoplexopathy, the anatomic site of the lesion is more proximal, and the diagnostic possibilities of diabetes mellitus and other processes such as malignant disease in the pelvis must be considered. Electromyography is well suited for this task, and testing should include sufficient interrogation of the quadriceps muscle group and the paraspinal, iliopsoas, and hip adductor muscles, to differentiate femoral neuropathy from more extensive lesions. Motor nerve conduction tests of the femoral nerve (stimulation point above the inguinal ligament and recording from the quadriceps muscle) may be performed, but these tests are generally less informative than needle electromyography123 and may need to be followed up with laboratory tests for diabetes mellitus and imaging of the pelvis by computed tomography (CT) or magnetic resonance imaging (MRI) scans.124–128 CT scan has long been shown to image the femoral nerve clearly, as have MRI and ultrasound. CT scan is indicated for suspected iliacus hemorrhages and other masses affecting the femoral nerve. Ultrasound and MRI are also effective in diagnosing iliacus hemorrhage and other masses.129–137
827
Treatment Obvious inciting lesions should be treated with such curative measures as are available. Exploration of the femoral nerve should be undertaken if complete disruption of the nerve, unintentional suturing, or stapling of the nerve is suspected. Management of retroperitoneal or iliopsoas hemorrhage may constitute a surgical emergency.138–140 Percutaneous relief of hemorrhage has been reported.140 In acute hemorrhage, anticoagulation, when present, must be reversed. Fluid and blood replacement may be necessary. Persistent pain requires pharmacologic treatment such as with gabapentin, pregabalin, other membrane stabilizers (newer anticonvulsants), tricyclic antidepressants, or other medications useful in neuropathic pain. Nerve blocks of the femoral nerve may be helpful to relieve pain. Physical therapy, bracing, and assistive devices may be necessary. Mobility and range of motion should be maintained.
Prognosis In iatrogenic femoral neuropathy, recovery is the usual outcome. The prognosis is better in incidents induced by the lithotomy position than it is in hip or inguinal surgical untoward events. The only significant prognostic factor is the percentage of axon loss in the vastus lateralis; this value is derived by a comparison of the vastus lateralis compound muscle action potential on the affected and unaffected sides.10
Saphenous Neuropathy Saphenous neuropathies can occur in the thigh as a result of lacerations, arterial surgery, compression by fibrous bands, and entrapment at the subsartorial canal exit.3 At the knee, saphenous neuropathies result from surgery, including arthroscopy or external compression. In the lower leg, this disorder is a complication of surgery. The infrapatellar branch can be injured by direct compression or by knee surgery, including arthroscopy and possibly entrapment in the sartorius muscle tendon.
Anatomy The saphenous nerve is the distal sensory continuation of the femoral nerve. It descends in the thigh through the quadriceps muscle in the subsartorial canal of Hunter lateral to the femoral artery. The saphenous nerve gives off an infrapatellar branch that supplies sensation to the anterior skin of the patella before it enters a fascial layer between the sartorius and gracilis muscles (Fig. 109.2). It emerges from the canal and becomes subcutaneous approximately 10 cm proximal to the knee.10 The nerve crosses the pes anserine bursa at the upper medial portion of the tibia and then runs distally along the medial aspect of the tibia. The saphenous vein is closely apposed to the nerve along most of its descent in the calf, especially in the distal third of the leg. At the lower third of the leg, the saphenous nerve divides into two main branches. One branch continues along the medial border of the tibia and terminates at the ankle. The other branch passes anteriorly with the vein to cross the medial surface of the tibia and in front of the medial malleolus to reach the foot; it then continues along the medial surface to the ball of the great toe. The saphenous nerve innervates the medial and anterior sensory portions of the knee and the medial surface of the lower leg, the medial malleolus, and a minor part of the medial arch of the foot and great toe.10
828
Section IV—Regional Pain Syndromes
Table 109.2 Causes of Saphenous Neuropathy
Saphenous n.
Thigh
Infrapatellar br.
Lacerations Arterial surgery (femoral artery) Compression Schwannoma Subsartorial canal entrapment Knee
Surgery: arthroscopy; medial meniscectomy External compression (stirrups) Lower Leg
Surgical injury (varicose vein operations, vein harvest for arterial surgery) Cannulation of saphenous vein Descending br.
Infrapatellar Branch
Compression and other direct injuries Fig. 109.2 Anatomy of the saphenous nerve.
Etiology Causes of saphenous neuropathy are outlined in Table 109.2. The differential diagnosis of saphenous neuropathy depends on the anatomic location. In the thigh, because of its proximity to the femoral artery in the subsartorial canal, the saphenous nerve can be damaged by arterial surgery, lacerations, compression by fibrous bands, schwannoma, or nerve entrapment in which the nerve pierces a fascial layer to leave the subsartorial canal.3 At the knee, saphenous nerve injury results from arthroscopic surgery, medial meniscectomy, and external compression from knee-supporting stirrups. It also occurs in surfers, who habitually grasp the board between their knees. In the lower leg, surgical damage or saphenous nerve cannulation can produce neuropathy. Spontaneous paresthesia of the infrapatellar branch has been termed gonyalgia paresthetica.141,142 The infrapatellar branch can be injured by direct compression, by knee surgery (arthroscopy), and questionably by entrapment in the sartorius tendon.
Clinical Presentation In saphenous neuropathy, patients may report trivial numbness, but severe neuropathic pain may also occur. The course of the nerve should be palpated for tenderness, a neuroma, or Tinel's sign. The pain may be present at the medial aspect of the knee and may radiate downward to the medial side of the foot. Patients often state that negotiating stairs causes significant aggravation of the pain.3 The sensory abnormality in the medial calf that may extend to the medial foot and the great toe may take the form of numbness or paresthesia.
Diagnosis and Testing Electromyography provides an anatomic method of differentiating plexopathy from radiculopathy or combined lesions. Saphenous nerve conduction studies are technically challenging but may be useful for confirming damage to the sensory fibers of the saphenous nerve.143–145
Arthroscopy Possible Entrapment in the Sartorius Tendon
Somatosensory evoked potentials may document dysfunction of the saphenous nerve but may not localize the lesion.141,146,147 CT scan of the abdomen is mandatory in patients with suspected lesions of the psoas muscle or retroperitoneal space. MRI has supplemented CT because of superior tissue resolution. Focal lesions of the saphenous nerve can be confirmed by nerve conduction studies, which may be technically difficult. Somatosensory evoked potentials have been used for saphenous nerve studies. If a differential diagnosis between L4 radiculopathy and a saphenous nerve lesion is under consideration, electromyography of the L4-innervated muscles should be performed. Suspicion of a schwannoma should lead to an MRI scan of the thigh, with and without gadolinium enhancement.7
Treatment Treatment depends on accurate diagnosis that, in turn, depends on setting up and resolving the diagnostic dilemma. Surgical correction of any lesion, when possible, is ideal. When residual pain and disability persist, rehabilitative efforts must be made. Although medical knowledge is constantly changing, neuropathic pain at this juncture is best dealt with by pharmacologic treatment such as with nonsteroidal anti-inflammatory drugs, mild analgesics, gabapentin, pregabalin, other membrane stabilizers (newer anticonvulsants), and tricyclic antidepressants, as well as by avoidance of precipitating factors for pain.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
110
IV
Obturator Neuropathy Bernard M. Abrams
CHAPTER OUTLINE Anatomy 829 Clinical Presentation 829 Etiology 830
Obturator neuropathy is an uncommon affliction that can cause medial thigh pain.1 Although its description as an entrapment neuropathy is historically interesting,2 the most frequent etiologic agent by far is trauma; and, unfortunately, iatrogenic trauma is the most common cause.
Anatomy Anatomically, the obturator nerve is formed within the psoas muscle by the ventral divisions of the ventral primary rami of the L2, L3, and L4 nerve roots (Fig. 110.1). It shares fibers from the same nerve roots as the femoral nerve. After descend ing through the psoas muscle, it emerges from the medial bor der of the psoas at the pelvic brim immediately anterior to the sacroiliac joint. In the female, it is separated from the ovary by a thin layer of peritoneum. The nerve then curves downward and forward around the pelvic cavity wall to emerge through the obturator foramen, where it is in company with the obtu rator vessels. The obturator canal is an osseofibrous canal formed by a hiatus in the obturator membrane up against the pubic bone. Of the anatomic structures in the canal, the nerve is the closest to the bone, which leads to its purported involve ment in osteitis pubis (Fig. 110.2).3 In the canal, it divides into anterior and posterior branches.4 The anterior branch innervates the adductor longus, adductor brevis, and graci lis muscles. The supply to the pectineus muscles is variable. The posterior branch supplies the obturator externus and adductor magnus muscles. The adductor brevis muscle may be supplied by either branch. Articular branches are given off to the hip joint.4 Sensory innervation of a limited area of the upper medial thigh is found. Because of its position, the nerve is seldom directly traumatized.
Clinical Presentation Although seldom damaged alone in extensive trauma, the hallmarks of obturator neuropathy are pain and weakness of the adductor musculature. The patient cannot stabilize the hip joint, and leg weakness is usually the predominant symptom, but paresthesias, often painful, may be the main symptom. © 2011 Elsevier Inc. All rights reserved.
Diagnosis 831 Treatment 831
Maneuvers that stretch the nerve such as extension or lateral leg movement may increase the pain. In an obturator hernia, if still mobile, an increase in abdominal pressure, as in coughing, sneezing, or straining, increases the pain.5 Careful examination of the strength of the hip adductors and quadriceps muscle, the patella reflexes, and the sensory deficit (Fig. 110.3) may serve to differentiate obturator neu ropathy from femoral neuropathy, but the two nerves are often damaged together because of their shared nerve root and lumbar plexus origin and course in pelvic trauma or hip surgery. Lumbar radiculopathy of L3 or L4 may also account for the weakness and shifts the focus to the lumbar spine for pathology.
Ant. sup. iliac spine
Obturator n.
Articular br.
Obturator foramen Post. br. Ant. br.
Cutaneous br.
Fig. 110.1 Anatomy of the obturator nerve.
829
830
Section IV—Regional Pain Syndromes
Etiology Broad categories of etiology are pelvic fractures, complications of hip replacements, malignant pelvic mass or endometriosis (note its proximity to the ovary in the female), obturator her nia, complications of labor, lithotomy position, entrapment, and as a complication in the newborn (Table 110.1). As stated previously, isolated obturator nerve injuries are rel atively rare, and pelvic fractures and penetrating injuries such as gunshot wounds much more frequently injure multiple nerves
or other neural structures, such as nerve roots or the lumbar plexus.6–9 The obturator nerve can be injured during hip or pel vic surgery as a result of stretch, retractor compression, injury from cement (encasement or thermal injury), or electrocau tery.10–14 Massive pelvic hemorrhage, either spontaneous or dur ing gynecologic surgery, can cause obturator neuropathy.15,16 Obturator hernias can cause pain down the medial thigh, espe cially with Valsalva's maneuvers.17,18 The lithotomy position has been implicated in obturator neuropathies, both in urologic
Table 110.1 Causes of Obturator Neuropathy Pelvic fractures Direct penetrating injuries Pelvis malignant diseases Endometriosis
Obturator n.
Complications of hip arthroplasty, including encasement by cement Articular br.
Obturator foramen Post. br. Ant. br.
Obturator externus m.
Obturator hernia Obturator nerve entrapment Lithotomy position Pregnancy and labor (multiple mechanisms)
Fig. 110.2 The obturator canal. (Redrawn from Kopell HP, Thompson WAL: Obturator nerve entrapment, N Engl J Med 262:56, 1960.)
Pelvic hemorrhage (including as a complication of procedures such as cardiac catheterization) Obturator palsy of the newborn
Obturator canal Obturator n. Branch to obturator externus m.
Ant. br. obturator n.
Branch to adductor brevis m. Branch to adductor longus m.
Branch to adductor magnus m.
Branch to gracilis m.
Fig. 110.3 Sensory testing of the obturator nerve.
and in gynecologic surgeries.19–23 It also has been reported dur ing pregnancy and delivery, but here, multiple factors are at play, including the fetal head, forceps application, hematoma, or other trauma occasioned by cesarean section or improper lithotomy position.24,25 Malignant tumors can compress or invade the obturator nerve, as can endometriosis and laparo scopic pelvic lymphadenectomy, making visualization of the nerve mandatory during electrocautery.26,27 Aneurysm of the hypogastric artery can also produce compression of the obtu rator nerve.6,28,29 Obturator neuropathy caused by cardiac catheterization is a special case of retroperitoneal hematoma formation compressing the nerve.30,31 Bradshaw and associates32 reported on 32 athletes who had entrapment of the obturator nerve by fascial entrapment of the nerve entering the thigh with distal pain radiating along the medial thigh induced by exercise with surgical relief from excision of the thickened fascia over the short adductor muscle. All of the afflicted athletes participated in sports with a “leg predominance,” such as soccer and rugby. Idiopathic obturator neuropathy has also been described.33 Finally, infants are not immune to obturator neuropathy, and one case possibly related to prolonged abnormal intrauterine leg position has been reported.34
Diagnosis The clinical examination and the setting in which the neuro pathy arose generally suggest its cause. Electromyography is essential for confirmation of anatomic location, and the differential diagnosis includes much more common multiple neuropathies, lumbar plexopathies, and L3-L4 nerve root lesions. For possible retroperitoneal hemorrhage or tumor,
Chapter 110—Obturator Neuropathy
831
computed tomographic scan, magnetic resonance imaging, and ultrasound scan are helpful.35,36 Angiography may be necessary in the patient suspected of having a hypogastric artery aneurysm. The question of the possible relationship to diabetes melli tus arises in the same context as that for femoral neuropathy. Muscles innervated by the obturator nerve are almost invariably affected by so-called diabetic amyotrophy. Two reports in the literature37,38 invoke diabetes as a cause of obturator neuropathy, but this, as in the case of femoral neuropathy, remains problem atic. The reader is referred to a recent retrospective study that analyzed causes and outcomes.39
Treatment Obvious inciting lesions should be treated with such curative measures as are available, that is, surgery for management of tumors, hemorrhage, or entrapment as indicated. In particular, when hip arthroplasty has been carried out, after a period of observation, reexploration may be indicated because of the possibility of the nerve being encased in cement. Persistent pain necessitates pharmacologic treat ment, such as with gabapentin, pregabalin, other membrane stabilizers (newer anticonvulsants), tricyclic antidepres sants, or other medications useful in neuropathic pain. One report in the literature seems to indicate some promise in the treatment of intractable pain, but further evaluation is warranted.40
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
111
Painful Conditions of the Knee Steven D. Waldman
CHAPTER OUTLINE Functional Anatomy of the Knee 834 Common Painful Conditions of the Knee 836 A Rational Approach to Knee Pain 837 The Targeted History 837 Acute or Chronic? 837 Age of the Patient 837 Presence of Trauma 837 Fever 838 Polyarthralgias 838 Rash 838 Muscle Weakness 838 Constitutional Symptoms 838 Recent Weight Gain or Loss 838 Addition of New Medications 839 Use of Anticoagulants 839
Knee pain is one of the most common reasons that patients seek medical attention from their primary care physicians, orthopedists, rheumatologists, and pain management specialists. Knee pain can arise from the joint or the periarticular tissues (e.g., the bursae and tendons) or may be referred from the hip joint, femur, or proximal tibia and fibula. The largest joint in the body, the knee is subject to an amazing array of forces and injuries.1 In this chapter, an overview is presented of some of the more common knee pain syndromes encountered in clinical practice.
Functional Anatomy of the Knee For accurate diagnosis and treatment of knee pain, the clinician must have a clear understanding of the functional anatomy of the knee. The knee is not just a simple hinge joint that flexes and extends. The largest joint in the body in terms of articular surface and joint volume, the knee is capable of amazingly complex movements that encompass highly coordinated flexion and extension.2 The knee joint is best thought of as a cam capable of locking in a stable position. Even the simplest movements of the knee involve an elegantly coordinated rolling and gliding movement of the femur on the tibia. Because of the complex nature of these movements, the knee is extremely susceptible to functional abnormalities with relatively minor alterations in the anatomy from arthritis or damage to the cartilage or ligaments. Although both clinicians and laypersons think of the knee joint as a single joint, from the viewpoint of understanding its functional anatomy, it is more helpful to think of the knee 834
Corticosteroids 839 Tick Bites 839 Targeted Physical Examination 839 Palpation of the Knee 839 Valgus Stress Test for Medial Collateral Ligament Integrity 840 Varus Stress Test for Lateral Collateral Ligament Integrity 840 Anterior Drawer Test for Anterior Cruciate Ligament Integrity 840 Posterior Drawer Test for Posterior Cruciate Ligament Integrity 841 McMurray's Test for Torn Meniscus 841 Use of Testing Modalities for Evaluation of the Painful Knee 841
Conclusion 842
as two separate but interrelated joints: the femoral-tibial and the femoral-patellar joints (Fig. 111.1). Both joints share a common synovial cavity, and dysfunction of one joint can easily affect the function of the other. The femoral-tibial joint is made up of the articulation of the femur and the tibia. Interposed between the two bones are two fibrocartilaginous structures known as the medial and lateral menisci (Fig. 111.2). The menisci serve to help transmit the forces placed on the femur across the joint onto the tibia. They possess the property of plasticity in that they are able to change their shape in response to the variable forces placed on the joint through its complex range of motion. The medial and lateral menisci are relatively avascular and receive the bulk of their nourishment from the synovial fluid, which means that little potential for healing exists when these important structures are traumatized. The femoral-patellar joint's primary function is to use the patella, which is a large sesamoid bone embedded in the quadriceps tendon, to improve the mechanical advantage of the quadriceps muscle. The medial and lateral articular surfaces of the sesamoid interface with the articular groove of the femur (Fig. 111.3). In extension, only the superior pole of the patella is in contact with the articular surface of the femur. As the knee flexes, the patella is drawn superiorly into the trochlear groove of the femur. Most of the knee joint's stability comes from the ligaments and muscles surrounding it, with little contribution from the bony elements. The main ligaments of the knee are the anterior and posterior cruciate ligaments, which provide much of the © 2011 Elsevier Inc. All rights reserved.
Chapter 111—Painful Conditions of the Knee
anteroposterior stability of the knee, and the medial and lateral collateral ligaments, which provide much of the valgus and varus stability (Fig. 111.4). All of these ligaments also help prevent excessive rotation of the tibia in either direction. A number of secondary ligaments also add further stability to this inherently unstable joint. The main extensor of the knee is the quadriceps muscle, which attaches to the patella via the quadriceps tendon. Fibrotendinous expansions of the vastus medialis and vastus lateralis insert into the sides of the patella and are subject to strain and sprain. The hamstrings are the main flexors of the hip, along with help from the gastrocnemius, sartorius, and gracilis muscles. Medial rotation of the flexed knee is via the medial hamstring muscle, and lateral rotation of the knee is controlled by the biceps femoris muscle. The knee is well endowed with a variety of bursa to facilitate movement. Bursae are formed from synovial sacs whose purpose it is to allow easy sliding of muscles and tendons across one another at areas of repeated movement. These synovial sacs are lined with a synovial membrane that is invested with a network of blood vessels that secrete synovial fluid. Inflammation of the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or misuse, these bursae may become inflamed, enlarged, and, on rare occasions, infected (Fig. 111.5). Given that the knee shares a common synovial cavity, inflammation of one bursa can cause significant dysfunction and pain of the entire knee.
Fig. 111.1 Functional anatomy of the knee is easier to understand if it is viewed as two separate but interrelated joints: the femoral-tibial and the femoral-patellar joints. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 322.)
Vastus medialis m.
•
•
••
Iliotibial tract
•
•
Vastus lateralis m.
Med. sup. genicular a.
••
Lat. sup. genicular a.
Adductor magnus t. Femur
•
•
Post. cruciate lig.
•
Popliteus t.
•
•
Iliotibial tract
Ant. cruciate lig.
Med. meniscus
•
••
•
Lat. meniscus
•• ••
Peroneus longus and extensor digitorum longus mm.
Tibial collateral lig.
Sartorius t. Tibia
••
••
Med. inf. genicular a.
•
Ant. tibial recurrent a.
835
••
Gracilis and semitendinosus tt.
Fig. 111.2 Coronal view of the knee. (From Kang HS, Joong AM, Resnick D: MRI of the extremities, Philadelphia, 2002, Saunders, p 301.)
836
Section IV—Regional pain syndromes
• •
Prefemoral fat body Quadriceps t.
•
Rectus femoris m.
•
••
•
Suprapatellar bursa Suprapatellar fat body
•
••
••
••
Oblique popliteal lig. and joint capsule Ant. cruciate lig. Post. meniscolemoral lig. of Wrisberg
••
•
Post. cruciate lig.
••
• •
••
•
Tibia
•
Gastrocnemius, lat. head and plantaris mm. Popliteal v and tibial n.
••
Joong AM, Resnick D: MRI of the extremities, Philadelphia, 2002, Saunders, p 341.)
Tibial n.
••
Fig. 111.3 Sagittal view of the knee. (From Kang HS,
•
••
••
Transverse lig. Lat. inf. genicular a. Infrapatellar fat body Patellar lig.
Lat. sup. genicular a. Femur
•
Patella
Tibial n.
••
Popliteus m. Soleus m.
Fig. 111.4 The main ligaments of the knee. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 325.)
Common Painful Conditions of the Knee The initial general physical examination of the knee guides the clinician in narrowing his or her differential diagnosis and helps suggest which specialized physical examination maneuvers and laboratory and radiographic testing will aid
Fig. 111.5 A, Deep infrapatellar bursitis. A sagittal T2-weighted (TR/ TE, 2300/70) spin-echo MRI shows fluid of high signal intensity (arrow) in the deep infrapatellar bursa. B, Prepatellar bursitis. A sagittal T2-weighted (TR/TE, 2000/80) spin-echo MRI shows fluid of high signal intensity (arrows) in the prepatellar bursa. (A, Courtesy of M Zlatkin, MD, Hollywood, FL. B, Courtesy of EM Bellon, MD, Cleveland, OH. From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 3285.)
in confirming the cause of the patient's knee pain and dysfunction.3 For the clinician to make best use of the initial information gleaned from the general physical examination of the knee, a grouping of the common causes of knee pain and dysfunction is exceedingly helpful. Although no classification of knee pain and dysfunction can be all inclusive or all exclusive because of the frequently overlapping and multifactoral nature of knee pathology, Table 111.1 should help improve the diagnostic accuracy of the clinician confronted with the patient with knee pain and dysfunction and help the clinician avoid overlooking less common diagnoses. The list of disease processes in Table 111.1 is by no means comprehensive, but it does aid the clinician in organizing the potential sources of pathology that manifest as knee pain and dysfunction. The most commonly missed categories of knee pain and the categories that most often result in misadventures in diagnosis and treatment are the last three categories. The knowledge of this potential pitfall should help the clinician keep these sometimes overlooked causes of knee pain and dysfunction in the differential diagnosis.
A Rational Approach to Knee Pain The Targeted History
Chapter 111—Painful Conditions of the Knee
Table 111.1 Classification of Painful Conditions That Affect the Knee Knee Pain From Localized Bony or Joint Space Pathology
Fracture Primary bone tumor Primary synovial tissue tumor Joint instability Localized arthritis Osteophyte formation Joint space infection Hemarthrosis Villonodular synovitis Intra-articular foreign body Osgood-Schlatter disease Chronic dislocation of the patella Patellofemoral pain syndrome Patella alta Knee Pain From Periarticular Pathology
The starting point for the clinician faced with the patient with knee pain is to obtain a targeted history and perform a targeted physical examination of the affected knee or knees based on that history. Salient features of the targeted history are summarized in Table 111.2. The relevance of each is discussed briefly.
Bursitis
Acute or Chronic?
Muscle sprain
The onset of acute knee pain in the absence of trauma is a cause for concern in that many of the diseases associated with acute knee pain can cause significant damage to the joint if not promptly diagnosed and treated.4 The connective tissue diseases, septic arthritis, the crystal arthropathies, and hemarthrosis in the patient undergoing anticoagulation therapy are just a few of the diseases that can permanently damage a knee. Any acute knee pain associated with fever or constitutional symptoms or occurring in a patient on anticoagulation therapy should be taken seriously and not automatically attributed to “arthritis.”
Tendinitis Adhesive capsulitis Joint instability Muscle strain Periarticular infection not involving joint space Knee Pain From Systemic Disease
Rheumatoid arthritis Collagen vascular disease Reiter's syndrome Gout Other crystal arthropathies Charcot's neuropathic arthritis Knee Pain From Sympathetically Mediated Pain
Age of the Patient
Causalgia
The age of the patient can provide significant direction to the clinician's search for a diagnosis. Table 111.3 provides a grouping of the most common causes of knee pain in different age groups. The presence of knee pain in childhood and early adolescence in the absence of trauma is a cause for concern and should not be attributed to “growing pains.”
Reflex sympathetic dystrophy
Presence of Trauma Traumatic knee pain is common. Many knee pain syndromes after trauma can be managed conservatively. However, the clinician should remember that many cannot. Early use of magnetic resonance imaging (MRI) of the traumatic knee serves two purposes: (1) it allows the clinician to aggressively rehabilitate those knees in which no internal derangement has be identified; and (2) it allows rapid surgical treatment of those patients with significant ligamentous and cartilaginous injuries before they do more damage to an already compromised joint.4–6
Knee Pain From Other Body Areas
Lumbar plexopathy Lumbar radiculopathy Lumbar spondylosis Fibromyalgia Myofascial pain syndromes Inguinal hernia Entrapment neuropathies Intrapelvic tumors Retroperitoneal tumors
837
838
Section IV—Regional pain syndromes
Fever Acute knee pain and fever should be considered a dangerous combination.7 Although some acute febrile illnesses, such as streptococcal pharyngitis, may have large joint arthralgias as part of their constellation of symptoms, the clinician must rule out the septic knee joint, the collagen vascular diseases, and Lyme disease before assuming that the fever and joint pain are unrelated. In younger patients, rheumatic fever must always be considered in the d ifferential diagnosis of knee pain in the presence of fever.
Polyarthralgias The patient presenting with knee pain who also has pain in other joints is a cause for concern. Although in the older, otherwise healthy patient, osteoarthritis is the most common reason for this clinical presentation, the clinician should be careful to avoid jumping to this conclusion without careful consideration.8 The
Table 111.2 Targeted History for Knee Pain Acute or chronic Age of patient History of trauma Fever Pain in other joints
connective tissue diseases, including polymyalgia rheumatic, are a common cause of polyarthralgias in older patients.9,10 Polyar thralgias in the younger patient should point the clinician toward the diagnosis of juvenile rheumatoid arthritis, among others.
Rash The presence of rash and knee pain should suggest a number of potentially problematic diseases, such as Lyme disease and the connective tissue diseases, especially systemic lupus erythematosus and dermatomyositis.11 In younger patients, the rash often is a harbinger of the onset of a collagen vascular disease or rheumatic fever. Gonococcal arthritis may also present with rash as its first symptom.
Muscle Weakness The symptom of muscle weakness should clue the physician to strongly consider the connective tissue diseases, especially polymyalgia rheumatica and polymyositis.12,13 The paraneoplastic syndromes associated with malignancy disease can also present as large joint pain and muscle weakness. Dermatomyositis in the younger age group is another diagnostic consideration in the setting of knee pain and muscle weakness. Approximately 20% of patients with dermatomyositis have an occult malignancy disease, which could include primary or metastatic tumors that involve the knee and its related structures.12
Rash
Constitutional Symptoms
Muscle weakness
As with all other areas of medicine, the presence of constitutional symptoms should alert the clinician to the potential that a serious systemic illness is present. The association of constitutional symptoms and knee pain should suggest the possibility of primary tumor or metastatic disease; the connective tissue diseases, especially polymyalgia rheumatic; and hypothyroidism.10
Other constitutional symptoms (e.g., malaise, anorexia) Recent weight gain or loss Addition of any new medications Use of anticoagulant therapy Recent administration of corticosteroids Recent tapering of corticosteroids Recent tick bite
Recent Weight Gain or Loss Recent unexplained weight loss in the presence of knee pain has the same implications as the presence of constitutional
Table 111.3 Common Causes of Knee Pain in Different Age Groups Cause Age group
Intra-articular
Periarticular
Referred
Childhood (2 to 10 years)
Juvenile chronic arthritis Osteochondritis dissecans Septic arthritis Torn discoid lateral meniscus
Osteomyelitis
Perthes' disease Transient synovitis of the hip
Adolescence (10 to 18 years)
Osteochondritis dissecans Torn meniscus Anterior knee pain syndrome Patellar malalignment
Osgood-Schlatter disease Sinding-Larsen-Johansson disease Osteomyelitis Tumors
Slipped upper femoral epiphysis
Early adulthood (18 to 30 years)
Torn meniscus Instability Anterior knee pain syndrome Inflammatory conditions
Overuse syndromes Bursitis
Rare
Adulthood (30 to 50 years)
Degenerate meniscal tears Early degeneration after injury or meniscectomy Inflammatory arthropathies
Bursitis Tendinitis
Degenerative hip disease from hip dysplasia or injury
Older age (≥50 years)
Osteoarthritis Inflammatory arthropathies
Bursitis Tendinitis
Osteoarthritis of the hip
symptoms, as discussed previously. Recent weight gain may place new forces on the knee joint and exacerbate preexisting problems, such as degenerative arthritis or a torn meniscus.
Chapter 111—Painful Conditions of the Knee
839
Targeted Physical Examination
Anticoagulants and knee pain spell trouble for two reasons. First, seemingly minor trauma can cause a hemarthrosis of the knee that if untreated can result in permanent knee damage. Second, the presence of anticoagulants precludes rapid surgical treatment of otherwise treatable causes of knee pain.15
The targeted physical examination when combined with the targeted history allows the clinician to correctly diagnose the cause of the painful knee in most instances or at least direct further radiographic and laboratory investigations. Because of the lack of soft tissue overlying the knee joint, visual inspection can provide the clinician with important clues to the cause of knee pain and dysfunction. The starting point to visual inspection of the knee is an observation of the patient both standing and walking. The degree of valgus or varus of the knee with weight bearing should be noted as should any other obvious bony deformity (Fig. 111.7). The clinician should then look for evidence of quadriceps wasting, which, if identified, can be quantified with careful measurement at a point 12 cm above the upper margin of the patella with the knee fully extended. The presence of rubor suggestive of infection or swelling above, below, and alongside of the patella suggestive of an inflammatory process, including bursitis and tendonitis, is also noted. The posterior knee is then inspected for presence of a popliteal fossa mass suggestive of Baker's cyst.18
Corticosteroids
Palpation of the Knee
Knee pain after treatment with the corticosteroids can be the result of the return of the inflammatory condition originally responsible for the pain or the result of pseudorheumatism.16 The pain of pseudorheumatism can be quite severe and can also occur with the tapering of corticosteroids used to treat unrelated acute conditions, such as poison ivy, or in the chronic setting, as in the treatment of chronic obstructive pulmonary disease.
Careful palpation of the knee often provides the examiner with valuable clues to the cause of the patient's knee pain and dysfunction. The examiner palpates the temperature of both knees because localized increase in temperature may indicate inflammation or infection. The presence of swelling in the suprapatellar, prepatellar, or infrapatellar regions suggestive of suprapatellar, prepatellar, or infrapatellar bursitis is then identified. Generalized joint effusion may be identified by performing the ballottement test (Fig. 111.8). The bony elements of the knee, including the medial and lateral femoral condyles, the patella, and the tibial tubercle, are then palpated. The patellar tendon is then palpated to identify patellar tendonitis or jumper's knee (Fig. 111.9). The popliteal fossa is then palpated for evidence of a mass or Baker's cyst.18 The knee joint is then ranged through flexion, extension, and medial and lateral rotation to identify crepitus or limitation of range of motion.
Addition of New Medications Many medications can cause joint pain as a side effect unrelated to their intended therapeutic action. In most instances, this is an idiosyncratic reaction and will abate with discontinuation of the offending drug. In some, such as procainamide and hydralazine, the drug may cause a syndrome indistinguishable from systemic lupus erythematosus.14
Use of Anticoagulants
Tick Bites Although uncommon, Lyme disease after a tick bite can cause significant knee pain.11,17 The condition is usually associated with a specific rash known as erythema migrans that is the result of an infection with Borrelia burgdorferi; failure to accurately diagnose and treat this uncommon cause of knee pain can result in permanent knee damage (Fig. 111.6).
Fig. 111.6 Erythema migrans. This annular, erythematous lesion developed over a period of 3 weeks around the site of a tick bite. (Reproduced with permission from McKee PH: Pathology of the skin, ed 2, London, 1996, Mosby. From Klippel JH, Dieppe PA: Rheumatology, ed 2, London, 1998, Mosby.)
Fig. 111.7 Visual inspection of the knee. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 326.)
840
Section IV—Regional pain syndromes
Fig. 111.10 Valgus stress test for medial collateral ligament integrity. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 334.)
Valgus Stress Test for Medial Collateral Ligament Integrity
Fig. 111.8 The ballottement test for large joint effusions. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 332.)
The valgus stress test provides the clinician with useful information regarding the integrity of the medial collateral ligaments. For the valgus stress test, the patient is placed in a supine position on the examination table with the knee flexed 35 degrees and the entire affected extremity relaxed. The examiner then places his or her hand above the knee to stabilize the upper leg. With the other hand, the examiner forces the lower leg away from the midline while observing for widening of the medial joint compartment and pain (Fig. 111.10). The maneuver is then repeated with the other lower extremity, and the results are compared.
Varus Stress Test for Lateral Collateral Ligament Integrity The varus stress test provides the clinician with useful information regarding the integrity of the lateral collateral ligaments. For the varus stress test, the patient is placed in a supine position on the examination table with the knee flexed 35 degrees and the entire affected extremity relaxed. The examiner then places his or her hand above the knee to stabilize the upper leg. With the other hand, the examiner forces the lower leg forward from the midline while observing for widening of the medial joint compartment and pain (Fig. 111.11). The maneuver is then repeated with the other lower extremity, and the results are compared.
Anterior Drawer Test for Anterior Cruciate Ligament Integrity Fig. 111.9 Palpation of the knee. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 327.)
The anterior drawer test is useful in helping the clinician assess the integrity of the anterior cruciate ligament. For the anterior drawer test, the patient is placed in the supine position on the examination table with the patient's head on a pillow to help
Chapter 111—Painful Conditions of the Knee
841
Fig. 111.11 Varus stress test for lateral collateral ligament integrity. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 335.)
Fig. 111.12 Anterior drawer test for anterior cruciate ligament integrity. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 336.)
relax the hamstring muscles. The patient's hip is then flexed to 45 degrees with the patient's foot placed flat on the table. The examiner then grasps the affected leg below the knee with both hands and pulls the lower leg forward while stabilizing the foot (Fig. 111.12). The test is considered positive if more than 5 mm of anterior motion is seen.
Posterior Drawer Test for Posterior Cruciate Ligament Integrity The posterior drawer test is useful in helping the clinician assess the integrity of the posterior cruciate ligament. For the posterior drawer test, the patient is placed in the supine position on the examination table with the patient's head on a pillow to help relax the hamstring muscles. The patient's hip is then flexed to 45 degrees with the patient's foot placed flat on the table. The examiner then grasps the affected leg below the knee with both hands and pushes the lower leg backward while stabilizing the foot (Fig. 111.13). The test is considered positive if more than 5 mm of posterior motion is seen.
McMurray's Test for Torn Meniscus The McMurray's test for torn meniscus can provide the clinician with useful information as to the whether a torn medial or lateral meniscus is responsible for the patient's knee pain. For the McMurray's test for torn meniscus, the examiner has the patient assume the supine position on the examination table with the knee maximally flexed. With the affected extremity relaxed, the examiner grasps the ankle and palpates the knee while simultaneously rotating the lower leg internally and externally and extending the knee (Fig. 111.14). The test is considered positive for a torn meniscus if the examiner appreciates a palpable or auditory click while rotating and extending the knee.
Fig. 111.13 Posterior drawer test for posterior cruciate ligament integrity. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 337.)
Use of Testing Modalities for Evaluation of the Painful Knee Plain radiographs are indicated in all patients who present with knee pain. On the basis of the patient's clinical presentation, additional testing may be indicated, including complete blood cell count, sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging of the knee is indicated if internal derangement is suspected. Radionuclide
842
Section IV—Regional pain syndromes bone scan is indicated if metastatic disease or primary tumor involving the knee is being considered. Synovial fluid analysis should be performed in all patients suspected of having a septic joint or a crystal arthropathy. Titers for Lyme disease are indicated in patients with rash suggestive of erythema migrans or in patients with a history of tick bite who also have knee pain.11,17
Conclusion The diagnosis of knee pain should be a relatively straightforward clinical endeavor as long as the clinician performs a careful targeted history and physical examination. The clinician faced with the patient with knee pain should have a relatively low threshold for the ordering of MRI, especially in the presence of trauma. A failure to heed the warning signs discussed can result in much unneeded pain and functional disability and permanent damage to the knee. Fig. 111.14 McMurray's test for torn meniscus. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p 342.)
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
112
IV
Bursitis Syndromes of the Knee Steven D. Waldman
CHAPTER OUTLINE Suprapatellar Bursitis 843 Clinical Presentation 843 Diagnosis 843 Differential Diagnosis 844 Treatment 844
Prepatellar Bursitis 845 Clinical Presentation 845 Diagnosis 846 Differential Diagnosis 846 Treatment 846 Complications and Pitfalls 846
Superficial Infrapatellar Bursitis 847 Clinical Presentation 847 Diagnosis 848
Bursitis of the knee is one of the most common causes of knee pain encountered in clinical practice. The bursae of the knee are vulnerable to injury from both acute trauma and repeated microtrauma.1 The bursae of the knee may exist as single bursal sacs or, in some patients, as a multisegmented series of sacs that may be loculated.2 Acute injuries to the bursae of the knee frequently take the form of direct trauma to the bursa from falls or blows directly to the knee; of patellar, tibial plateau, and proximal fibular fractures; or of overuse injuries, including running on soft or uneven surfaces or from jobs that require crawling on the knees, such as laying carpet. If the inflammation of the bursae of the knees becomes chronic, calcification of the bursa may occur.3
Suprapatellar Bursitis The suprapatellar bursa extends superiorly from beneath the patella under the quadriceps femoris muscle (Figs. 112.1 and 112.2). The patient with suprapatellar bursitis frequently has pain in the anterior knee above the patella, which can radiate superiorly into the distal anterior thigh.4 Often, the patient is unable to kneel or walk down stairs (Fig. 112.3). The patient may also have a sharp, catching sensation with range of motion of the knee, especially on first arising. Suprapatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture.2
© 2011 Elsevier Inc. All rights reserved.
Differential Diagnosis 848 Treatment 848
Pes Anserine Bursitis 848 Clinical Presentation 849 Diagnosis 849 Differential Diagnosis 849 Treatment 849
Deep Infrapatellar Bursitis 850 Clinical Presentation 851 Diagnosis 851 Differential Diagnosis 851 Treatment 851
Complications and Pitfalls in the Treatment of Bursitis of the Knee 852
Clinical Presentation Physical examination may reveal point tenderness in the anterior knee just above the patella. Passive flexion and active resisted extension of the knee reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain.1 Swelling in the suprapatellar region with a boggy feeling to palpation may be seen. Occasionally, the suprapatellar bursa may become infected, as evidenced by systemic symptoms including fever and malaise and local signs of rubor, color, and dolor.
Diagnosis Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon consistent with chronic inflammation. Magnetic resonance imaging (MRI) is indicated if internal derangement, occult mass, or tumor of the knee is suspected.5 Electromyography helps distinguish suprapatellar bursitis from femoral neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described subsequently serves as a diagnostic and therapeutic maneuver. A complete blood cell count and an automated chemistry profile, including determinations of uric acid, erythrocyte sedimentation rate, and antinuclear antibody value, are indicated if collagen vascular disease is suspected. If infection is considered, aspiration, Gram stain, and culture of bursal fluid are indicated on an emergent basis.
843
844
Section IV—Regional Pain Syndromes
*
Fig. 112.1 Suprapatellar bursa. Sagittal proton density (3000/26) fast spin echo fat-saturated magnetic resonance imaging scan shows a suprapatellar bursa (*), which normally communicates with the joint unless the suprapatellar plica (arrow) fails to involute, thus isolating this compartment. (From Beaman FD Peterson JJ: MR imaging of cysts, ganglia, and bursae about the knee, Radiol Clin North Am 45:969, 2007.)
Fig. 112.3 Suprapatellar bursitis is usually the result of direct trauma to the suprapatellar bursa from either acute injury or repeated microtrauma. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 255.)
Differential Diagnosis Because of the unique anatomy of the region, not only the suprapatellar bursa but also the associated tendons and other bursae of the knee can become inflamed and confuse the diagnosis. The suprapatellar bursa extends superiorly from beneath the patella under the quadriceps femoris muscle and its tendon. The bursa is held in place by a small portion of the vastus intermedius muscle called the articularis genus muscle. Both the quadriceps tendon and the suprapatellar bursa are subject to the development of inflammation after overuse, misuse, or direct trauma. The quadriceps tendon is made up of fibers from the four muscles that comprise the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella forming the medial and lateral patella retinacula that help strengthen the knee joint. These fibers are called expansions and are subject to strain, and the tendon proper is subject to the development of tendinitis (Fig. 112.4). The suprapatellar, infrapatellar, and prepatellar bursae may also concurrently become inflamed with dysfunction of the quadriceps tendon. Remember that anything that alters the normal biomechanics of the knee can result in inflammation of the suprapatellar bursa.
Treatment Fig. 112.2 Noncommunicating suprapatellar pouch cyst. A lateral view from a double-contrast knee arthrogram shows minimal extrinsic impression on the suprapatellar pouch (arrow) by an adjacent fluidfilled mass. (From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 284.)
A short course of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), or cyclooxygenase-2 (COX-2) inhibitors and a knee brace to prevent further trauma is a reasonable first step in the treatment of patients with suprapatellar bursitis. If the patient does not have rapid improvement, the following injection technique is
Chapter 112—Bursitis Syndromes of the Knee
845
Rectus femoris t. Inflamed suprapatellar bursa
A
Fig. 112.5 Injection technique for relief of the pain from suprapatellar bursitis. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 452.)
dressing and ice pack are placed at the injection site. Physical therapy to restore function is a reasonable next step after the acute pain and swelling has subsided after injection with local anesthetic and corticosteroid. B Fig. 112.4 Moderate patellar tendinopathy. A, Sagittal T2 fatsaturated image shows focal increased signal in the deep posterior portion of the proximal patellar tendon (arrow) and indistinct posterior margins of the tendon at this point. B, Axial proton density fat-saturated image of the same patient shows focal high signal in the tendon extending into the retropatellar fat (arrowhead). (From O'Keeffe SA, Hogan BA, Eustace SJ, et al: Overuse injuries of the knee, Magnetic Resonance Imaging Clin North Am 17:725, 2009.)
a reasonable next step.6 The goals of this injection technique are explained to the patient. The patient is placed supine with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial aspect of the knee joint is prepared with antiseptic solution. A sterile syringe containing the 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch 25-gauge needle with strict aseptic technique. The superior margin of the medial patella is identified. Just above this point, the needle is inserted horizontally to slide just beneath the quadriceps tendon (Fig. 112.5). If the needle strikes the femur, it is then withdrawn slightly and redirected in a more anterior trajectory. When the needle is in position just below the quadriceps tendon, the contents of the syringe are then gently injected. Little resistance to injection should occur. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure
Prepatellar Bursitis The prepatellar bursa is vulnerable to injury from both acute trauma and repeated microtrauma. The prepatellar bursa lies between the subcutaneous tissues and the patella (Fig. 112.6).1,7 This bursa may exist as a single bursal sac or, in some patients, as a multisegmented series of sacs that may be loculated. Acute injuries frequently take the form of direct trauma to the bursa from falls directly onto the knee or from patellar fractures and from overuse injuries, including running on soft or uneven surfaces. Prepatellar bursitis may also result from jobs that require crawling on the knees, such as laying carpet or scrubbing floors; hence, the other name for prepatellar bursitis is housemaid's knee (Fig. 112.7). It has also been reported in break dancers.8 If the inflammation of the prepatellar bursa becomes chronic, calcification of the bursa may occur.
Clinical Presentation The patient with prepatellar bursitis frequently has pain and swelling in the anterior knee over the patella that can radiate superiorly and inferiorly into the area surrounding the knee.9 Often, the patient is unable to kneel or walk down stairs. The patient may also have a sharp, catching sensation with range of motion of the knee, especially on first arising. Prepatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture.
846
Section IV—Regional Pain Syndromes
Differential Diagnosis
Fig. 112.6 Prepatellar bursitis. A sagittal short tau inversion recovery (TR/TE, 5300/30; inversion time, 150 ms) magnetic resonance imaging scan shows fluid and synovial tissue in the prepatellar bursa. (From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 4257.)
Because of the unique anatomy of the region, not only the prepatellar bursa but also the associated tendons and other bursae of the knee can become inflamed and confuse the diagnosis. The prepatellar bursa lies between the subcutaneous tissues and the patella. The bursa is held in place by the ligamentum patellae. Both the quadriceps tendon and the prepatellar bursa are subject to the development of inflammation after overuse, misuse, or direct trauma. The quadriceps tendon is made up of fibers from the four muscles that comprise the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon extending around the patella forming the medial and lateral patella retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain, and the tendon proper is subject to the development of tendinitis. The suprapatellar, infrapatellar, and prepatellar bursae may also concurrently become inflamed with dysfunction of the quadriceps tendon. Remember that anything that alters the normal biomechanics of the knee can result in inflammation of the prepatellar bursa.
Treatment
Fig. 112.7 Prepatellar bursitis is also known as housemaid's knee because of its prevalence in people whose work requires prolonged crawling or kneeling. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 312.)
Diagnosis Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon consistent with chronic inflammation. MRI is indicated if internal derangement, occult mass, or tumor of the knee is suspected. Electromyography helps distinguish prepatellar bursitis from femoral neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described in the section on treatment serves as a diagnostic and therapeutic maneuver. Testing for antinuclear antibody is indicated if collagen vascular disease is suspected. If infection is considered, aspiration, Gram stain, and culture of bursal fluid are indicated on an emergent basis.
A short course of conservative therapy consisting of simple analgesics, NSAIDs, or COX-2 inhibitors and use of a knee brace to prevent further trauma is a reasonable first step in the treatment of patients with prepatellar bursitis. If the patient does not have rapid improvement, the following injection technique is a reasonable next step.5 The patient is placed supine with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the patella is prepared with antiseptic solution. A sterile syringe containing the 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch 25-gauge needle with strict aseptic technique. Then the center of the medial patella is identified (Fig. 112.8). Just above this point, the needle is inserted horizontally to slide subcutaneously into the prepatellar bursa. If the needle strikes the patella, it is then withdrawn slightly and redirected in a more anterior trajectory. When the needle is in position in proximity to the prepatellar bursa, the contents of the syringe are then gently injected. Little resistance to injection should occur. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.
Complications and Pitfalls Failure to identify primary or metastatic distal femur or joint disease that is responsible for the patient's pain may yield disastrous results. The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients have a transient increase in pain after injection of the suprapatellar bursa of the knee; patients should
Chapter 112—Bursitis Syndromes of the Knee
847
Inflamed and swollen prepatellar bursa
Fig. 112.9 Superficial infrapatellar bursitis. A fluid level within the bursa is evident on a sagittal fast spin echo (TR/TE, 2600/22) magnetic resonance imaging. (From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 4257.)
Fig. 112.8 Injection technique for relief of the pain from prepatellar bursitis. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 455.)
be warned of such. The use of physical modalities including local heat and gentle range-of-motion exercises should be introduced several days after the patient undergoes this injection technique for prepatellar bursitis pain. Vigorous exercises should be avoided because they exacerbate the patient's symptoms.
Superficial Infrapatellar Bursitis The superficial infrapatellar bursa is vulnerable to injury from both acute trauma and repeated microtrauma. The superficial infrapatellar bursa lies between the subcutaneous tissues and the upper part of the ligamentum patellae (Fig. 112.9).1 The deep infrapatellar bursa lies between the ligamentum patellae and the tibia. These bursae may exist as single bursal sacs or, in some patients, as a multisegmented series of sacs that may be loculated. Acute injuries frequently take the form of direct trauma to the bursa from falls directly onto the knee or from patellar fractures and from overuse injuries, including running on soft or uneven surfaces and break dancing.1,10 Superficial infrapatellar bursitis may also result from jobs that require crawling on the knees, such as laying carpet or scrubbing floors (Fig. 112.10). If the inflammation of the superficial infrapatellar bursa becomes chronic, calcification of the bursa may occur.
Fig. 112.10 Superficial infrapatellar bursitis is a common cause of inferior knee pain. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 314.)
Clinical Presentation The patient with superficial infrapatellar bursitis frequently has pain and swelling in the anterior knee over the patella that can radiate superiorly and inferiorly into the area surrounding the knee.10 Often, the patient is unable to kneel or walk down stairs. The patient may also have a sharp, catching sensation with range of motion of the knee, especially on first arising.
848
Section IV—Regional Pain Syndromes
Superficial infrapatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture.
Diagnosis Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon consistent with chronic inflammation. MRI is indicated if internal derangement, occult mass, or tumor of the knee is suspected. Electromyography helps distinguish superficial infrapatellar bursitis from femoral neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described in the section on treatment serves as a diagnostic and therapeutic maneuver. Testing for antinuclear antibody is indicated if collagen vascular disease is suspected. If infection is considered, aspiration, Gram stain, and culture of bursal fluid are indicated on an emergent basis.
Inflamed and swollen superficial infrapatellar bursa
Differential Diagnosis Because of the unique anatomy of the region, not only the superficial infrapatellar bursa but also the associated tendons and other bursae of the knee can become inflamed and confuse the diagnosis. Both the quadriceps tendon and the superficial infrapatellar bursa are subject to the development of inflammation after overuse, misuse, or direct trauma. The quadriceps tendon is made up of fibers from the four muscles that comprise the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single, exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon extending around the patella forming the medial and lateral patella retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain, and the tendon proper is subject to the development of tendinitis. The suprapatellar, infrapatellar, and superficial infrapatellar bursae may also concurrently become inflamed with dysfunction of the quadriceps tendon. Remember that anything that alters the normal biomechanics of the knee can result in inflammation of the superficial infrapatellar bursa.
Treatment A short course of conservative therapy consisting of simple analgesics, NSAIDs, or COX-2 inhibitors and use of a knee brace to prevent further trauma is a reasonable first step in the treatment of patients with superficial infrapatellar bursitis. If the patient does not have rapid improvement, the following injection technique is a reasonable next step.11 For injection of the superficial infrapatellar bursa, the patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the patella is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch 25-gauge needle with strict aseptic technique. The center of the lower pole of the patella is identified. Just below this point, the needle is inserted at a 45-degree angle to slide subcutaneously into the superficial infrapatellar bursa (Fig. 112.11). If the needle strikes the
Fig. 112.11 Injection technique for relief of the pain from infra patellar bursitis. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 459.)
patella, it is then withdrawn slightly and redirected in a more inferior trajectory. When the needle is in position in proximity to the superficial infrapatellar bursa, the contents of the syringe are then gently injected. Little resistance to injection should occur. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The use of physical modalities including local heat and gentle range-ofmotion exercises should be introduced several days after the patient undergoes this injection technique for prepatellar bursitis pain. Vigorous exercises should be avoided because they exacerbate the patient's symptoms.
Pes Anserine Bursitis The pes anserine bursa lies beneath the pes anserine tendon, which is the insertional tendon of the sartorius, gracilis, and semitendinous muscles to the medial side of the tibia (Fig. 112.12).1 This bursa may exist as a single bursal sac or, in some patients, may exist as a multisegmented series of sacs that may be loculated. Patients with pes anserine bursitis present with pain over the medial knee joint and increased pain on passive valgus and external rotation of the knee (Fig. 112.13).12 Activity, especially involving flexion and external rotation of the knee, makes the pain worse, with rest and heat providing some relief. Often, the patient is unable to kneel or walk down stairs.
Chapter 112—Bursitis Syndromes of the Knee
849
*
Fig. 112.13 Pes anserine bursitis. Axial proton density image. A homogenous high signal intensity fluid collection (*) is seen deep to the tendons of the pes anserinus. The tendons of sartorius (arrowhead) and semitendinosus (arrow) are visualized. (From O'Keeffe SA, Hogan BA, Eustace SJ, et al: Overuse injuries of the knee, Magnetic Resonance Imaging Clin North Am 17:725, 2009.)
Diagnosis Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the pes anserine tendon consistent with chronic inflammation. MRI is indicated if internal derangement, occult mass, or tumor of the knee is suspected. Electromyography helps distinguish pes anserine bursitis from neuropathy, lumbar radiculopathy, and plexopathy. The injection technique described subsequently serves as a diagnostic and therapeutic maneuver.
Differential Diagnosis
Fig. 112.12 Patients with pes anserine bursitis frequently have medial knee pain that is made worse with kneeling or walking down stairs. (From Waldman SD: Atlas of uncommon pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 290.)
Clinical Presentation The pain of pes anserine bursitis is constant and characterized as aching. The pain may interfere with sleep. Coexistent bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint. Frequently, the medial collateral ligament is also involved if the patient has sustained trauma to the medial knee joint. If the inflammation of the pes anserine bursa becomes chronic, calcification of the bursa may occur. Physical examination may reveal point tenderness in the anterior knee just below the medial knee joint at the tendinous insertion of the pes anserine.12 Swelling and fluid accumulation surrounding the bursa are often present. Active resisted flexion of the knee reproduces the pain. Sudden release of resistance during this maneuver markedly increases the pain. Rarely, the pes anserine bursa becomes infected in a manner analogous to infection of the prepatellar bursa.
The pes anserine bursa is prone to the development of inflammation after overuse, misuse, or direct trauma. The medial collateral ligament also often is involved if the medial knee has been subjected to trauma. The medial collateral ligament is a broad, flat bandlike ligament that runs from the medial condyle of the femur to the medial aspect of the shaft of the tibia where it attaches just above the groove of the semimembranosus muscle. It also attaches to the edge of the medial semilunar cartilage. The medial collateral ligament is crossed at its lower part by the tendons of the sartorius, gracilis, and semitendinosus muscles. Because of the unique anatomic relationships of the medial knee, accurate determination of which anatomic structure is responsible for the patient's pain is often difficult on clinical grounds. MRI helps sort things out and rule out lesions such as tears of the medial meniscus that may need surgical intervention. Remember that anything that alters the normal biomechanics of the knee can result in inflammation of the pes anserine bursa.
Treatment A short course of conservative therapy consisting of simple analgesics, NSAIDs, or COX-2 inhibitors and a knee brace to prevent further trauma is a reasonable first step in the treatment of patients with pes anserine bursitis. If the patient does not have rapid improvement, the following injection technique is a reasonable next step.13
850
Section IV—Regional Pain Syndromes
For injection of the pes anserine bursa, the patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin just below the medial knee joint is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch, 25-gauge needle with strict aseptic technique. With strict aseptic technique, the pes anserine tendon is identified by having the patient strongly flex his or her leg against resistance. The point distal to the medial joint space at which the pes anserine tendon attaches to the tibia is the location of the pes anserine bursa. The bursa usually is identified with point tenderness at that spot. At this point, the needle is inserted at a 45-degree angle to the tibia to pass through the skin and subcutaneous tissues and into the pes anserine bursa (Fig. 112.14). If the needle strikes the tibia, it is then withdrawn slightly into the substance of the bursa. When the needle is in position in proximity to the pes anserine bursa, the contents of the syringe is then gently injected. Little resistance to injection should occur. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site. The use of physical modalities including local heat and gentle range-of-motion exercises should be introduced several days after the patient undergoes this injection technique for pes anserine bursitis pain. Vigorous exercises should be avoided because they exacerbate the patient's symptoms.
Deep Infrapatellar Bursitis The deep infrapatellar bursa is vulnerable to injury from both acute trauma and repeated microtrauma. The superficial infrapatellar bursa lies between the subcutaneous tissues and the upper part of the ligamentum patellae. The deep infrapatellar bursa lies between the ligamentum patellae and the tibia (Fig. 112.15).1,14 These bursae may exist as single bursal sacs or, in some patients, as a multisegmented series of sacs that may be loculated in nature. Acute injuries frequently take the form of direct trauma to the bursa via falls directly onto the knee (Fig. 112.16)14 or from patellar fractures and from overuse
Fig. 112.15 Deep infrapatellar bursitis. Sagittal, T2-weighted, spin echo magnetic resonance imaging shows fluid of high signal intensity (arrow) in the deep infrapatellar bursa.
Medial collateral lig.
Inflamed pes anserine bursa
Fig. 112.14 Injection technique for relief of the pain from pes anserine bursitis. (From Waldman SD: Atlas of pain management injection
Fig. 112.16 Deep infrapatellar bursitis commonly presents as inferior knee pain accompanied by a catching sensation, especially on rising from a sitting position. (From Waldman SD: Atlas of common pain syndromes, ed 2,
techniques, ed 2, Philadelphia, 2007, Saunders, p 4670.)
Philadelphia, 2008, Saunders, p 316.)
injuries, including running on soft or uneven surfaces. Deep infrapatellar bursitis may also result from jobs that require crawling and kneeling on the knees, such as carpet laying or scrubbing floors. If the inflammation of the superficial infrapatellar bursa becomes chronic, calcification of the bursa may occur.
Clinical Presentation The patient with deep infrapatellar bursitis frequently has pain and swelling in the anterior knee below the patella that can radiate inferiorly into the area surrounding the knee. Often, the patient is unable to kneel or walk down stairs. The patient may also have a sharp, catching sensation with range of motion of the knee, especially on first arising. Infrapatellar bursitis often coexists with arthritis and tendinitis of the knee joint, and these other pathologic processes may confuse the clinical picture. Physical examination may reveal point tenderness in the anterior knee just below the patella. Swelling and fluid accumulation surrounding the lower patella are often present. Passive flexion and active resisted extension of the knee reproduce the pain. Sudden release of resistance during this maneuver markedly increases the pain. The deep infrapatellar bursa is not as susceptible to infection as the superficial infrapatellar bursa.
Diagnosis Plain radiographs of the knee may reveal calcification of the bursa and associated structures, including the quadriceps tendon, consistent with chronic inflammation. MRI is indicated if internal derangement, occult mass, or tumor of the knee is suspected. Electromyography helps distinguish deep and superficial infrapatellar bursitis from femoral neuropathy, lumbar radiculopathy, and plexopathy. The following injection technique serves as a diagnostic and therapeutic maneuver. Antinuclear antibody testing is indicated if collagen vascular disease is suspected. If infection is considered, aspiration, Gram stain, and culture of bursal fluid are indicated on an emergency basis.
Chapter 112—Bursitis Syndromes of the Knee
851
development of tendinitis. The suprapatellar, prepatellar, and superficial infrapatellar bursae may also concurrently become inflamed with dysfunction of the quadriceps tendon. Remember that anything that alters the normal biomechanics of the knee can result in inflammation of the deep infrapatellar bursa.
Treatment A short course of conservative therapy consisting of simple analgesics, NSAIDs, or COX-2 inhibitors and a knee brace to prevent further trauma is a reasonable first step in the treatment of patients with deep infrapatellar bursitis. If the patient does not have rapid improvement, the following injection technique is a reasonable next step.15 For injection of the deep infrapatellar bursa, the patient is placed in the supine position with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial portion of the lower margin of the patella is prepared with antiseptic solution. A sterile syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg methylprednisolone is attached to a 1.5-inch 25-gauge needle with strict aseptic technique. With strict aseptic technique, the medial lower margin of the patella is identified. Just below this point, the needle is inserted at a right angle to the patella to slide beneath the ligamentum patellar into the deep infrapatellar bursa. If the needle strikes the patella, it is then withdrawn slightly and redirected in a more inferior trajectory. When the needle is in position in proximity to the deep infrapatellar bursa, the contents of the syringe are then gently injected. Little resistance to injection should occur. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed, and a sterile pressure dressing and ice pack are placed at the injection site.
Differential Diagnosis
Complications and Pitfalls in the Treatment of Bursitis of the Knee
Because of the unique anatomy of the region, not only the deep infrapatellar bursa but also the associated tendons and other bursae of the knee can become inflamed and confuse the diagnosis. Both the quadriceps tendon and the deep and superficial infrapatellar bursae are subject to the development of inflammation after overuse, misuse, or direct trauma. The quadriceps tendon is made up of fibers from the four muscles that compose the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. These muscles are the primary extensors of the lower extremity at the knee. The tendons of these muscles converge and unite to form a single exceedingly strong tendon. The patella functions as a sesamoid bone within the quadriceps tendon, with fibers of the tendon expanding around the patella to form the medial and lateral patella retinacula, which help strengthen the knee joint. These fibers are called expansions and are vulnerable to strain, and the tendon proper is subject to the
Coexistent bursitis, tendinitis, arthritis, and internal derangement of the knee may also contribute to the patient's pain and may necessitate additional treatment. The simple analgesics and NSAIDs are a reasonable starting place in the treatment of bursitis of the knee. If these agents are ineffective, the injection of the inflamed bursa with a local anesthetic and corticosteroid is a reasonable next step. The previously described injection techniques are generally safe procedures if careful attention is paid to the clinically relevant anatomy in the areas to be injected. The use of physical modalities including local heat and gentle range-of-motion exercises should be introduced several days after the patient undergoes the injection techniques. Vigorous exercises should be avoided because they exacerbate the patient's symptoms. The clinician should remember that failure to identify infection or primary or metastatic tumors of the distal femur, joint, or proximal tibia and fibula that may be responsible for the patient's pain may yield disastrous results (Fig. 112.17).16
852
Section IV—Regional Pain Syndromes
A
B
C
Fig. 112.17 Chondroblastoma: radiographic abnormalities of long tubular bones. A, Tibia. Note the radiolucent lesion involving the metaphysis and epiphysis of the proximal portion of the tibia. B and C, Frontal and lateral radiographs of the femur in a 22-year-old man show a large epiphyseal and metaphyseal lesion (arrows) that contains foci of calcification. An unusual degree of periostitis is apparent in the metaphysis and diaphysis. (From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 3856.)
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
113
IV
Baker's Cyst of the Knee Steven D. Waldman
CHAPTER OUTLINE Clinical Presentation 853 Diagnosis 853 Differential Diagnosis 854
A common cause of knee pain, Baker's cyst is the result of an abnormal accumulation of synovial fluid in the medial aspect of the popliteal fossa.1 Overproduction of synovial fluid from the knee joint results in the formation of a cystic sac. This sac often communicates with the knee joint with a one-way valve effect, causing a gradual expansion of the cyst.2 Often a tear of the medial meniscus or a tendinitis of the medial hamstring tendon is the inciting factor responsible for the development of Baker's cyst.3 Patients with rheumatoid arthritis are especially susceptible to the development of Baker's cysts.4
Treatment 854 Conclusion 855
Diagnosis Plain radiographs are indicated in all patients who present with Baker's cyst. Ultrasound scan aids in diagnosis in patients whose body habitus makes accurate palpation of the popliteal fossa difficult (Fig. 113.3). On the basis of the patient's clinical presentation, additional testing may be indicated, including complete blood cell count, erythrocyte sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the knee is indicated
Clinical Presentation Patients with Baker's cysts have a feeling of fullness behind the knee.5 Often, they notice a lump behind the knee that becomes more apparent when they flex the affected knee (Fig. 113.1).1,5 The cyst may continue to enlarge and may dissect inferiorly into the calf (Fig. 113.2).6 Occasionally, the dissection may be so significant as to cause a lower extremity compartment syndrome.7 Patients with rheumatoid arthritis are prone to this phenomenon.4 The pain associated with dissection into the calf may be confused with thrombophlebitis and inappropriately treated with anticoagulants.8,9 The pain of ruptured Baker's cyst that has been misdiagnosed as thrombophlebitis has been called pseudothrombophlebitis. On physical examination, the patient with Baker's cyst has a cystic swelling in the medial aspect of the popliteal fossa. Baker's cysts can become quite large, especially in patients with rheumatoid arthritis. Activity, including squatting or walking, makes the pain of Baker's cyst worse; rest and heat provide some relief. The pain is constant, is characterized as aching, and may interfere with sleep. Baker's cyst may spontaneously rupture, and rubor and color in the calf may mimic thrombophlebitis.7,8 Homan's sign is negative, and no cords are palpable.
© 2011 Elsevier Inc. All rights reserved.
Fig. 113.1 The patient with Baker's cyst often has a sensation of fullness or a lump behind the knee. (From Waldman SD: Atlas of common pain syndromes, ed 2, Philadelphia, 2008, Saunders, p 319.)
853
854
Section IV—Regional Pain Syndromes
Fig. 113.3 Ultrasound scan of popliteal fossa. Baker's cyst is marked. No evidence of rupture is seen, although it contains debris. H, Head; F, feet. (From Chaudhuri R, Salari R: Baker's cyst simulating deep vein thrombosis, Clin Radiol 41:400, 1990.)
Fig. 113.2 Arthrogram revealing a typical downward rupture of Baker's cyst. (From Chaudhuri R, Salari R: Baker's cyst simulating deep vein thrombosis, Clin Radiol 41:400, 1990.)
Fig. 113.4 Magnetic resonance imaging of the knee is useful in confirming the presence of Baker's cyst. (From Haaga JR, Lanzieri CF, Gilkeson RC: CT and MR imaging of the whole body, ed 4, Philadelphia, 2003, Mosby, p 1808.)
if internal derangement or occult mass or tumor is suspected and is also useful in confirming the presence of Baker's cyst (Fig. 113.4).
Differential Diagnosis As mentioned previously, Baker's cyst may rupture spontaneously and may be misdiagnosed as thrombophlebitis. Occasionally, tendinitis of the medial hamstring tendon may be confused with Baker's cyst, as may injury to the medial meniscus. Primary or metastatic tumors in the region, although rare, must be considered in the differential diagnosis (Fig. 113.5).
Treatment Although surgery is often necessary to successfully treat Baker's cyst, conservative therapy consisting of an elastic bandage combined with a short trial of nonsteroidal anti-inflammatory
drugs or cyclooxygenase-2 inhibitors is warranted. If these conservative treatments fail, the following injection technique represents a reasonable next step.10 For injection of a Baker's cyst, the patient is placed in the prone position with the anterior ankle resting on a folded towel to slightly flex the knee. The middle of the popliteal fossa is identified, and at a point 2 fingers' breath medial and two fingersbreath below the popliteal crease, the skin is prepped with antiseptic solution. A syringe containing 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 2-inch, 22-gauge needle. The needle is then carefully advanced through the previously identified point at a 45-degree angle from the medial border of the popliteal fossa directly toward the Baker's cyst (Fig. 113.6). With continuous aspiration, the needle is advanced very slowly to avoid trauma to the tibial nerve or popliteal artery or vein. When the cyst is entered, synovial fluid suddenly is aspirated into the syringe. At this point, if is no paresthesia is elicited in
Chapter 113—Baker's Cyst of the Knee
855
Semimembranosus m.
Semitendinosus m. Popliteal v. Popliteal a. Inflamed cyst
Tibial n.
Common peroneal n.
Fig. 113.6 Technique for injecting Baker's cyst. (From Waldman SD: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, p 485.) Fig. 113.5 Lipoma arborescens. Magnetic resonance image showing diffuse fatty infiltration of the synovium. (From: Nielsen GP, O-Connell JX: Tumors of synovial tissue bone and soft tissue pathology, Philadelphia, 2010, Saunders, pp 255–275.)
the distribution of the common peroneal or tibial nerve, the contents of the syringe are then gently injected. Minimal resistance to injection should be felt. A pressure dressing is then placed over the cyst to prevent reaccumulation of fluid. Failure to diagnose primary knee pathology (e.g., tears of the medial meniscus) may lead to further pain and disability. MRI should help in identification of internal derangement of the knee. The proximity to the common peroneal and tibial nerves and to the popliteal artery and vein makes it imperative that this procedure be carried out only by those well versed in the regional anatomy and experienced in performing injection techniques. Many patients also have a transient increase in pain after this injection technique. Although rare, infection may occur if careful attention to sterile technique is not followed.
Conclusion When bursae become inflamed, they may overproduce synovial fluid, which can become trapped in saclike cysts as a result of a one-way valve phenomenon. This occurs commonly in the medial aspect of the popliteal fossa and is called Baker's cyst. The injection technique described is extremely effective in the treatment of pain and swelling from this disorder. Coexistent semimembranosus bursitis, medial hamstring tendinitis, or internal derangement of the knee may also contribute to knee pain and may necessitate additional treatment with more localized injection of local anesthetic and depot corticosteroid.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
114
Quadriceps Expansion Syndrome Steven D. Waldman
CHAPTER OUTLINE Clinical Presentation 856 Diagnosis 856
The quadriceps expansion syndrome is an uncommon cause of anterior knee pain encountered in clinical practice. This painful condition is characterized by pain at the superior pole of the patella.1 It is usually the result of overuse or misuse of the knee joint, such as running marathons or direct trauma to the quadriceps tendon from kicks or head butts during football. The quadriceps tendon is also subject to acute calcific tendinitis, which may coexist with acute strain injuries. Calcific tendinitis of the quadriceps tendon has a characteristic radiographic appearance of whiskers on the anterosuperior patella. The quadriceps tendon is made up of fibers from the four muscles that comprise the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris (Fig. 114.1). Fibers of the quadriceps tendon expanding around the patella form the medial and lateral patella retinacula, which help strengthen the knee joint. These fibers are called expansions and are subject to strain, and the tendon proper is subject to the development of tendinitis. Patients with quadriceps expansion syndrome present with pain over the superior pole of the sesamoid, more commonly on the medial side. The patient notes increased pain on walking down slopes or down stairs (Fig. 114.2). Activity of the knee makes the pain worse; rest and heat provide some relief. The pain is constant, is characterized as aching, and may interfere with sleep.
Clinical Presentation On physical examination, patients with quadriceps expansion syndrome have tenderness under the superior edge of the patella that occurs more commonly on the medial side.2 Patients exhibit a positive knee extension test on active resisted extension of the knee that reproduces the pain (Fig. 114.3). Coexistent suprapatellar and infrapatellar bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse the clinical picture after trauma to the knee joint.3
Diagnosis Plain radiographs of the knee are indicated in all patients who present with quadriceps expansion syndrome pain. On the basis of the patient's clinical presentation, additional testing 856
Differential Diagnosis 856 Treatment 856
may be indicated, including complete blood cell count, erythrocyte sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) of the knee is indicated if tendinosis, tendon rupture, internal derangement, or occult mass or tumor is suspected (Fig. 114.4). Ultrasound scan may be useful in identification of disruption of the quadriceps tendon (Fig. 114.5). Bone scan may be useful in identification of occult stress fractures that involve the joint, especially if trauma has occurred.
Differential Diagnosis The most common cause of anterior knee pain is arthritis of the knee. This should be readily identifiable on plain radiographs of the knee and may coexist with quadriceps expansion syndrome. Another common cause of anterior knee pain that may mimic or coexist with quadriceps expansion syndrome is suprapatellar or prepatellar bursitis.3 Internal derangement of the knee and a torn medial meniscus may also confuse the clinical diagnosis but should be readily identifiable on MRI of the knee.
Treatment Initial treatment of the pain and functional disability associated with quadriceps insertion syndrome should include a combination of the nonsteroidal anti-inflammatory agents or cyclooxygenase-2 inhibitors and physical therapy. Local application of heat and cold may also be beneficial. For patients who do not respond to these treatment modalities, injection of the quadriceps expansion, as described subsequently, with a local anesthetic and a corticosteroid may be a reasonable next step.4 For injection of the quadriceps expansion, the patient is placed supine with a rolled blanket underneath the knee to gently flex the joint. The skin overlying the medial aspect of the knee joint is prepped with antiseptic solution. A sterile syringe containing the 2.0 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 1.5-inch 25-gauge needle with strict aseptic technique. The medial edge of the superior patella is identified (Fig. 114.6). At this point, the needle is inserted horizontally toward the medial edge of © 2011 Elsevier Inc. All rights reserved.
Chapter 114—Quadriceps Expansion Syndrome Quadriceps t.
••
Vastus medialis t. (apon)
•
••
•
•
Suprapatellar bursa
•
•
••
Vastus medialis m. Femur
••
Vastus lateralis t. Prefemoral fat body
Suprapatellar fat body
••
Lat. patellar retinaculum
Patella
857
•
Gastrocnemius m. and t., med. head
•
••
••
••
••
••
••
Lat. sup. genicular a. Biceps femoris m. and t.
••
Iliotibial tract Med. sup. genicular a. Plantaris t.
••
•• ••
••
••
Tibial n.
Semimembranosus m. and t. Semitendinosus t.
Popliteal a. and v.
Quadriceps t.
••
•
••
•
•
•
Prefemoral fat body
•
Iliotibial tract Lat. sup. genicular a.
Gracilis t.
•
Suprapatellar fat body
Vastus medialis t. (apon)
••
Lat. patellar retinaculum Vastus lateralis t.
• •• •
Lesser saphenous v.
Patella
Sartorius m.
•
•• ••
Common peroneal n. Lat sural cutaneous n.
•
Suprapatellar bursa
•
Vastus medialis m.
•
Plantaris t.
••
••
••
••
••
••
•• ••
••
Lat. sural cutaneous n. Tibial n.
Lesser saphenous v.
••
••
Common peroneal n.
••
Femur Med. sup. genicular a. Gastrocnemius m. and t. med. head Greater saphenous v.
••
•
••
••
Biceps femoris m. and t.
Greater saphenous v.
•• •
••
Sartorius m. Gracilis t. Semimembranosus m. and t.
Popliteal a. and v. Semitendinosus t.
Fig. 114.1 The quadriceps tendon is made up of fibers from the four muscles that comprise the quadriceps muscle: the vastus lateralis, the vastus intermedius, the vastus medialis, and the rectus femoris. (From Kang HS, Ahn JM, Resnick D, et al, editors: MRI of the extremities, ed 2, Philadelphia, 2002, Saunders, p 315.)
858
Section IV—Regional Pain Syndromes
Vastus lateralis Rectus femoris Vastus medialis
Patella
Fig. 114.2 Patients with quadriceps expansion syndrome present with pain over the superior pole of the sesamoid, more commonly on the medial side. (From Waldman SD: Atlas of uncommon pain syndromes, Philadelphia, 2003, Saunders, p 216.)
Fig. 114.3 The knee extension test for quadriceps expansion syndrome. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and
Fig. 114.4 Partial and complete tears of the quadriceps tendon. A and B, Partial tear. Sagittal intermediate-weighted (TR/TE, 2500/20; A) and T2-weighted (TR/TE, 2500/80; B) spin-echo magnetic resonance images (MRIs) show disruption of the normal trilaminar appearance of the quadriceps tendon. The tendon (solid arrows) of the vastus intermedius muscle appears intact. The other tendons have retracted (open arrows). Note the high signal intensity at the site of the tear (arrowhead) and in the soft tissues and muscles in B. C and D, Complete tear. Sagittal intermediate-weighted (TR/TE, 2500/30; C) and T2-weighted (TR/ TE, 2500/80; D) spin-echo MRIs show a complete tear (arrows) of the quadriceps tendon at the tendo-osseous junction. Note the high signal intensity at the site of the tear in D. The patella is displaced inferiorly.
symptoms, Philadelphia, 2010, Saunders.)
(From Resnick D, editor: Diagnosis of bone and joint disorders, ed 4, Philadelphia, 2002, Saunders, p 3229.)
the patella. The needle is then carefully advanced through the skin and subcutaneous tissues until it impinges on the medial edge of the patella. The needle is withdrawn slightly out of the periosteum of the patella, and the contents of the syringe are then gently injected. Little resistance to injection should
be felt. If resistance is encountered, the needle is probably in a ligament or tendon and should be advanced or withdrawn slightly until the injection proceeds without significant resistance. The needle is then removed and a sterile pressure dressing and ice pack are placed at the injection site.
Chapter 114—Quadriceps Expansion Syndrome
Right leg Tendon Patella
Blood Tendon
Torn quadriceps
859
The major complication of this injection technique is infection. This complication should be exceedingly rare if strict aseptic technique is adhered to. Approximately 25% of patients have a transient increase in pain after injection of the quadriceps tendon of the knee; patients should be warned of such. The clinician should also identify coexisting internal derangement of the knee, primary and metastatic tumors, and infection, which if undiagnosed may yield disastrous results.
References Full references for this chapter can be found on www.expertconsult.com.
Fig. 114.5 Two-dimensional ultrasound scan of patient's right knee showing disrupted quadriceps tendon and an acute bleed. (From LaRocco BG, Zlupko G, Sierzenski P: Ultrasound diagnosis of quadriceps tendon rupture, J Emerg Med 35:293, 2008.)
Rectus femoris m.
Vastus lateralis m.
Vastus medialis m.
Inflamed quadriceps expansion Patellar lig.
Carrico & Shavell
Fig. 114.6 Injection technique for relieving the pain from quadriceps expansion syndrome. (From Waldman SD: Atlas of pain management injection techniques, Philadelphia, 2000, Saunders, p 266.)
IV
Chapter
115
Arthritis of the Ankle and Foot Saima Chohan
CHAPTER OUTLINE Etiology and Clinical Presentation 860’ Treatment 861
The foot and the ankle have many functions, providing a base for standing, a lever for forward propulsion, and a shock absorber for the body's weight. The ankle is probably the most commonly injured joint in athletics because of the forces it withstands and the mass it supports. Painful disorders of the ankle and foot are a common presentation in general, rheumatologic, and orthopedic practices. The pain may arise from the bones and joints of the ankle and foot, periarticular structures (tendon sheaths, tendon insertions, or bursae), plantar fascia, nerve roots and peripheral nerves, or vascular system or be referred from the lumbar spine or knee joint.1,2 A classification of painful disorders of the ankle and foot, based on the site of origin and predominant location of the pain, is outlined in Table 115.1. Static disorders from inappropriate footwear, foot deformities, and weak intrinsic muscles account for most painful foot conditions. Precise diagnosis depends on knowledge of anatomy, a detailed history, and an assessment of the joints, periarticular soft tissue structures, nerve and blood supply, and lumbar spine. Diagnostic studies include routine laboratory tests, synovial fluid analysis, nerve conduction studies, vascular (Doppler) studies, bone scintiscan, sonography, plain radiographs, computed tomographic (CT) scan, and magnetic resonance imaging (MRI). Special radiographic views, arthrography, arteriography, gait analysis, and footprint studies are occasionally necessary.1,2
Etiology and Clinical Presentation The main causes of arthritis of the ankle and subtalar and other joints of the foot include rheumatoid arthritis, psoriatic arthritis, gout, trauma, and osteoarthritis. The foot and ankle can be viewed in three functional parts: forefoot (metatarsal bones, sesamoids, and phalanges), midfoot (navicular, cuboid, and three cuneiform bones), and hindfoot (talus and calcaneus). Similarly, the foot has four major joints: ankle, subtalar, midtarsal, and midfoot. The ankle or talocrural joint (mortise) is a hinge joint between the distal ends of the tibia and fibula and the trochlea of the talus that provides plantarflexion and dorsiflexion 860
movement. The synovial cavity does not normally communicate with other joints, adjacent tendon sheaths, or bursae. Tendons that cross the ankle region are invested for part of their course in tenosynovial sheaths (Figs. 115.1 and 115.2). Posteriorly, the common tendon of the gastrocnemius and soleus (Achilles tendon) is inserted into the posterior surface of the calcaneus.1–3 The retrocalcaneal bursa is located between the Achilles tendon insertion and the posterior surface of the calcaneus. It is surrounded anteriorly by Kager's fat pad. The bursa serves to protect the distal Achilles tendon from frictional wear against the posterior calcaneus. The retroachilleal bursa lies between the skin and the Achilles tendon and protects the tendon from external pressure. The subcalcaneal bursa is located beneath the skin over the plantar aspect of the calcaneus. Two bursae, the medial and lateral subcutaneous malleolar or “last” bursae, are located near the medial and lateral malleoli, respectively (see Figs. 115.1 and 115.2).1,3 The subtalar (talocalcaneal) joint lies between the talus and the calcaneus. It permits about 30 degrees of foot inversion (sole of the foot turned inward) and 10 to 20 degrees of eversion (sole turned outward). Subtalar arthritis is associated with painful restriction of inversion and eversion, diffuse swelling, and tenderness in the subtalar region, but direct palpation of the joint is difficult. The midtarsal (transverse tarsal) joint comprises the combined talonavicular and calcaneocuboid joints and serves to demarcate the hindfoot from the midfoot.1,3 The cuboid and navicular are usually joined by fibrous tissue, but a synovial cavity may exist between them. The midtarsal joint contributes to inversion (supination) and eversion (pronation) movements at the subtalar joint. It also allows 20 degrees of adduction (foot turned toward the midline) and 10 degrees of abduction (foot turned away from the midline). Arthritis of the transverse tarsal joint is associated with painful restriction of inversion and eversion, diffuse tenderness, and swelling of the midtarsal region. The midfoot joint provides stability to the body. The other smaller joints in the foot include the intertarsal joints, the metatarsophalangeal (MTP) joints, and the interphalangeal joints. The intertarsal joints are plane gliding joints © 2011 Elsevier Inc. All rights reserved.
Chapter 115—Arthritis of the Ankle and Foot
Table 115.1 Painful Disorders of the Ankle and the Foot Type
Example
Articular
Rheumatoid arthritis, osteoarthritis, psoriatic arthritis, gout
Toe disorders
Hallux valgus, hallux rigidus, hammertoe
Arch disorders
Pes planus, pes cavus
Periarticular
Corn, callosity
Cutaneous
Rheumatoid arthritis nodules, gouty tophi
Subcutaneous
Ingrown toenail
Plantar fascia
Plantar fasciitis Plantar nodular fibromatosis
Tendons
Achilles tendinitis Achilles tendon rupture Tibialis posterior tenosynovitis Peroneal tenosynovitis
Bursae
Bunion, bunionette Retrocalcaneal and retroachilleal bursitis Medial and lateral malleolar bursitis Hydroxyapatite pseudopodagra (first metatarsophalangeal joint)
Osseous
Fracture (traumatic and stress) Sesamoiditis Neoplasm Infection Epiphysitis (osteochondritis) Second metatarsal head (Frieberg's disease) Navicular (Kohler's disease) Calcaneus (Sever's disease) Painful accessory ossicles Accessory navicular Os trigonum (near talus) Os intermetatarseum (first to second)
Neurologic
Tarsal tunnel syndrome Interdigital (Morton's) neuroma Peripheral neuropathy Radiculopathy (lumbar disc)
Vascular
Ischemic (atherosclerosis, Buerger's disease) Vasospastic disorder (Raynaud's phenomenon) Cholesterol emboli
Referred
Lumbosacral spine Knee Reflex sympathetic dystrophy syndrome
between the navicular, cuneiforms, and cuboid that intercommunicate with one another and with the intermetatarsal and tarsometatarsal joints. The MTP joints are ellipsoid joints lined by separate synovial cavities. They lie about 2 cm proximal to the webs of the toes.1 The transverse metatarsal ligament binds the metatarsal heads together, preventing excessive splaying of the forefoot. The intermetatarsophalangeal bursae are frequently present between the metatarsal heads. Chronic arthritis of the MTP joints is characterized by local tenderness, swelling, synovial thickening, and a painful metatarsal compression test (pain on gentle compression of the metatarsal heads together with one hand). Forefoot splaying or spread, from weakness of the transverse metatarsal ligaments, and
861
toe deformities are frequent. A bursa (bunion) is commonly located over the medial aspect of the first MTP joint. Less frequently, a small bursa is present over the lateral aspect of the fifth metatarsal head (bunionette or tailor's bursa). The proximal and distal interphalangeal (PIP and DIP) joints are hinge joints.1 The digital flexor tendon sheaths enclose the long and short flexor tendons, extending proximally along the length of the toes to the distal third of the sole. Arthritis of the PIP and DIP joints is associated with tender swelling, synovial thickening, restriction of movements, and often toe deformities. The plantar fascia is the primary aponeurosis originating on the plantar aspect of the calcaneus and attaching to the base of each of the five metatarsal heads. Inflammation of the plantar fascia can cause pain in the plantar region, especially with initiation of walking. Ankle arthritis is characterized by a diffuse swelling, joint line tenderness, restricted movements, and synovial thickening anteriorly with obliteration of the two small depressions that are normally present in front of the malleoli. A large ankle effusion may bulge both medial and lateral to the extensor tendons and produce fluctuance; pressure with one hand on one side of the joint produces a fluid wave transmitted to the second hand placed on the opposite side of the ankle. A traumatic tear of the talofibular ligament allows forward movement of the tibia and fibula on the talus (positive anterior draw sign).1 Ankle tenosynovitis, by contrast, presents as a linear, superficial, tender, swelling localized to the distribution of the tendon sheath and extending beyond the joint margins. Movements of the involved tendon often produce pain.
Treatment Management of arthritis of the ankle, subtalar, midtarsal, MTP, PIP, and DIP joints of the toes depends primarily on the underlying cause. For symptomatic treatment, rest, local heat therapy, and nonsteroidal anti-inflammatory drugs are often helpful. For persistent inflammatory synovitis, corticosteroid injections are often beneficial. The ankle joint can be injected via an anteromedial approach with the joint slightly plantarflexed. The needle is inserted at a point just medial to the tibialis anterior tendon and distal to the lower margin of the tibia. The needle is directed posteriorly and laterally to a depth of 1 to 2 cm, and 20 mg of methylprednisolone acetate or similar corticosteroid is injected. For the subtalar joint, with the patient supine and the leg-foot-ankle at 90 degrees, the needle is inserted horizontally into the subtalar joint just inferior to the tip of the lateral malleolus at a point just proximal to the sinus tarsi. The midtarsal, other intertarsal, and tarsometatarsal joints cannot easily be injected without fluoroscopic or CT scan guidance. The MTP, PIP, and DIP joints can be entered via a dorsomedial or dorsolateral route. The joint space is first identified, and then a 28-gauge needle is inserted on either side of the extensor tendon to a depth of 2 to 4 mm. Slight traction on the appropriate toe facilitates entry before injection of 10 mg of methylprednisolone acetate.4
References Full references for this chapter can be found on www.expertconsult.com.
862
Section IV—Regional Pain Syndromes
Achilles t.
Tibialis ant. t. and sheath
Peroneus longus
Extensor hallucis longus t. and sheath
Peroneus brevis
Sup. extensor retinaculum
Common peroneal t. and sheath
Extensor digitorum longus and peroneus tertius tendons and sheath
Lat. subcutaneous malleolar bursa
Inf. extensor retinaculum
Sup. peroneal retinaculum
Peroneus tertius t.
Retrocalcaneal bursa Retroachilleal bursa Inf. peroneal retinaculum Calcaneus
Fig. 115.1 Bursae, tendons, and tendon sheaths of the anterior tibial (extensor) and peroneal compartments of the ankle.
Achilles t. Tibialis post. t. and sheath Sup. extensor retinaculum Tibialis ant. t. and sheath Inf. extensor retinaculum
Flexor digitorum longus t. and sheath Medial malleolus and medial subcutaneous malleolar bursa Retroachilleal bursa Retrocalcaneal bursa Flexor retinaculum Flexor hallucis longus t. and sheath
Fig. 115.2 Bursae, tendons, and tendon sheaths of the medial (flexor) compartment of the ankle.
Chapter
116
IV
Achilles Tendinitis and Bursitis and Other Painful Conditions of the Ankle Saima Chohan
CHAPTER OUTLINE Achilles Tendinitis 863 Etiology 863 Clinical Presentation 863 Diagnosis 864 Treatment 864
Achilles Tendon Rupture 864 Etiology 864 Clinical Presentation 864 Diagnosis 865 Treatment 865
Retrocalcaneal, Sub-Achilles, or Subtendinous Bursitis 865 Etiology 865 Clinical Presentation 865 Treatment 865
Retroachilleal or Subcutaneous Calcaneal Bursitis 865 Treatment 865
Achilles Tendinitis Etiology The Achilles tendon is the strongest and thickest tendon in the body; it is formed by the convergence of the gastrocnemius and soleus tendons. Injuries to the Achilles tendon are the most common lower extremity tendinous injuries. Achilles tendinitis is usually caused by repetitive trauma and microscopic tears from excessive use of the calf muscles, as in ballet dancing, distance running, track and field, jumping, and other athletic activities; from wearing faulty footwear with a rigid shoe counter; or from use of medications, including corticosteroids and fluoroquinolone antibiotics (Fig. 116.1).1–7 Tendon microtears are often associated with both focal mucoid degeneration and neovascularization.8 Insertional Achilles tendinitis, often associated with enthesopathy and retrocalcaneal bursitis, occurs frequently in patients with spondyloarthropathies, such as ankylosing spondylitis or psoriatic arthritis. The tendon is also a common site for gouty tophi, rheumatoid nodules, and xanthomas.1
Clinical Presentation Tendinitis of the Achilles tendon is characterized by activityrelated pain, swelling, tenderness, and sometimes crepitus over the tendon 2 to 6 cm from its insertion (Fig. 116.2).1–7 © 2011 Elsevier Inc. All rights reserved.
Fig. 116.1 The pain of Achilles tendinitis is constant and severe and is localized to the posterior ankle.
863
864
Section IV—Regional Pain Syndromes
Diagnosis Abnormalities of the tendon and peritendinous tissues can be seen with both ultrasound scan9 and magnetic resonance imaging (MRI).3 With ultrasound scan, Achilles tendinitis is characterized by swelling and a hypoechogenic area within the substance of the tendon, with loss of the normal, wellorganized, ribbon-like intratendinous echostructure. The ultrasound scan demonstration of a spindle-shaped thickening of the Achilles tendon in asymptomatic athletes may also predict those at risk of subsequent development of symptoms.9
Treatment
Fig. 116.2 Swelling and erythema along the left Achilles tendon in a patient receiving a fluoroquinolone. (From Damuth E, Heidelbaugh J, Malani PN, et al: An elderly patient with fluoroquinolone-associated achilles tendinitis, Am J Geriatr Pharmacother 6:264, 2008.)
Treatment consists of a period of rest, weight reduction in obese patients, avoidance of the provocative occupational or athletic activity, shoe modification, a heel raise to reduce stretching of the tendon during walking, nonsteroidal anti-inflammatory drugs (NSAIDs), and physiotherapy, including local ice or heat application, gentle stretching exercises, and sometimes a temporary splint with slight ankle plantarflexion.1–3 Rehabilitation is aimed at stretching the Achilles tendon, the hamstrings, and the calf muscles. Avoidance of hills and uneven running surfaces and diligent stretching before sport activities are often beneficial. Symptoms may persist for several months. The Achilles tendon is vulnerable to rupture, particularly in elderly individuals. Corticosteroid injections in or near the tendon may predispose to tendon rupture and are, therefore, strongly discouraged.1–7,10 Surgical treatment, including open tenotomy with excision of the inflamed peritendinous tissue, open tenotomy with paratenon stripping, or percutaneous longitudinal tenotomy, is rarely necessary in conditions that do not respond to more than 6 months of nonoperative management.1–7,11
Achilles Tendon Rupture Etiology
Fig. 116.3 Eliciting the creak sign for Achilles tendinitis. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, Philadelphia, 2006, Saunders, p 377.)
Tissues surrounding the tendon may be thick and irregular, and sometimes a palpable nodule may be present. Passive dorsiflexion of the ankle intensifies the pain, and a creak sign for Achilles tendinitis may be present (Fig. 116.3). The painful arc sign (movements of the tender swollen area within the tendon with dorsiflexion and plantarflexion of the ankle) and the Royal London Hospital test (tenderness on repalpating a tender swollen area within the tendon with the ankle in maximum active dorsiflexion) are often positive.7
The area of the Achilles tendon, located 2 to 6 cm proximal to its calcaneal insertion, has the poorest blood supply, predisposing this region to tendinopathy and possible rupture.6 Rupture of the Achilles tendon has increased significantly because of increased physical activity in the older population. Achilles tendon rupture occurs most commonly in active men between 30 and 50 years old, typically during a burst of unaccustomed physical activity involving forced ankle dorsiflexion. It may also result from a sharp blow, a fall, or intense athletic activities, because of repetitive microtrauma.1–7,12,13 It may occur spontaneously or after minor trauma in elderly patients with preexisting Achilles tendinitis or retrocalcaneal bursitis, in patients with systemic lupus erythematosus or rheumatoid arthritis receiving corticosteroids, in those on long-term hemodialysis, after local corticosteroid injections in the vicinity of the tendon, and in patients treated with fluoroquinolone antibiotics.14
Clinical Presentation The onset is often sudden, with pain in the region of the tendon, sometimes with a faint “pop” sound and difficulty walking or standing on the toes. Swelling, ecchymosis,
Chapter 116—Achilles Tendinitis and Bursitis and Other Painful Conditions of the Ankle
t enderness, and sometimes a palpable gap are present at the site of the tear. In partial tendon rupture, active plantarflexion of the ankle may be preserved but painful. In those cases with complete rupture, active plantarflexion of the ankle with the adjacent intact flexor tendons is still possible. However, gentle squeezing of the calf muscles with the patient prone, sitting, or kneeling on a chair produces little or no ankle plantarflexion (positive Thompson calf squeeze test).1–7,12,13 If the Thompson test is equivocal, the blood pressure cuff test can be performed. For this test, a sphygmomanometer cuff is inflated to 100 mm Hg around the calf with the patient lying prone and knee flexed 90 degrees.13 If the tendon is intact, the pressure rises to about 140 mm Hg with passive dorsiflexion of the ankle, but it changes very little if the tendon is ruptured.13 Rupture is typically associated with inability to perform single-leg toe raise on the affected side.
Diagnosis Estimates are that 20% to 30% of Achilles tendon ruptures are not diagnosed on initial assessment.6,13 The tendon defect can be disguised by hematoma, and the patient may retain some plantarflexion power because of the actions of the flexor digitorum, flexor hallucis longus, tibialis posterior, and peronei muscles. Thus, the Thompson test should be performed in all patients with suspected Achilles tendon injury. If the diagnosis is still in doubt, the extent and orientation of the rupture can be confirmed and accurately assessed with either ultrasound scan15 or MRI.1,3
Treatment Treatment for Achilles tendon rupture may be nonoperative or surgical. Nonoperative management consists of immobilization with casting to prevent dorsiflexion. Such conservative treatment is usually limited to patients at risk for surgical complications and nonathletes.4–7,12 Immobilization is associated with a higher rerupture rate, a more prolonged recovery time, and a less favorable functional outcome.1–7,12,16 Although open operative or percutaneous repair of the ruptured Achilles tendon is indicated in most patients, particularly in young athletes, recent literature has shown the value of minimally invasive surgery for tendionopathy, acute ruptures, and chronic tears.1–7,13,16,17 Repair of the ruptured tendon should be done within 3 weeks to prevent atrophy of the medial gastrocnemius muscle. Surgery is followed by 6 weeks of immobilization, including 2 weeks of non–weight bearing with use of crutches. The incidence of rerupture is significantly reduced with surgical repair. Use of transforming growth factor in animal models to accelerate and improve tendon healing and improved biomechanical properties of Achilles tendon is an exciting area of research.18
Retrocalcaneal, Sub-Achilles, or Subtendinous Bursitis Etiology Retrocalcaneal bursitis usually occurs in middle-aged and elderly individuals. Known causes include rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis.1,2,6,19 It may
865
also occur in association with both Haglund's deformity (abnormal prominence of the posterior superior calcaneal tubercle causing chronic irritation of Achilles tendon and bursa)20 and Achilles tendinitis resulting from overactivity. Haglund's deformity is often associated with a varus hindfoot. When viewed from behind, it presents as a round bony swelling just lateral to the distal part of the Achilles tendon.20
Clinical Presentation Retrocalcaneal bursitis is associated with posterior heel pain that is aggravated by passive dorsiflexion of the ankle.1,2,6,19 It is often worse in the beginning of an activity, such as walking and running, and diminishes as the activity continues. Patients may present because they are unable to comfortably wear shoes. Symptoms seem to improve on weekends and during vacations. Patients may develop a limp, and wearing shoes can become painful. On examination, the bursitis is associated with tenderness and sometimes erythema on the posterior aspect of the heel at the tendon insertion. Bursal distention produces a tender swelling behind the ankle, with bulging on both sides of the tendon.1,2,6,19 The diagnosis can be confirmed with radiography (showing obliteration of the retrocalcaneal recess, a Haglund's deformity, and sometimes calcified distal Achilles tendon), ultrasound scan,21 or MRI.19
Treatment Rest, activity modification, heat application, a slight heel elevation with a felt heel pad or cup, and NSAIDs constitute sufficient therapy for most patients.1,2,6 A walking cast or a cautious ultrasound scan–guided corticosteroid injection into the bursa is sometimes necessary. Surgical bursectomy and resection of the superior prominence of the calcaneal tuberosity are rarely indicated.1,2,6,20
Retroachilleal or Subcutaneous Calcaneal Bursitis Retroachilleal bursitis, also known as “pump bumps,” produces a painful tender subcutaneous swelling overlying the Achilles tendon, usually at the level of the shoe counter.1–4 The overlying skin may be hyperkeratotic or reddened. It occurs predominantly in women and is frequently caused and aggravated by improperly fitting shoes or pumps with a stiff, closely contoured heel counter. It may also occur in patients with bony exostoses and varus hindfoot.1,2,4,6,20
Treatment Treatment consists of rest, heat application, NSAIDs, padding, and relief from shoe pressure by wearing a soft, nonrestrictive shoe without a counter. Local corticosteroid injections should be avoided. Surgical excision is rarely indicated.1,2,6
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
117
Morton's Interdigital Neuroma and Other Painful Conditions of the Foot Saima Chohan
CHAPTER OUTLINE Metatarsalgia 866 Etiology 866 Clinical Presentation 866
Metatarsalgia Etiology Metatarsalgia, or pain and tenderness in and about the metatarsal heads or metatarsophalangeal (MTP) joints, is a common symptom of diverse causes (Table 117.1).1–6 The condition often follows years of disuse and weakness of the intrinsic muscles as a result of chronic foot strain from improper footwear with the toes cramped into tight or pointed shoes.
Clinical Presentation Metatarsalgia may either be limited to a single joint or generalized across the ball of the foot. The main clinical findings are pain in the forefoot on standing and walking and tenderness on palpation of the metatarsal heads and MTP joints (Fig. 117.1).1,3–6 Prominent, dropped central metatarsal heads, plantar calluses, and clawed toes are frequently present.
Morton's Interdigital Neuroma Historical Aspects Detailed description of interdigital neuroma was first reported by T. G. Morton in 1876.7
Etiology Morton's neuroma is commonly unilateral and occurs most often in middle-aged women. It often results from chronic foot strain and repetitive trauma caused by inappropriately fitting shoes or from mechanical foot problems such as pronated pes planus and pes cavus.1–8 It represents an entrapment 866
Morton's Interdigital Neuroma 866 Historical Aspects 866 Etiology 866 Clinical Features 866 Treatment 868
europathy (rather than a true neuroma) of an interdigital n nerve, typically between the third and fourth metatarsal heads, although it may occasionally occur between the second and third metatarsal heads (Fig. 117.2). The nerve is entrapped under the transverse metatarsal ligament, causing endoneural edema, demyelination, axonal injury, and perineurial fibrosis. An intermetatarsophalangeal bursa or synovial cyst may also cause compression of the nerve.
Clinical Features Although Morton's neuroma can be clinically silent, typical symptoms include paroxysms of lancinating, burning, or neuralgic pain in the affected interdigital cleft and occasionally paresthesia or anesthesia of contiguous borders of adjacent toes.1–9 Hyperesthesias of the toes, numbness and tingling, and aching and burning in the distal forefoot are common symptoms. Relief of pain when the shoe is removed and the foot is massaged is characteristic. Walking on hard surfaces or wearing tight or high-heeled shoes increases the discomfort. The metatarsal arch is often depressed, and tenderness is present over the entrapped nerve between the third and fourth metatarsal heads.1–9 The pain is made worse with compression of the metatarsal heads together with one hand while squeezing the affected web space between the thumb and index finger of the opposite hand (web space compression test). Injection of 1% lidocaine into the symptomatic interspace often temporarily relieves the pain.1,7 Altered sensation may be found on the lateral aspect of the third toe and the medial aspect of the fourth toe. A soft tissue mass (neuroma) may be palpable between the metatarsal heads. Movements of the adjacent toes may produce a clicking sensation produced © 2011 Elsevier Inc. All rights reserved.
Chapter 117—Morton's Interdigital Neuroma and Other Painful Conditions of the Foot
867
Table 117.1 Causes of Metatarsalgia Chronic foot strain and weakness of intrinsic muscles from improper footwear with the toes crammed into tight or pointed shoes Altered foot biomechanics from flat, cavus, or splay foot Interdigital (Morton's) neuroma Attrition of the plantar fat pad in elderly patients Painful plantar callosities, including intractable plantar keratosis (discrete or diffuse painful callus beneath one or more of the lateral metatarsals) Plantar plate rupture with secondary metatarsophalangeal joint instability (usually the second) Hallux valgus, hallux rigidus, hammertoes, and mallet toes Arthritis of the metatarsophalangeal joints: osteoarthritis, rheumatoid arthritis, psoriatic arthritis, gout, trauma Overlapping and underlapping toes Bunion, bunionette, and intermetatarsophalangeal bursitis Osteochondritis of the second metatarsal head (Freiberg's disease) Metatarsal stress (march) fracture Sesamoiditis, sesamoid fracture, or osteonecrosis Failed forefoot surgery Tarsal tunnel syndrome, neuropathy Ischemic forefoot pain: peripheral vascular disease, vasospastic disorder, vasculitis
3
2
Fig. 117.2 The pain of Morton's neuroma is made worse with prolonged standing or walking.
1
4 5
Callus Metatarsal heads
Fig. 117.1 On physical examination, pain can be reproduced with pressure on the metatarsal heads.
868
Section IV—Regional Pain Syndromes
Fig. 117.3 Eliciting the Mulder sign for Morton neuroma. (From Waldman SW: Physical diagnosis of pain: an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, p. 348.)
by extrusion of the neuroma between the metatarsal heads as it moves beneath the transverse metatarsal ligament (Mulder's sign; Fig. 117.3).1–8 The affected nerve may show slow sensory conduction velocity on electrophysiologic testing. The exact location and extent of the lesion can be determined with both magnetic resonance imaging (MRI) and sonography.10 MRI is more sensitive and often shows a well-demarcated bulbous mass arising between the metatarsal heads on the plantar side of the transverse metatarsal ligament. The lesion shows low signal intensity on both T1-weighted and T2-weighted images.11
Treatment Symptomatic management of metatarsalgia includes a metatarsal pad placed proximal to the metatarsal heads, weight reduction in obese patients, strengthening of the intrinsic muscles with toe flexion exercises, and shoe modification, including a wide toe box and, in patients with a
Fig. 117.4 Magnetic resonance image (STIR image) with Morton's neuroma in 3/4 intermetatarsal space. (From George VA, Khan AM, Hutchinson CE, editor: Morton's neuroma: the role of MR scanning in diagnostic assistance, Foot 15:14, 2005.)
pronated foot, an arch support.1–9 If these measures fail, metatarsal osteotomy or metatarsal head resection is indicated. In Morton's neuroma (Fig. 117.4), nonoperative measures, including proper footwear, metatarsal pad, and local corticosteroid injections into the intermetatarsal space, are often helpful. Surgical excision of the neuroma (interdigital neurectomy), epineurolysis, or simple division of the transverse metatarsal ligament are necessary in patients whose conditions are refractory to conservative treatment.1–9 After neurectomy, regeneration of the proximal cut end of the interdigital nerve, blocked by scar tissue, can result in a painful, recurrent, interdigital neuroma. This can be managed with implantation of the proximal cut end of the nerve into an intrinsic arch muscle.12
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
118
IV
Hallux Valgus, Bunion, Bunionette, and Other Painful Conditions of the Toe Saima Chohan
CHAPTER OUTLINE Hallux Valgus 869 Etiology 869 Clinical Presentation 869 Treatment 869
Hallux Limitus and Rigidus 869 Etiology 869
Hallux Valgus Etiology Hallux valgus refers to lateral deviation of the first (great) toe on the first metatarsal (Fig. 118.1). Although the exact etiology is unknown, this deformity is likely caused by abnormal foot mechanics and anatomy, use of shoes (a lower prevalence is seen in barefoot populations), genetic influences, and female gender. It is more common in women and is aggravated by wearing short, narrow, high-heeled, or pointed shoes.1–5 Other causes include congenital splay foot deformity, metatarsus primus varus with or without metatarsus adductus of the adjacent second and third metatarsals,6 and arthritis of the first metatarsophalangeal (MTP) joint from rheumatoid arthritis or osteoarthritis.1–5
Clinical Presentation Medial deviation and splaying of the first metatarsal (metatarsus primus varus) with an increased intermetatarsal angle of more than 9 degrees is seen. The deformity involves rotation of the great toe so that the nail faces medially. The condition is often asymptomatic, but pain may arise from wearing of improper footwear, bursitis over the medial aspect of the first MTP joint (bunion), or secondary osteoarthritis.1–5 As the first metatarsal moves into varus at its joint with the first cuneiform, its head also moves dorsally, resulting in a transfer of weight to the second metatarsal head. This is known as transfer lesion. Altered weight bearing results in a callosity under the second metatarsal head with the second toe forced dorsally, and a hammertoe deformity develops. If the deformity is marked, the great toe may overlie or underlie the second toe and the sesamoids are displaced laterally.1–5 The severity © 2011 Elsevier Inc. All rights reserved.
Clinical Presentation 870 Treatment 870
Bunionette 871 Etiology 871 Clinical Presentation 871 Treatment 871
of the deformity and its progression over time can be assessed radiographically with measurement of the hallux valgus angle between the first metatarsal and first proximal phalanx.7 Structural abnormalities of metatarsal head and sesamoids and the presence of bunion bursitis can be clearly delineated with magnetic resonance imaging (MRI).8
Treatment Treatment of hallux valgus consists of shoe modification to accommodate the bunion, a bunion pad, night splinting, analgesics, and, in the presence of a transfer lesion, a metatarsal pad.1–5 Surgical correction (osteotomy of the first metatarsal base, resection of metatarsal head or base of proximal phalanx with or without distal soft tissue lateral release, and realignment of the sesamoids) is indicated in patients with severe deformity, failure with conservative management, and intractable pain.1–5,9 Corrective osteotomies for the adduction deformities of the second and third metatarsals are often necessary to correct the metatarsus primus varus deformity in those with hallux valgus associated with metatarsus adductus.6 Patients with symptomatic, recurrent hallux valgus after failed prior surgery may benefit from a reduction of the first to second intermetatarsal angle and arthrodesis of both the first tarsometatarsal and first to second intermetatarsal joints.10
Hallux Limitus and Rigidus Etiology Hallux limitus refers to painful limitation of dorsiflexion of the first MTP joint. In hallux rigidus, marked limitation of movement or immobility of the first MTP joint is seen, 869
870
Section IV—Regional Pain Syndromes
Fig. 118.1 An AP clinical picture of a hallux varus deformity showing the medial deviation of the hallux onto the first metatarsal and the supination of the toe, particularly visible at the toenail. (From Devos B, Leemrijse T: The hallux varus: classification and treatment, Foot Ankle Clin North Am 14:51, 2009.)
Fig. 118.2 Valgus hallucal rotation in hallus rigidus. (From Beeson P, Phillipsa C, Corra S, et al: Hallux rigidus: a cross-sectional study to evaluate clinical parameters, Foot 19:80, 2009.)
Fig. 118.3 A, Tailor's bunion deformity may be assessed radiographically with a lateral splaying in the distal fifth metatarsal. B, Clinically, the patient generally presents with symptoms that occur laterally or plantarlaterally, often with an adduction of the fifth toe. (From Thomas JL, Blitch EL, Chaney M, et al: Clinical practice guideline: diagnosis and treatment of forefoot disorders: section 4: tailor's bunion, J Foot Ankle Surg 48: 257, 2009.)
A
sually from advanced osteoarthritis, rheumatoid arthritis, u or gout (Fig. 118.2).1–3,8,11
Clinical Presentation Intermittent aching pain, joint tenderness, crepitus, osteophytic lipping, and painful limitation of movement, particularly toe dorsiflexion, are common. It usually occurs in elderly patients with osteoarthritis. A primary type is seen in younger persons; the condition may follow repetitive trauma as in ballet dancing. The “toe-off ”’ is accomplished by the outer four toes and the distal phalanx of the great toe, thereby bypassing and protecting the first MTP joint from painful dorsiflexion. Calluses often develop beneath
B
the second, third, and fourth metatarsal heads. In advanced stages, the first MTP joint becomes completely rigid in slight plantarflexion.1–3,8,11
Treatment Treatment consists of a stiff-soled shoe with a wide toe box and a bar across the metatarsal heads to allow walking with little movement at the first MTP joint.1–3,8,11 Intraarticular corticosteroid injections may produce temporary relief. In patients with severe pain and disability, excision of irregular osteophytic lipping that interferes with MTP movements, arthrodesis, or arthroplasty of the first MTP joint is indicated.1–3,8,11
Chapter 118—Hallux Valgus, Bunion, Bunionette, and Other Painful Conditions of the Toe
Bunionette Etiology A bunionette (tailor's bunion) is a painful callus and an adventitious bursa that overlies a prominent, laterally deviated fifth metatarsal head and a medially deviated fifth toe.1–3,12–15 It often occurs in conjunction with hallux valgus or splay foot deformity from an incompletely developed transverse metatarsal ligament (Fig. 118.3). The fourth to fifth intermetatarsal angle varies between 3 and 11 degrees, with a mean of 6.5 to 8.0 degrees. The angle is often more than 10 degrees in patients with symptomatic bunionette deformity. The fifth metatarsophalangeal angle is normally less than 14 degrees and is more than 16 degrees in those with bunionette.12,13
Clinical Presentation Enlargement of the fifth metatarsal head from exostosis is commonly present. Bunionette deformity is common in athletes, especially downhill skiers. It is often asymptomatic, but patients may present with pain, tenderness, and swelling over
871
the head of the fifth metatarsal. The pain is made worse by both activity and wearing constricting shoes. Callosity with hyperkeratosis of the skin over the fifth metatarsal head is found, and an adventitious bursa, skin ulceration, or infection may develop.1–3,12
Treatment Shoe modification with a wide toe box, shaving of the callus, a bunion pad, nonsteroidal anti-inflammatory drugs, and intrabursal corticosteroid injections may reduce symptoms, particularly in those with inflamed bunionette bursitis.1–3,12 Distal osteotomy of the fifth metatarsal,12,14 proximal domeshaped osteotomy of the fifth metatarsal,15 or resection of the lateral one third of the fifth metatarsal prominence (head)12 may be necessary in those conditions that are refractory to nonoperative treatment.
References Full references for this chapter can be found on www.expertconsult.com.
IV
Chapter
119
Plantar Fasciitis Dhaneshwari Solanki
CHAPTER OUTLINE Anatomy of the Plantar Fascia 872 Clinical Presentation 872 Diagnosis 872 Investigations 873
Plantar fasciitis is the most common condition treated by the orthopedist and is the most common cause of heel pain in the age group of 40 to 60 years.1 Almost one in 10 persons will suffer from heel pain during their lifetime. It can occur in athletes and nonathletes, yet little is known about its pathophysiology. Wood in 1812 first described plantar fasciitis associated with inflammation from tuberculosis,2 but the infectious theory was soon discredited and the association of heel spur causing this pain was popularized. This was proven not to be the case, and it is accepted that heel spurs can occur with plantar fasciitis but they do not cause it. Plantar fasciitis is presumed to be synonymous with the inflammation of the plantar fascia. But is it really an inflammatory disorder? Histologic signs of inflammation are typically absent. Histologic changes show myxoid degeneration, necrosis of the collagen, and hyperplasia of the angiofibroblasts. Microtears and presence of perifascial edema also can be seen on magnetic resonance imaging (MRI). All this evidence indicates that plantar fasciitis is not an inflammatory but a degenerative disease. Thus, the correct term to describe this condition would be plantar fasciosis.3
Anatomy of the Plantar Fascia The plantar fascia is a longitudinal fibrous tissue with its origin at the medial tubercle of the calcaneus. It traverses the sole of the foot, dividing into five bands at midfoot. It is thickest at its center. Each of the five bands attaches to the proximal phalanx of the toes (Fig. 119.1). It is a static support for the longitudinal arch and acts as the bow string on the plantar surface of the foot (Fig. 119.2).4 A normal plantar fascia has a dorsoplanar thickness of 3 mm. In plantar fasciitis, it can increase to 15 mm.5
Clinical Presentation Plantar fasciitis has been reported in patients aged 7 to 85 years. It is mostly unilateral, but in one third of the cases, it could be bilateral. The skin of the heel is thicker than in other 872
Treatment 873 Surgery 874 Conclusion 874
areas and is designed to deal with constant friction. Thickness of this heel pad decreases after the age of 40 years, so plantar fasciitis is more common after that age. It is also more common in women. Some of the risk factors for development of plantar fasciitis include the following: ■ ■ ■ ■ ■
Obesity Poorly fitting shoes Increase in running intensity or distance Changes in running or walking surfaces Occupation that involves prolonged standing (e.g., policeman)
The foot and ankle should be examined while the patient is standing and during the gait because a pes planus or pes cavus deformity can place excess load on the plantar fascia. The pain in plantar fasciitis is located at the medial tubercle of the calcaneus, which is the origin of the plantar fascia. It is tender to palpation. Other causes of the heel pain include heel spur, stress fracture of the calcaneum, and injury to the first branch of the lateral plantar nerve. Heel pain could also occur in patients with systemic disease, such as gout and rheumatoid arthritis. Bilateral heel pain in a young person may be from Reiter's syndrome.
Diagnosis The diagnosis of plantar fasciitis is based on history and physical examination. No history of trauma is seen. Patients report gradually worsening heel pain. The pain is noticeably worse on awakening in the morning. Patients limp to the bathroom because weight bearing increases the pain. This pain eases after taking a few steps, decreases through the day, and gets worse toward the end of the day. The pain also worsens with prolonged standing. Rest in the evening produces pain relief. Pain of the calcaneal stress fracture worsens with walking. If the pain persists during sleep, other causes such as infection, tumors, and neuropathic pain must be sought and investigations should be done to rule out other pathologic processes that could cause the heel pain. © 2011 Elsevier Inc. All rights reserved.
Chapter 119—Plantar Fasciitis
873
MCT
Fig. 119.3 Ultrasound scan of normal asymtomatic plantar fascia. Plantar aponeurosis
MCT
Fig. 119.1 Anatomy of the plantar fascia.
Fig. 119.4 Ultrasound scan of the inflamed and symptomatic plantar fascia.
Tibia Fibula
Calcaneus Long plantar lig.
Fig. 119.2 Increased dorsoplanar thickness of the fascia in plantar fasciitis.
The most cardinal finding is the presence of localized tenderness on the anteromedial aspect of the heel. Application of firm pressure is often necessary to determine maximum point of tenderness. Passive dorsiflexion of the toes exacerbates the pain. Tightness of the Achilles tendon is found and limits the dorsiflexion of the foot in 78% of patients. No other clinical findings in the foot or the ankle are seen. Tenderness of the posterior part of the heel may be indicative of subcalcaneal bursitis. Mediolateral tenderness on the heel is indicative of a
calacaneal stress fracture. A positive Tinel's sign on the medial aspect of the heel may be the result of tarsal tunnel syndrome or the entrapment of the nerve to the abductor digiti quinti.
Investigations Imaging has a limited role in the diagnosis of plantar fasciitis. Plain radiographs of the heel are obtained to rule out causes such as stress fracture, bony erosion from bursitis, or heel spurs that could cause heel pain. If a calcaneal stress fracture is suspected and plain radiographs are normal and the patient has not responded to 4 to 6 months of nonsurgical treatment, a triple phase bone scan should be considered. An MRI is rarely indicative, but it can define the thickness of the plantar fascia. Ultrasound scan examination shows hypoechoic thickened fascia and is as effective as bone scan and MRI. Ultrasound scan examination can be done in the office. It is inexpensive and avoids radiation exposure. Normal plantar fascia on ultrasound scan examination appears thin and hypoechoic (Fig. 119.3). Inflamed plantar fascia appears as a thick band yet is hypoechoic (Fig. 119.4).6 A complete blood count and erythrocyte sedimentation rate should be done when the patient presents with bilateral heel pain or atypical symptoms.
Treatment Plantar fasciitis is a self-limiting condition. The conservative treatment, if started within 6 weeks of the onset of symptoms, hastens the recovery process.7 Conservative treatment should
874
Section IV—Regional Pain Syndromes
be tried for 12 months before surgical intervention is contemplated. Twenty-six different conservative treatments have been recommended,8 but heel pads, orthoses, corticosteroid injections, night splints, and extracorporeal shock wave therapy (ESWT) have been evaluated with randomized control trials. The conservative treatments include: 1. 2. 3. 4. 5.
Nonsteroidal anti-inflammatory drugs Orthoses and insets Physical therapy Injections ESWT
Oral nonsteroidal anti-inflammatory drugs should be used only during the acute phase. They show improved pain relief, but they have not been examined prospectively with randomized trials. Orthoses recreate the shape of the heel, decreasing excessive pronation and stress on the plantar fascia. Pfeffer9 compared various types of shoe inserts with a control group and found superior pain relief. Magnetic insoles were not beneficial. Pain relief with application of ice, heat, or massage is largely based on patient reports. Patients should be taught the exercises for the Achilles tendon stretching and plantar fascia stretching. Dorsiflexion of the foot with the knee extended stretches the gastrocnemius muscle. The same movement with the knee partially flexed stretches the soleus muscle. These stretches should be done in 8 to 10 repetitions and three to five times a day. Plantar fascia stretching is done by dorsiflexing the toes while the ankle is dorsiflexed. Night splints can help because they keep the Achilles tendon in a stretched position. Patients with severe pain can benefit from a below-the-knee cast for 4 to 6 weeks; it can minimize repetitive microtrauma. Corticosteroid injection in combination with local anesthetics has been used to treat plantar fasciitis, but hardly any evidence is found of its effectiveness. In the past, injection was done via palpation. Now, it is done with ultrasound scan to improve the accuracy of the injection site. Kane et al10 compared the two methods and did not find any difference. In addition, complications, such as rupture of the plantar fascia and fat pad atrophy, have been reported with these injections. The Cochrane group has concluded that steroid injections are useful in the short term and to a limited degree.8 In a case series of 20 patients, Ryan et al11 reported pain relief in 80%
of the patients when a solution of hyperosmolar dextrose and lidocaine was injected in the hypoechoic areas of the plantar fascia with ultrasound scan guidance. The hyperosmolar solution triggers proliferation of fibroblasts and collagen synthesis because of upregulation and migration of various growth factors. ESWT has become increasingly popular for recalcitrant pain. It should be used in patients when disabling symptoms have persisted more than 6 months and other conservative therapies have failed to relieve the pain. The shockwaves are directed to the origin of the plantar fascia. The mechanism is speculative, but the hypothesis is that it produces microdisruption of the fascial tissue that starts the healing response. No consensus exists as to the use of the low-energy or highenergy waves, but randomized controlled trials have supported the use of both and no serious side effects have been reported.12
Surgery Surgery should be considered only when the patient has not responded to the previously described treatment for 12 months.9 The surgical procedures that are considered for treatment of plantar fasciitis are release of plantar fascia, calcaneal spur excision, Steindler stripping, neurolysis, and endoscopic procedures.13 Surgery could provide relief in 50% to 60% of patients, but a possibility also exists of significant complications from such procedures.
Conclusion Plantar fasciitis is the most common cause of heel pain. Review of the literature provides ample evidence that conservative management is the treatment of choice. In many cases, plantar fasciitis could be a self-limiting condition. Surgical intervention should only be considered when the pain and disability from plantar fasciitis persists despite adequate trial with nonsurgical therapies.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
120
Simple Analgesics Robert B. Supernaw
CHAPTER OUTLINE Nonprescription Simple Analgesics: Overview 878 Over-the-Counter Nonsteroidal Anti-Inflammatory Drugs 879 Salicylates 879 Aspirin 879 Sodium Salicylate 881 Propionic Acids 881 Ibuprofen 881
For most pain phenomena, pharmacotherapy represents an indispensable therapeutic tool. However, pharmacotherapy— even over-the-counter (OTC) pharmacotherapy—has the dual feature of combating the principal condition while potentially provoking undesired adverse effects. Therefore, even in cases of mild, uncomplicated pain, the best therapeutic approach is to combat the pain with physical methods (e.g., ice packs, heat, massage) if the condition is amenable to such treatment. However, the option of not employing pharmacotherapy in managing many painful conditions is not realistic. If the clinician has determined that the symptom of pain cannot be effectively treated with physical intervention, drug therapy is indicated. To determine the best pharmacotherapeutic response to pain, the nature and severity of the pain must be assessed and considered. If the pain is uncomplicated and nonpsychogenic and if the pain intensity is mild or moderate, simple analgesics, including OTC agents, represent first-line treatment options. Even in cases of mild or moderate pain, treatment plans are formulated on the basis of the specific nature of the complaint. For example, moderate headache pain may be treated differently from moderate pain of a sprained ankle. In one case, it may be important to consider the pain of inflammation, whereas in another case inflammation may not be at the root of the pain. Unlike the basic therapeutic approach to other commonly encountered problems (e.g., hypertension, hyperlipidemia) in which drug therapy is initiated in relatively small doses and is slowly increased until the therapeutic threshold or desired outcome is achieved, the therapeutic approach to pain is predicated on the basis of matching the complete pain presentation to the appropriate agent, with a reasoned dose of the agent chosen. In many instances, no need exists to begin drug therapy for the pain complaint with a less potent, OTC analgesic before attempting more potent drug therapy. The severe 878
Naproxen Sodium 882 Ketoprofen 882
Acetaminophen 882 Action 882 Dosing 882 Pharmacokinetics 883 Indications in Pain 883 Cautions 883
pain of a cluster headache does not respond to aspirin or acetaminophen therapy; therefore, little is gained in trying. This treatment principle underscores the need for an accurate categorization of the pain complaint. When, in the judgment of the clinician, the nature (i.e., relatively uncomplicated pain) and intensity (i.e., mild or moderate pain) of the pain complaint are deemed appropriate, first-line pharmacotherapy (i.e., simple OTC analgesics) may be initiated. These conditions include uncomplicated headache, facial pain, muscle ache, toothache, joint pain, foot pain, and uncomplicated back pain, to name a few of the more commonly encountered pain problems. The OTC simple analgesics are the most widely used drugs for mild to moderate nociceptive pain, and sales of these agents (i.e., aspirin, acetaminophen, ibuprofen, naproxen sodium, and ketoprofen) totaled more than $2.18 billion in the United States in 2004.
Nonprescription Simple Analgesics: Overview Mild acute pain is limited in its duration. Therefore, it need not be aggressively treated if it does not affect an individual's quality of life and the patient has not indicated significant or distracting discomfort. In some instances, the pain need not be treated at all. Mild chronic pain may prove to be more problematic in its negative impact on an individual's quality of life, family relations, and ability to work. It usually requires active treatment. If a decision is made to treat mild acute or chronic pain, the first consideration should be given to simple analgesics. These agents are available without a prescription on an OTC basis. The principal OTC simple analgesics include members of two major families of drugs—the nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. © 2011 Elsevier Inc. All rights reserved.
Chapter 120—Simple Analgesics
A useful categorization of the OTC NSAIDs includes two principal groupings—the salicylates and the nonsalicylates. The salicylates can be further divided into two families of drugs, the acetylated and the nonacetylated salicylates. A helpful representation of the categorization of the simple analgesics is depicted in Figure 120.1. When a decision is made to treat mild to moderate nociceptive pain, consideration should be given to the nature of the pain and the patient. If the patient is not allergic to aspirin and tolerates aspirin well, then aspirin is a good firstline choice and is the most widely recommended analgesic.1 Acetaminophen should be considered if the patient is aspirin sensitive, aspirin intolerant, or allergic to aspirin. However, as is the case with most choices in pharmacotherapy, the rules are not quite that simple. Many other factors must be taken into account before the choice of a simple analgesic can be made. These considerations are detailed in the following sections of this chapter.
Over-the-Counter Nonsteroidal Anti-Inflammatory Drugs OTC NSAIDs are the most commonly employed of the simple analgesics. This category of drugs includes the salicylates and the propionic acids (see Fig. 120.1). The salicylates are further divided into the acetylated and the nonacetylated compounds.
Salicylates Two forms of salicylates are available in the OTC analgesic armamentarium. The most commonly used member of the acetylated salicylate family is aspirin, including the combination products enteric-coated aspirin and buffered aspirin. The OTC nonacetylated salicylate family includes sodium salicylate.
SIMPLE ANALGESICS
OTC NSAIDs
Salicylates
Acetylated salicylates (e.g., aspirin)
Acetaminophen
Propionic acids (e.g., Ibuprofen, naproxen sodium, ketoprofen)
Nonacetylated salicylates (e.g., sodium salicylate)
Fig. 120.1 Classification and relationships of simple analgesics.
879
Aspirin Acetylsalicylic acid, more commonly known as aspirin, is the most commonly used simple analgesic and has been for many years. According to the Aspirin Foundation, approximately 100 billion aspirin tablets are produced annually. Aspirin represents a reasonable first choice for common mild to moderate pain, if the pain is nociceptive. The forerunner of aspirin, sodium salicylic acid, was widely used as an analgesic and antipyretic from the 1700s onward. A much improved acetyl derivative of sodium salicylic acid—acetylsalicylic acid or aspirin—was introduced commercially in the United States in 1899. By definition, aspirin is an NSAID that predates all other modern NSAIDs. Aspirin is the prototypical salicylate and, as such, has a long history of safe and effective use. However, as is the case with almost all drugs, whether OTC or prescription, aspirin is not without its risks. The benefits of aspirin therapy are well known. It is cheap, is readily available, has a very long track record, is effective in the relief of mild to moderate nociceptive pain, improves function, and reduces inflammation, especially at higher doses. Additional benefits include its ability to reduce fever and its antiplatelet adhesion properties. Given as a 650-mg dose (two regular-strength tablets) every 4 hours, aspirin may be considered first-line drug therapy in various mild to moderate pain-related problems including chronic joint pain, minor arthritis flare-ups, common and tension-type headaches, dysmenorrhea, minor postoperative pain and inflammation, and chronic minor low back pain. Action Aspirin and the acetylated salicylates have analgesic, antiinflammatory, antiplatelet, and antipyretic activity. These drugs are most effective for general pain, common headache pain, and especially pain of musculoskeletal origin, including arthritis and muscle pain. When peripheral tissue is insulted in trauma or when a pain-triggering event occurs, prostaglandins enhance the transmission of pain impulses and the sensitivity of the pain receptors, and an inflammatory response may ensue. Aspirin's principal mechanism of action is inhibition of prostaglandin (eicosanoid) synthesis in peripheral tissue.2 Therefore, pain relief is not instantaneous, as eicosanoid levels dissipate. Aspirin appears to acetylate the active site of the enzyme cyclooxygenase (COX), also known as PGH synthase, which is the specific enzyme necessary for the conversion of arachidonic acid to eicosanoids. This acetylation permanently (irreversibly) deactivates the COX enzyme and thereby effectively inhibits prostaglandin production.3 This irreversibility is an important distinction between aspirin, an acetylated salicylate, and the other NSAIDs. It is likely that aspirin also mitigates pain through central mechanisms. Investigators have hypothesized that the acetate components of aspirin pass into the brain and spinal cord and exert their activity on central nervous system prostaglandins that are involved in the perception and transmission of pain. Dosing Aspirin is available in 325-mg and 500-mg tablet, caplet, and effervescent tablet strengths. It is also available as an 81-mg chewable tablet and an 81-mg enteric coated tablet.
880
Section V—Specific Treatment Modalities for Pain and Symptom Management
Aspirin is available in a controlled-release 800-mg oral dosage form and is embedded in chewing gum in the 228-mg strength. For rectal use, aspirin is available in 125- and 300-mg suppositories. For administration in adult patients, for general musculoskeletal and common headache pain, aspirin is most often given orally in doses ranging from 325 to 650 mg every 3 to 4 hours as needed, not to exceed 4 g in a 24-hour period. If the condition warrants the more potent dosage form (i.e., extra strength 500 mg), the suggested dose is 500 mg every 3 to 4 hours or 1000 mg every 6 to 8 hours. For significant inflammatory processes, including arthritis, aspirin can be given in divided doses equivalent to 3.2 to 6.0 g daily, provided every 3 to 4 hours. For severe headache pain, aspirin has been demonstrated to show added analgesic activity when doses are pushed to 1000 mg.4 For the pain and discomfort of niacininduced flushing, 325 mg aspirin should be given before the administration of the niacin dose. Because the potential for gastrointestinal irritation is related to both a local effect and a pharmacologic effect, aspirin should always be taken with a full glass of water. Studies have also shown that doses should be slightly increased in obese patients because peak levels do not match those seen in nonobese individuals.5 For administration in pediatric patients who are more than of 2 years old, a 10 to 15 mg/kg/dose every 4 hours, up to 60 to 80 mg/kg per day is appropriate for general pain, discomfort, or fever. For infants and children into their teens, aspirin is contraindicated—should not be given—in cases of viral infections, including flu and chickenpox because it has been implicated in Reye's syndrome. For infants and children suffering from juvenile rheumatoid arthritis, an initial dose of 90 to 130 mg/kg per day, in divided doses every 4 to 6 hours, is appropriate for oral administration. This dose may be increased as needed to maximize anti-inflammatory efficacy to achieve a plasma salicylate level objective of 150 to 300 mg/mL. An alternative dosing guideline for pediatric patients is based on age and weight. For children ages 2 to 11 years, a total of 64 mg/kg per day in four to six doses is appropriate. Another guideline6,7 is as follows, if the child's weight is within normal limits: Children more than 11 years old (weight, greater than 43.2 kg): 650 mg every 4 hours, not to exceed 4 g per day n Children age 11 years (weight, 32.4 to 43.2 kg): 480 mg every 4 hours n Children age 9 to 10 years (weight, 26.9 to 32.3 kg): 400 mg every 4 hours n Children age 6 to 8 years (weight, 21.5 to 26.8 kg): 325 mg every 4 hours n Children age 4 to 5 years (weight, 16.0 to 21.4 kg): 240 mg every 4 hours n Children age 2 to 3 years (weight, 10.6 to 15.9 kg): 160 mg every 4 hours n Children younger than 2 years (up to 23 months and up to 10.5 kg in weight): aspirin not recommended n
Pharmacokinetics Oral aspirin is absorbed very rapidly in the stomach and upper small intestine by passive diffusion.8 Moderate differences in absorption are noted between buffered and nonbuffered varieties. Buffered tablets are absorbed in 30 to 45 minutes,
and nonbuffered tablets are absorbed within 60 minutes.9 However, significant levels are detectable in plasma in less than 30 minutes after a single dose of aspirin.1 In buffered aspirin, minute quantities of antacid are added to aid in the dissolution of the tablet. In theory, this would enhance absorption, but studies have not demonstrated significant differences in total absorption. Although enteric coating does delay aspirin's absorption, it does not affect total absorption or the resultant salicylate levels.10 Taking aspirin with food or with meals does not affect its absorption.11 Peak levels of oral aspirin occur approximately 1 hour after administration. Unlike salicylic acid, aspirin is not effectively absorbed through the skin. Percutaneous absorption is significantly less than 10% of oral absorption.12 Rectal absorption of aspirin administered in a suppository dosage form is incomplete and variable; therefore, it is not advisable unless other routes are not feasible.13 The distribution of the salicylates is throughout most body tissues and depends on the patient and the drug concentration. Approximately 68% (± 3%) of the aspirin dose is available (at the initial stages after administration) as the unchanged drug, but this may be significantly different in older patients and in patients with compromised liver function.14 Of course, aspirin (acetylsalicylic acid) is hydrolyzed to salicylic acid, which is not accounted for in this 68% figure. At usual or higher concentrations of salicylates, albumin binding varies but may approach 80%.13 At lower concentrations, inactive binding to albumin may approach 90%. On average, at therapeutic concentrations, approximately 80% of the aspirin dosed is inactively bound.1,13 Because of this significant albumin binding, caution is warranted when aspirin is given to a patient who is taking an oral anticoagulant (OAC) in that the OAC is approximately 97% albumin bound. The aspirin binding will displace some of the OAC, and this displacement will augment the active dose (drug level) of the OAC and significantly increase bleeding time. If as little as 3% of the OAC is displaced by the aspirin, the effective dose of the OAC will be doubled. The process of inactive albumin binding can saturate the system; therefore, high doses of aspirin (e.g., single doses greater than 650 mg) will saturate the binding system and lead to very high blood levels. In other words, increasing the dose of aspirin to more than 650 mg will increase the blood levels of aspirin in a disproportionate manner and will significantly increase the half-life of the drug. The volume of distribution of aspirin is 0.15 L/kg (±0.03 L/kg).1 Aspirin crosses the placental barrier and is not advised in the third trimester of pregnancy (pregnancy category C/D). Aspirin is hydrolyzed in circulation and in the liver to form salicylate and acetic acid. Within 30 minutes, only 27% of the orally administered dose remains as acetylsalicylic acid; the active remainder is salicylate.1 As with all salicylates, aspirin is metabolized in the liver by esterases. The major metabolite of salicylates is salicyluric acid. Salicylates are excreted in the urine, and alkalinization of the urine increases the rate of excretion.13 Aspirin exhibits a two-compartment half-life. It has a half-life of 15 minutes as aspirin (acetylsalicylic acid) and 3 to 5 hours as its salicylate metabolite. Therefore, although normally the half-life of pure aspirin is 15 minutes, and 3 to 5 hours for salicylate, when the inactive albumin binding system is saturated, the half-life may increase up to threefold of normal (e.g., 3 to 5 hours for dosing at 600 mg daily versus 12 to 16 hours for dosing at 3.6 g daily for significant anti-inflammatory effects).13 Only approximately
10% of aspirin is excreted as free salicylic acid; 75% is excreted as salicyluric acid.1 Because aspirin is excreted in breast milk, the drug is unsafe to use in breast-feeding mothers. Indications in pain As a nonselective COX-1 and COX-2 inhibitor, aspirin is indicated for the treatment of general complaints of pain associated with inflammatory processes, menstruation (e.g., dysmenorrhea), dental pain, headache, joint pain, muscle pain, and integumentary pain. It is less effective in treating visceral pain. In synovial fluid, aspirin reaches approximately 78% of plasma concentrations,15,16 thus making it a good option for treating arthritis pain and, at higher doses, inflammation. Cautions Aspirin should never be given to children or teenagers who exhibit symptoms of influenza or chickenpox. In these cases, aspirin administration has been associated with Reye's syndrome, which, although rare, is associated with mortality rates up to 30% and severe brain damage in patients who survive. Ringing in the ears may indicate toxicity. Any complaints of such a symptom indicate the basis for discontinuation of aspirin. Dizziness may also indicate the onset of toxicity. Because of its irreversible antiplatelet effects, aspirin should be discontinued at least 7 days before surgery to preclude the chance of aspirin-induced postoperative bleeding. Caution is warranted with the use of aspirin in asthmatic patients. Bronchospasms occur in up to 19% of these patients. As with all drugs metabolized in the liver, caution is warranted in patients with compromised liver function. Aspirin should not be considered in the third trimester of pregnancy and should not be administered to lactating mothers who are breast-feeding. Because of local and pharmacologic induced gastrointestinal irritation, aspirin should be used with caution in patients who complain of gastrointestinal burning and in those with ulcers. Rectal bleeding and fecal blood loss should be monitored. When plasma concentration monitoring is possible, the therapeutic range should not exceed 300 mg/mL (30 mg/dL). Acidification of the urine increases plasma levels, and alkalinizing the urine decreases levels. Aspirin has also been implicated in blood-related problems including decreased white blood cell and platelet counts and hemolytic anemia. Clinicians should warn patients to discard aspirin that has an odor of vinegar; this indicates that the aspirin has undergone chemical degradation. Extra caution is indicated if the patient (1) is taking an OAC; (2) is taking an oral antidiabetic agent; (3) has a history of peptic ulcer disease; (4) has systemic lupus erythematosus; (5) is pregnant or is contemplating pregnancy; (6) is scheduled for surgery; (7) is receiving a new prescription; or (8) experiences a new significant adverse effect. Analgesic effects result from plasma levels approaching 10 mg/dL. Anti-inflammatory effects result from plasma levels from 10 to 40 mg/dL. Ringing in the ears occurs at approximately 50 mg/dL. Toxicity occurs as a function of levels higher than 50 mg/dL, and doses leading to levels higher than 160 mg/dL are lethal.17 Aspirin interacts with several other drugs and chemical entities. Alcohol increases the risk of gastrointestinal irritation. Ascorbic acid acidifies the urine and decreases the excretion of aspirin. Antacids and urinary alkalinizers increase the
Chapter 120—Simple Analgesics
881
excretion of aspirin and thereby decrease the effects of aspirin. OAC levels are increased with the concomitant use of aspirin because of inactive binding displacement. Aspirin and other NSAIDs exhibit additive gastrointestinal irritative effects. Aspirin decreases the antihypertensive effects of angiotensin-converting enzyme inhibitors (ACE inhibitors) and beta blockers. Aspirin and the salicylates antagonize the action of uricosuric agents, and salicylates should not be given with methotrexate.
Sodium Salicylate Sodium salicylate is the “other” nonprescription salicylate. Its characteristics are similar to those of aspirin, with one major exception: sodium salicylate is not acetylated. As such, it does not have a two-compartment half-life, as does aspirin. In other words, although aspirin has a “first” half-life as acetylsalicylic acid that is approximately 15 minutes, followed by an active metabolite, salicylate, with a half-life of 3 to 5 hours, sodium salicylate has a single compartment active drug half-life of 3 to 5 hours, but that half-life can be prolonged up to 19 hours.13 The second major difference between aspirin and sodium salicylate is that aspirin acetylates and irreversibly blocks COX. Therefore, platelet aggregation is effectively inhibited for the life of the platelet with aspirin, whereas the antiplatelet adhesion effect is only temporary with the nonacetylated salicylates. Sodium salicylate is considered somewhat less effective in reducing pain when compared with aspirin. However, some patients who are hypersensitive to aspirin may tolerate sodium salicylate. The dose of sodium salicylate is the same as for aspirin—325 to 650 mg every 4 hours, as needed.
Propionic Acids Ibuprofen Ibuprofen is available as an OTC analgesic in modest doses of 200 mg per tablet. For a complete description of the NSAIDs used in pain management, please see Chapter 121. Although OTC doses of ibuprofen are effective in mild to moderate pain, the drug at this low dose does not have anti-inflammatory effects. Ibuprofen is marketed generically and as Motrin, Nuprin, and Advil. It is relatively safe to give to children. The children's OTC doses are as follows: 50 mg every 6 to 8 hours for children weighing 12 to 17 pounds (not more than four doses per day) n 75 mg every 6 to 8 hours for children weighing 18 to 23 pounds (not more than four doses per day) n 100 mg every 6 to 8 hours for children weighing 24 to 35 pounds (not more than four doses per day) n 150 mg every 6 to 8 hours for children weighing 35 to 47 pounds (not more than four doses per day) n 200 mg every 6 to 8 hours for children weighing 48 to 59 pounds (not more than four doses per day) n 250 mg every 6 to 8 hours for children weighing 60 to 71 pounds (not more than four doses per day) n 300 mg every 6 to 8 hours for children weighing 72 to 95 pounds (not more than four doses per day) n
Children age 12 and older may be dosed at 200 mg every 4 to 6 hours, with a maximum 24-hour total dose of 1200 mg. The recommended OTC dose for patients who are more than
882
Section V—Specific Treatment Modalities for Pain and Symptom Management
16 years old and who have mild to moderate pain is 200 to 400 mg every 4 to 6 hours as needed up to a maximum of 1200 mg in a 24-hour period. Absorption is approximately 85%, but it is 90% to 99% albumin bound. The time to peak concentrations is 1 to 2 hours, and the drug's half-life is 2 to 4 hours. In OTC doses (i.e., 200 mg), this medication is safe to use in older patients, with caution.
Naproxen Sodium Naproxen sodium is available as an OTC analgesic in modest doses of 220 mg per tablet. For a complete description of NSAIDs used in pain management, please see Chapter 121. Although OTC doses of naproxen sodium are effective in mild to moderate pain, the drug at this low dose does not have antiinflammatory effects. It is marketed on an OTC basis as Aleve. This drug should not be given to children less than 12 years old. The recommended OTC dose for mild to moderate pain in patients who are more than 12 years old is two tablets initially (440 mg), followed by one tablet (220 mg) every 8 to 12 hours. For individuals who are more than 65 years old, the recommended OTC dose is one tablet every 12 hours. The drug is virtually completely absorbed, but it is highly albumin bound. The time to peak concentrations is 1 to 4 hours, and its duration of action is approximately 12 hours. Therefore, naproxen sodium is an excellent choice when an OTC NSAID is indicated and extended duration of action is desired.
Ketoprofen Ketoprofen is available as an OTC analgesic in modest doses of 12.5 mg per tablet. For a complete description of the NSAIDs used in pain management, please see Chapter 121. Although OTC doses of ketoprofen are effective in mild to moderate pain, the drug at this low dose does not have antiinflammatory effects. It is marketed for OTC use as Orudis KT. Ketoprofen should not be given to children. The recommended OTC dose for mild to moderate pain in adults who are more than 16 years old is 12.5 mg every 4 to 6 hours as needed up to a maximum of six tablets in a 24-hour period.It is virtually completely absorbed, but it is highly albumin bound. The time to peak concentrations is 30 minutes up to 2 hours, and its half-life is 2.5 hours. In OTC doses, this medication is safe to use in older patients.
Acetaminophen Acetaminophen is not an NSAID. It has a mechanism of action different from that of the NSAIDs, and it has little antiinflammatory and no antiplatelet activity. However, it is a very good OTC analgesic and has significantly less potential for gastrointestinal irritation when compared with aspirin and the other NSAIDs. On an equivalent-dose basis, acetaminophen is comparable to aspirin in its analgesic abilities. However, acetaminophen has come under fire for its dose-related adverse effects, specifically those associated with liver damage. Acetaminophen is N-acetyl-aminophenol. (The last three letters of acetyl and the last four letters of aminophenol have lent themselves to the naming of the most popular tradenamed acetaminophen product, Tylenol.) Acetaminophen is an active metabolite of phenacetin. Analogues of acetaminophen were used in the late 1800s. Although these analogues exhibited good analgesic and antipyretic effects, most had
significant adverse effects. Acetaminophen was used sparingly from 1893 until 1950. In 1951, research revealed that acetaminophen was as effective as aspirin for temporary pain relief and fever reduction. McNeil Pharmaceuticals then marketed acetaminophen as an aspirin alternative in 1953 and as an elixir for children in 1955. Today, acetaminophen is available generically and as brandnamed products including Tylenol, Acephen, Aspirin Free Anacin, Tempra, Panadol, Genipap, Liquiprin, and Datril, to name but a few.
Action The mechanism of acetaminophen's analgesic action has not been fully determined. However, research indicates that acetaminophen inhibits prostaglandin synthesis in a manner somewhat similar to that of aspirin. Although aspirin clearly nonselectively blocks the COX-1 and COX-2 enzymes to inhibit prostaglandin synthesis, it appears that acetaminophen only partially blocks the COX-1 and, perhaps, COX-2 enzymes. Most likely, acetaminophen inhibits specific prostaglandin synthesis associated with the newly identified COX-3 enzyme, as well as a subtype of the COX-1 enzyme.18 Other researchers have opined that the COX-3 enzyme is a subtype of the COX-2 enzyme.19 Regardless of the nature of the COX-3 entity, blocking the activity of this newly discovered enzyme provides a reasonable explanation that accounts for acetaminophen's ability to inhibit or diminish pain impulse transmission and perception while having little effect on inflammation and platelet aggregation and not diminishing the production of the prostaglandin that protects the gastrointestinal tract lining.
Dosing Acetaminophen is available in tablet, capsule, extended-release dosage forms, chewable tablets, rectal suppositories, and liquid elixir for oral pediatric use. The recommended OTC dose for adults is similar to that of aspirin—325 to 650 mg every 4 hours as needed, up to 1 g every 6 hours or 1300 mg every 8 hours. At these higher doses, the self-medicating patient should be carefully reviewed by the physician if the condition does not improve within 10 days. It is essential not to exceed 4 g of acetaminophen per day. The accumulation of the drug causes hepatotoxicity.20 Initial symptoms of liver damage include nausea, vomiting, and significantly diminished appetite, often mistaken for symptoms of the flu. In June of 2009, an advisory committee to the United States Food and Drug Administration (FDA) recommended that labeling include recommendations that the single adult dose of acetaminophen be limited to no more than 650 mg, a dose significantly less than the 1000 mg currently consumed when a patient takes two 500-mg tablets or capsules. The panel also recommended that the 24-hour dose of acetaminophen be limited to a dose less than the current 24-hour limit of 4000 mg (4 g). The panel cited 56,000 emergency room visits, 26,000 hospitalizations, and 458 deaths annually, according to studies spanning the 1990s. The FDA has yet to act on these recommendations. Another recommendation of the advisory committee that has yet to be acted on is that of eliminating the acetaminophen contained in prescription analgesics (e.g., Vicodin, Percocet, Darvocet). This recommendation was more contentious, given that the affirmative panel vote was 20 to 17.
Dosing in children should be guided by the following formula: 1.5 g per day, in divided doses, for each square meter of body surface. Alternatively, a more convenient guideline21 was developed by McNeil Laboratories: Infants up to 3 months old: 40 mg every 4 hours orally as needed n Infants 4 to 14 months old: 80 mg every 4 hours orally as needed n Children 1 to 2 years old: 120 mg every 4 hours orally as needed n Children 2 to 4 years old: 160 mg every 4 hours orally as needed n Children 4 to 6 years old: 240 mg every 4 hours orally as needed n Children 6 to 9 years old: 320 mg every 4 hours orally as needed n Children 9 to 11 years old: 320 to 400 mg every 4 hours orally as needed n Children 11 to 12 years old: 320 to 480 mg every 4 hours orally as needed n
It is recommended that children up to the age of 12 years receive no more than five doses in any 24-hour period. For children, liquid dosage forms are preferred; however, instructions to parents and caregivers on the dosage calibration when administering liquids using teaspoons or droppers must be clear.
Pharmacokinetics Acetaminophen is rapidly and almost completely absorbed when it is taken orally.22,23 Absorption may be decreased if the drug is taken following a meal high in carbohydrates. Rectal absorption is variable and depends largely on the vehicle base. After oral administration, peak levels are reached in 30 to 60 minutes.22,23 The plasma half-life is approximately 2 hours, and the agent's duration of action is approximately 4 hours. The drug is widely distributed, and it is approximately 20% to 50% plasma protein bound. Acetaminophen does appear in breast milk, but only reaches levels of 10 to 15 mg/mL approximately 1 to 2 hours after administration of a 650-mg dose. The metabolism of acetaminophen occurs primarily in the liver. One of the metabolites may accumulate when the system is saturated; this metabolite is hepatotoxic and nephrotoxic. With doses up to 650 mg, plasma concentrations will reach levels of 5 to 20 mg/mL. Elimination is by the renal pathway; approximately 3% of the dose is excreted unchanged.
Indications in Pain Acetaminophen is an excellent OTC analgesic drug to be considered in place of aspirin in patients who are sensitive to aspirin or aspirin-like medications; in patients who have ulcers; in patients who experience pain without an inflammatory process; in patients who should not receive antiplatelet drug therapy, including those who are receiving anticoagulant therapy; and in patients receiving uricosuric agents. Although acetaminophen has little or no anti-inflammatory
Chapter 120—Simple Analgesics
883
capability and should not be considered in rheumatoid arthritis, it can be used in patients who have mild osteoarthritis. In fact, acetaminophen is recommended as a first-line agent for the treatment of pain associated with osteoarthritis of the hip and knee by the American College of Rheumatology, Subcommittee on Osteoarthritis Guidelines.24 Additionally, acetaminophen is widely used and is effective in treating general complaints of pain associated with menstruation (e.g., dysmenorrhea), dental pain, headache, joint pain, muscle pain, and integumentary pain. It is less effective in treating visceral pain.
Cautions The metabolites of acetaminophen are toxic and may accumulate when high doses are employed and when the drug is taken by in liver-impaired individuals. Special concern should be exercised in alcoholic patients, patients with eating disorders, and patients who are fasting. Acute hepatotoxicity may occur when a single dose of 10 to 15 g or more is taken (150 to 250 mg/kg).22,23 Doses of 20 to 25 g or more can be fatal.22,23 Long-term daily use of 4 g or more for extended periods may also lead to serious toxicity. Symptoms of chronic toxicity include significant gastrointestinal disturbance. If an acute toxic dose is detected within 4 hours, gastric lavage is indicated.22,23 For many poison control centers, N-acetylcysteine (Mucomyst) is the treatment of choice if it can be administered less than 36 hours after acetaminophen ingestion. However, it is most effective if it is given within 10 hours after acetaminophen ingestion.25 Treatment consists of 140 mg/kg orally (loading), followed by 70 mg/kg every 4 hours for 17 doses. In any cases of acetaminophen overdose or suspected toxicity, the caregiver should immediately call a poison control center and emergency services. While awaiting recommendations, activated charcoal may be administered. It is effective in binding acetaminophen in cases of acute toxicity. The therapeutic effects of acetaminophen may be decreased when the drug is given concomitantly with barbiturates, carbamazepine, hydantoins, rifampin, and sulfinpyrazone, which may decrease the drug's analgesic effects. Cholestyramine may decrease acetaminophen absorption, so it is prudent to separate concomitant dosing of acetaminophen and cholestyramine by at least 1 hour. Barbiturates, carbamazepine, hydantoins, isoniazid, rifampin, and sulfinpyrazone, when given concomitantly with acetaminophen, may have additive effects that increase their cumulative hepatotoxic potential. The effects of warfarin may also be enhanced when given to a patient taking acetaminophen. Consuming alcohol while taking acetaminophen may increase the risk of hepatotoxicity, as will the concomitant use of NSAIDs and acetaminophen.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
121
Nonsteroidal Anti-Inflammatory Drugs and Cyclooxygenase-2 Inhibitors Steven D. Waldman
CHAPTER OUTLINE Prostaglandin Synthesis and the Analgesic Effects of the Nonsteroidal AntiInflammatory Drugs 884 Body's Response to Inflammation 885 Individual Characteristics of Various Nonsteroidal Anti-Inflammatory Drugs 885 Salicylates 885 Diflunisal 886
The nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most widely used drugs in the world. This heterogeneous group of drugs includes aspirin, the nonacetylated salicylates, and an ever-increasing number of chemically diverse nonsalicylate compounds commonly referred to as the NSAIDs, a subclass of which is known as the cyclooxygenase-2 (COX-2) inhibitors. All these drugs have become an integral part of the routine treatment of numerous painful conditions. Although investigators initially assumed that the painrelieving properties of the NSAIDs could be attributed solely to their inhibition of prostaglandins, more recent research suggested that many of the NSAIDs may exert an antinociceptive effect that is separate from their anti-inflammatory properties and may be useful in the treatment of pain that is not inflammatory in origin. This chapter focuses on the pharmacology, mechanisms of action, adverse effects, and clinical use of NSAIDs. It also provides the clinician with a practical framework for the safe and optimal use of this class of drugs.
Prostaglandin Synthesis and the Analgesic Effects of the Nonsteroidal Anti-Inflammatory Drugs Investigators initially believed that the pain-relieving properties of the NSAIDs were primarily the result of the ability of these drugs to inhibit the peripheral formation of prostaglandins.1 Further understanding of the way in which the NSAIDs 884
Nonacetylated Salicylates 886 Other Nonsteroidal Anti-Inflammatory Drugs 886
Drug Selection 886 Side Effects 886 Cyclooxygenase-2 Inhibitors 889 Celecoxib 889
Conclusion 889
produce both beneficial and harmful effects led to the concept that this class of drugs most likely works by inhibition of the enzyme COX. Currently, at least two forms of the enzyme are known to exist. These have been named COX-1 and COX-2.2 COX-1 activation leads to the production of prostacyclin, which exhibits antithrombogenic and gastric cytoprotective properties. COX-2 is induced by inflammatory stimuli and cytokines and exhibits an anti-inflammatory response. The anti-inflammatory actions of the NSAIDs appear to result from inhibition of COX-2, whereas many of the unwanted side effects, such as gastrointestinal bleeding, result from inhibition of COX-1. Therefore, in theory, drugs that have the highest COX-2 activity and a more favorable ratio of COX-2 to COX-1 activity should have a potent anti-inflammatory activity with fewer side effects than drugs with a less favorable ratio of COX-2 to COX-1 activity. Although this conclusion was the logical result of years of basic science research and led to the development of newer NSAIDs with this seemingly desirable profile, the withdrawal of rofecoxib and valdecoxib from the market in response to unwanted cardiovascular side effects called this line of reasoning into question. At the very least, it pointed to our incomplete understanding of the way in which the NSAIDs affect the various organ systems.3 Although the foregoing discussion explains the mechanism by which NSAIDs can relieve pain mediated by the inflammatory response, it does not fully explain the antinociceptive properties of this group of drugs in the treatment of acute pain from a single noxious stimulus on otherwise healthy tissue. This apparent disparity between the relative © 2011 Elsevier Inc. All rights reserved.
Chapter 121—Nonsteroidal Anti-inflammatory Drugs and Cyclooxygenase-2 Inhibitors
anti-inflammatory and antinociceptive effects is termed dissociation.4 The proposed reasons for dissociation include the following: (1) NSAIDs produce pain relief in the absence of the physicochemical changes induced by inflammation; (2) NSAIDs appear to exert some central modulation of pain by attenuation of the phenomenon of central sensitization independent of peripheral events including prostaglandin synthesis; and (3) little correlation exists between the efficacy of a given NSAID to relieve pain and the drug's ability to inhibit prostaglandin synthesis.4 The clinical importance of these findings is the subject of much clinical research.
Body's Response to Inflammation Inflammation is the body's response to tissue injury. Many of the major events in the inflammatory process have been identified, but the reasons for these events and the roles of the different chemical mediators in this process remain unclear. Factors such as the severity of tissue injury and the patient's ability to mount an inflammatory response determine the intensity of inflammation in each individual case.5 Histamine mediates the initial inflammatory response by producing a transient period of vasoconstriction. Subsequently, vasodilation and increased permeability of blood vessels constitute a process sustained by prostaglandins.5 In addition to these vascular events, cellular events contribute to the production of inflammation. At the site of inflammation, complement activation causes the release of chemotactic peptides called leukotrienes. These peptides diffuse into the adjoining capillaries and cause passing phagocytes to adhere to the endothelium. This process is pavementing. The phagocytes insert pseudopods between the endothelial cells and dissolve the basement membrane (diapedesis). The neutrophils then pass out of the blood vessel and move up the concentration gradient of the chemotactic peptides toward the site of inflammation.4,6 The result of this phagocytic process is the eventual destruction of the neutrophil. When this occurs, intracellular free radicals and lysosomal enzymes are released from the cell into the extracellular space. These substances cause further tissue damage.6 As the process continues, other chemical mediators, including complement fragments and interleukin-1, stimulate increased release of leukocytes from the bone marrow.7 As leukocytes, leukocyte fragments, damaged tissue, and plasma accumulate in the area of injury, an exudate (pus) forms.6,7 These events characterize acute inflammation. When the precipitating stimulus is removed or destroyed, inflammation resolves. If, however, the precipitating stimulus cannot be eliminated by these body defenses, inflammation will progress from an acute to a chronic state.5,8,9
Individual Characteristics of Various Nonsteroidal Anti-Inflammatory Drugs Salicylates Aspirin (acetylsalicylic acid) is the prototype of the nonopioid anti-inflammatory drugs (Fig. 121.1). Aspirin and aspirin-like drugs are most often administered as analgesics, antipyretics, and inhibitors of platelet aggregation.10 To achieve antiinflammatory activity, doses of aspirin greater than 3.6 g per
885
CH3
O N N
S
NH2
O
F3C Fig. 121.1 Chemical structure of aspirin.
day are necessary.10 The serum half-life of salicylates ranges from 2 hours for analgesic doses to more than 20 hours for anti-inflammatory doses.10 Orally administered salicylates are rapidly absorbed from the small intestine and, to a lesser extent, from the stomach. No conclusive evidence indicates that sodium bicarbonate given with aspirin (buffered aspirin) results in a faster onset of action, greater peak intensity, or longer analgesic effect. Aspirin available in buffered effervescent preparations, however, undergoes more rapid systemic absorption and achieves higher plasma concentrations than the corresponding tablet formulations. These effervescent preparations also cause less gastrointestinal irritation.11 Food delays the absorption of salicylates. Aspirin, by acetylating COX, decreases the formation of both thromboxane (a potent vasoconstrictor and stimulant of platelet aggregation) and prostacyclin (a potent vasodilator and inhibitor of platelet aggregation). Low doses of aspirin, 60 to 100 mg daily, selectively suppress the synthesis of platelet thromboxane without inhibiting the production of endothelial prostacyclin.9 This selective suppression may explain the favorable effect of low doses of aspirin in preventing coronary artery thrombosis.12 Aspirin-induced platelet dysfunction seen with higher doses of aspirin lasts for the normal life span of platelets, which is 8 to 11 days. The decreased platelet aggregation observed with aspirin is not seen with the nonacetylated salicylate products such as choline magnesium trisalicylate (Trilisate) and salsalate (Disalcid).13,14 These nonacetylated salicylates are a much safer alternative in patients with a bleeding disorder or in those patients scheduled to undergo a surgical procedure.14 Aspirin should be avoided in patients with severe hepatic dysfunction, vitamin K deficiency, hypoprothrombinemia, or hemophilia because platelet inhibition in such patients can result in hemorrhage.13 Aspirin should also be avoided in children with chickenpox and flulike illnesses, because the drug has been implicated as a possible causative or contributory factor in the evolution of Reye's syndrome. Patients with asthma and nasal polyposis should also avoid aspirin and aspirin-like drugs because acute allergic reactions may result. Salicylates may cause gastric irritation and ulceration by a reduction in prostaglandins, which normally inhibit gastric acid secretion and the ability to inhibit COX-1.14 Alcohol ingestion may exacerbate the problem. To minimize these effects, the salicylates should be taken with food or milk or administered with cytoprotection agents. Being highly bound to albumin (80% to 90%), aspirin and aspirin-like drugs may
886
Section V—Specific Treatment Modalities for Pain and Symptom Management
displace other drugs such as warfarin, oral hypoglycemics, and methotrexate from protein-binding sites.13
Diflunisal Diflunisal (Dolobid) is a difluorophenyl derivative of salicylic acid. This drug has pharmacodynamic and pharmacokinetics profiles similar to those of the other salicylates. Diflunisal has been used primarily for musculoskeletal pain. It is less likely to cause the tinnitus associated with higher doses of aspirin. The initial loading dose for diflunisal is 1000 mg, followed by 250 to 500 mg every 8 to 12 hours.
Nonacetylated Salicylates Choline magnesium trisalicylate (Trilisate) and salsalate (Disalcid) are two nonacetylated salicylate derivatives that appear to lack many of the side effects of the other members of the salicylate family. These drugs exert significantly fewer effects on platelets and cause fewer gastrointestinal side effects.15 These unique qualities are especially useful in the oncology patient who may have chemotherapy-induced clotting abnormalities. Both drugs appear to exert analgesic and anti-inflammatory effects similar to those of the acetylated salicylates. Choline magnesium trisalicylate is available in a liquid form, thus making it useful for those patients who are unable to swallow pills.
Other Nonsteroidal Anti-Inflammatory Drugs Although technically the salicylates and para-amino-phenol derivatives (acetaminophen) are included in this class of drugs, the term nonsteroidal anti-inflammatory drug has gained common acceptance as a descriptor for the chemically heterogeneous group of drugs that exhibit aspirin-like analgesic and anti-inflammatory properties. NSAIDs provide analgesic effects at lower doses and anti-inflammatory effects at higher doses. The NSAIDs are all antipyretic. Many NSAIDs from several chemical classes are available. More products are in various phases of clinical testing in Europe and the United States. Although the drugs referred to in common parlance as the COX-2 inhibitors are also technically NSAIDs, in this chapter they are considered separately and are discussed later. In general, the NSAIDs are indicated after simple analgesics have failed to relieve pain, toxic effects have developed, or inflammation is present.13 All NSAIDs appear to be as effective as aspirin in terms of analgesia or anti-inflammatory properties and may cause fewer gastrointestinal complaints than aspirin, although this relationship may be dose dependent.13,14 These characteristics have encouraged many physicians to select NSAIDs before aspirin in spite of the increased cost to the patient. The pharmacokinetic properties of all individual NSAIDs are similar.16 All these drugs are well absorbed after oral administration, are highly protein bound (>90%), and have a low volume of distribution (60 years). The exact mechanism for muscular rigidity is not known, but it is postulated to be centrally located in the striatum, which is known to be rich in opioid binding sites.36 The rigidity of the striatal muscles is characterized by increased muscle tone, which may progress to severe stiffness. In particular, thoracic and abdominal muscles are involved, resulting in the so-called wooden chest, which impedes ventilation.
Respiratory System All µ-receptor agonists produce dose-dependent respiratory depression. The agonist-antagonists also depress respiration but have a ceiling effect. Opioids primarily cause respiratory depression by reducing brainstem respiratory center responsiveness to carbon dioxide (CO2). They also depress the respiratory centers in the pons and medulla, which are involved in regulating respiratory rhythmicity.37 The resting CO2 increases, and the CO2 response curve shifts to the right. Equianalgesic doses of µ-receptor agonists produce the same degree of respiratory depression. A decrease in respiratory rate is characteristic of µ-receptor agonist–induced respiratory depression. Some compensatory increase occurs in the minute volume, which is incomplete, as evidenced by an increase in the partial pressure of CO2 (Paco2). Patients must rely on hypoxic drive to stimulate ventilation. Pain is an effective antagonist to the respiratory depressant effects of opioids. κ- Receptor agonists produce less respiratory depression, even after administration of large doses. Opioid antagonists antagonize the respiratory
Atropine
Meperidine
Fig. 122.6 At high doses, meperidine may cause tachycardia because of its structural resemblance to atropine. (Adapted from Ferrante M: Opioids. In Ferrante M, VadeBoncouer T, editors: Postoperative pain management, New York, 1993, Churchill Livingstone, p 145.)
depressant effects of opioids. Central sleep apnea and ataxic breathing are observed in a dose-dependent fashion in patients using opioids on a long-term basis.38,39 Partial opioid agonists have also been used to antagonize the respiratory depression caused by pure opioid agonists. Physostigmine also has been shown to reverse the respiratory depressant effect while preserving the analgesic effect.40 Systemic morphine but not nebulized morphine is superior to placebo in the treatment of cancer-related dyspnea.41
Cardiovascular System The cardiovascular effects of opioids not only depend on the dosage but also are also linked with the product and the prevailing vegetative basic tone of the patient. Opioids produce dose-dependent bradycardia by increasing centrally mediated vagal stimulation. Meperidine produces tachycardia because of its structural similarity to atropine (Fig. 122.6). Morphine and some other opioids (meperidine and codeine) provoke release of histamine, which plays a major role in producing hypotension. Naloxone does not inhibit the histamine release produced by opioids. Morphine exerts its well-known therapeutic effect in the treatment of angina pectoris by decreasing preload, inotropy, and chronotropy, thereby decreasing myocardial oxygen consumption.9 Pentazocine and butorphanol cause an increase in systemic and pulmonary artery pressure, left ventricular filling pressure, systemic vascular resistance and a decrease in left ventricular ejection fraction. Opioids should be used with caution in patients with decreased blood volume because these agents can aggravate hypovolemic shock. Methadone can prolong the QT interval and lead to torsades de pointes and potentially lethal ventricular arrhythmias.
Gastrointestinal Tract µ-Receptor agonists decrease gastric, biliary, pancreatic, and intestinal secretions. Even small doses decrease gastric motility and prolong gastric emptying time. Resting tone in the small and large intestine is increased to the point of spasm, and the propulsive peristaltic waves are decreased. Opioids exert their effect on the submucosal plexus, decrease the secretion by enterocytes, and inhibit the stimulatory effects of acetylcholine, prostaglandin E2, and vasoactive intestinal peptide. These effects are mediated in large part by the release of
orepinephrine and stimulation of alpha2-adrenergic receptors n on the enterocytes.42 The gastrointestinal effects of opioids are primarily mediated by µ and δ receptors in the bowel. However, neuraxial application of opioids can also cause these effects as long as the extrinsic innervation of the bowel is intact. Patients usually develop very little tolerance to the constipating effects of opioids. Opioids constrict the sphincter of Oddi and raise the common bile duct pressure. Opioids in patients with biliary disease may cause severe sphincter constriction and pain. Delayed respiratory depression associated with opioids is postulated to be caused by enterosystemic circulation of opioids. Secondary peaks are often seen in plasma concentration-time graphs during pharmacokinetic studies of the more lipid-soluble opioids.43 This phenomenon is thought to be caused by absorption of the opioids first sequestered in the acidic gastric juices and then absorbed from the small intestine.
Chapter 122—Opioid Analgesics
897
Immune System Opioids affect host defense mechanisms in a complex manner. Acute, central immunomodulatory effects seem to be mediated by activation of the sympathetic nervous system, whereas long-term effects may involve modulation of hypothalamicpituitary-adrenal axis function.48 Morphine alters numerous mature immunocompetent cells that are involved in cellmediated and humoral immune responses and also modulates the neuronal mechanism centrally. Heroin addicts have an altered and impaired immune system and also have a higher prevalence of infectious diseases than do nonaddicts.49
Tolerance
Opioids in therapeutic doses prolong labor by decreasing uterine contractions.45 Parenteral opioids given within 2 to 4 hours of delivery can produce neonatal respiratory depression because they cross the placenta.
Tolerance refers to a phenomenon in which exposure to a drug results in the diminution of an effect or the need for a higher dose to maintain an effect. Tolerance can be innate (genetically determined) or acquired. The three types of acquired tolerance are pharmacokinetic, pharmacodynamic, and learned. Pharmacokinetic tolerance comes from changes in the metabolism and distribution of the drug after repeated administration (i.e., enzyme induction). Pharmacodynamic tolerance originates from adaptive changes (i.e., drug-induced changes in receptor density). Learned tolerance is a result of compensatory mechanisms that are learned.50 Short-term tolerance probably involves phosphorylation of the µ and δ receptors through protein kinase C,51 whereas long-term tolerance is associated with increases in adenylyl cyclase activity, a counterregulation to the decrease in cAMP levels seen after acute opioid administration.52 In opioid tolerance, functional decoupling of opioid receptors from the G-protein–regulated cellular mechanisms occurs, in addition to down-regulation of endogenous opioids or opioid receptors and behavioral changes.53 Tolerances to different opioid side effects develop at different rates; this phenomenon is termed selective tolerance. Tolerance to nausea, vomiting, sedation, euphoria, and respiratory depression develop rapidly, whereas tolerance to constipation and miosis is minimal.54 Repeated doses of a drug in a given category confer tolerance not only to the drug used but also to other drugs in the same structural and mechanistic category; this effect is known as cross-tolerance. Cross-tolerance has been shown to be incomplete in animal studies and has been reported in humans as well.55 Incomplete cross-tolerance is frequently attributed to opioids, which have differing opioidreceptor subtype affinity.55,56 NMDA antagonists have been shown to block the antinociceptive tolerance to morphine.57
Skin
Hyperalgesia
Morphine in therapeutic doses can cause dilation of cutaneous blood vessels. This is in part the result of histamine release and a decrease in peripheral vascular resistance. The skin of the face, neck, and upper thorax becomes flushed. Morphine- and meperidine-induced histamine release accounts for the urticaria at the site of injection; this effect is not reversed by naloxone.9 Oxymorphone, methadone, fentanyl, and sufentanil are not associated with histamine release. Pruritus is a disabling side effect of opioid use. Pruritus is more intense with the intrathecal application of opioids,46 and the effect appears to be mediated in large part by dorsal horn neurons.47
The process of increased sensitivity to pain with the shortterm and long-term use of opioids is termed opioid-induced hyperalgesia. Multiple mechanisms for the development of this condition have been proposed. Investigators have observed activation of the central glutamatergic system, a cellular mechanism common to the development of tolerance.58 Spinal dynorphins also have an important role in the development of opioid-induced hyperalgesia. Opioid use is associated with a rise in spinal dynorphin levels, and this increase, in turn, mediates release of spinal excitatory neuropeptides. Basically, up-regulation of the pronociceptive pathways appears to occur. Decreasing the opioid dose (40% to 50%) and adding
Genitourinary System Retention of urine, a frequent finding with opioid analgesics, increases urinary sphincter pressure and decreases the central inhibition of detrusor tone. The hypothesized site of action of opioids is in the thoracic spinal cord, where some preganglionic cell bodies are surrounded by terminals containing enkephalins and substance P.44
Endocrine System µ-Receptor agonists inhibit the release of gonadotropinreleasing hormone and corticotropin-releasing hormone and thereby decrease the circulating concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), ACTH, and ß-endorphin. As a result of decreased pituitary trophic hormones, plasma levels of testosterone and cortisol also decrease. With long-term administration, patients develop a tolerance to these effects. κ-Receptor agonists inhibit the release of antidiuretic hormone and cause diuresis, and µ-receptor agonists tend to produce an antidiuretic effect.
Uterus
898
Section V—Specific Treatment Modalities for Pain and Symptom Management
adjuvants or a low dose of methadone can be used to treat opioid-induced hyperalgesia.59 Ketamine, a NMDA receptor antagonist is another option for the management of this condition.
physicians who prescribe large quantities of opioid analgesics to patients in pain has had a chilling effect on the appropriate use of opioid analgesics in pain management in many communities. Efforts by the national and international pain management community to highlight the appropriateness of the use of opioid analgesics for the management of all types of pain have helped to decriminalize such activities. Further efforts to define and codify best practices in opioid prescribing have also helped. Patient contracts and urine drug screening have also assisted in decreasing the incidence of diversion of prescribed opioids and opioid overuse. Physical dependence is defined as the potential for an abstinence syndrome, or withdrawal, after abrupt dose reduction, discontinuation of the drug, or administration of an antagonist or agonist-antagonist drug. This is a physiologic phenomenon and is associated with disabling symptoms (Table 122.5). The lowest dose and shortest duration of treatment that may predispose patients to a significant abstinence syndrome are not known.33 Clinically, the dose can be decreased by 10% to 20% every other day and eventually stopped without signs and symptoms of withdrawal.9
Addiction and Physical Dependence Addiction has been defined by the World Health Organization as “a state, psychic and sometimes also physical, resulting from the interactions between a living organism and a drug, characterized by a behavioral and other responses that always include a compulsion to take the drug on a continuous or periodic basis in order to experience its psychic effects, and sometimes to avoid the discomfort of its absence. Tolerance may or may not be present.” Increasing evidence implicates the mesolimbic dopamine system in the rewarding effects of drugs of abuse such as opioids; in addition, endogenous opioids may play a key role in the underlying adaptive mechanisms.33 Opioid agonists with affinity for µ and δ receptors are rewarding, whereas opioid agonists with affinity for κ receptors are aversive. Experiments with opioid antagonists have demonstrated the presence of an endogenous opioidergic tone in the reward system. The dopaminergic mesolimbic system, originating in the ventral tegmental area of the midbrain, has been implicated in the rewarding effects seen with opioid use (Fig. 122.7). The D1 subtype of dopamine receptors mediates a tonic activation of this pathway. The basal release of dopamine in the NAcc is under tonic control of both opposing opioid systems: µ-receptor (and possibly δ-receptor) activity originating from the ventral tegmental area increases and κ-receptor activity (originating from the NAcc) decreases basal activity of the mesolimbic reward system.60 Some evidence suggests a possible genetic predisposition to the development of addiction. The term pseudoaddiction has been used to describe the iatrogenic syndrome of behavioral changes similar to addiction that can develop as a result of inadequate pain management. Opiophobia is the phenomenon of failure to administer legitimate opioid analgesics because of fear of the power of these drugs to produce addiction. Aggressive prosecution of
Pharmacokinetics Pharmacokinetics is the study of drug disposition in the body (what the body does to the drug) over time, including absorption, distribution, biotransformation, and elimination. Opioids have similar pharmacodynamic properties but have widely different kinetic properties (Tables 122.6 and 122.7).
Absorption and Routes of Administration Absorption refers to the rate and extent of removal of the drug from the site of administration. This process is determined by the drug's molecular shape and size, ionization constant, lipid solubility, and physicochemical properties of the membrane it must cross.61 OPIOID-DOPAMINE INTERACTION
NAC
VTA β-Endorphin (?)
Reinforcement
µ tonus
Dynorphin
κ tonus Fig. 122.7 Model for the modulation of mesolimbic A10 neurons by endogenous opioid systems. D1, dopamine receptor subtype; DA, dopamine; GABA, g-aminobutyric acid; NAC, nucleus accumbens; VTA, ventral tegmental area. (Adapted from Spanagel R, Herz A, Shippenberg TS: Opposing tonically active endogenous opioid systems modulate the mesolimbic dopaminergic pathway, Proc Natl Acad Sci U S A 89:2046, 1992.)
D1 receptor
DA release
Aversion
GABA Interneuron A10 neuron
Chapter 122—Opioid Analgesics
Oral Route The oral route is the preferred route for long-term administration of opioids because it is convenient and cost effective. Most opioids are well absorbed after oral administration. Aqueous solutions are absorbed the best, followed by oily solutions, suspensions, and oral solids. Drugs absorbed from the gut are subject to first-pass metabolism in the liver and some degree of metabolism by enzymes in the intestinal wall. The onset of action is slower and variable in comparison with parenteral administration. Some opioids (e.g., codeine, oxycodone) have a high oral-to-parenteral potency ratio because they are protected from conjugation by substitution on C3 aromatic hydroxyl residue.62 Oral opioids are
Table 122.5 Symptoms and Signs of Opioid Withdrawal Symptoms
Signs
Craving for opioids
Pupillary dilatation
Restlessness
Sweating
Irritability
Piloerection
Increased sensitivity to pain
Tachycardia
available in tablet and liquid form and in immediate-release and controlled-release preparations. Morphine, oxycodone, and oxymorphone are available in controlled-release forms. The controlled-release form of hydromorphone is not available in the United States.
Table 122.7 Plasma Half-Life Values for Opioids and Their Active Metabolites Plasma Half-Life (hr) Short Half-Life Opioids
Morphine
2–3.5
Morphine-6-glucuronide
2
Hydromorphone
2–3
Oxycodone
2–3
Fentanyl
3.7
Codeine
3
Meperidine
3–4
Pentazocine
2–3
Nalbuphine
5
Butorphanol
2.5–3.5
Buprenorphine
3–5
Nausea
Vomiting
Long Half-Life Opioids
Abdominal cramps
Diarrhea
Methadone
24
Myalgia
Hypertension
Levorphanol
12–16
Dysphoria
Yawning
Propoxyphene
12
Insomnia
Fever
Norpropoxyphene
30–40
Anxiety
Rhinorrhea
Normeperidine
14–21
From Collett BJ: Opioid tolerance: the clinical perspective, Br J Anaesth 81:58, 1998.
899
From Inturrisi CE: Clinical pharmacology of opioids for pain, Clin J Pain 18(Suppl 4):S3, 2002.
Table 122.6 Pharmacokinetic and Physiochemical Variables of Opioid Analgesics Drug
Vc (L/kg)
Vd (L/kg)
Cl (mL/min/kg)
T1⁄2b 134 min
Partition Coefficient (Octanol/Water)
Morphine
0.23
2.8
15.5
Hydromorphone
0.34
4.1
22.7
15 min
1
Meperidine
0.6
2.6
12
180 min
21
Methadone
0.15
Levorphanol
3.4
1.6
23 hr
10.0
10.5
11 hr
1
115
Alfentanil
0.12
0.9
7.6
94 min
130
Fentanyl
0.85
4.6
21
186 min
820
Sufentanil
0.1
2.5
11.3
149 min
1,750
Buprenorphine
0.2
2.8
17.2
184 min
10,000
Nalbuphine
0.45
4.8
23.1
222 min
Butorphanol
5.0
38.6
159 min
Dezocine
12.0
52
156 min
Cl, clearance; T ⁄2β, elimination half-life; Vc, central volume of distribution; Vd, volume of distribution. Adapted from Hill H, Mather L: Patient-controlled analgesic, pharmacokinetic and therapeutic considerations, Clin Pharmacokinet 24:124, 1993; and O'Brien JJ, Benfield P: Dezocine: A preliminary review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy, Drugs 38:226, 1989. 1
900
Section V—Specific Treatment Modalities for Pain and Symptom Management
Subcutaneous Route
Inhalational Route
In comparison with the oral route, subcutaneous administration is faster and does not have to rely on gastrointestinal function. Absorption can be variable and erratic. The subcutaneous route can be used for continuous infusion, patient-controlled analgesia, and intermittent boluses. The drawbacks are that only small volumes can be infused and that pain and necrosis may occur at the site of injection The intramuscular route is painful and inconvenient, and absorption can show some variability. As compared with the subcutaneous route, larger volumes and oil-based solutions can be used intramuscularly. The intravenous route provides the most rapid onset of analgesia, but the duration of analgesia after a bolus dose is shorter than with other routes. This route provides more reliable absorption and drug levels in the plasma. Intravenous drugs must be water soluble, or the oil-based solutions need to be diluted and given in larger volumes.
Administration of opioids by the inhalational route is a novel technique. Use of this technique has been encouraging because of the suggestion that this method may target opioid receptors in the lung. After inhalation of morphine and diamorphine, morphine has been detected in the plasma after 1 minute, with a time of maximal concentration in 10 and 6 minutes, respectively.63,64 Fentanyl administered by this route achieves a time of maximal concentration in 2 minutes.65 Inhaled opioids have been investigated for several indications: dyspnea at rest, postoperative pain, and provision of pain relief in the general population. Nebulized morphine is not superior to placebo for treatment of dyspnea in patients with cancer.41
Rectal Route The rectal route is an alternative when the upper gastrointestinal tract cannot be used and the parenteral route is not available or acceptable. The rectal route is contraindicated if the patient has lesions of the anus or rectum. Absorption of medications is similar to that with the oral route. The bioavailability of drugs is variable; the bioavailability of morphine is 55% to 60%, a finding suggesting that this route partially avoids the first-pass metabolism.
Intranasal Route Intranasal administration is particularly familiar to the recreational abuser of opioids. Reliable absorption across the nasal mucosa is determined by lipid solubility. This route avoids first-pass metabolism. Opioids administered by this route can be used either as a dry powder or dissolved in water. Butorphanol is the only opioid available formulated in a metered-dose spray form. Clinical trials are ongoing to evaluate a nasal fentanyl preparation. Many opioids dissolved in water or saline solution have been investigated. Intranasal administration of opioids for acute pain settings is not superior to parenteral administration. The intranasal route may have a role in patients with difficult intravenous access. Drug reservoir
Transdermal Route The transdermal route is used in two forms: passive system and active (iontophoresis) system. Fentanyl is the only opioid currently available in a transdermal form. Fentanyl can be used for transdermal delivery because of its physicochemical properties: low molecular weight, high lipid solubility, and high potency. Transdermal fentanyl uses the passive system. The two principal system components are a fentanylcontaining reservoir and a rate-controlling membrane. Five patch sizes are available and provide delivery of fentanyl at 12.5, 25, 50, 75, or 100 µg/hour. The transdermal system is not ideal for rapid dose titration. Transdermal fentanyl should be considered when patients have relatively constant pain with infrequent episodes of breakthrough pain. The transdermal therapeutic system used to administer fentanyl is designed to release the drug for 72 hours at a controlled rate dictated by the system, rather than by the skin.66 Fentanyl is dissolved in ethanol, is gelled with hydroxyl cellulose, and is held in a reservoir between a clear occluding polyester-ethylene backing layer and a rate-controlling membrane (ethylene-vinyl acetate copolymer film) on an adhesive base (Fig. 122.8). The amount of fentanyl administered per hour is proportional to the surface area of the patch. Multiple patches must be applied if higher doses are needed. The major obstacle to diffusion is the stratum corneum, where diffusion occurs primarily through the intracellular lipid medium.67 Because a depot is established in the dermis, absorption continues even after patch removal. After the first patch application, initial detection of fentanyl in the blood has been reported to occur at 1 to 2 hours. The plasma fentanyl
Backing
Microporous release membrane
Contact adhesive Fig. 122.8 Fentanyl transdermal therapeutic system. Schematic representation (not to scale) of the delivery system and the pathway of absorption across the skin.
Transdermal drug delivery system Viable epidermis Dermis
Removable protective liner
Subdermal tissue
Stratum corneum Cutaneous microcirculation Sytemic circulation
Skin
concentration increases over 12 to 18 hours until a plateau develops. Under normal physiologic conditions, skin temperature and regional blood flow do not influence fentanyl absorption significantly.66 Absorption rises by approximately one third with a rise in body temperature to 40°C (104°F).68 The plasma concentration remains constant as long as the patch is changed every 72 hours. After patch removal, the plasma fentanyl concentration slowly declines, with an apparent half-life of 15 to 21 hours.67 A transdermal formulation of sufentanil is currently in clinical trials and may represent another option for patients who have become tolerant to the less potent drug fentanyl. A transdermal formulation of sufentanil in combination with the local anesthetic bupivacaine is also undergoing clinical trials. Buprenorphine is available as a transdermal preparation in some countries. Iontophoresis is a method of transdermal delivery of drugs in an ionized state with the use of an electric current. Morphine has been administered using this route for postoperative analgesia.69 The delivery of fentanyl by iontophoresis is being investigated more extensively than is that of other opioids. Iontophoresis has the advantage of achieving a rapid steady state and the ability to vary delivery rate.70
Neuraxial Route Neuraxial delivery by intrathecal, epidural, and intraventricular administration of opioids has the advantage of producing profound analgesia with relatively small doses. The mechanism of analgesia produced by epidural morphine is bimodal and synergistic. During the first 20 minutes, the vascularly absorbed morphine activates the descending inhibitory system. Then, as the cerebrospinal fluid (CSF) morphine concentration increases, the spinal cord receptors are activated.1 The short-term use of this route is most commonly advocated for postsurgical pain relief. It is indicated for long-term use when other routes do not control the pain or are associated with significant side effects. Opioids injected in the neuraxis should be free of preservatives. Duramorph (preservative-free morphine) is commercially available. Other opioids such as fentanyl, sufentanil, meperidine, methadone, and hydromorphone are used intrathecally and epidurally. Remifentanil cannot be given intraspinally; it is prepared with glycine, which can cause temporary motor paralysis. The most common side effects are pruritus, nausea, vomiting, somnolence, urinary retention, and respiratory depression. The most worrisome side effect is delayed respiratory depression, which may occur 12 hours after the intraspinal administration of morphine. Lipophilic drugs such as fentanyl do not spread much after intrathecal administration, but hydrophilic drugs such as morphine can spread rostrally and cause delayed respiratory depression. This effect is also seen sporadically after epidural administration. Other late side effects of long-term administration of neuroaxial opioids are tolerance and the development of subarachnoid granulation tissue, which may decrease the efficacy of the opioids administered and may cause neurologic compromise. This last side effect is seen most commonly with intrathecal morphine at high doses.71 Intraventricular opioid administration is a satisfactory analgesic method that should be reserved for patients who have intractable pain and a short life expectancy and who have exhausted other modalities of pain management. Small doses of intraventricular morphine provide satisfactory control of otherwise intractable pain in patients with terminal cancer.72
Chapter 122—Opioid Analgesics
901
Distribution After being injected into the circulation or being absorbed, opioids are distributed within the body in two phases. In the early phase, the drug is distributed to highly perfused tissues such as the heart, liver, kidney, and brain. This is a function of the cardiac output and regional blood flow. The second phase is characterized by a slow diffusion to less-perfused areas such as muscle, fat, viscera, and skin. Volume of distribution is the extent to which a drug is distributed within the body. The differences in distribution determine the onset of activity. A highly diffusible drug that acts on a highly diffusible organ has a very rapid onset of action. The nonionized and unbound fraction of the drug is diffusible, and this fraction leaves the circulation to be distributed. Highly protein-bound drugs are poorly diffusible and have a small volume of distribution. Lipid-insoluble drugs diffuse poorly and also have a small volume of distribution, whereas highly lipid-soluble drugs have a large volume of distribution. The measure of acid strength (pKa) determines the ionized versus the nonionized fraction at a particular pH. The clinical effects of the highly lipophilic opioids are determined by the apparent volume of distribution (tissue: blood partition coefficient). For a given opioid, the larger the volume of distribution, the lesser the concentration in the plasma will be. Alfentanil has a small volume of distribution and therefore a rapid onset of action and a short duration.
Metabolism Opioids containing a hydroxyl group are conjugated in the liver with glucuronic acid to form opioid glucuronides that are then excreted by the kidney. Uridine 5-diphosphateglucuronyltransferase (UGT) performs an important group of conjugation reactions.62 UGTs are involved in metabolism of many opioid analgesics. Some natural opioids and semisynthetic opioids are metabolized by the cytochrome P-450 isoforms. The phenylpiperidine derivatives undergo oxidative metabolism. N-demethylation is a minor pathway for metabolism of opioids. Remifentanil undergoes rapid hydrolysis by plasma esterases.
Excretion The kidneys excrete most polar metabolites, and a small amount is excreted unchanged. Glucuronide conjugates are also excreted in bile and may undergo enterohepatic circulation.
Phenanthrene Alkaloids Morphine Morphine is a naturally occurring alkaloid derived from opium, and, to date, chemical synthesis is difficult. The milky juice obtained from the unripe seed capsule of the poppy plant is dried and powdered to make powdered opium, which contains certain alkaloids: the principal phenanthrenes are morphine (10% of opium), codeine (0.5%), and thebaine (0.2%). The morphine molecule consists of five fused ring systems (see Fig. 122.2).73 The carbon atoms are numbered 1 to 16. It has 5 asymmetrical carbon atoms,5,6,8,9,13 resulting in strong levorotation, the l-isomer being pharmacologically active and
902
Section V—Specific Treatment Modalities for Pain and Symptom Management
the D-isomer inactive.74 The pKa for the morphine base is 7.9, and at physiologic pH, it is 76% nonionized. Morphine is relatively water soluble and poorly lipid soluble because of the hydrophilic OH- groups present.75 This poor lipid solubility limits movement of morphine across membranes and is a barrier to accessing the CNS. Morphine is absorbed, to some extent, through all mucosa and the spinal dura. Therefore, multiple routes are available for drug administration. Protein binding of morphine in plasma is 45%. The mean elimination half-life ranges from 1.4 to 3.4 hours. After intravenous administration, morphine is rapidly distributed to tissues and organs. Within 10 minutes of administration, 96% to 98% of the drug is cleared from the plasma. Mean volume of distribution is large, ranging from 2.1 to 4.0 L/kg. Intramuscular absorption is rapid, and the peak occurs at 10 to 20 minutes.76 Peak plasma concentrations after subcutaneous administration occur at approximately 15 minutes, and plasma levels equivalent to those obtained with the intravenous route can be achieved.77,78 Morphine is rapidly distributed out of the plasma after intravenous administration. Intramuscular or subcutaneous injection creates a depot, which continues to release morphine into the plasma for distribution. After oral administration, plasma levels of morphine peak at 30 to 90 minutes. Absorption is mainly from the upper small intestine; morphine is poorly absorbed from the stomach.75 Bioavailability from the oral route is low owing to extensive first-pass metabolism in the liver. Great interindividual variability exists for bioavailability (20% to 30% reported in various studies). Low bioavailability of oral morphine is a factor in determining oral-to-parenteral conversion ratios, 1:3 in chronic pain states.77,79,80 Peak plasma levels after controlled-release morphine occur two to three times later (at 150 minutes) than with immediate-release oral morphine preparations. Bioavailability of controlled-release morphine is 85% to 90% that of immediate-release formulations. Rectal absorption appears to be as good as or better than oral absorption. Morphine can be administered intrathecally, epidurally, or intraventricularly. Epidural morphine is rapidly absorbed into the systemic circulation and produces significant plasma levels. Plasma levels after intrathecal administration are too low to be of any clinical significance. Rostral distribution of morphine occurs in the CSF, and this causes delayed respiratory depression (12 to 18 hours). Morphine is not suited to be administered transdermally or by the nasal route because it is poorly lipid soluble. Morphine has been delivered by iontophoresis for postoperative analgesia after total hip and knee replacement surgery.69 Absorption after buccal and sublingual administration is similar to oral administration in terms of peak plasma level and time to peak, low bioavailability, and large degree of inter-individual variation.80 After being absorbed, morphine is rapidly distributed throughout the body to highly perfused tissues, such as the lungs, kidney, liver, and spleen.76,77 Morphine and its highly polar metabolites M3G and morphine-6-glucuronide (M6G) cross the blood-brain barrier to a small extent. CSF morphine levels are 4% to 60% after systemic administration.81 The mean volume of distribution is large, ranging from 2.1 to 4.0 L/kg. It is affected by the hemodynamic status of the patient, alterations in plasma protein binding, and variations in tissue blood flow. Morphine binds to albumin and gamma globulin. Morphine is 20% to 40% protein bound.82,83 Major changes in
binding would be required to influence plasma morphine levels because of the normally low extent of binding. The predominant metabolic fate of morphine in humans is glucuronidation, and the liver is the predominant site for this biotransformation. Approximately 90% of injected morphine is converted into metabolites, the major metabolites being M3G (45% to 55%) and M6G (10% to 15%) (Fig. 122.9). Other metabolites include morphine-3,6-diglucuronide, morphine-3-ethereal sulfate, normorphine, normorphine6-glucuronide, normorphine-3-glucoronide,84 and codeine.85 M3G is the major metabolite quantitatively. It has a very low affinity for the µ receptor and as a consequence has no analgesic potency. M3G was found to antagonize morphine- and M6G-induced analgesia and respiratory depression in the rat and has led to the hypothesis that M3G may influence the development of morphine tolerance.86 M3G was shown to cause nonopioid mediated hyperalgesia and allodynia after intrathecal administration in rats. M6G has a higher affinity for µ receptors than for δ or κ receptors. M6G is poorly lipid soluble, and very little crosses the blood-brain barrier. M6G can accumulate in patients with renal insufficiency and is a likely factor in prolonged opioid effects after morphine administration. Increases in M6G levels in patients with renal failure elevate the CSF concentration and result from the mass effect of the accumulated M6G. Within the CSF, M6G is 45 to 100 times more potent than morphine in its analgesic activity and 10 times more potent in depressing ventilation. Normorphine is produced in small amounts and is pharmacologically active. Normorphine may be neurotoxic, analogous to normeperidine.87 Excretion of morphine is predominantly renal, by glomerular filtration of water-soluble conjugates. Up to 85% of a dose of morphine is recovered from the urine as free morphine and metabolites. Some morphine (10% to 20%) is unaccounted for by renal excretion and is presumably excreted in urine as unidentified metabolite or is excreted by other routes.73 Enterohepatic circulation of morphine and its glucuronides accounts for the presence of small amounts of morphine in the feces and in the urine for several days after the last dose. Morphine remains the reference against which all other opioids are compared. The clinical effects and side effects are those that are seen with all µ-receptor agonists. These effects are detailed in the previous section on the pharmacodynamics of opioids.
Clinical Uses and Preparations Morphine is available as its sulfate and hydrochloride forms. It is the most commonly used medication for moderate to severe pain in the acute and chronic setting. Oral morphine is available as tablets and suspension in immediate-release and sustainedrelease forms. Immediate-release formulations have the disadvantage of frequent dosing. Various sustained-release forms are available that can be administered every 8 to 12 hours (MS Contin, Oramorph) or every 24 hours (Kapanol, MXL, Kadian, Avinza). Most sustained-release formulations adsorb morphine onto a hydrophilic polymer that is embedded in some form of a wax or hydrophobic matrix, granulated and finally compressed into tablets.88 Following oral administration, gastric fluid dissolves the tablet surface and hydrates the hydrophilic polymer to produce a gel, the formation of which is controlled by higher aliphatic alcohols. Varying the hydrophilic polymer, the type of hydrophobic matrix, or their ratio can control the release rate.
Chapter 122—Opioid Analgesics HO
903
HO
O
O
N-Demethylation N
CH3
N
HO
H
HO NOR-MORPHINE
MORPHINE UDP glucuronyl transferase
HO
UDP glucuronyl transferase O
COOH O HO
N
O
CH3
COOH
OH
O O OH
O
HO N
CH3
OH OH MORPHINE 6 GLUCURONIDE
HO
Ferrante M: Opioids. In Ferrante M, VadeBoncouer T, editors: Postoperative pain management, New York, 1993, Churchill Livingstone, p 145.)
MORPHINE 3 GLUCURONIDE
Also available is a suspension formulation, in which morphine is attached to small beads of an ion exchange resin. Rectal suppositories are available; a specific sustained-release formulation contains morphine, sodium alginate, and a calcium salt in a suitable vehicle that melts in the rectum. Parenteral formulations are available for intravenous, intramuscular, and subcutaneous use. A preservative-free formulation for intrathecal and epidural use is available. Morphine has also been used intraarticularly, with varying results.
Codeine Like morphine, codeine is a naturally occurring alkaloid. Codeine is methylmorphine, the methyl substitution being on the phenolic hydroxyl group. With the exception of aspirin, codeine is perhaps the most widely used oral analgesic and is generally accepted as the alternative to aspirin as a standard of comparison of drugs in this category89 (e.g., 60 mg of codeine is comparable to 600 mg of aspirin). Codeine is approximately 60% as effective orally as parenterally, both as an analgesic and as a respiratory depressant. Compared with morphine, codeine has a high oral-to-parenteral potency ratio as a result of less first-pass metabolism in the liver. Codeine is metabolized by the liver to inactive forms (90%), which are excreted in the urine. Free and conjugated forms of morphine are found in urine after codeine administration: 10% of administered codeine is O-demethylated to morphine. The cytochrome P-450 enzyme CYP2D6 effects the conversion of codeine to morphine. Ten percent of the white population has a well-characterized genetic polymorphism in the CYP2D6 enzyme, and these persons are not able to convert codeine
Fig. 122.9 Metabolism of morphine. Morphine-3-glucuronide and morphine- 6-glucuronide are major metabolites. Morphine-6-glucuronide possesses signifi cant analgesic activity and may substantially contribute to the analgesic effects of morphine. Both metabolites are excreted in the urine, and accumulation may occur after repetitive dosing in patients with renal failure. Demethylation is a minor pathway for morphine metabolism. (Adapted from
to morphine and thus do not attain an analgesic effect from codeine administration. Codeine's major disadvantage is its lack of effectiveness in treating severe pain. Codeine has a low affinity for opioid receptors and is a weak analgesic; the analgesic effect is the result of its conversion to morphine. It has a limited propensity to produce sedation, nausea, vomiting, constipation, and respiratory depression. It also produces a lower incidence and degree of physical dependence than most other opioids. Codeine is used for mild to moderate pain conditions. The addictive potential of codeine is low. Codeine has an excellent antitussive effect at doses as low as 15 mg; greater cough suppression is seen at higher doses. The antitussive effects are mediated by the active metabolites depressing the cough reflex in the medulla. Distinct receptors that bind to codeine itself may exist.61 Codeine is available in the United States in oral, subcutaneous, intramuscular, and intravenous formulations. Oral forms of codeine are formulated with acetaminophen. Parenteral forms of codeine are also available; 130 mg of codeine is equianalgesic to 10 mg of intramuscular morphine. Codeine should not be used intravenously because the histamine-releasing potency of codeine is even greater than that of morphine.4
Thebaine Thebaine is a naturally occurring alkaloid derived from opium. Thebaine has little analgesic action but is a precursor to several important 14-OH agents such as oxycodone and naloxone. A few derivatives of thebaine are more than 1000 times as potent as morphine (e.g., etorphine).9
904
Section V—Specific Treatment Modalities for Pain and Symptom Management
Semisynthetic Opioids
Heroin should be given orally; it is approximately 1.5 times more potent than morphine in controlling chronic pain. Given parenterally, heroin is 2 to 4 times more potent than morphine and is faster in onset of action. Heroin has a short half-life, but the effects of its active metabolites last longer. Heroin has a high addictive potential and it is not known to have any real advantage over morphine. It is banned from manufacture and medicinal use in the United States.4
Heroin Diacetylmorphine, or heroin, is derived from acetylation of morphine at the 3 and 6 positions (Fig. 122.10). Heroin is deacetylated to 6-monoacetylmorphine (6-MAM) and subsequently to morphine. The liver has the greatest capacity for the production of morphine from 6-MAM. In serum, the conversion to 6-MAM is mediated by a serum cholinesterase, which is present also in kidney, liver, and brain tissues and could be responsible for conversion in these organs as well.90 Direct renal clearance of heroin is less than 1% of the administered dose.91 Both heroin and 6-MAM are more lipid soluble than morphine and cross the blood-brain barrier more readily.
Hydrocodone Hydrocodone is a semisynthetic opioid with multiple actions qualitatively similar to those of codeine. It has a bioavailability of 50% and is available as oral formulations in combination with nonopioid analgesics.
H3C O H3C C O
H3C N
H3C N
N H
H
HO
O
CH3O
O O
H OH
Morphine
Codeine
H3C N
H3C N H HO O
H3C N OH
HO
H3CO
O O
O
Hydromorphone
H3C N CH3 CH3 O
H
Levorphan
O C2H5
C2H5
Meperidine
Methadone N N
S N
N
N
N C
N O
H3C O N
O C2H5
Fentanyl
N
N
O C2H5
Sufentanil
O
Oxycodone
N CH3
O
OH
O
Oxymorphone
H3C N H HO
O
H OH
C CH3 O
Heroin
H
O
O COCH3
O N CH3OCCH2CH2 N
CCH2CH3 O
C2H5 Alfentanil
Fig. 122.10 m-Opioid receptor agonists.
Remifentanil
Hydrocodone undergoes O-demethylation, N-dealkylation, and 6-ketoreduction to the corresponding 6-α and 6-ß hydroxymetabolites. The O-demethylation to dihydromorphine is mediated by the polymorphically expressed cytochrome P-450 CYP2D6 enzyme. Some of the hydrocodone metabolites (dihydromorphine, dihydrocodeine, and hydromorphone) are pharmacologically active and may produce adverse effects if their excretion is impaired.62 Hydrocodone is considered a weak analgesic. It has excellent antitussive properties. Like other opioids, hydrocodone can cause respiratory depression, sedation, and impairment of mental and physical performance, constipation, and urinary retention. Sensorineural hearing loss associated with long-term hydrocodone use has been reported.92,93 Drug dependence and addiction are seen with long-term use. Hydrocodone is available only for oral use in combination with acetaminophen or acetylsalicylic acid. These combinations provide a synergistic effect, and the side effects are reduced.
Hydromorphone (Dilaudid) Hydromorphone, a direct derivative of morphine, was first synthesized in the 1920s. Like morphine, hydromorphone has a basic amino group as well as a phenolic group. However, hydromorphone is more lipophilic than morphine because its 6-alcoholic hydroxyl group has been converted to a less hydrophilic ketone group (see Fig. 122.10).94 The global pharmacokinetic properties of hydromorphone are generally similar to those of morphine. It is six to eight times as potent as morphine; the best-accepted conversion is that 1.5 mg of hydromorphone is equianalgesic to 10 mg of morphine. Hydromorphone is easily absorbed from the gastrointestinal tract and so is effective after oral and rectal administration. It has a rapid distribution phase; approximately 90% of a specific dose is lost from the plasma in 10 minutes.95 Hydromorphone elimination, like that of morphine, depends on tissue uptake, with subsequent slow release from tissue to plasma. Hydromorphone has no active metabolites and therefore is a particularly useful drug in patients with renal insufficiency. The side effect profile is very similar to that of other opioids. Despite anecdotal reports of reduced incidences of nausea, vomiting, respiratory depression, urinary retention, and constipation, little evidence exists as proof.96 Hydromorphone is available as tablets for oral administration and as rectal suppositories. A controlled-release form for administration every 12 hours is available in some countries. Injectable preparations are available, and hydromorphone is particularly useful for subcutaneous use because of its relatively high solubility. Hydromorphone is used intrathecally and epidurally with good effect. The drug is hydrophilic: when given epidurally, its long half-life resembles that of epidural morphine, and its short latency of analgesia is similar to that of meperidine.97
Oxycodone Oxycodone (14-hydroxyl-7, 8-dihydrocodeine) is derived from modification of the morphine molecule. Its pharmacokinetic and opioid-receptor binding characteristics differ from those of morphine. Oxycodone is a μ-receptor agonist and also exhibits some κ-mediated antinociceptive effects.98 It is available in immediate-release and sustained-release forms and also in combination with nonopioid analgesics. The parenteral forms are currently not available in the United States.
Chapter 122—Opioid Analgesics
905
The oral bioavailability, 50% to 80%, is superior to that of morphine. Bioavailability and peak plasma concentration are altered by high-fat meals; absorption is delayed, but bioavailability is improved. Normal-release oxycodone absorption is monoexponential; the mean half-life is 3.5 to 5.6 hours. Controlled-release oxycodone is absorbed in a biexponential fashion. The drug has a rapid phase with a half-life of 37 minutes and a slow phase with a half-life of 6.2 hours.99 In uremic patients, the mean half-life of oxycodone is increased by increased volume of distribution and reduced clearance, and plasma concentrations of noroxycodone are higher.94 Oxycodone is metabolized by the liver to the active metabolite, oxymorphone (10%), through O-demethylation by the cytochrome P-450 enzyme CYP2D6 and to the dominant nonactive metabolite, noroxycodone, through N-demethylation.100 The metabolites are excreted in the urine, noroxycodone in an unchanged form and oxymorphone in the form of a conjugate. Women eliminate oxycodone 25% more slowly than do men.101 Protein binding is low (i.e., 38% to 45%). Lipid solubility is very similar to that of morphine. Oxycodone is a µ-receptor agonist, but part of its antinociceptive effect is mediated by κ-opioid receptors.98 The relative potency of parenteral oxycodone is 70% that of morphine. The wide variability of oral morphine bioavailability, unequal incomplete cross-tolerance depending on the drug sequence, and delayed oxycodone clearance in women account for bioequivalent ratios between 1:1 and 2.3:1.100 Less crosstolerance occurs with a switch from morphine to oxycodone than from oxycodone to morphine.102 The side effects of oxycodone are similar to those normally attributed to opioids. The incidence of constipation is higher than with morphine, but the incidence of nausea is lower. Oxycodone causes drowsiness, lightheadedness, nausea, vomiting, pruritus, constipation, and sweating. Fluoxetine and its metabolite norfluoxetine inhibit CYP2D6 and prevent O-demethylation of oxycodone to oxymorphone, processes that may lead to higher plasma oxycodone levels.103 Presumably, sertraline does the same.
Oxymorphone Oxymorphone is a congener of morphine with a substitution of a ketone group at the C-6 position, conferring a more rapid onset of action, greater potency, and a slightly longer duration of action than morphine.104 Oxymorphone has a short half-life but has a prolonged duration of action owing to slow dissociation from its receptor sites.61 It has a high affinity for µ-opioid receptors and is approximately 10 times more potent than morphine in the parenteral form and three times more potent in the oral form. Like heroin, oxymorphone has a high addictive potential. Oxymorphone and naloxone have significant structural similarities; naloxone is the N-allyl (−CH2−CH=CH2)–substituted analogue of oxymorphone.4 The structural similarities between the µ-receptor antagonist naloxone and the agonist oxymorphone have been used to study and develop new agonists and antagonists. Oxymorphone is available in the United States in oral, injectable, and rectal forms (Numorphan). It is available in immediate-release and sustained-release oral formulations. The adult subcutaneous or intramuscular dose is 1 to 1.5 mg every 4 to 6 hours, with a starting intravenous dose of 0.5 mg. Rectal administration is approximately one tenth as potent as intramuscular administration.
906
Section V—Specific Treatment Modalities for Pain and Symptom Management
Synthetic Opioids Levorphanol and Congeners Levorphanol is the only commercially available opioid agonist of the morphinan series. Only the l-isomer has analgesic effect. The d-isomer (dextromethorphan) is relatively devoid of analgesic effect but may have inhibitory effects at NMDA receptors and it also has an antitussive activity. Levorphanol has activity mainly at the µ-opioid receptors and some effect at κ and δ receptors. Because of its effect on multiple receptors, levorphanol is used as a second-line agent or in patients who are tolerant to morphine.105 The pharmacologic profile of levorphanol closely parallels that of morphine. The analgesic effects are similar to those of morphine, but levorphanol has a lower incidence of nausea and vomiting. Levorphanol is available in forms that can be administered subcutaneously, intramuscularly, intravenously, or orally. It is less effective when given orally; the oralto-parenteral potency ratio is comparable to that of codeine and oxycodone. Levorphanol is seven times more potent than oral morphine and five times more potent than parenteral morphine. Levorphanol has a half-life of 12 to 16 hours, but its duration of analgesia is similar to that of morphine (i.e., 4 to 6 hours). The longer half-life may lead to systemic accumulation with repeated dosing. Levorphanol is available for oral administration in 2-mg tablets and as an injectable solution for parenteral administration.
Meperidine and Congeners Meperidine is a synthetic phenylpiperidine opioid analgesic. The other opioids in the phenylpiperidine series are fentanyl, sufentanil, alfentanil, and remifentanil. Oral bioavailability of meperidine is 45% to 75%, owing to extensive first-pass metabolism. Its absorption is slow and peaks at 2 hours. Meperidine is absorbed by all routes of administration, but absorption after intramuscular injection is very erratic.106 Approximately 60% of meperidine is protein bound. Meperidine is metabolized in the liver and is N-demethylated to meperidinic acid and normeperidine. Normeperidine has a halflife of 15 to 40 hours. Meperidine has a half-life of 3 hours, but in patients with liver disease, the half-lives of both meperidine and normeperidine are prolonged. Patients with renal insufficiency accumulate normeperidine, with resulting systemic toxicity. Normeperidine is an active metabolite possessing one half the analgesic potency of meperidine. It has twice the potency of the parent compound as a proconvulsant. Normeperidine has CNS stimulant effects, and toxicity may be manifested as myoclonus and seizures.107,108 Meperidine is no longer recommended for chronic pain; use for longer than 48 hours or doses greater than 600 mg/24 hours are not advocated, according to Agency for Health Care Policy and Research in 1992.9 Meperidine is 7 to 10 times less potent than morphine in producing analgesia; 75 to 100 mg of meperidine is equivalent to 10 mg of morphine. The peak analgesic effect is seen 1 to 2 hours after oral administration and in less than an hour after parenteral administration. The analgesic effect lasts 2 to 3 hours, a duration shorter than that of morphine. Meperidine also produces sedation, respiratory depression, and euphoria, and a few patients experience dysphoria. Like other opioids, meperidine produces nausea and vomiting, as
well as pupillary dilation with large doses. It also affects the pituitary hormones. The accumulation of normeperidine can cause CNS excitation, which may manifest as tremors, myoclonus, and seizures. Unlike other opioids, meperidine causes tachycardia because of its structural similarity to atropine. Meperidine can cause hypotension owing to its histamine-releasing effect. In large doses, meperidine can cause a decrease in myocardial contractility and stroke volume and a rise in filling pressures.109 No deleterious effects were seen when therapeutic doses of meperidine were given to patients with acute myocardial infarction.110 Like other opioids, meperidine is known to cause spasm of smooth muscle but to a lesser degree. It is a preferred agent in patients with pain from renal colic and biliary spasm. Therapeutic doses of meperidine administered during active labor do not delay the birth process. The adverse effects associated with meperidine are qualitatively similar to those produced by morphine. Meperidine is associated with a lower incidence of constipation and urinary retention. Tolerance develops to the actions of meperidine, and the drug has a high addictive potential. CNS excitation is seen with long-term use of meperidine, especially in patients with compromised renal and liver function owing to the accumulation of normeperidine. Naloxone does not reverse meperidine-induced seizures. Meperidine administration is relatively contraindicated in patients taking monoamine oxidase inhibitors. Two types of interactions are seen. The most prominent interaction is excitatory,. It manifests as hyperthermia, hypertension or hypotension, muscular rigidity, convulsions, coma, and death.111 This reaction is probably the result of the ability of meperidine to block neuronal reuptake of serotonin and thereby cause an increase in local serotonin activity.112 The other type of interaction is seen as a potentiation of opioid effect resulting from inhibition of hepatic microsomal enzymes in patients taking monoamine oxidase inhibitors. The major use of meperidine is for acute pain control. It is no longer recommended for long-term use because of its active metabolite. Meperidine in single doses is used to treat postanesthesia shivering. Congeners of meperidine, diphenoxylate and loperamide, are used to treat diarrhea. Meperidine is available for oral administration in the form of tablets and elixir. It is available for parenteral administration in varying concentrations. Intramuscular doses of 50 to 100 mg are used to treat severe pain and need to be repeated every 2 to 4 hours.
Fentanyl Fentanyl is a synthetic opioid, a meperidine congener of the phenylpiperidine series. It is a pure opioid agonist with a high affinity for the µ receptor. It is approximately 75 to 100 times more potent than morphine as an analgesic. Fentanyl is very commonly used in anesthetic practice owing to its high potency and quick onset and offset of action. Fentanyl is a highly lipid-soluble opioid and crosses the blood-brain barrier rapidly. The plasma level equilibrates with the CSF levels within 5 minutes. It has a rapid onset of action (30 seconds) and a short duration of action owing to redistribution to fat and skeletal muscle. The fairly rapid decline in plasma concentration reflects the redistribution. With repeated dosing or continuous infusion, however, saturation of the fat and muscle depots occurs. This leads to a
prolonged effect resulting from systemic accumulation and a slower decline in the plasma concentration. Fentanyl is 50% protein bound. Fentanyl is primarily metabolized in the liver by cytochrome P-450 CYP3A4 to phenylacetic acid, norfentanyl, and small amounts of the pharmacologically active compound, p-hydroxyl fentanyl,113 which are excreted in the bile and urine. A small portion (8%) is excreted unchanged in the urine. Fentanyl is the drug of choice in patients with renal disease because almost all the metabolites are inactive. Fentanyl has a large volume of distribution, as reflected by its long (3 to 4 hours) elimination half-life.4 As with other highly lipid-soluble opioids, the half-life of fentanyl is influenced by duration of administration, which is a function of the extent of fat sequestration. The elimination half-life is 7 to 12 hours in steady-state conditions.113 Liver disease does not prolong the half-life, but a prolonged effect is seen in older patients.114 Fentanyl has a high affinity for the µ-opioid receptor, is almost 100 times more potent than morphine, and produces the same degree of respiratory depression as morphine in equianalgesic doses. Because fentanyl is highly lipid soluble, the risk of delayed respiration resulting from rostral spread of intrathecally administered drug to medullary respiratory centers is greatly reduced. When fentanyl is administered intravenously, the peak analgesic effect is seen after 5 minutes, and a quick recovery is also seen after single doses. With repeated dosing or prolonged infusions, a prolonged effect is seen. Muscle rigidity is commonly seen with intravenous fentanyl administration. Like other µ-receptor agonists, fentanyl produces nausea, vomiting, and itching. Respiratory depression is noted, and the onset is much more rapid than with morphine. As with morphine and meperidine, delayed respiratory depression seen after the use of fentanyl is possibly caused by enterohepatic circulation.9 High doses of fentanyl can cause neuroexcitation and, rarely, seizure-like activity. Fentanyl decreases heart rate and mildly decreases blood pressure. It also causes minimal myocardial depression. Fentanyl does not release histamine and provides a marked degree of cardiovascular stability. Fentanyl is used very commonly as an anesthetic agent because of its rapid onset and offset of action and relative cardiovascular stability. Because of its short duration of action, fentanyl is generally not the drug of choice for single-shot parenteral administration for chronic pain. It is one of the drugs of choice for intravenous patient-controlled analgesia in patients with renal disease. It is administered frequently by the epidural and intrathecal routes. Its high lipophilicity and small molecular weight make it well suited for use in a transdermal preparation. Fentanyl is not used for oral administration because of extensive first-pass metabolism and poor bioavailability (32%). It is available as a preparation for oral transmucosal use; bioavailability is 52% to 65%. This form is used for breakthrough cancer pain and is not recommended for acute postoperative pain. Transdermal fentanyl has a lower incidence of constipation than do oxycodone and morphine.115
Alfentanil Alfentanil and remifentanil were developed in search of analgesics with a more rapid onset of action and predictable termination of effects.111 Alfentanil is 5 to 10 times less potent than fentanyl and has a shorter duration of effect.
Chapter 122—Opioid Analgesics
907
Alfentanil has a rapid onset (1 to 2 minutes) of analgesic effect after intravenous administration. This is because 90% of the drug is nonionized at physiologic pH as a result of a low pKa value. Alfentanil has a smaller volume of distribution, lower lipid solubility, and slightly greater protein binding compared with fentanyl.116 Its analgesic effect is terminated rapidly as a result of redistribution. Hepatic metabolism accounts for most of the elimination of alfentanil. A small percentage (1%) is excreted unchanged in urine. The elimination halflife is 70 to 98 minutes.117 The elimination half-life is significantly increased in patients with cirrhosis. Renal disease does not affect alfentanil clearance. Alfentanil is used for epidural analgesia and for intravenous patient-controlled analgesia. Owing to its short duration of analgesic effect, alfentanil is not an ideal choice for patientcontrolled analgesia use. It is available for injection in a concentration of 500 µg/mL.
Sufentanil Sufentanil is a synthetic opioid that is a member of the phenylpiperidine series. Sufentanil is the most potent µ-receptor agonist available for human clinical use.61 It is 5 to 10 times more potent than fentanyl and 1000 times more potent than morphine. It has an affinity for opioid receptors 30 times greater than that of fentanyl.118 Sufentanil is highly lipid soluble, more so than fentanyl and alfentanil. It rapidly crosses the blood-brain barrier, equilibrates with the CSF, and therefore has a rapid onset of action. The analgesic effect is terminated quickly as a result of rapid redistribution to fat and skeletal muscle. Sufentanil has a volume of distribution, distribution half-life, and elimination half-life that fall between those of fentanyl and alfentanil.119 More than 90% of sufentanil is protein bound. The shorter elimination half-life is the result of a small volume of distribution and higher hepatic mobilization. Sufentanil is metabolized in the liver; products of N-dealkylation are inactive, and the O-demethylation product (methylsufentanil) is active. Sufentanil metabolites are excreted in the urine. The pharmacologic profile of sufentanil is very similar to that of fentanyl. Like other opioids, sufentanil produces bradycardia, respiratory depression, nausea, vomiting, itching, and smooth muscle spasm. Sufentanil is available only in an injectable form. It is administered parenterally and by the epidural and intrathecal routes. A transdermal formulation of sufentanil is currently in clinical trials.
Remifentanil Remifentanil is an esterase-metabolized opioid of the phenylpiperidine series. Its potency is approximately equal to that of fentanyl. The analgesic effect occurs within 1 to 1.5 minutes. Remifentanil undergoes rapid hydrolysis by nonspecific esterases in blood and tissues.120,121 Clearance is unaffected by cholinesterase inhibition. Renal and liver disease does not alter remifentanil pharmacokinetics. Remifentanil has a distribution half-life of 2 to 4 minutes and an elimination half-life of 10 to 20 minutes. Remifentanil is available only for parenteral administration. Its short duration of effect does not make it an ideal drug for use in intravenous patient-controlled anesthesia. It is currently formulated with glycine and is therefore not recommended for epidural or intrathecal use.
908
Section V—Specific Treatment Modalities for Pain and Symptom Management
Methadone and Congeners Methadone, a synthetic drug developed in the 1940s, is an opioid of the structural class of diphenylpropylamines. It was originally synthesized during World War II by the German pharmaceutical industry. Methadone bears no structural resemblance to morphine. Methadone is used clinically as a racemic mixture, the levorotatory (l) form being 8 to 50 times more potent than the dextrorotatory (d) form. Methadone is popular as a maintenance drug for heroin addicts and is a time-honored therapy for cancer pain.122,123 It has excellent bioavailability and a long half-life, thus making it an ideal drug for outpatient use.124 The oral bioavailability of methadone is high (i.e., 81% to 95%).125 Methadone is rapidly absorbed from the gastrointestinal tract, and measurable concentrations in plasma are seen in 30 minutes,126 but the analgesic effect peaks at 4 hours. After parenteral administration, methadone can be detected in plasma within 10 minutes, and CSF levels peak at 1 to 2 hours. Methadone is a basic and lipophilic drug subject to considerable tissue distribution.127 The sequestration of methadone at extravascular binding sites, followed by slow release into plasma, contributes to the prolonged duration of methadone half-life in plasma. The protein (alpha1-acid-glycoprotein, AAG) binding of methadone is 60% to 90%, which is double that of morphine. Methadone binds to AAG with a relatively high affinity. Methadone can be displaced from AAG by the following drugs: propranolol, chlorpromazine, prochlorperazine, thioridazine, and tricyclic antidepressants.128 Biotransformation and renal and fecal excretion are important determinants of the elimination of methadone. Methadone undergoes extensive metabolism in the liver by N-demethylation and cyclization to form the inactive metabolites pyrroline and pyrrolidines. These inactive metabolites are excreted in the urine and bile along with small amounts of unchanged drug. Urinary pH is an important determinant of elimination half-life of methadone; the half-life increases with rising pH. The elimination half-life of methadone after a single dose is approximately 15 hours, and with long-term administration, it is 22 hours. Methadone has a secondary half-life of more than 55 hours (from release of tissue stores). Methadone is a µ-receptor agonist with pharmacologic properties qualitatively similar to those of morphine. Although it is a potent µ-receptor agonist, methadone also has considerable affinity for the δ-opioid receptor.129 Methadone also has some agonist actions at the κ- and σ-opioid receptors.130 Methadone binds with low affinity to NMDA receptors and acts as a noncompetitive NMDA receptor antagonist in the brain and spinal cord.131,132 The analgesic potency is equal to or slightly greater than that of morphine. The duration of analgesia after a single dose of methadone is 4 to 6 hours, governed by the rapid initial absorption-distribution phase.127,133 Methadone and many of its congeners retain a considerable degree of their effectiveness when given orally. Methadone, when given orally, is approximately 50% as effective as the same dose administered intramuscularly; the oral-to-parenteral potency ratio is 1:2.134 With repeated dosing, cumulative effects are seen because of slow release from tissues. Dosage should be tailored accordingly; either the dose or the frequency of doses should be decreased. The occurrence of side effects with equianalgesic doses is similar for both morphine and methadone.
Therapeutic Uses and Preparations Methadone is an excellent analgesic with good bioavailability. Its low cost and long half-life make it a good choice for outpatient use in chronic pain states. Methadone is also used for treatment of opioid abstinence syndromes and in heroin users. The NMDA blocking property of methadone makes it a choice of opioid for the treatment of neuropathic pain. Methadone may be an option in patients with opioid-induced hyperalgesia. It is available for oral administration in tablets (5 and 10 mg) and as a solution (10 mg/5 mL). Methadone is also available for parenteral administration and is used for intravenous patient-controlled analgesia. Methadone has also been used epidurally and intrathecally.
Levo-Alpha Acetyl Methadol An alternative to methadone for individuals who are addicted to opioids, levo-alpha acetyl methadol (LAAM) is a medication that is a derivative of methadone. LAAM was first developed in 1948 by German chemists as a painkiller. In 1993, the US Food and Drug Administration (FDA) approved LAAM for use in medication therapy for opiate addiction.135 LAAM itself is not effective; its metabolites, nor-LAAM and dinor-LAAM, are the active agents. LAAM is ineffective through intravenous injection and therefore is not attractive for illegal use.136 The delay occurs before the effects of LAAM can be detected, and the drug remains in the body much longer than methadone (72 hours for most people at doses of ≥80 mg). LAAM has pharmacologic cross-tolerance to other opioids and thereby blocks the euphoric effects seen with these drugs, but it still controls opiate craving. It is available for oral administration in a suspension form. Doses range from 10 to 140 mg, three times a week.61 LAAM requires administration every 2 to 3 days and can be given at treatment centers by itself with no take-home medications.
Propoxyphene Propoxyphene is structurally related to methadone (Fig. 122.11) and is a weak analgesic. The analgesic activity of the racemate was found to reside in the D-isomer, and it is this compound that is currently used as a mild analgesic. The l-isomer, which lacks analgesic activity, has been introduced as an antitussive.89 After oral administration, propoxyphene undergoes firstpass metabolism and has a bioavailability of 30% to 70 %.4
CH3 CH3CH2COCCHCH2N CH2 O
CH3 CH3
Propoxyphene Fig. 122.11 Chemical structure of propoxyphene.
Plasma concentration peaks at 1 to 2 hours. Propoxyphene undergoes extensive redistribution and tissue binding because its redistribution volume (960 L) is much greater than that of the other opioid analgesics.94 Propoxyphene is metabolized in the liver by N-demethylation to form norpropoxyphene. Propoxyphene has an average half-life of 6 to 12 hours, which is much longer than that of codeine. Norpropoxyphene has a half-life of approximately 30 hours, and its accumulation with repeated doses may be responsible for the toxicity seen with propoxyphene administration. Norpropoxyphene also undergoes extensive first-pass metabolism, and liver disease can enhance accumulations. Propoxyphene is a weak analgesic, with a relative potency one half to one third that of codeine. The classic triad of physical dependence, psychological dependence, and tolerance accompanies the use of propoxyphene. Moderately toxic doses produce CNS and respiratory depression, but increasing doses cause CNS excitation, cardiotoxicity, and pulmonary edema. These toxicities are attributed to the effects of the active metabolite, norpropoxyphene. Propoxyphene is recommended for the treatment of mild to moderate pain. A dose of 90 to 120 mg of propoxyphene is equianalgesic to 60 mg of codeine or 600 mg of aspirin. Propoxyphene hydrochloride is available in 32- and 65-mg tablets; it is formulated with acetaminophen or aspirin to give a synergistic effect. It is also available as propoxyphene napsylate in a suspension form and in 100-mg tablets.
Tramadol Tramadol is a synthetic opioid structurally related to morphine and codeine. It is a centrally acting opioid agonist with some selectivity for the µ receptor and also binds weakly to κ and δ receptors. It also acts on the monoamine system by inhibiting the reuptake of norepinephrine and serotonin (5-hydroxytryptamine, 5-HT).137 Tramadol undergoes some first-pass metabolism after oral administration and has a bioavailability of 68%.9 It is O-demethylated by the cytochrome P-450 enzyme CYP2D6 to the therapeutically active O-desmethyltramadol and is N-demethylated by CYP34A to the inactive N-desmethyltramadol. O-desmethyltramadol is two to four times more potent than tramadol itself. A significant amount (10% to 30%) of tramadol is excreted unchanged in the urine. Whereas plasma protein binding is low (20%), its apparent volume of distribution is large (2.7 L/kg), indicating considerable tissue uptake.137 The elimination half-life for tramadol is 6 hours, and the active metabolite has a slightly longer half-life of 7.5 hours. Tramadol produces analgesia by its opioid-like activity and also by inhibiting the reuptake of norepinephrine and serotonin. It is contraindicated in patients taking monoamine oxidase inhibitors. Tramadol produces nausea, vomiting, sedation, dizziness, dry mouth, hot flashes, and headache. It produces less respiratory depression than morphine in equianalgesic doses. The incidence of seizures in patients receiving tramadol is less than 1%. Tramadolinduced seizures are not reversed by the µ-opioid antagonist naloxone. With its dual mode of action (opioid agonist, norepinephrine and 5-HT reuptake inhibition), tramadol is a useful drug in nociceptive and neuropathic pain. It is superior
Chapter 122—Opioid Analgesics
909
to morphine in the treatment of some neuropathic pain syndromes. Unlike other opioids, tramadol produces only a weak and clinically irrelevant respiratory depression at the recommended analgesic doses.138 Tramadol has a low potential for drug abuse and dependence. It is available as 50-mg tablets, to be administered every 6 hours. The daily dose should not exceed 400 mg. It is also available formulated in combination with acetaminophen.
Tapentadol Tapentadol is a centrally acting opioid agonist that has as its sites of action the µ and norepinephrine receptors. It has been approved by the FDA as an oral analgesic for moderate to severe pain. Early clinical experience suggests that tapentadol is comparable to hydrocodone and oxycodone and has a slightly more favorable side effect profile. Tapentadol is rapidly absorbed orally and appears to have no analgesically active metabolites. The drug reaches a maximum concentration in approximately 1.5 hours. It is excreted primarily by the kidneys. With its dual mode of action (opioid agonist and norepinephrine inhibition), tapentadol should theoretically be useful for treatment of neuropathic pain. In diabetic animal models, tapentadol showed selective inhibition of disease-related hyperalgesia with not much change in normal sensation.139 Based on its pharmacology, tapentadol should have a relatively low potential for drug abuse and dependence, but the FDA has classified it as a schedule II opioid. It is available as 50-, 75-, and 100-mg tablets, to be administered every 4 to 6 hours. The daily dose should not exceed 600 mg.
Agonist-Antagonists The agonist-antagonists produce opposing action at the µ and κ receptors; they are µ-receptor antagonists and κ-receptor agonists. These drugs were initially developed in search of an analgesic with less respiratory depression and addictive potential. These compounds are less efficacious than pure µ-receptor agonists in their analgesic effect and seem to have a lower potential for abuse.61
Pentazocine Pentazocine is a synthetic opioid of the benzomorphan (Fig. 122.12) series that is a weak competitive antagonist at the µ receptor and an agonist at the κ1 and possibly κ2receptors. Pentazocine is well absorbed after oral and parenteral administration. It undergoes extensive first-pass metabolism, and only 20% of the drug enters the systemic circulation. It has a peak analgesic effect in 15 minutes to 1 hour after intramuscular injection and in 1 to 3 hours after oral administration.9 Pentazocine has a plasma half-life of 3 to 4 hours. Its action is terminated by hepatic metabolism to inactive glucuronide conjugates and renal excretion. Less than 2% of the given dose is excreted in the bile. Pentazocine is an agonist at the κ receptors and produces analgesia. Higher doses of pentazocine elicit psychotomimetic and dysphoric effects. The exact mechanism of these effects is not known but is thought to be caused by weak σ-receptor agonist activity4 and activation of supraspinal κ receptors.111 Like other agonist-antagonists, pentazocine exhibits a ceiling effect
910
Section V—Specific Treatment Modalities for Pain and Symptom Management HO
H3C
NCH2CH
C
CH3 CH3
CH3 PENTAZOCINE
NCH
NCH2 HO
OH
OH O HO
BUTORPHANOL
NALBUPHINE Mixed agonist-antagonists
Fig. 122.12 Chemical structure of pentazocine, butorphanol, and nalbuphine.
for respiratory depression and analgesic effect. The ceiling effect is seen with 60 to 100 mg of pentazocine.140 Pentazocine does not reverse the respiratory depression produced by morphine. Pentazocine may, however, precipitate withdrawal if it is given to patients taking pure µ-receptor agonists. Unlike other opioids, pentazocine does not cause bradycardia. High doses of pentazocine increase heart rate and blood pressure. In patients with acute myocardial infarction, pentazocine produces substantial elevation in cardiac preload and afterload and thereby increases the cardiac workload.110 In addition, an increase in systemic and pulmonary artery pressure, left ventricular filling pressure, and systemic vascular resistance and a decrease in left ventricular ejection fraction are seen. These effects may be caused by a rise in the plasma concentration of catecholamine. Pentazocine also produces smooth muscle spasm but appears to cause less of a biliary spasm than does morphine.141 The most common adverse effects are sedation, sweating, dizziness, and nausea. With parenteral doses higher than 60 mg, psychotomimetic effects occur, manifested by anxiety, strange thoughts, nightmares, and hallucinations. With prolonged use, tolerance develops to the analgesic and subjective effects of the drug. Pentazocine is used to treat mild to moderate pain; an oral dose of 50 mg is equianalgesic to 60 mg of codeine orally. Oral forms are available compounded with aspirin and acetaminophen. To reduce the incidence of parenteral injection, tablets for oral use are formulated with naloxone. Naloxone is completely degraded with oral administration, but if injected, the combination would have no effect because of the antagonist effects of naloxone. Abuse patterns seem to be low with the oral forms of pentazocine.
Nalbuphine Nalbuphine is a semisynthetic mixed agonist-antagonist that is chemically related to naloxone and oxymorphone. Bioavailability of oral nalbuphine is less than 20% as a result
of extensive first-pass metabolism. It is lipophilic and has a large volume of distribution. Nalbuphine is metabolized in the liver to inactive glucuronide conjugates. Nalbuphine and its metabolites are excreted to a great extent in the feces. The elimination half-life of nalbuphine is 3 to 6 hours.142 Compared with pentazocine, nalbuphine is a more potent antagonist at the µ receptor. Intramuscularly administered nalbuphine produces analgesia comparable to that of morphine (potency ratio of 1:1). It exhibits a ceiling effect at approximately 0.45 mg/kg,4 and no further respiratory depression or analgesia is obtained. In contrast to pentazocine and butorphanol, nalbuphine does not increase cardiac index, pulmonary artery pressure, or cardiac work. The systemic blood pressure does not change significantly.111 The most common adverse effects are sedation, sweating, and headache. Higher doses can produce dysphoria and psychotomimetic effects. Nalbuphine can precipitate withdrawal symptoms in individuals taking µ-opioid receptor agonists. Nalbuphine also reverses the respiratory depression143 associated with opioids and can be used to treat pruritus related to opioid use.144 Long-term use of nalbuphine can cause physical dependence.
Butorphanol Butorphanol is a synthetic mixed agonist-antagonist compound of the morphinan series. It has a profile of action similar to that of pentazocine but with greater analgesic efficacy and fewer side effects.61 Bioavailability after oral administration is low (5% to 17%)145 as a result of extensive first-pass metabolism. No first-pass metabolism occurs with parenteral or transnasal administration, and these routes produce similar plasma levels.9 Butorphanol is rapidly absorbed after parenteral administration and has a distribution half-life of 5 minutes. Transnasal administration results in rapid absorption with onset of analgesia within 15 minutes. Plasma protein binding is approximately 85%. Butorphanol is converted to the inactive metabolites hydroxybutorphanol and norbutorphanol. The plasma terminal half-life of butorphanol is 3 hours with parenteral administration and 4.5 to 5.5 hours with transnasal administration. Butorphanol has agonistic activity at the κ receptor and antagonistic activity at the µ receptor. It also exhibits partial agonistic activity at the σ receptor.146 A dose of 2 to 3 mg of parenteral butorphanol is equivalent to 10 mg of parenteral morphine. Like other agonist-antagonists, butorphanol has a ceiling effect for respiratory depression and analgesia. Common adverse effects of butorphanol are sedation and diaphoresis. It also causes dysphoria because of its σ-agonist activity. As with pentazocine, analgesic doses of butorphanol produce an increase in heart rate, systemic blood pressure, and pulmonary artery pressure.147 Its effects on the biliary tract are milder than are those of morphine. Butorphanol can reverse the analgesia produced by pure µ-receptor agonists but does not reverse the respiratory depression. Physical dependence is noted with long-term use of butorphanol. Because of its high analgesic potency, butorphanol is indicated for the treatment of moderate to severe pain. The recommended parenteral dose is 1 to 2 mg intramuscularly and 0.5 to 2 mg intravenously every 3 to 4 hours. Butorphanol is also available for intranasal administration in a spray form.
Chapter 122—Opioid Analgesics CH2NCH2
C(CH3)3 C
CH3
OH
NCH2CH HO
OCH3
CH
OH O
HO
O Naloxone
O Buprenorphine
911
Fig. 122.14 Chemical structure of naloxone.
Fig. 122.13 Chemical structure of buprenorphine.
Buprenorphine
Antagonists
Buprenorphine is a semisynthetic, highly lipophilic opioid derived from the naturally occurring alkaloid thebaine (Fig. 122.13). It is 25 to 50 times more potent than morphine111 and is a partial µ-receptor agonist. Bioavailability after oral administration is 16% because of extensive first-pass metabolism.148 Buprenorphine displays a bell-shaped dose-response curve, with peak antinociceptive opioid effects at approximately 0.5 mg/kg (subcutaneously) 60 minutes after the dose and a gradual decline of the effects in the dosage range of 0.5 to 10 mg/kg.149 Buprenorphine is highly lipophilic and is approximately 96% bound to plasma proteins. After parenteral administration, the analgesic response is governed by the kinetics of receptor dissociation.150 The half-life of dissociation from the µ receptor is 166 minutes for buprenorphine versus 7 minutes for fentanyl.151 It has an elimination half-life of 3 to 4 hours but a prolonged duration of effect because of slow dissociation from receptor site. Information concerning the metabolism of buprenorphine is limited. In animal studies, buprenorphine disposition is by hepatic conjugation to glucuronides, eliminated in the bile (92%). A dose of 0.3 mg of parenteral buprenorphine produces analgesia equivalent to that of 10 mg of parenteral morphine.152 Buprenorphine acts as a partial agonist at the µ receptor and as an antagonist at the κ receptor. Buprenorphine has a less well-defined effect on respiratory function than that usually expected of opioids; it has a ceiling effect on respiratory depression with an increase in dose. The adverse effects associated with buprenorphine are sedation and nausea. Usual parenteral doses of buprenorphine can reduce the adrenocortical response after surgery.153 Buprenorphine partially reverses the effects of large doses of μ-receptor agonists and can reverse the ventilatory depression seen with these opioids. The cardiovascular hemodynamic responses are similar to those of morphine. Buprenorphine is used to treat moderate to severe pain conditions. Parenteral buprenorphine can be given in a dose of 0.3 mg every 6 to 8 hours. The drug may not be a good choice for intravenous patient-controlled analgesia because of its slow onset of action. Few studies have described effective analgesia with minimal respiratory depression associated with buprenorphine in intravenous patient-controlled analgesia. Sublingual buprenorphine, 0.4 mg every 8 hours, provides analgesia equivalent to 10 mg of morphine intramuscularly every 4 hours. A sublingual formulation of buprenorphine and naloxone hydrochloride dihydrate in a 4:1 ratio is also awaiting FDA approval for the treatment of pain. Transdermal buprenorphine is available for clinical use in some countries.
Pohl154 developed the first opioid antagonist, N-allylnorcodeine in 1915 by making minor changes in the codeine molecule (Fig. 122.14).
Naloxone, Naltrexone, Methylnaltrexone, and Alvimopan Naloxone is the first opioid antagonist to be developed that is devoid of agonist activity. Naloxone is a synthetic N-allyl derivative of oxymorphone. Naltrexone is a lipid-soluble opioid antagonist that readily crosses the blood-brain barrier. Methylnaltrexone is a quaternary derivative of naltrexone formed by addition of a methyl group at the amine ring that makes it less lipid soluble and with restricted ability to cross the blood-brain barrier. Naloxone is rapidly absorbed after oral administration, but high presystemic metabolism makes this route unreliable. The oral-to-parenteral potency ratio has been estimated at 1:50. Effects are seen 1 to 2 minutes after an intravenous dose and 2 to 5 minutes after a subcutaneous dose. Naloxone is highly lipid soluble and is rapidly distributed throughout the body. As a result of this rapid redistribution, naloxone has a very short duration (30 to 45 minutes) of action. Supplementation of the initial dose of naloxone is usually necessary if sustained antagonism is desired. Approximately 50% of the drug is bound to plasma proteins, mainly albumin. The plasma half-life is 1 to 2 hours. Naloxone undergoes extensive biotransformation in the liver to inactive metabolites. The metabolites are, in large part, excreted in the urine. The effects produced by naloxone are the result of antagonism of endogenous and exogenous opioids. Naloxone has no effects when administered in clinical doses to normal human volunteers. On administration to humans with pain who have not received exogenous opioids, naloxone demonstrates a biphasic response. Low doses produce analgesia, and higher doses produce hyperalgesia.155 Naloxone reverses all the effects of exogenous opioids (i.e., analgesia, respiratory depression, pupillary constriction, delayed gastric transit, and sedation). Naloxone also reverses the analgesic effects of placebo medications and acupuncture. Small doses (0.4 to 0.8 mg) of naloxone given parenterally reverse the effects of µ-receptor agonists. Naloxone can be titrated to reverse the respiratory depression produced by opioids while maintaining some analgesic effect. Naloxone infusions of 5 µg/kg/hour have been shown to reverse the respiratory depression produced by epidural morphine and not affect the quality of analgesia.156 Rebound release of catecholamines may cause hypertension, tachycardia, and ventricular arrhythmias. Pulmonary edema
912
Section V—Specific Treatment Modalities for Pain and Symptom Management
has also been observed after naloxone administration. Small doses of naloxone can precipitate a withdrawal syndrome in patients who are opioid dependent. Long-term administration of naloxone increases the density of opioid receptors and produces a temporary exaggeration of response to subsequently administered opioids.111 Naltrexone reverses the analgesia as well as the adverse effects associated with opioids and therefore can cause withdrawal symptoms. Methylnaltrexone, in contrast, reverses side effects of opioids that are mediated by the peripheral receptors (gastrointestinal tract) and has no effect on the analgesia. The treatment of life-threatening consequences of known or suspected opioid overdose is the prime indication for naloxone use. Naloxone is also used in small doses to reverse some of the side effects (respiratory depression and pruritus) associated with opioid use. Oral naloxone given in a dose of 8 to 12 mg has been used to ameliorate constipation in patients taking opioids. Naloxone is also used in a formulation with oral pentazocine to prevent diversion. To reverse sedation and respiratory depression, an intravenous dose of 10 µg of naloxone (followed by increasing doses) is given. An infusion may be necessary to maintain the antagonism. Naloxone is available for parenteral administration in concentrations of 0.02, 0.4, and 1 mg/mL. Methylnaltrexone was approved in 2008 for the treatment of opioid-induced constipation in the palliative setting in patients not responsive to laxative therapy. It is available for subcutaneous injection at 8 to 12 mg (0.15 mg/kg), not to exceed one dose over a 24-hour period. Alvimopan is a µ-receptor antagonist approved by the FDA in 2008 for the treatment of postoperative ileus. The drug antagonizes the peripheral effects of opioids (constipation) without reversing centrally mediated analgesia. The peak plasma concentration is seen approximately 2 hours after oral ingestion, and the bioavailability is 6%. Alvimopan does not cross the blood-brain barrier because of its large molecular weight and low lipophilicity. It has a terminal half-life of 10 to 18 hours. It has one active metabolite as a result of intestinal
metabolism. It is approved for oral use in a hospital setting, at an initial 12-mg dose 30 minutes to 5 hours preoperatively, followed by twice daily for 7 days.
Conclusion Since their initial discovery thousands of years ago, opioids remain important agents in the treatment of pain. They have become the drugs of choice in the management of acute perioperative pain and of moderate to severe cancer pain. The use of opioids to treat chronic noncancer pain conditions remains controversial. Multiple preparations of various opioids are available in immediate-release and extended-release preparations. The choice of agent is based on the patient's previous response, the patient's medical condition, the degree of pain, and the physician's experience. Careful titration of drugs for pain control with vigilance about side effects is needed. Opioid use is associated with side effects, including tolerance, addiction, and abuse. Aggressive prosecution of physicians who prescribe large quantities of opioid analgesics to patients in pain has had a chilling effect on the appropriate use of opioid analgesics in pain management in many communities. Efforts by the national and international pain management community to highlight the appropriateness of the use of opioid analgesics for the management of all types of pain have helped to decriminalize such activities. Research is ongoing to discover an efficacious opioid that has minimal side effects and does not have a potential for abuse. Tamper-resistant and nonaddictive preparations are needed. Genetic differences account in part for the individual differences in response to opioid analgesics and in the development of addiction. Pharmacogenetic studies are looking further into individual responses to various opioids and hold promise for the use of genetics in the treatment of pain.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
123
V
Role of Antidepressants in the Management of Pain Steven D. Waldman and Corey W. Waldman
CHAPTER OUTLINE Classification of Antidepressants 913 Tricyclic (Heterocyclic) Antidepressants 913 Mechanism of Action 914 Absorption and Metabolism 914 Side Effects 914 Abuse Potential and Side Effects of Withdrawal of the Drug 915 Overdosage 915 Some Common Tricyclic and Tetracyclic Antidepressants 915 Selective Serotonin Reuptake Inhibitors 915 Mechanism of Action 916 Absorption and Metabolism 916
The antidepressant compounds have been used in patients suffering from a variety of painful conditions since these drugs were first released in the 1950s. The use of these agents in this clinical setting was predicated on the logical notion that most patients with unremitting pain were depressed. Not until the early 1970s, however, did Merskey and Hester1 and other investigators put forth the notion that this group of drugs could also have analgesic properties separate and apart from their primary mood-altering purpose. This notion has stood the test of time, and the results of numerous controlled studies have confirmed it.2 Given the widespread use of the antidepressant compounds as a first-line treatment for pain, one must wonder that if the pharmaceutical companies that first introduced these drugs as antidepressants could turn back the hands of time, they would have introduced them as analgesics. This chapter reviews the clinically relevant pharmacology of the various antidepressant compounds that are thought to be useful in the management of pain with an eye to providing the clinician with a practical roadmap on how to implement, manage, and discontinue therapy with this heterogeneous group of drugs.
Classification of Antidepressants For the purposes of this chapter, the antidepressant compounds can be divided into the following six groups: (1) the tricyclic antidepressants (TCAs); (2) the selective serotonin reuptake inhibitors (SSRIs); (3) the serotonin and noradrenergic reuptake © 2011 Elsevier Inc. All rights reserved.
Side Effects 916 Abuse Potential and Side Effects on Withdrawal of the Drug 916 Overdosage 916 Some Common Selective Serotonin Reuptake Inhibitors 916 Serotonin and Noradrenergic Reuptake Inhibitors 917 Venlafaxine (Effexor) 917 Noradrenergic Reuptake Inhibitors 917 Reboxetine (Edronax) 917 Monoamine Oxidase Inhibitors 917
Practical Considerations for Clinical Use of Antidepressants as Analgesics 918
inhibitors (SNaRIs); (4) the noradrenergic and specific serotoninergic antidepressants (NaSSAs); (5) the noradrenergic reuptake inhibitors (NaRIs); and (6) the monoamine oxidase inhibitors (MAOIs) (Table 123.1). In addition, an emerging group of pharmacologically heterogeneous drugs is known as the atypical antidepressants. Although many of the characteristics of the various types of antidepressant compounds are similar to the properties of the TCAs, the unique properties of each class of drugs are discussed individually.
Tricyclic (Heterocyclic) Antidepressants The TCAs are the prototypical antidepressant compounds in clinical use for the treatment of pain and are, by far, the most studied. Their name is derived from their molecular structure, which is composed of three rings (Fig. 123.1). The modification of the middle ring and the alteration of the amine group on the terminal side chain resulted in numerous clinically useful drugs. More recently, the addition of a fourth ring to the TCAs in drugs such as trazodone and amoxapine complicated the nomenclature of this class of drugs (Fig. 123.2). In terms of chemical structure, these drugs are now correctly referred to as heterocyclic antidepressants; however, the more familiar term tricyclic antidepressants is still used by most clinicians to indicate the amitriptyline-like drugs, regardless of their actual chemical structure, and to differentiate them from other classes of antidepressants such as the SSRIs and the MAOIs. 913
914
Section V—Specific Treatment Modalities for Pain and Symptom Management
Mechanism of Action
Side Effects
The mechanism of action of the TCAs is thought to be through their ability to alter monoamine transmitter activity at the synapse by blocking the reuptake of serotonin and norepinephrine.3 Although this pharmacologic effect begins with the first dose of the drug, most clinicians believe that clinically demonstrable improvement in the patient's pain complaints requires 2 to 3 weeks of treatment. This lag in onset of clinically demonstrable improvement suggests that more may be at play than the simple alteration of monoamine transmitter activity.4 Some investigators have postulated that the normalization of a disturbed sleep pattern is ultimately responsible for the analgesic properties of these drugs, rather than their direct action on monoamine transmitter activity itself.
In addition to blocking the synaptic reuptake of serotonin and norepinephrine, the TCAs also interact with other receptors. These interactions account for the wide and varied side effect profile of TCAs (Table 123.2). Many of the early TCAs, as typified by amitriptyline, exert significant anticholinergic side effects through the muscarinic receptors. Such side effects include xerostomia, xerophthalmia, constipation, urinary retention, tachycardia, decreased gastric emptying, and difficulties in visual accommodation.5 In addition to the anticholinergic side effects of the TCAs, many of these drugs cause significant blockade of the alphaadrenergic receptors, with resulting orthostatic hypotension. The orthostatic hypotension is most likely the result of venous blood pooling in the lower extremities and viscera. This potentially dangerous side effect can range from a mildly annoying sensation of transient light-headedness when arising to near syncopal episodes, with falling and head injury distinct possibilities. Other side effects include the blocking of the histamine (H2) receptors with resultant decrease in gastric acid production, as well as various psychomimetic side effects that can be most upsetting to the patient. These psychomimetic side effects include vivid “Technicolor” dreams, prolonged and intense dreaming, restlessness, and occasionally psychic activation. Some drugs in this class seem to produce increased appetite and weight gain, whereas others seem to suppress appetite. Increased and decreased libido, as well as sexual dysfunction, can occur and should be discussed with patients when assessing the efficacy of therapy with the TCA compounds. The unique side effect of priapism, which occurs in approximately 1 in 10,000 men when taking trazodone, should also be discussed when implementing treatment with this drug.
Absorption and Metabolism The TCAs are well absorbed orally and are bound to serum proteins. This class of drugs undergoes rapid first-pass hepatic metabolism, but these agents have relatively long elimination half-lives of 1 to 4 days, owing to their lipophilic nature. Diseases that affect serum proteins or decrease liver function can alter the serum levels of these drugs. These drugs are excreted in the urine and feces.
Table 123.1 Classification of Antidepressant Compounds Tricyclic antidepressants Selective serotonin reuptake inhibitors Serotonin and noradrenergic reuptake inhibitors Noradrenergic and specific serotoninergic antidepressants Noradrenergic reuptake inhibitors
Table 123.2 Common Side Effects of the Tricyclic Antidepressants
Monoamine oxidase inhibitors
Xerostomia Xerophthalmia Urinary retention Blurred vision Constipation Sedation Cardiac arrhythmias N
CH3
Orthostatic hypotension Sleep disruption
CH3
Weight gain
Fig. 123.1 The chemical structure of amitriptyline, the prototypical tricyclic antidepressant.
Headache Nausea Gastrointestinal disturbance/diarrhea Abdominal pain
CI N
N N
Inability to achieve an erection Inability to achieve an orgasm (men and women)
N
N
Loss of libido Agitation
O Fig. 123.2 The chemical structure of trazodone.
Anxiety
Chapter 123—Role of Antidepressants in the Management of Pain
These side effects can usually be managed by proper dosing techniques when implementing therapy with the TCAs, as discussed subsequently. However, they may necessitate switching to a drug with a different side effect profile to achieve patient compliance with the drug regimen.
Abuse Potential and Side Effects of Withdrawal of the Drug The TCAs do not appear to interact significantly with the opioid, benzodiazepine, γ-aminobutyric acid, or beta-adrenergic receptors. No clinical evidence of addiction occurs when these drugs are discontinued. Some drugs in this class, however, have a propensity to cause various symptoms including insomnia, restlessness, lack of energy, and increased cholinergic activity as manifested by excessive salivation and occasional gastrointestinal distress. These side effects can be avoided by slowly tapering the TCA over 10 to 14 days.
Overdosage Overdosage of significant amounts of the TCAs is a serious event that, if not aggressively managed, can result in death.6 In general, the dosages that are required to treat pain are lower than those required to treat severe depression. However, the advent of mail order pharmacies, with their 90-day prescription requirements, has made overdose a real issue because amitriptyline doses greater than 2000 mg can be fatal— well within the amounts supplied in a 90-day prescription. Sedation progressing to coma, combined cardiac abnormalities including delays in cardiac conduction as manifested by a prolonged QT interval, and bizarre cardiac dysrhythmias can make the management of TCA overdose most challenging. Further complicating this clinical picture is the potential for grand mal seizures and a hypercholinergic state consisting of mydriasis, urinary retention, dry mouth and eyes, and delirium. Because of the potential for disastrous results of TCA overdosage, all such events should be taken seriously, and all patients suspected of overdosage should be immediately evaluated and treated in an emergency department equipped to manage the attendant life-threatening symptoms.
Some Common Tricyclic and Tetracyclic Antidepressants Amitriptyline (elavil) Amitriptyline is the prototype of all antidepressants (see Fig. 123.1). Its efficacy as an analgesic has been studied extensively, and significant clinical experience exists in this setting.7,8 Blocking both norepinephrine and serotonin, amitriptyline is an efficacious analgesic, but it has significant side effects including sedation, orthostasis, and most of the troublesome anticholinergic side effects. This drug should be used cautiously in patients with cardiac conduction defects owing to its propensity to cause tachycardia, and it should not be used in patients with narrow-angle glaucoma and significant prostatism. In spite of its side effect profile, amitriptyline remains a reasonable starting point for implementation of TCA therapy because of its proven efficacy, low cost, availability of liquid and parenteral formulations, ability to treat sleep disturbance, dosing flexibility, and universal availability, even for those patients on Medicaid or in managed care plans with restrictive formularies. Because of its sedative properties, amitriptyline should be given
915
as a bedtime dose starting at 10 to 25 mg. The drug can be titrated upward as side effects allow in 10- to 25-mg doses, with care being to identify the increases in side effects as the dose is raised. In particular, orthostatic hypotension can be insidious in onset as the dose of the drug is raised and may lead to falls at night when the patient gets up to use the bathroom. If analgesia is not achieved by the time the dose is raised to 150 mg, the patient should be switched to a different antidepressant compound, preferably from another class of drugs, or another adjuvant analgesic can be added, such as gabapentin if appropriate. If the patient has partial relief of pain, this drug can be carefully titrated upward to a single bedtime dose of 300 mg. Desipramine (norpramin) and nortriptyline (pamelor) Both desipramine and nortriptyline are good choices for initial TCA therapy if sedation is not desired or if the sedative side effects of amitriptyline are too great (Fig. 123.3).9,10 Given as a morning dose, these drugs are good first choices in those patients suffering from pain who have complained of lack of energy or who are at risk for the orthostatic side effects of amitriptyline (e.g., patients taking warfarin [Coumadin]). Dosed at 10 to 25 mg every morning and titrated upward to a maximum dose of 150 mg, pain relief is usually noted at doses of 50 to 75 mg after 2 to 3 weeks of therapy, although improvement in sleep may occur much sooner. These drugs should be used cautiously in patients with cardiac arrhythmia and in those prone to psychic activation or agitation. Such psychic activation or agitation may be exacerbated by the concomitant administration of steroids (e.g., epidural steroid injections). Trazodone (deseryl) Although the unique side effect of priapism may limit the use of this drug in men, trazodone has the sedating characteristic of amitriptyline, which is desirable in those patients suffering from sleep disturbance as part of their pain symptoms, without the cardiac, anticholinergic, and orthostatic side effects (see Fig. 123.2).11 The drug should be started at 75 mg at bedtime and titrated upward to 300 mg as side effects allow. Pain relief usually occurs at a dose range of 150 to 200 mg.
Selective Serotonin Reuptake Inhibitors Although generally less efficacious than the TCAs or heterocy clic antidepressants in the treatment of pain, the SSRIs have proven efficacy in this clinical setting. Their lack of side effects relative to the TCAs makes the SSRIs a good choice for those patients with pain who cannot or will not tolerate the side effects of the TCAs, albeit at greater monetary cost.12
N
CH3
H Fig. 123.3 The chemical structure of nortriptyline.
916
Section V—Specific Treatment Modalities for Pain and Symptom Management
Mechanism of Action
Overdosage
The SSRIs selectively block the reuptake of serotonin by blocking the sodium/potassium adenosine triphosphate pump. The result is an increased level of serotonin at the synaptic cleft. The SSRIs also affect other serotonin receptors, most notably in the gut, a characteristic that probably accounts for the propensity of these drugs to cause gastrointestinal side effects, especially during initiation of therapy.
In general, overdosage with the SSRIs is much less serious than is overdosage with the TCAs.14 Remarkably few fatal overdoses have been reported in the literature or to the US Food and Drug Administration involving ingestion only of an SSRI. Moderate overdoses of up to 30 times the daily dose are associated with minor or no symptoms, whereas ingestions of greater amounts typically result in drowsiness, tremor, nausea, gastrointestinal disturbances, and vomiting. At very high doses of greater than 75 times the common daily dose, the more serious adverse events, including seizures, electrocardiogram changes, and decreased consciousness may occur. SSRI overdoses in combination with alcohol or other drugs are associated with increased toxicity, and almost all fatalities involving SSRIs have involved co-ingestion of other substances.
Absorption and Metabolism The SSRIs are well absorbed orally. This class of drugs undergoes rapid first-pass hepatic metabolism and may compete with other drugs for these enzymes. The result is an increase in blood levels of warfarin (Coumadin) and the benzodiazepines, among others. These drugs have relatively long serum elimination half-lives, and given that many of the SSRIs have active metabolites, side effects may persist for a long time after this class of drugs is discontinued. The SSRIs are excreted in the urine and feces.
Side Effects As mentioned, the SSRI interaction with the serotonin receptors of the gut may result in the side effects of cramping, nausea, and diarrhea, especially during the initial implementation of therapy. These symptoms are usually self-limited and actually decrease as the gut accommodates to the increased serotoninergic milieu. In addition to the gastrointestinal side effects associated with the SSRIs, side effects associated with central nervous system activation, including tremors, insomnia, and physic activation can limit the use of these drugs, as can the increased incidence of sexual side effects relative to the TCAs. These sexual side effects include alterations in libido, erectile and orgasmic difficulties, ejaculatory delay, and impotence. The allegation that the SSRI fluoxetine may cause increased suicidal ideation has not appeared to be a problem with the use of this drug as an analgesic, although the relative lack of efficacy of fluoxetine for this purpose when compared with the TCAs has. The SSRIs can interact with the MAOIs to produce a potentially life-threatening constellation of symptoms known as the central serotonergic syndrome. The central serotonergic syndrome is characterized by hypertension, fever, myoclonus, tachycardia, and seizures. In extreme instances, cardiovascular collapse and death may occur.13 For this reason, these classes of drugs should never be used together, and a long, drug-free period of at least 10 half-lives should be implemented when stopping the SSRI and starting the MAOIs. This class of drugs also appears to interact with St. John's wort, and hypertensive crises have been reported when the drugs are taken together.
Some Common Selective Serotonin Reuptake Inhibitors Fluoxetine (prozac, serafem) Fluoxetine is available in capsule, tablet, and liquid forms, which are usually taken once a day in the morning or twice a day, in the morning and at noon. In addition, a fluoxetine delayed-relayed capsule is usually taken once a week (Fig. 123.4). Because the side effect profile is minimal, it is usually possible to start this drug at the lower range of the doses thought to provide analgesia 20 mg, and titrate upward to 60 mg as side effects allow and efficacy demands. The onset of analgesic action of fluoxetine usually occurs within 2 to 3 weeks.15 Paroxetine (paxil) Well tolerated by most patients, paroxetine is another reasonable choice for patients who do not tolerate the TCAs. This drug comes in both an immediate-release form and a controlled-release form. It is taken either once a day or twice a day in the morning and at noon, to minimize the side effects of tremors or irritability. Anecdotal reports indicate that paroxetine may have a lower incidence of ejaculatory side effects when compared with fluoxetine. Paroxetine should be started at a dose of 20 mg and titrated upward to 40 mg as side effects allow and efficacy dictates. Sertraline (zoloft) Sertraline is available as an immediate-release tablet or capsule, as well as an oral liquid concentrate. Generally well tolerated, sertraline is take once a day as a morning dose starting at 50 mg and titrated upward to 200 mg as side effects and efficacy allow.16 This drug may have efficacy for those patients suffering from pain who also exhibit obsessive-compulsive tendencies.
Abuse Potential and Side Effects on Withdrawal of the Drug Like the TCAs, the SSRIs do not appear to interact significantly with the opioid, benzodiazepine, γ-aminobutyric acid, or beta-adrenergic receptors. No clinical evidence of addiction occurs when these drugs are discontinued, but some drugs in this class have a propensity to cause various symptoms including lack of energy and decreased serotoninergic activity, as manifested by constipation. These side effects can be avoided by slowly tapering the SSRI over 10 to 14 days.
O
• HCI H N CH3
F3C
Fig. 123.4 The chemical structure of fluoxetine.
Chapter 123—Role of Antidepressants in the Management of Pain
Serotonin and Noradrenergic Reuptake Inhibitors Venlafaxine (Effexor) Venlafaxine was shown to be useful as an analgesic in controlled clinical trials.17,18 Its structure differs from that of any of the other clinically useful antidepressant compounds (Fig. 123.5). With a better side effect profile than the SSRIs, this drug is a good starting point for those patients who seem to have side effects with most adjuvant analgesics. Like amitriptyline, venlafaxine affects both serotonin and norepinephrine, a feature that theoretically should make it more efficacious for pain than the SSRIs. It remains to be seen whether widespread clinical use will bear out this premise. A reasonable starting dose for pain is 25 mg of venlafaxine every 12 hours, with the dose increased by 25 mg every week as side effects allow and efficacy dictates.
Noradrenergic Reuptake Inhibitors Reboxetine (Edronax) The newest class of antidepressants, the NaRIs are among the least studied of the antidepressant compounds in the role of analgesics.19,20 Given that reboxetine acts primarily on the noradrenergic system, theoretically it is most useful for those patients with pain who are also suffering from significant anergia and depression and who cannot tolerate desipramine or nortriptyline (Fig. 123.6). Not yet unavailable in the United States but available in more than 50 countries, reboxetine is given as a 4-mg twice-daily dose titrated upward by 1 mg each week to 10 mg as side effects allow and efficacy dictates. Anecdotal reports indicate that painful ejaculation can occur at higher doses of this drug.
Monoamine Oxidase Inhibitors Isoniazid and its derivative iproniazid were introduced in 1951 as pharmacologic treatments for tuberculosis. Investigators found that iproniazid inhibited the enzyme MAO and that patients with tuberculosis who were treated with this drug experienced an elevation of mood. This discovery, along with the introduction of the phenothiazines,
ushered in the modern era of the pharmacologic treatment of psychiatric disorders. Widespread experience with this class of drugs led to an understanding that these drugs were also useful in patients suffering from chronic pain, most notably intractable headache, as well as the realization that their side effect profile limited their clinical utility.21 The introduction of the TCAs in the early 1960s led to the almost complete abandonment of the MAOIs, except in the most severely disturbed psychiatric patients and a few recidivist patients with headache. Through the almost single-handed efforts of Diamond et al at the Diamond Headache Clinic in Chicago, the efficacy and the safety of the MAOIs in combination with the TCAs in the treatment of intractable headache were firmly established. The MAOIs are a heterogeneous group of drugs that work by blocking the oxidative deamination of the biogenic amines at the nerve synapse.22 This process leads to the release of a larger than normal amount of these amines by the synapse when an action potential is present. The MAOIs are well absorbed by mouth and are metabolized in the liver, primarily by acetylation. Some potential for liver damage from this class of drugs exists, and appropriate monitoring of liver function tests should be part of the patient's overall treatment plan.23 In spite of the efficacy of the MAOIs in the treatment of intractable pain, the unpredictable and sometimes severe side effects of this class of drugs limit their use in pain management to patients in whom other, less problematic treatments have failed and who are willing and able to adhere strictly to the dietary and medication restrictions required with these drugs. These restrictions are extremely important because many drugs and foods can potentiate the adrenergic and serotonergic effects of MAOIs (Tables 123.3 and 123.4).24 Commonly used MAOIs include phenelzine, isocarboxazid, and tranylcypromine, which are nonselective MAOIs. Phenelzine is the most commonly used MAOI in pain
Table 123.3 Dietary Restrictions When Taking Monoamine Oxidase Inhibitors Aged food or meat Overripe fruit
NH2
Fermented food
OH
Chicken liver Soy sauce Smoked or pickled meat, poultry, or fish OH
Fig. 123.5 The chemical structure of venlafaxine.
O
Cold cuts, including bologna, pepperoni, salami, summer sausage Alcoholic beverages (especially Chianti, sherry, liqueurs, and beer) Alcohol-free or reduced-alcohol beer or wine
CH3
Anchovies Caviar
O
Cheeses (especially strong or aged varieties) Figs
O
Raisins, bananas NH
Fig. 123.6 The chemical structure of reboxetine.
917
Meat prepared with tenderizers Meat extracts
918
Section V—Specific Treatment Modalities for Pain and Symptom Management NH
Table 123.4 Drug Interactions with Monoamine Oxidase Inhibitors Allergy medications (including nose drops or sprays)
NH2
Fig. 123.7 The chemical structure of phenelzine.
Amantadine (Symmetrel) Antihistamines (e.g., Actifed DM, Benadryl, Benylin, ChlorTrimeton, Compoz) Antipsychotics Appetite suppressants Asthma drugs Blood pressure medication Buclizine Bupropion (Wellbutrin) Buspirone (BuSpar) Carbamazepine (Tegretol) Cocaine Cold medications Cyclizine (Marezine) Cyclobenzaprine (Flexeril) Dextromethorphan Disopyramide (Norpace) Flavoxate (Urispas) Fluoxetine (Prozac) and other SSRIs Insulin (MAOIs may change amount of insulin needed) Ipratropium (Atrovent) Levodopa (Dopar, Larodopa) Maprotiline (Ludiomil) Meclizine (Antivert) Meperidine (Demerol; deaths have occurred when combining MAOIs and a single dose of meperidine) Methylphenidate (Ritalin) Other MAOIs (e.g., Norflex) Oxybutynin (Ditropan) Procainamide (Pronestyl) Promethazine (Phenergan) Quinidine (Quinidex) Sinus medication Tricyclic antidepressants Tryptophan MAOIs, monoamine oxidase inhibitors; SSRIs, selective serotonin reuptake inhibitors.
anagement (Fig. 123.7).25 Phenelzine is started at an inim tial morning dose of 15 mg. The dose may be increased by 15 mg per week, with the second dose given at noon as side effects allow and as efficacy dictates to a total dose of 60 mg. If the patient has no relief of pain at this point, amitriptyline at a dose of 10 mg should be added, with careful monitoring for side effects. Phenelzine should not be abruptly discontinued; the patient should be cautioned about this, and the drug should be tapered over a 2- to 3-week period.26
Practical Considerations for Clinical Use of Antidepressants as Analgesics As many ways exist to use antidepressants to treat pain as there are antidepressant drugs. The following is an approach that has proved beneficial in the management of patients with various painful conditions in numerous clinical settings. The first step in the practical implementation of antidepressant treatment for pain is to explain to the patient that pain, not depression, is being treated as the primary symptom. Patients have an unfortunate tendency to attribute motive to the act of prescribing antidepressants, because they may feel that they are being labeled as crazy or being told that “it's all just in your head.” Referring to the drugs as “tricyclic analgesics” and providing patient information sheets that reflect this nomenclature will also help. Beware that efforts by pharmacies to provide written patient information materials with each prescription may undermine the best of intentions. When the physician is treating patients who questions his or her prescribing motive, a call to the pharmacist to enlist his or her help in patient education is beneficial. The second step in the practical implementation of antidepressant treatment for pain is to explain to the patient that the medication will not work immediately, but it will take a period of weeks for the patient to experience meaningful pain relief. The physician should explain that treatment is starting at a low dose and that an increased dosage may be needed in the future. This helps alleviate concerns that the patient is taking “too much medicine.” Again, the pharmacist can be of great help in this setting. The third step is to educate the patient with regard to normalizing sleep when treating pain. The physician should reinforce the salutary effects of normalization of the patient's sleep cycle as a benefit of most of the drugs discussed earlier. The physician should also let the patient know that this drug is not a “sleeping pill” but actually will help treat the sleep disturbance and, most importantly, the pain. The fourth step is to discuss side effects without setting the stage for medication noncompliance. For the most part, these drugs are well tolerated because the chosen drug is started at the lower range of the dosage spectrum, and increases in dosage are done slowly. Supportive measures for early side effects such as eye drops for xerophthalmia or cough drops for xerostomia can improve compliance. Informing the patient that the “hungover” feeling that may be experienced early on will soon subside may be helpful, too. The final step is to remain positive regarding the potential for the patient to obtain pain relief. Let the patient know that changes in dosing or even medication may occur and is a routine part of treating pain. Most importantly, the message should be one of hope, not negativity.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
124
V
Anticonvulsants Steven D. Waldman and Corey W. Waldman
CHAPTER OUTLINE Category 1 Anticonvulsants 919 Phenytoin (Dilantin) 919 Carbamazepine (Tegretol) 920 Lamotrigine (Lamictal) 921 Topiramate (Topamax) 922
Category 2 Anticonvulsants 922 Gabapentin (Neurontin) 922 Tiagabine (Gabitril) 922 Divalproex Sodium (Depakote) 923 Pregabalin (Lyrica) 923
Conclusion 923
It is not surprising that with the introduction of each new anticonvulsant into clinical practice, the drug has been tried as a treatment for neuropathic pain, albeit with varying degrees of success. This chapter reviews the anticonvulsant compounds that have proven efficacy in the treatment of various painful conditions and provides the clinician with a practical step-bystep guide for their use. What is striking about the anticonvulsants used to treat pain is their heterogenicity. Unlike the antidepressants, which can readily be grouped into classes based on their chemical structure (e.g., the tricyclic antidepressants) or their mechanism of action (e.g., the selective serotonin reuptake inhibitors), the anticonvulsants defy simple classification. However, some generalizations can be made. The anticonvulsants useful in the treatment of pain can be placed into two broad categories (Table 124.1). Category 1 includes those drugs whose primary mechanism of action is to modulate the function of the voltage-dependent sodium channels, whereas category 2 drugs have mechanisms other than modulation of the sodium channel.
Category 1 Anticonvulsants Category 1 anticonvulsants modulate the voltage-dependent sodium channels. Although the exact mechanism of neuropathic pain has not been fully explained, some generalizations can be made that may help to describe how the anticonvulsants exert their analgesic effect in this clinical setting. If one begins with an assumption that neuropathic pain is the result of abnormal nerve firing, it is reasonable to assume that anything that modulates this abnormal nerve firing downward should decrease the pain, regardless of the drug's exact mechanism of action. Conceptually, the category 1 anticonvulsant drugs exert their pain-relieving effect by raising the firing threshold required to open the sodium channel and allow the nerve to reach its action potential and fire (Fig. 124.1).1 Although overly simplistic and ignoring the role of pain modulation © 2011 Elsevier Inc. All rights reserved.
at the spinal cord and central levels, the idea that it requires more subthreshold stimuli to elicit an action potential in the presence of Category 1 anticonvulsants and the concept of a dose-response curve that is roughly linear fit with our overall clinical observations in this setting, given the diverse nature of pain syndromes treated with the anticonvulsant drugs. Again, to attribute a solely peripheral mechanism of action to the anticonvulsants is probably incorrect given that all the drugs discussed subsequently have the ability to cross the bloodbrain barrier and that many of the drugs exert other pharmacologic actions at both the peripheral and higher levels (e.g., the ability of phenytoin to modulate the calcium and potassium channels).
Phenytoin (Dilantin) The first modern anticonvulsant drug used to treat neuropathic pain, phenytoin has seen extensive use as an adjuvant analgesic since the 1950s, with mixed results (Fig. 124.2). Reasonably well absorbed after oral administration, phenytoin is extensively protein bound, with only approximately 10% existing in its free state. The drug is metabolized by the liver, and only a small amount is excreted in the urine. Phenytoin is available in a large array of formulations including immediate-release and sustained-release oral products in a variety of doses, as well as liquid solutions and an injectable preparation. In clinical dosage ranges, it is relatively nonsedating and reasonably well tolerated. Side effects of phenytoin are summarized in Table 124.2 and include nystagmus, behavioral changes, peripheral neuropathy, gingival hyperplasia (Fig. 124.3), gastrointestinal disturbance, osteomalacia, rash, Stevens-Johnson syndrome, liver dysfunction, blood dyscrasias, and a unique side effect of pseudolymphoma that is clinically difficult to distinguish from Hodgkin's disease. Because phenytoin is so highly protein bound, any drugs that compete with the binding sites on serum albumin have the potential to increase the free fraction of the drug and can result in toxicity. 919
920
Section V—Specific Treatment Modalities for Pain and Symptom Management
To treat neuropathic pain with phenytoin, a dose of 100 mg at bedtime is a reasonable starting point. After 1 week, an additional 100-mg morning dose may be added. If the patient is not experiencing limiting side effects, an additional 100-mg noontime dose may be added. At this point, a complete blood count and liver function tests should be performed. If the patient is tolerating the 300-mg dosing regimen and has experienced partial pain relief, the drug may be titrated upward by 30 mg per week to a maximum dose of 400 mg as side effects allow and efficacy dictates. If at the 300-mg dose the patient is experiencing no diminution of pain, it may be reasonable to switch to another anticonvulsant. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
support the efficacy of carbamazepine in certain other painful conditions including neuropathic pain related to human immunodeficiency virus (HIV) infection or chemotherapy. Chemically related to the tricyclic antidepressants, carbamazepine is highly protein bound and is metabolized in the liver. After glucuronidation, it is excreted in the urine. As with phenytoin, interaction with other drugs that are protein bound, such as isoniazid and warfarin (Coumadin), can affect free fraction concentrations and lead to toxicity. In addition to raising the firing threshold of the
Carbamazepine (Tegretol)
H N
Particularly useful in the treatment of lancinating and neuritic pain syndromes such as trigeminal neuralgia, carbamazepine has proven efficacy in the treatment of numerous neuropathic pain syndromes including diabetic polyneuropathy, trigeminal neuralgia, glossopharyngeal neuralgia, postherpetic neuralgia, and central pain states (Fig. 124.4).2–4 Many anecdotal reports
Table 124.1 Classification of Anticonvulsants Based on Their Mechanism of Action
O
O N H
Fig. 124.2 Chemical structure of phenytoin.
Table 124.2 Side Effects Associated with Phenytoin
Category 1 Anticonvulsants (drugs that modulate voltage-dependent sodium channels)
Nystagmus
Phenytoin
Behavioral changes
Carbamazepine
Peripheral neuropathy
Lamotrigine
Gingival hyperplasia
Topiramate
Gastrointestinal disturbance
Category 2 Anticonvulsants (drugs whose primary mechanism of action is unrelated to modulation of the voltage-dependent sodium channel)
Osteomalacia
Gabapentin
Stevens-Johnson syndrome
Tiagabine
Liver dysfunction
Valproic acid
Blood dyscrasias
Pregabalin
Pseudolymphoma
Rash
Sodium ions Outside Channel Cell membrane
Inside
A
B
C
Fig. 124.1 Modulation of voltage-gated sodium channels by category 1 anticonvulsants. A, Voltage-gated sodium channel closed. B, Depo larization opens the voltage-gated sodium channel. C, Sodium ions inside the cell result in a positive change within the cell, and the “gate” closes.
Chapter 124—Anticonvulsants
voltage-dependent sodium channel, carbamazepine suppresses norepinephrine reuptake and, in all likelihood, exerts some of its actions centrally, given it tendency to cause sedation at the higher end of the therapeutic dosage range. In addition to sedation, carbamazepine can cause various central nervous system (CNS) side effects including vertigo, ataxia, diplopia, dizziness, and blurred vision. Gastrointestinal side effects and rash may occur, but the most worrisome side effect of carbamazepine is its potential to cause aplastic anemia. This side effect can generally be avoided if careful and systematic monitoring of hematologic parameters is followed in all patients considered for treatment with this drug. Table 124.3 provides a recommended monitoring protocol for patients who are to receive carbamazepine. Failure to monitor the carbamazepine-treated patient scrupulously can have fatal consequences. This drug should be used with extreme caution in those patients suffering from neuropathic pain who have previously undergone chemotherapy or radiation therapy for malignant disease, even if their hematologic parameters have returned to normal. These patients are extremely sensitive to the hematologic side effects of carbamazepine. Given the reasonably high incidence of CNS side effects associated with carbamazepine therapy, this drug should be started at a low nighttime dose of 100 mg. The drug may then be increased in 100-mg increments, with the drug given on a dosing schedule of four times a day to a maximum dose of 1200 mg as side effects allow and efficacy dictates. In patients with pain emergencies such as intractable trigeminal neuralgia that is limiting the patient's ability to maintain adequate nutrition and hydration, hospitalization is recommended so more rapid upward titration may be safely accomplished. Regardless of the speed at which the drug is titrated upward, the monitoring
921
protocol outlined in Table 124.3 must be followed to avoid disaster. Like all other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
Lamotrigine (Lamictal) Lamotrigine is another anticonvulsant whose mechanism of action involves modulation of the voltage-dependent sodium channel (Fig. 124.5). Useful in the treatment of various neuropathic pain states including HIV-induced polyneuropathy, trigeminal neuralgia, and poststroke pain, lamotrigine is worth a try in those patients who have lancinating or sharp neuropathic pain that has not responded to carbamazepine or in those patients in whom carbamazepine is contraindicated.5–7 Lamotrigine is rapidly and completely absorbed following oral administration, and it reaches peak plasma concentrations (tmax) 1.4 to 4.8 hours after administration. When it is administered with food, the rate of absorption is slightly reduced, but the extent remains unchanged. Lamotrigine is approximately 55% bound to human plasma proteins. Unlike many of the other anticonvulsants, protein binding is unaffected by therapeutic concentrations of phenytoin, phenobarbital, or valproic acid, although valproic acid significantly increases the plasma half-life of lamotrigine. Therefore, the dose should be decreased with the concurrent use of these drugs. Lamotrigine is metabolized predominantly in the liver by glucuronic acid conjugation. The major metabolite is an inactive 2-H-glucuronide conjugate that can be hydrolyzed by beta-glucuronidase. Approximately 70% of an oral lamotrigine dose is recovered in urine as this drug metabolizes.
Table 124.3 Monitoring Protocol for Carbamazepine Use 1. Obtain baseline CBC, chemistry profile including creatinine and liver function tests, and urinalysis before the first dose of carbamazepine. 2. Repeat CBC and chemistry profile after 1 week of therapy. 3. Repeat CBC and chemistry profile after the second week of therapy. 4. Repeat CBC and chemistry profile after the fourth week of therapy. 5. Repeat CBC and chemistry profile after the sixth week of therapy. 6. Repeat CBC after the eighth week of therapy and every 2 months thereafter. 7. Stop carbamazepine immediately at the first sign of hematologic or liver function abnormalities. Fig. 124.3 Gingival hyperplasia as a side effect of phenytoin. O
CBC, complete blood count.
CI CI N N
O
NH2
Fig. 124.4 Chemical structure of carbamazepine.
H2N
N
N NH2
Fig. 124.5 Chemical structure of lamotrigine.
922
Section V—Specific Treatment Modalities for Pain and Symptom Management
Side effects of lamotrigine include CNS side effects similar to those of carbamazepine, although less severe, as well as occasional gastrointestinal upset and liver function test abnormalities. Although free of the hematologic side effects associated with carbamazepine, lamotrigine has 10% of significant dermatologic side effects ranging from rash to fatal Stevens-Johnson syndrome. Severe dermatologic side effects associated with lamotrigine occur with great enough frequency that they must be carefully looked for and the drug discontinued immediately at the first sign of even the slightest rash or skin irritation. Most dermatologic side effects of lamotrigine occur within the first week of therapy. No monitoring of hematologic parameters is required with this drug. Lamotrigine is supplied in a chewable tablet and an oral tablet formulation in a variety of dosage strengths, thus making titration of the drug reasonably easy. In treating patients suffering from neuropathic pain with lamotrigine, a reasonable starting dose is 25 mg at bedtime, with upward titration in 25-mg increments using a twice-daily dosing schedule to a maximum dose of 400 mg as side effects allow and efficacy dictates. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
Topiramate (Topamax) With demonstrated efficacy in the treatment of pain associated with diabetic polyneuropathy, topiramate is a reasonable next choice for those patients with neuropathic pain who have not responded to the tricyclic antidepressants, either alone or in combination with other anticonvulsants (Fig. 124.6).8,9 Topiramate's mechanism of action is thought to be related to its ability to modulate the voltage-dependent sodium channel and, in part, to its ability to inhibit carbonic anhydrase. Topiramate is well absorbed orally, and its absorption is unaffected by food. Topiramate is not extensively metabolized, and approximately 70% is primarily eliminated unchanged in the urine. Available in tablet and sprinkle formulations, topiramate is dispensed in various of doses, thus making titration easy. A reasonable starting dose of topiramate is 25 mg at bedtime. The dosage is then increased in weekly intervals by 25 mg with a twice-daily dosing schedule to a maximum dose of 400 mg as side effects allow and efficacy dictates. CNS side effects similar to carbamazepine occur in approximately 15% of patients taking topiramate. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
Category 2 Anticonvulsants Category 2 anticonvulsants are drugs whose primary mechanism of action is unrelated to modulation of the voltage-dependent sodium channel. They include gabapentin, tiagabine, valproic acid, and pregabalin.
O H 3C
CH2OSO2NH2
Tiagabine (Gabitril) Anecdotal reports have suggested that tiagabine may be efficacious in the treatment of neuropathic pain (Fig. 124.8).14 Tiagabine blocks GABA uptake into presynaptic neurons and permits more GABA to be available for receptor binding on the surfaces of postsynaptic cells. Some investigators have suggested that tiagabine is especially effective in preventing the wind-up phenomenon often seen in many neuropathic pain states. Although tiagabine is well absorbed orally, fatty food may decrease absorption and should be avoided when taking the drug. Like phenytoin, tiagabine is highly protein bound, and the possibility for drug-drug interactions H2N
COOH
X Fig. 124.7 Chemical structure of gabapentin.
CH3
S
C
H
CH
COOH
CH2 CH2 N
CH3 O
H3C
One of the most extensively used anticonvulsants in the management of neuropathic pain, gabapentin has proven efficacy in the management of diabetic polyneuropathy, postherpetic neuralgia, phantom limb pain, and pain following spinal cord injury (Fig. 124.7).10–13 An analogue of γ-aminobutyric acid (GABA), gabapentin is thought to exert its analgesic effect by modulating high-voltage calcium channels as well as interacting at the N-methyl-d-aspartate (NMDA) receptors. Gabapentin is generally well tolerated. The drug's oral absorption is not dose dependent in that as the oral dose increases, the proportion that is absorbed decreases. Less than 3% of orally administered gabapentin is protein bound, with negligible drug metabolism. The drug is excreted unchanged in the urine. Treatment with gabapentin is begun with a 100-mg bedtime dose and is then increased on a weekly basis by 100mg increments using a dosing schedule of four times a day. Gabapentin can be increased to a maximum dose of 3600 mg as side effects allow and efficacy dictates. CNS side effects are similar to those of the other anticonvulsants, but they are generally milder. Occasional gastrointestinal side effects including nausea and gastrointestinal upset can occur. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
S
O
O
Gabapentin (Neurontin)
O CH3
Fig. 124.6 Chemical structure of topiramate.
CH3 Fig. 124.8 Chemical structure of tiagabine.
Chapter 124—Anticonvulsants
with other highly protein-bound drugs exists. Tiagabine is partially metabolized in the liver and is excreted in the feces and urine. Therapy with tiagabine should begin with a 4-mg daily dose, with the dose increased in weekly intervals by 4 mg to a maximum dose of 56 mg as side effects allow and efficacy dictates. Side effects of tiagabine include dizziness, sedation, difficulty thinking, and gastrointestinal intolerance. Reports of painful urination and hematuria have also been associated with the use of tiagabine. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
Divalproex Sodium (Depakote) Divalproex sodium, which is metabolized to valproic acid in the gastrointestinal tract, has been used to treat various neuropathic pain syndromes.15 Although the mechanism of action has not yet been established, investigators have suggested that divalproex sodium's activity is related to its ability to increase levels of GABA. Valproic acid is well absorbed orally and is rapidly distributed throughout the body. More than 90% of the drug is strongly bound to human plasma proteins, thus giving the potential for drug-drug interactions with other drugs that are highly protein bound. Divalproex sodium is metabolized in the liver and is excreted in the urine. An initial dose of 250 mg twice daily for a period of 7 to 10 days represents a reasonable starting dose. The dose may be slowly increased to a maximum of 250 mg four times daily. CNS side effects are similar to those observed with tiagabine. Fatal hepatic side effects have been reported with this drug, and patients started on divalproex sodium require careful monitoring of liver function studies throughout therapy. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect.
Pregabalin (Lyrica) Like gabapentin, pregabalin (Fig. 124.9) acts by binding at the alpha2delta subunit of the voltage-dependent calcium NH2 H
c hannel in the CNS and thus reducing the influx of calcium into the nerve endings.16 Pregabalin is believed to have a much higher affinity for the alpha2delta subunit binding sites when compared with gabapentin, and this feature theoretically should make pregabalin a more effective drug in the treatment of pain.17 Not all clinicians believe that this premise has been borne out in clinical practice. Pregabalin increases intraneuronal GABA by causing a dose-dependent increase in glutamic acid decarboxylase. Glutamic acid decarboxylase is responsible for converting glutamate into GABA. Pregabalin is well absorbed orally, and food decreases absorption. The drug is excreted unchanged by the kidneys. Drowsiness and dizziness occur in significant numbers of patients who are started on pregabalin, and these effects appear to be dose dependent when initiating therapy. Like other anticonvulsants, this drug should be discontinued slowly to avoid any rebound effect. Treatment with pregabalin is begun at a dose of 150 mg/day given in two or three divided doses, and titrated up to 300 mg/day over a 1 to 2 weeks as side effects and pain relief dictate. Side effects are for the most part dose dependent. Many clinicians believe that patients experience a faster onset of pain relief with pregabalin when compared with gabapentin.18
Conclusion The anticonvulsant compounds have demonstrable efficacy in the treatment of various neuropathic pain syndromes. Much like with the antidepressants, the art of using these drugs correctly is paramount if high levels of patient compliance and satisfaction are to be achieved and potentially serious side effects are to be avoided. The admonition to “start low and go slow” is quite apt when contemplating starting a patient on an anticonvulsant drug to treat neuropathic pain. Clear and frequent communication with the patient to emphasize the “trial and error” nature of the use of this class of drugs is mandatory, to avoid noncompliance. Maintaining a positive and hopeful attitude toward the probability of success often enhances the therapeutic outcome for the patient in this challenging clinical setting.
O OH
Fig. 124.9 Chemical structure of pregabalin.
923
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
125
Centrally Acting Skeletal Muscle Relaxants and Associated Drugs Howard J. Waldman, Steven D. Waldman, and Katherine A. Kidder
CHAPTER OUTLINE Mechanism of Action 924 Pharmacokinetics 924 Clinical Efficacy 924 Side Effects 925 Potential for Abuse 925 Individual Skeletal Muscle Relaxants 925 Carisoprodol (Soma) 925 Chlorzoxazone (Parafon Forte DSC) 925 Cyclobenzaprine Hydrochloride (Flexeril) 926 Metaxalone (Skelaxin) 926
Numerous painful conditions have associated muscle spasm. These are most frequently musculoskeletal disorders (e.g., muscle strain) or central nervous system (CNS) disorders associated with spasticity. Various therapeutic interventions, including pharmacologic agents, have been used in an attempt to reduce or obliterate muscle spasm in the belief that this will secondarily alleviate pain and improve function.1–4 Although there is controversy regarding the efficacy of this class of drug, centrally acting skeletal muscle relaxants (SMRs) are the most frequently prescribed drugs for the treatment of muscle spasm (Table 125.1).5 Studies have suggested that these drugs are effective, have tolerable side effects, and can be an adjunct in the treatment of painful musculoskeletal conditions with associated muscle spasm.5–8 Their use is limited by somnolence9–13 and the potential for abuse and dependency.14–17 The SMRs should not be confused with peripherally acting SMRs (e.g., curare and pancuronium), which block neuromuscular junction function and are generally confined to use in surgical anesthesia.
Mechanism of Action The exact mode of action of the SMRs is not known. The SMRs appear to depress polysynaptic reflexes preferentially. At higher dosages, the SMRs may influence monosynaptic reflexes. In animal studies, these drugs appear to produce their muscle relaxation effects by inhibiting interneuronal activity and blocking polysynaptic neurons in the spinal cord and descending reticular formation in the brain.5,10,12 In humans, the SMRs 924
Methocarbamol (Robaxin) 926 Orphenadrine Citrate (Norflex) 926 Tizanidine Hydrochloride (Zanaflex) 926
Associated Drugs Used in the Treatment of Muscle Spasm and Spasticity 926 Diazepam (Valium) 927 Baclofen (Lioresal) 927 Dantrolene Sodium (Dantrium) 927 Quinine Sulfate (Quinamm) 928
Conclusion 928
do not appear to relax skeletal muscle directly. Rather, they may produce their effects through sedation, with resultant depression of neuronal activity at therapeutic doses.6,9,12,18
Pharmacokinetics The SMRs are generally well absorbed after oral ingestion. They have a rapid onset of action, generally within 1 hour. Some SMRs may be administered parenterally, and this route yields a more rapid onset of action. The drugs undergo biotransformation in the liver and are excreted primarily in the urine as metabolites. Significant variability exists among individual drugs, their plasma half-lives, and their duration of action (Table 125.2).10–13
Clinical Efficacy Numerous clinical trials of SMRs have been conducted. Unfortunately, study design deficiencies have made interpretation of results and comparisons among studies difficult. These deficiencies include ill-defined patient selection criteria, noncomparable musculoskeletal disorders studied, variability of disease severity and duration, and subjective assessment of patients' responses to therapy.5,18–24 Despite these difficulties, certain conclusions are possible. In almost all studies, SMRs were more effective than placebo in the treatment of acute painful musculoskeletal disorders and muscle spasm. Efficacy was less consistent in the treatment of chronic disorders. When used alone, SMRs were not consistently superior to simple © 2011 Elsevier Inc. All rights reserved.
Chapter 125—Centrally Acting Skeletal Muscle Relaxants and Associated Drugs
Table 125.1 Commonly Used Centrally Acting Skeletal Muscle Relaxants Generic Name
Trade Name
Carisoprodol
Soma
Chlorphenesin
Maolate
Chlorzoxazone
Paraflex, Parafon Forte DSC
Cyclobenzaprine
Flexeril
Metaxalone
Skelaxin
Methocarbamol
Robaxin
Orphenadrine
Norflex
Tizanidine
Zanaflex
Table 125.2 Skeletal Muscle Relaxant Onset of Action, Duration, and Half-Life* Drug
Onset
Carisoprodol
30 min
Duration (hr)
Chlorphenesin
30 min
NR
2.5–5 hr
Chlorzoxazone
1 hr
3–4
1–2 hr
4–6
Half-Life 8 hr
Cyclobenzaprine
1 hr
4–6
2–3 hr
Metaxalone
30 min
NR
1–2 hr
Methocarbamol
1 hr
4–5
Orphenadrine
1 hr
12–24
925
doses of SMRs may result in significant toxicity, with CNS depression consisting of stupor, coma, respiratory depression, and even death.l4,17–28 Abrupt cessation of some SMRs may cause withdrawal symptoms similar to those seen in barbiturate or alcohol withdrawal.
Potential for Abuse The SMRs have the potential for abuse and dependence. Although the abuse potential of the SMRs is lower than that for benzodiazepines or opioids, numerous incidences have been reported in the medical literature.14,17,29–31 The SMRs may be the primary drug of abuse, presumably for their sedative or mood-altering effects. More frequently, SMRs are used in combination with other CNS depressants, such as opioids or alcohol. These combinations may be taken to prolong the effect of the opioid or benzodiazepines or to achieve the same effect with a lesser amount of the primary drug of abuse. Prescriptions for the SMRs are more readily obtainable than are prescriptions for opioids or benzodiazepines, and prescriptions for SMRs elicit less suspicion when they are frequently refilled.14,15,17 Because of the potential for abuse, investigators have recommended that SMRs be prescribed only for acute conditions and for short periods of time. The SMRs should be used cautiously in known or suspected drug abusers, especially if these patients are already using other CNS depressants.
14 hr 1–3 days
*Data are based on oral administration. NR, duration of action not reported. From Basmajian JV: Acute back pain and spasm: a controlled multicenter trial of combined analgesic and antispasm agents, Spine 14:438, 1989.
analgesics (e.g., aspirin, acetaminophen, and nonsteroidal anti-inflammatory medications) in pain relief. However, when SMRs were used in combination with an analgesic, pain relief was superior to that of either drug used alone. Comparative studies of SMR efficacy failed to document superiority of one drug over another.25–27
Side Effects The most commonly reported side effect of the SMRs is drowsiness. Manufacturers of these agents warn against activities that require mental alertness (e.g., driving, operating machinery) while taking these medications. Other CNS side effects include dizziness, blurred vision, confusion, hallucinations, agitation, and headaches. Gastrointestinal (GI) side effects have also been frequently reported, including anorexia, nausea, vomiting, and epigastric distress. Allergic reactions, including skin rash, pruritus, edema, and anaphylaxis, have also been observed. SMRs are generally not recommended for use in children or in pregnant or lactating women. Because SMRs undergo hepatic metabolism and renal excretion, they must be used cautiously in patients with compromised hepatic or renal function. SMRs should be used with caution in combination with alcohol and other CNS depressants because the effects of these substances may be cumulative.9–13 Excessive
Individual Skeletal Muscle Relaxants Carisoprodol (Soma) Carisoprodol is a precursor of meprobamate (Miltown and Equanil). Meprobamate is one of the three primary metabolites produced by hepatic biotransformation of carisoprodol. Meprobamate dependency secondary to carisoprodol use has been reported with associated drug-seeking behavior and withdrawal symptoms. Withdrawal symptoms are similar to those seen in withdrawal from barbiturates and include restlessness, anxiety, insomnia, anorexia, and vomiting. Severe withdrawal symptoms have included agitation, hallucinations, seizures, and, rarely, death. Because of this potential for physical dependency, carisoprodol should be tapered rather than abruptly discontinued following long-term use. Idiosyncratic adverse effects include weakness, speech disturbances, temporary visual loss, ataxia, and transient paralysis. The onset of action of carisoprodol is 30 minutes. The plasma half-life is 8 hours, and the duration of action is 4 to 6 hours. The drug is supplied as 350-mg tablets, and the recommended dose is one tablet taken four times daily. Carisoprodol is also available in combination with aspirin (Soma Compound) or aspirin and codeine (Soma Compound with Codeine).4,10–13
Chlorzoxazone (Parafon Forte DSC) Chlorzoxazone is similar to the other SMRs, except for some reported cases of significant hepatotoxicity in individuals taking this drug.9,11,32 Chlorzoxazone has an onset of action within 1 hour and a plasma half-life of 1 to 2 hours. The duration of action is 3 to 4 hours. The drug is available in 250- and
926
Section V—Specific Treatment Modalities for Pain and Symptom Management
500-mg caplets, and the recommended adult dose is 250 to 750 mg taken three to four times daily. A pediatric dose of 20 mg/kg divided into three or four doses is suggested by the manufacturer.9,11–13
Cyclobenzaprine Hydrochloride (Flexeril) Cyclobenzaprine is related structurally and pharmacologically to the tricyclic antidepressants (TCAs). Like other SMRs, cyclobenzaprine produces its effects within the CNS, primarily at the brainstem level. Like the TCAs, cyclobenzaprine has anticholinergic properties and may cause dry mouth, blurred vision, increased intraocular pressure, urinary retention, and constipation. The drug should therefore be used with caution in individuals with angle-closure glaucoma or prostatic hypertrophy. As with the TCAs, cyclobenzaprine should not be used in patients with cardiac arrhythmias, conduction disturbances, or congestive heart failure or during the acute phase of recovery from myocardial infarction. Cyclobenzaprine may interact with monoamine oxidase inhibitors and should not be used concurrently or within 14 days of discontinuation of these drugs. Withdrawal symptoms consisting of nausea, headache, and malaise have been reported following abrupt cessation of cyclobenzaprine after prolonged use.9,11–13,28 Cyclobenzaprine has an onset of action within 1 hour. The plasma half-life is 1 to 3 days, and the duration of action is 12 to 24 hours. Cyclobenzaprine is supplied as 10-mg tablets and has a recommended dose of 10 mg three times per day. Up to 40 mg daily in divided doses may be prescribed.9,11–13,28 A long-acting formulation of cyclobenzaprine has been introduced and is believed by some clinicians to have a lower side effect profile than the immediate-release formulation of this drug.
in 500- and 750-mg tablets and has a recommended dosage range of 4000 to 4500 mg daily in three to four divided doses. For severe conditions, a dose as high as 6 to 8 g may be given for the first 48 to 72 hours. This drug is available for IV or IM injection in 10-mL single-dose vials containing 10 mg/mL. Methocarbamol tablets are also available in combination with aspirin (Robaxisal).9,12–15
Orphenadrine Citrate (Norflex) Orphenadrine is an analogue of the antihistamine diphenhydramine (Benadryl). Orphenadrine shares some of the antihistaminic and anticholinergic effects of diphenhydramine. Unlike the other SMRs, orphenadrine produces some independent analgesic effects that may contribute to its efficacy in relieving painful skeletal muscle spasm. In addition to adverse effects commonly associated with other SMRs, dry mouth, blurred vision, and urinary retention may occur as a result of the drug's anticholinergic activity. Rare instances of aplastic anemia have been reported. Like methocarbamol, orphenadrine is available for IV or IM injection. Anaphylactoid reactions have been reported following parenteral administration. Orphenadrine has an onset of action of 1 hour following oral administration. The onset of action is approximately 5 minutes after IM injection and is almost immediate with IV administration. The drug's plasma half-life is 14 hours, and the duration of action is 4 to 6 hours. Orphenadrine is available in 100-mg tablets with a recommended dose of one tablet twice daily. Orphenadrine is available for parenteral use in 2-mL ampules containing 60 mg of the drug and is also administered once every 12 hours. Orphenadrine tablets are also produced in combination with aspirin and caffeine (Norgesic and Norgesic Forte, respectively).9–13,31
Metaxalone (Skelaxin)
Tizanidine Hydrochloride (Zanaflex)
Metaxalone is comparable in effect to the other SMRs. Adverse effects are also similar, with the exception of drug-associated hemolytic anemia and impaired liver function. Hepatotoxicity associated with metaxalone has not been as severe as that reported with chlorzoxazone. Monitoring of liver function is recommended with long-term usage. Metaxalone has an onset of action of 1 hour, a plasma half-life of 2 to 3 hours, and a duration of action of 4 to 6 hours. This drug is supplied as 400-mg tablets and has a recommended dose of 800 mg three to four times daily.9,11–13
Tizanidine hydrochloride is a centrally acting alpha2-adrenergic agonist. Tizanidine is thought to exert its antispasticity properties by increased presynaptic inhibition of motoneurons; this action reduces facilitation of spinal motoneuron firing. Tizanidine does not appear to have any direct effect on the neuromuscular junction or on skeletal muscle fibers. The drug is well absorbed after oral administration and has a half-life of approximately 2.5 hours. Tizanidine is metabolized by the liver, and 95% is excreted in the urine and feces. The drug is available in 2-mg and 4-mg tablets for oral administration. Because of the drug's short half-life, it must be administered every 6 to 8 hours. Because of the common side effects of weakness and sedation, it is best to start the patient on a 2-mg bedtime dose and then titrate upward every 4 to 6 days in 2-mg doses given every 6 to 8 hours. Faster upward titration is best accomplished in an inpatient setting. The maximum daily divided dose should not exceed a total of 36 mg.
Methocarbamol (Robaxin) Methocarbamol is available in oral and parenteral form for intravenous (IV) or intramuscular (IM) injection. Subcutaneous injection is not recommended. Taken orally, this drug is similar to the other SMRs. Parenteral use of methocarbamol has been associated with pain, sloughing of skin, and thrombophlebitis at the injection site. Additionally, overly rapid IV injection has been associated with syncope, hypotension, bradycardia, and convulsions. Because of the risk of convulsion, parenteral use of the drug is not recommended for use in patients with epilepsy. The onset of action is 30 minutes following oral ingestion and is almost immediate following parenteral administration. The plasma half-life of the drug is 1 to 2 hours. The duration of action has not been reported. Methocarbamol is produced
Associated Drugs Used in the Treatment of Muscle Spasm and Spasticity Two additional drugs with muscle relaxant effects, specifically the benzodiazepine diazepam and the antispasmodic agent baclofen, may be useful in the treatment of pain. A third drug, dantrolene sodium, a peripherally acting spasmolytic agent, is
Chapter 125—Centrally Acting Skeletal Muscle Relaxants and Associated Drugs
limited to controlling chronic spasticity associated with upper motoneuron disorders. Finally, the cinchona alkaloid quinine sulfate may help to reduce nocturnal leg cramps. A discussion of each drug follows.
Diazepam (Valium) Diazepam is the most frequently prescribed benzodiazepine used in the treatment of muscle spasm and pain.33 Other available benzodiazepines have not been proven superior to diazepam for this use.10,33 Diazepam has anxiolytic, hypnotic, and antiepileptic properties in addition to its antispasmodic actions. The muscle relaxant effects of this drug are thought to result from enhancement of γ-aminobutyric acid (GABA)– mediated presynaptic inhibition at spinal and supraspinal sites. Numerous studies have been performed comparing diazepam with placebo and with other SMRs in the treatment of painful musculoskeletal disorders. Results have been inconsistent; in general, however, diazepam has been found to be superior to placebo, but not consistently superior to other SMRs in the relief of muscle spasm and pain.5–21,33–35 Diazepam appears to offer greater relief of associated anxiety than the other SMRs tested.5,6,33 Diazepam is superior, however, to other SMRs in the treatment of spasticity associated with CNS disorders such as spinal cord injury and cerebral palsy.11,12,36,37 Efficacy is similar to that of baclofen and dantrolene sodium for CNS disorders. Diazepam's long-term use in these disorders is limited primarily by sedation, abuse potential, and dependence.36,38 Diazepam is well absorbed from the GI tract, although it may also be administered by IV or IM injection. The drug undergoes biotransformation in the liver and is excreted in the urine. Diazepam is highly lipid soluble and rapidly crosses the blood-brain barrier. The onset of action is rapid following oral and parenteral administration. Diazepam's plasma half-life is 20 to 50 hours, and active metabolites of the drug have plasma half-lives ranging from 3 to 200 hours. The duration of action is variable, depending on rate and extent of drug distribution and elimination. Abuse and dependence have been reported with the use of diazepam and the other benzodiazepines. The incidence of these problems is somewhat controversial. The potential for abuse varies among individuals and also varies with doses and length of therapy.33,39–41 Withdrawal symptoms may occur with abrupt cessation of the drug and are similar to symptoms of barbiturate or alcohol withdrawal, including anxiety, dysphoria, insomnia, diaphoresis, vomiting, diarrhea, tremor, and seizures. Diazepam may have an additive effect when taken with other CNS depressants. Diazepam may have reduced plasma clearance and an increased half-life when taken in combination with disulfiram (Antabuse) or cimetidine (Tagamet). Diazepam's most common adverse effects are related to its CNS-depressant activity: sedation, impairment of psychomotor performance, cognitive dysfunction, confusion, dizziness, and behavioral changes. Paradoxical CNS stimulation has also been reported. Other reported adverse effects include GI complaints, skin rash, blood dyscrasias, and elevation of liver enzymes. Parenteral administration has been associated with pain and thrombophlebitis at the injection site. IV and IM administration has produced more serious side effects, especially in seriously ill or geriatric patients; these side effects include cardiopulmonary depression, apnea, hypotension, bradycardia, and cardiac arrest.
927
Diazepam is available in 2-, 5-, and 10-mg tablets. The recommended dose for relief of painful musculoskeletal conditions is 2 to 10 mg three to four times daily. An extended-release 15-mg capsule (Valrelease) is produced and has a daily single dose of 1 to 2 capsules. Diazepam is available for parenteral administration in 2-mL ampules or 10-mL vials with 5 mg/mL. The recommended IM or IV dose is 5 to 10 mg every 3 to 4 hours as necessary.9–13
Baclofen (Lioresal) Baclofen is a chemical analogue of GABA, which is an inhibitory neurotransmitter. The drug produces its effects primarily by inhibiting monosynaptic and polysynaptic transmission in the spinal cord, although some supraspinal activity may also occur. Baclofen is used chiefly in the management of spasticity associated with CNS disorders such as spinal cord lesions and multiple sclerosis.9–13 The drug is reported to be equal or superior in efficacy when compared with diazepam and dantrolene sodium. It is less sedating than diazepam and has fewer serious side effects than dantrolene sodium.12,36,38,42,43 Baclofen may be administered intrathecally to manage severe spasticity in patients who are intolerant or unresponsive to oral therapy.44–48 Baclofen has been useful in the treatment of trigeminal neuralgia. Because the a more favorable side effect profile, some researchers consider baclofen to be the drug of first choice in the treatment of this condition. The coadministration of baclofen and carbamazepine may be more effective than either drug used singly owing to a synergistic effect; however, adverse effects may be cumulative.33,49–51 l-Baclofen has been reported to be more effective and to have fewer side effects than racemic baclofen.52 Baclofen is well absorbed from the GI tract and undergoes limited hepatic biotransformation. Most of the drug is excreted unchanged in the urine. The onset of action is highly variable, ranging from hours to weeks. The drug has a plasma half-life of 2.5 to 4 hours. The onset of action following intrathecal injection is 0.5 to 1 hour. The most frequent side effects associated with the use of baclofen are drowsiness, dizziness, weakness, confusion, nausea, and hypotension. Side effects may be minimized by starting the drug at a low dose and gradually increasing it to the desired level. Abrupt discontinuation of the drug has been associated with hallucinations, psychiatric disturbances, and seizures; therefore, the drug should be gradually withdrawn.9,10,53 Baclofen is produced in 10- and 20-mg tablets. The recommended starting dose is 5 mg three times daily for 3 days with an incremental increase of 5 mg per dose every 3 days. The therapeutic range is 40 to 80 mg daily.9–13
Dantrolene Sodium (Dantrium) Dantrolene sodium is a peripherally acting skeletal muscle relaxant that produces its effect on skeletal muscle by interfering with the release of calcium ions from the sarcoplasmic reticulum. The primary indication for this drug is reduction of spasticity associated with upper motoneuron disorders, including spinal cord injury, stroke, multiple sclerosis, and cerebral palsy. This drug is also used in the treatment of malignant hyperthermia by reducing the hypometabolic processes associated with this disorder. Dantrolene sodium is not
928
Section V—Specific Treatment Modalities for Pain and Symptom Management
indicated in the treatment of other painful musculoskeletal disorders.10–13 Dantrolene sodium is incompletely absorbed from the GI tract. It is metabolized by the liver and is excreted in the urine primarily as metabolites. The onset of action may require a week or more in the treatment of CNS-associated spasticity. The drug's plasma half-life is 8.7 hours. The most frequent side effects associated with its use are muscle weakness, drowsiness, dizziness, malaise, and diarrhea, which may be severe. Serious idiosyncratic and hypersensitive hepatocellular injury may occur that may be fulminant and fatal. This adverse effect has occurred most frequently in women more than 35 years old. The drug is supplied in 25-mg, 50-mg, and 100-mg tablets. For treatment of spasticity, the recommended starting dose is 25 mg, which is gradually increased to a maximum daily dose of 400 mg.9–13,18
Quinine Sulfate (Quinamm) Quinine sulfate is a cinchona alkaloid best known for its use as an antimalarial agent. Although the use of this drug for the treatment of nocturnal leg cramps is controversial, many clinicians believe that the drug is useful in this setting.54–57 The drug reportedly produces its effect on skeletal muscle by an increased refractory period, reduced excitability of the motor end plate to acetylcholine, and redistribution of calcium within the muscle fiber. After oral ingestion, the drug is well absorbed, metabolized by the liver, and excreted in the urine. Quinine sulfate has a plasma half-life of 4 to 5 hours. Some individuals are hypersensitive to quinine sulfate and develop thrombocytopenic purpura, which may be lifethreatening. Visual disturbances, nausea, vomiting, and skin
rash have also been reported. The drug may increase plasma levels of digoxin and may potentiate the effects of neuromuscular blocking agents owing to its curariform-like effects. Cinchonism does not usually occur at doses used to treat leg cramps. The drug is supplied as 260-mg tablets, and the recommended dose is one or two tablets nightly.9–12
Conclusion The SMRs are efficacious in the treatment of painful musculoskeletal disorders. They are generally more effective in combination with analgesics and may potentiate the effects of other CNS depressants. The use of these drugs may be limited by sedation and other undesirable side effects, as well as by their potential for abuse and dependence. Diazepam may also be useful as a muscle relaxant and an anxiolytic, but it also causes sedation and has potential for abuse. Baclofen is used primarily to treat spasticity resulting from CNS lesions. It is also useful in the treatment of trigeminal neuralgia and may be the drug of first choice for this condition. Dantrolene sodium is a peripherally acting agent used to treat spasticity. It is not useful in the treatment of other painful musculoskeletal disorders. Quinine sulfate is an antimalarial agent that may be useful in the treatment of nocturnal leg cramps. Numerous evaluations have failed to demonstrate clear superiority of one SMR over another. Practitioners should base their choice of an agent on careful consideration of individual variables in a given clinical situation.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
126
V
Topical and Systemic Local Anesthetics James E. Heavner
CHAPTER OUTLINE Chemistry 929 Pharmacodynamics 931 Pharmacokinetics 931
Toxicity 932 Local Anesthetics in Clinical Use 933
Local anesthetics are widely used to prevent or treat acute pain— cancer, chronic, and inflammatory pain—and for diagnostic and prognostic purposes. Koller is credited with introducing local anesthetics into medical practice when he used cocaine to numb the cornea before performing eye surgery.1 Drugs classified as local anesthetics reversibly block action potential propagation in axons by preventing the sodium entry that produces the potentials.2 However, other actions of these drugs, such as anti-inflammatory actions by interaction with G-protein receptors,3 also are thought to help prevent or treat pain. Nociceptive pain and neuropathic pain are targeted with this group of drugs. Any part of the nervous system, from the periphery to the brain, may be where local anesthetics act to produce a desired anesthetic or analgesic effect. Various formulations of local anesthetics, routes of administration, and methods of administration are used. The drugs are formulated according to intended route of administration or to address specific concerns or needs. This chapter provides a concise review of the pharmacology of local anesthetics. Details regarding some specific indications (e.g., dentistry) are not considered.
link between the ends (Fig. 126.1). The link contains either an aminoester or an aminoamide bond, and local anesthetics are designated as belonging to one of two groups, the aminoesterlinked local anesthetics or the aminoamide-linked local anesthetics. Procaine is the prototypic aminoester-linked local anesthetic, and lidocaine is the prototypic aminoamide-linked local anesthetic (Fig. 126.2). Procaine was first synthesized in 1904, and lidocaine was first synthesized in 1943. Fundamental to the development of synthetic local anesthetics was the isolation of cocaine from coca beans and the elucidation of its chemical structure. Synthesis of molecules with local anesthetic activity paved the way for “tinkering” with the molecules by systematically modifying chemical structure and testing for a desired result (e.g., reduced toxicity) to develop new local anesthetics. Figure 126.3 presents a chronology of the introduction of local anesthetic into clinical practice. Four
CH3 O
Chemistry
C2H5
NHCCH2N C2H5
All local anesthetic molecules in clinical use have three parts: a lipophilic (aromatic) end, a hydrophilic (amine) end, and a
CH3 Lidocaine
Linkage O OOOO
N
H2N
C2H5
COCH2CH2N C2H5
Lipophilic part
Hydrophilic part
Fig. 126.1 All local anesthetic molecules in clinical use have three parts: a lipophilic (aromatic) end, a hydrophilic (amine) end, and a link between the ends. © 2011 Elsevier Inc. All rights reserved.
Procaine Fig. 126.2 Chemical structures of the prototypic aminoester-linked local anesthetic (procaine) and the prototypic aminoamide-linked local anesthetic (lidocaine).
929
930
Section V—Specific Treatment Modalities for Pain and Symptom Management
Cocaine 1884
Procaine 1905
Tetracaine 1932
1933
Dibucaine
Chloroprocaine 1948 Lidocaine
1955 1956
1960
Mepivacaine
1963
1971
1997
1999
Etidocaine Prilocaine Bupivacaine Ropivacaine Levobupivacaine
Fig. 126.3 Chronology of the introduction of different anesthetics into clinical practice. Chloroprocaine (1955) is the last aminoester-linked local anesthetic introduced that is still in clinical use. (Courtesy of David A. Scott, Melbourne, Australia.)
CH3 O NH
C
R1
R I N
N
R2
O C
O
CH2
Mepivacaine Ropivacaine Bupivacaine R= Equieffective Lipid/H2O Protein-bound (%)
CH3 1 0.8 77.5
C3H6 0.37 2.8 94
C4H9 0.25 27.5 95.6
Fig. 126.4 Results of structure alterations: amide linked. The aminoamidelinked local anesthetics mepivacaine, ropivacaine, and bupivacaine vary only by substitution at R on the basic molecule shown at the top. As the number of carbon atoms increases at R, potency, lipid solubility, and protein binding increase. (Adapted from Heavner JE: Pain mechanisms and local anesthetics: scientific foundations for clinical practice. In Raj PP, editor: Textbook of regional anesthesia, New York, 2002, Churchill Livingstone, p 105.)
aminoester-linked local anesthetics are shown in this figure: cocaine, procaine, tetracaine, and chloroprocaine. The other local anesthetics are aminoamide-linked substances. What is evident from the figure is that, since 1955, the focus has been on the development of aminoamide—rather than aminoesterlinked—local anesthetics. Reasons for this focus include the allergenic potential of aminoester-linked local anesthetics and the instability of aminoester bonds. Testing of various modifications to the basic procaine and lidocaine structure revealed that increasing the molecular weight of the molecules by adding carbon atoms to either end of the structure or to the link generally increases lipid solubility, protein binding, duration of action and toxic ity, and influences biotransformation of the molecule (Figs. 126.4 and 126.5). A positive correlation exists between intrinsic local anesthetic potency and lipid solubility of local anesthetics. Most local anesthetics have a tertiary amine on the hydrophilic end. Exceptions include prilocaine, which has a secondary amine, and benzocaine, which has a primary amine. Tertiary amines have a positive charge (cation) or are uncharged (base). The ratio of cation to base is determined by the acid dissociation constant (pKa) of the local anesthetic and the pH of the solution. The “state” of the amine determines how well local anesthetic molecules move through biologic membranes. The unchanged forms of local anesthetics pass readily through cell membranes. Therefore, speed of onset of local anesthetic
R1 R2 Hydrolysis rate (uM/ml/hr) =potent Duration (min) LD50 (mice)
N R2
H CH3
CH2
Procaine
Tetracaine
H C2H5 1.1 2 50 615
C4H9 CH3 0.25 0.25 175 48
Fig. 126.5 Results of structure alterations: ester linked. The aminoesterlinked local anesthetics procaine and tetracaine vary only by substitution at R1 and R2 on the basic molecule shown above. (Adapted from Heavner JE: Pain mechanisms and local anesthetics: scientific foundations for clinical practice. In Raj PP, editor: Textbook of regional anesthesia, New York, 2002, Churchill Livingstone, p 105.)
block, at least theoretically, is increased by raising the concentration of uncharged local anesthetic molecules injected. Because local anesthetics are weak bases, increasing the pH (“alkalinization”) of solution increases the ratio of base to cation. The Henderson-Hasselbalch equation can be used to quantitate the ratio: Log([cation] / [base]) = pKa(local anesthetic) - pH(solution) Sodium bicarbonate is used clinically to increase the pH of local anesthetic solutions. Commercial solutions of local anesthetics are acidified, so the hydrophilic (cationic) state is favored. Overzealous alkalinization can cause local anesthetic molecules to precipitate from solution. The newest additions to clinically available local anesthetics, ropivacaine (Fig. 126.6) and levobupivacaine, represent (1) the exploitation of technology that permits cost-favorable separation of racemic mixtures of local anesthetics into pure enantiomers and (2) the search for local anesthetics with greater safety margins. Simply stated, molecules with an asymmetrical carbon atom exist in forms that are mirror images (i.e., exhibit “handedness,” chirality), with images (enantiomer, stereoisomers) distinguished by how they rotate light according to the orientation of the structures in three dimensions. Various terms are used to refer to the different enantiomers; this discussion uses S- and R- to designate two different enantiomers. A racemic mixture contains equal amounts of the R- and S- isomers.
Chapter 126—Topical and Systemic Local Anesthetics CH3 NH
O C
CH
CH3
N C3H7
S-Ropivacaine
CH3 NH
C3H7
O C
CH
N
CH3 R-Ropivacaine Fig. 126.6 Chisal forms of ropivacaine. The only difference between the S- and R- isomers is their spatial orientation.
Table 126.1 Anesthetic Duration and Toxicity of Local Anesthetic Isomers Drug
Duration
Toxicity
Etidocaine
S=R
S=R
Mepivacaine
S>R
S=R
Bupivacaine
S>R
SR
S inactivated > resting. Many investigators have shown that the block of propagation of action potentials is a function of frequency of depolarization, a finding that supports the conclusion that the open state of the sodium channel is the primary t arget of local anesthetic molecules. This is referred to as state-dependent block. Certain sodium channel subtypes are generally divided into those that are tetrodotoxin sensitive (TTXs) and those that are tetrodotoxin resistant (TTXr).4 Most sensory neurons generate TTXs currents. However, TTXr currents are present in a high
931
proportion of smaller dorsal root ganglion neurons associated with nociceptive A-delta and C fibers. Available evidence indicates that channels from both groups are involved in pain states as a result of changes in channel function and expression caused by disease or injury. Arguments have been put forth that local anesthetics may exert their pharmacologic action not only on sodium conductance, but also on other ionic conductances (e.g., potassium and calcium).5,6 Differential block, the block of pain perception without motor block, for example, is observed clinically, but the mechanism responsible for this is poorly understood. The clinical manifestations of differential block vary depending on the local anesthetic used.7 For many years, differential block was ascribed to greater sensitivity of smaller axons than large ones to local anesthetics,8 but this “size principle” was challenged.9 Berde and Strichartz7 cited different factors that could contribute to differential block, including anatomic factors, and the relative sensitivity of different local anesthetics for sodium and potassium channels. Oda et al10 suggested that preferential block of TTXr sodium channels by ropivacaine in small dorsal root ganglia neurons (associated with nociceptive sensation) underlies the differential block observed during epidural anesthesia with this drug. Using a combination of local anesthetic and another drug to produce nociceptive selective block is under investigation. For example, activating transient receptor potential vanilloid subtype 1 channels on C fibers with capsaicin to deliver the local anesthetic, QX-314, into the fibers is effective in animal models.11 Another approach is to combine local anesthetic and a2-adrenergic agonist such as dexmedetomidine and has yielded favorable results. The mechanism for the a2-adrenergic agonist action is not known but may include direct inhibition of TTXr Na+ channel or through hyperpolarization activated cation current.12 Another pharmacodynamic puzzle is the mechanism whereby systemically administered local anesthetic relieves pain. An analgesic effect has been reported following intravenous lidocaine administration in many acute and chronic conditions.13–20 Subcutaneously injected bupivacaine reportedly produces analgesia by a systemic effect.21 Normal or altered sodium channels located in various areas of the brain, spinal cord, dorsal root ganglia, or peripheral axons are mentioned most frequently as the action sites. Zhang et al22 reported that in rats, systemic lidocaine delivered by implanted osmotic pump reduces sympathetic nerve sprouting in dorsal root ganglion that is associated with some neuropathic pain behaviors. Local anesthetics have effects on other biologic processes that are potentially important pharmacodynamic actions of value in treating pain. These include inhibition of G-protein– coupled receptor signaling.3
Pharmacokinetics Usual pharmacokinetic parameters (Table 126.2) for drugs incompletely describe important details regarding distribution of local anesthetics from application sites to target and nontarget structures. It is well established that systemic absorption of local anesthetics correlates positively with the vascularity of the injection site: intravenous > tracheal > intracostal > paracervical > epidural > brachial plexus > sciatic > subcutaneous.23 The spinal cord meninges influence distribution of local anesthetics from the epidural and subarachnoid spaces. Intact
932
Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 126.2 Disposition Kinetics in Adult Male Subjects Local Anesthetic
Vdss (L)
Clearance (L/min)
Half-Life (hr)
Hepatic Extraction
Lipid Solubility
Protein Binding (%)
Blood/Plasma Partitioning
Mepivacaine
84
0.78
1.9
0.40
0.8
78
0.92
Ropivacaine
59
0.73
1.8
0.40
2.8
94
0.69
Bupivacaine
73
0.58
2.7
0.51
27.5
96
0.73
Lidocaine
91
0.95
1.6
0.72
2.9
60
0.84
Vdss, Steady state volume of distribution.
skin is nearly a complete barrier to local anesthetic penetration. For delivery of local anesthetic through intact skin, special local anesthetic formulations (e.g., EMLA cream, a eutectic mixture of lidocaine and prilocaine) or delivery methods (e.g., electrophoresis) are employed to facilitate transcutaneous transfer. Because of the large number of different injection sites used by pain physicians (e.g., epidural, intrathecal, intrapleural, intraarticular, intramuscular, perineural, topical) and the variety of dosing methods (e.g., single injection, continuous infusion, intermittent infusion), more than a superficial discussion of the distribution kinetics of local anesthetics from injection sites is beyond the scope of this chapter. Aminoester-linked local anesthetics are hydrolyzed by esterases in tissues and blood. Aminoamide-linked local anesthetics are biotransformed primarily in the liver by cytochrome P-450 enzymes. Metabolites may retain local anesthetic activity and toxicity potential, albeit usually at lower potency than the parent compound. Vasoconstrictors (e.g., epinephrine 1:400,000 [2.5 mg/mL]) are used to reduce absorption of local anesthetics into the systemic circulation. The value of this practice depends on the vascularity of injection site and the tissue binding of different local anesthetics. The value of the addition of sodium bicarbonate to solutions to enhance speed of onset of local anesthetics also depends on injection site, as well as on the physiochemical properties of different local anesthetics. The addition of sodium bicarbonate increases the pH of solutions and thus increases the ratio of uncharged to charged molecules. This change raises the number of local anesthetic molecules in the form that most readily passes through biologic membranes. Hyaluronidase (tissue spreading factor) is sometimes added to local anesthetic solutions to facilitate spread of solution at the injection site, thereby affecting speed of onset and extending a block. This seems to be useful only when local anesthetic is injected behind the eyes preparatory to ophthalmologic surgery. Hyaluronidase may be injected with local anesthetic during epidural neurolysis to treat pain, with positive benefit. An issue of Techniques in Regional Anesthesia and Pain Medicine (volume 8, issue 3, July 2004) discussed in detail additives to local anesthetics. Various attempts have been made to prolong the duration of action of local anesthetics by loading them into liposomes or microcapsules, but no such formulations have been approved by the US Food and Drug Administration (FDA) for marketing.
Toxicity The toxic effects of local anesthetics can be categorized as shown in Figure 126.7. True allergic reactions are associated with aminoester-linked local anesthetics, not amino amide–
Localized or Systemic Allergic reactions
Localized Tissue toxicity
Systemic Cardiac/vascular Central nervous system Methemoglobin Fig. 126.7 Categories of local anesthetic toxic reactions.
linked ones. In a study of anaphylactic and anaphylactoid reactions (n = 789) occurring during anesthesia, Mertes et al24 found no such reactions to local anesthetics. However, Mackley et al25 reported that of 183 patients patch tested, 4 had positive reactions to lidocaine, and 2 of these patients had histories of sensitivity to local injections of lidocaine manifested by dermatitis. These investigators concluded that contact type IV sensitivity to lidocaine may occur more frequently than previously thought. It is common, but inappropriate, to refer to all adverse events as “allergic reactions.” Tissue toxicity, primary myotoxicity and neurotoxicity, can be produced by all local anesthetics if “high” concentrations are used. Signs and symptoms of varying degrees of neuropathy (e.g., transient neurologic symptoms, cauda equina syndrome) have been reported following spinal anesthesia with 2% and 5% lidocaine. A systematic review26 compared the frequency of transcutaneous nerve stimulation (TNS) and neurologic complications after spinal anesthesia with lidocaine with TNS after other local anesthetics. These investigators found that the risk for developing TNS after spinal anesthesia with lidocaine was higher than with bupivacaine, prilocaine, procaine, or mepivacaine.27 Symptoms in all patients disappeared spontaneously by the tenth postoperative day. The lithotomy position seems to be a predisposing factor. In 1980, Foster and Carlson27 reported that of the local anesthetics tested, procaine produced the least severe and bupivacaine the most severe muscle injury. More recently, Zink et al28 concluded that the myotoxic potential of ropivacaine is less than the potential of bupivacaine. However, both drugs produced morphologically identical patterns of calcified myonecrosis, formation of scar tissue, and a marked rate of muscle fiber regeneration in animals after continuous peripheral nerve blocks.29 Various local anesthetics reportedly may produce methe moglobinemia. Prilocaine is the local anesthetic associated with the greatest risk for this complication. As the concentration of local anesthetic in the systemic circulation increases, various cardiovascular system (CVS) and central nervous system (CNS) signs and symptoms appear (Fig. 126.8). The relative CVS and CNS toxicity of local anesthetics has been of interest, especially after Albright30 reported unexpected cardiovascular toxicity of bupivacaine. In animal studies, the
Chapter 126—Topical and Systemic Local Anesthetics Lidocaine plasma conc (µg/ml) 26 24 22 20 18 16 14 12 10 8 6 4 2 0
CVS depression
Respiratory arrest Coma Convulsions Unconsciousness Muscular twitching Visual disturbance Lightheadedness Numbness of tongue
Fig. 126.8 Cardiovascular (CVS) and central nervous system side effects of local anesthetics, depending on their concentration (conc) in systemic circulation.
ratio of doses of bupivacaine that produced convulsive activity and cardiovascular collapse7 was lower than for other local anesthetics such as lidocaine. Human volunteer studies of doses required to produce early features of CNS and CVS toxicity by ropivacaine and levobupivacaine demonstrated that the doses were about equal and higher than for bupivacaine.31–33 Brown et al34 reviewed records of patients who had seizures while undergoing brachial plexus, epidural, and caudal regional anesthetic regimens. No adverse CVS, pulmonary, or nervous system events were associated with any of the seizures, including 16 patients who received bupivacaine blocks. Clinically, which of the usual features if systemic local anesthetic toxicity occurs, the order in which it occurs, and how soon after local anesthetic administration is quite variable.35 This is not surprising given what is known about how various health conditions, other drugs, and rate of increase of local anesthetic concentration in systemic circulation can influence the manifestation and progression of signs and symptoms of local anesthetic toxicity. Measures to prevent systemic toxic reactions to local anesthetics include following dose recommendations, injecting aliquots over time, avoiding inadvertent intravascular injections, and monitoring vital signs during injection. Blanket recommended doses versus block-specific recommended doses have been discussed.36,37 Drug administration must be stopped should signs or symptoms of toxicity develop. Seizures induced by local anesthetics are usually self-limiting and require maintenance of respiratory gas exchange and control of muscle contractions (e.g., intubation, oxygenation, short-acting muscle paralysis). Drugs such as propofol, thiopental, midazolam, and diazepam are effective against these seizures. Cardiovascular toxicity is treated according to American Heart Association guidelines, depending on the nature of the toxicity. Evidence suggests that lipid emulsion infusion may be beneficial in some instances.38 The American Society of Regional Anesthesia and Pain Medicine now include intralipid in their recommended approach to treating local anesthetic systemic toxicity.39
Local Anesthetics in Clinical Use Generic and trade names of local anesthetics are listed in Table 126.3. Undoubtedly, lidocaine is most commonly used to prevent procedure-related pain and for diagnostic
933
Table 126.3 Generic and Trade Names of Local Anesthetics* Generic Name
Trade Name(s)
Benoxinate (oxybuprocaine)
Dorsacaine; Novesine
Bupivacaine
Marcaine; Sensorcaine
Butacaine
Butyn
Chloroprocaine (2-chlorprocaine)
Nesacaine
Cyclomethycaine
Surfacaine
Dibucaine
Nupercaine; Percaine
Etidocaine
Duranest
Hexylcaine
Cyclaine
Levobupivacaine
Chirocaine
Lidocaine
Xylocaine; Xylotox
Mepivacaine
Carbocaine; Polocaine
Piperocaine
Metycaine
Prilocaine
Citanest
Procaine
Novocain
Proparacaine
Ophthaine
Ropivacaine
Naropin
Tetracaine
Pontocaine; Pantocaine
*These local anesthetics are administered chiefly as the chloride or sulfate salts, and it would be more accurate to specify procaine hydrochloride rather than just procaine. Because procaine is the active species, it is the commonly used term. Adapted from de Jong RH: Local anesthetics, St. Louis, 1994, Mosby–Year Book.
Table 126.4 Topical Local Anesthetics and Their Available Preparations Benzocaine Cream Ointment Topical aerosol Benzocaine and menthol Lotion Topical aerosol solution Butamben Ointment Dibucaine
Lidocaine/prilocaine Cream Lidocaine/tetracaine Patch Pramoxine Cream Lotion Pramoxine and menthol Gel Lotion
Cream Ointment Lidocaine Film-forming gel Ointment Patch Cream
Tetracaine Cream Tetracaine and menthol Ointment
Adapted from http://www.nlm.nih.gov/medlineplus/druginfo/uspdi/202042.html
tests. Immediate-acting to long-acting local anesthetics such as ropivacaine, levobupivacaine, and bupivacaine are used for therapy. Table 126.4 lists topical anesthetics and their preparations. Most of the forms are available without prescription. A 5% lidocaine patch (Lidoderm) is approved by the FDA for controlling postherpetic neuralgia.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
127
Alternative Pain Medicine Winston C.V. Parris and Salahadin Abdi
C h apt e r O u t l i n e Prevalence of Alternative Medicine 935 Definition 935 Classification 935 Office of Alternative Medicine 936 Scope 937 Alternative Therapy Modalities 937 Music Therapy 937 Intercessionary Prayer and Spiritual Healing 937 Relaxation Therapy 938
Pain and illness continue to be the scourge of humankind even with the tremendous strides that have been made in the cure and relief of several diseases. Since the 1990s, great progress has been made in the management of pain derived from disease, trauma, or idiopathic origin. However, pain continues to be a major problem in the very young, the very old, cancer patients, diabetic patients, poststroke patients, and almost all patients whose disorder produces unrelenting pain. Pain in the injured worker is a major problem because of the occupational, legal, emotional, economic, political, psychosocial, and societal factors that influence or modify the patient's ultimate perception of pain. Since the advent of the pain medicine specialty, significant developments have contributed to modest success in resolving chronic pain,1 although much remains to be done in optimizing pain control. While we await these advances, patients become disappointed, disenchanted, and at times disgusted with the inadequacy of their pain management. This disillusionment has led many people to seek nontraditional, unconventional, and at times dangerous remedies to control pain. Unfortunately, a few unscrupulous practitioners take advantage of this situation, but it is heartening to note that some of these nontraditional remedies are effective in controlling, if not eliminating, chronic pain syndromes in selected patients. This whole arena is known as alternative medicine or complementary medicine.2 This chapter explores the role of alternative medicine in chronic pain management and examines how these methods can contribute to traditional or conventional pain medicine. Some conventional physicians scoff at any remedy that is not well described in standard medical textbooks or is not thoroughly investigated in peer-reviewed journals and supported by placebo-controlled, randomized, scientifically conducted studies. These methods reflect the standard 934
Hypnosis 938 Chiropractic Therapy 938 Comfort Measures 939 Transcutaneous Electrical Nerve Stimulation 939 Acupuncture 939 Biostimulation Techniques 939 Magnetic Field Therapy 939 Low-Power Laser Therapy 939
Conclusion 940
approach by which medical information is disseminated and passed on from teacher to student or from colleague to colleague. If a given alternative medicine practitioner proposed that snake oil is effective for migraine headaches, most traditional physicians would laugh. This reaction would be based on the fact that no Pharmacopoeia or Physicians' Desk Reference (PDR) or medical journal describes snake oil as a pharmacologic agent or as having any therapeutic value. Yet, if snake oil were analyzed and one of its active principles were absorbed transdermally and had a specific effect on cerebral vasculature that ultimately relieved migraine headaches, this originally preposterous idea would become a multimilliondollar scientific breakthrough. Although this hypothetical scenario is unlikely, it is possible. The major challenge is to determine how to evaluate those “preposterous ideas” that, after all, may not have any deleterious effect on a patient and may, in fact, be beneficial. The existing scientific, medical, and academic structure does not leave much room for this kind of investigation. Except for a few cases (e.g., The University of New Mexico in Albuquerque), most medical school administrators adhere rigidly, and in many situations blindly, to the curricula handed down by tradition. Change takes place, but most changes are insignificant and do not reflect the realities of medicine today and the needs of today's patient. Thus, although recent medical school graduates may be highly skilled in many new and sophisticated techniques of medicine, they may be relatively uninformed about the principles and practice of pain medicine. A needlessly defensive posture may be adopted when new and unconventional techniques are proposed. It takes approximately 1 to 2 decades of physician experience to allow for exploration or, at least, intelligent examination of unconventional information. © 2011 Elsevier Inc. All rights reserved.
Prevalence of Alternative Medicine The prevalence of alternative medicine in the United States was studied by Eisenberg et al,3 and their results were published in the New England Journal of Medicine in 1993. These investigators found that one in three persons in the United States used unconventional or alternative medicine for various illnesses, most of which were associated with pain. This study also highlighted the cost of alternative medicine and the fact that most modalities used in alternative medicine are not subject to governmental scrutiny, regulation, or supervision. Nevertheless, many patients use alternative medicine as their main therapeutic option, and most patients use alternative medicine along with conventional medicine, occasionally with the assent of a conventional physician. Some regional bias exists, in that alternative medicine, including herbal medicine,4 is used more commonly in the western United States and, to a lesser extent, in the southern than in the northern and eastern regions of the United States. To address the burgeoning business of alternative medicine and its impact on citizens, the federal government of the United States, through the Department of Health and Human Services, created the Office of Alternative Medicine by congressional mandate under the 1992 National Institutes of Health (NIH) appropriations bill. The creation of this office was motivated by the groundswell from citizens who demanded that government look into the efficacy of unconventional medicine and its modalities.5 Toward the end of the 1980s, the Mexican herbal medicine called laetrile generated great interest. Thousands of US citizens crossed the Mexican border in search of that elusive cancer cure. Most were not successful in that search. These events, and many others like it, politicized the issue and led to the formation of the Office of Alternative Medicine. The major objective of the Office of Alternative Medicine6 was to facilitate evaluation of alternative medical treatment modalities to determine their effectiveness in treating disease. Its congressional mandate provided for a public information clearinghouse to gather and appropriately categorize information and to fund and organize research training programs for alternative medicine.
Definition In this chapter, alternative medicine may be defined as unconventional or unorthodox medical interventions not routinely taught at US medical schools or not generally available in hospitals in the United States.7 Some alternative therapies are benign; others are invasive. Some have been used for a long time; others are more recent. Some alternative therapies are well known; others are mysterious and, on occasion, dangerous. Although some alternative therapies have sound scientific principles to recommend their use in clinical practice, they may not have been subjected to the scientifically conducted placebo-controlled randomized studies that most conventional medical therapies undergo, and they may not have been exposed to the peer review process necessary before any therapy is accepted as clinically useful. Thus, the claims of many alternative therapies are usually anecdotal. At times, inappropriate or inconsistent assumptions have been made regarding their clinical efficacy.
Chapter 127—Alternative Pain Medicine
935
Alternative medicine covers a wide scope of healing philosophies, methodologic approaches, and clinical therapies. Besides not being taught in medical schools, most alternative medical practices are not reimbursed by medical insurance companies. This situation is changing slowly; for example, acupuncture services now not only are recognized as effective but also are reimbursed by several medical insurers. Alternative medicine has been labeled “holistic medicine,” and although some common areas exist, the comparison is not accurate. The term holistic generally implies that the health care practitioner considers the whole person, including physical, mental, emotional, and spiritual aspects. In today's healthconscious society, many therapies are labeled preventive. This label implies that the practitioner is involved primarily in educating the patient about the disease, its symptoms, its complications, and its treatment. Even more important, however, the practitioner is committed to instructing the patient regarding the techniques and methods of preventing the disease. Using the principle that prevention is better than cure, many preventive practitioners lay heavy emphasis on cessation of smoking and promotion of exercise, a healthy diet, and similar measures to prevent heart disease, metabolic disorders (e.g., diabetes), morbid obesity, and some forms of cancer. Whereas some forms of alternative medicine are consistent with the fundamental physiologic principles involving the circulation and the central nervous system as understood by Western medicine, other approaches are based on different and unfamiliar healing systems. Gradually, some non-Western systems are being absorbed into the mainstream of Western medicine.
Classification To a large extent, alternative medicine has not been evaluated or scrutinized according to accepted scientific principles or methods. Consequently, the architects of individual alternative modalities have been more concerned with acceptance and positive results rather than an open and unconditional evaluation of their efficacy. As a result, no consistent organization existed before the creation of the Office of Alternative Medicine,6 and no attempts were made to classify the modalities used for alternative medicine. Under the aegis of the NIH, a task force was created to address classification issues. The result is seven categories of complementary or alternative medical practices, including the following: 1. 2. 3. 4. 5. 6. 7.
Alternative systems of practice Bioelectromagnetic applications Diet, nutrition, and lifestyle changes Herbal medicine Manual healing methods Mind-body interventions Pharmacologic and biologic treatments
The task force also reported on corresponding issues, such as research methodology, research and training needs, the peer review process, and information dissemination activities.7 The classification of alternative medicine practices was designed primarily to facilitate the review process for grant allocation. It was not designed as an arbitrary or definitive classification of alternative medicine. A summary of the classification is listed in Table 127.1.
936
Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 127.1 Classification of Alternative Medicine Practices Alternative Systems of Medical Practice Acupuncture
Anthroposophically extended medicine Ayurveda Community-based health care practices Environmental medicine Homeopathic medicine Latin American rural practices Native American practices Natural products Naturopathic medicine Past life therapy Shamanism Tibetan medicine Traditional Asian (Oriental) medicine Biolectromagnetic Applications Blue light treatment and artificial lighting Electroacupuncture Electromagnetic fields Electrostimulation and neuromagnetic stimulation devices Low-level laser Magnetic resonance spectroscopy Diet, Nutrition, and Lifestyle Changes Changes in lifestyle Diet Macrobiotics Megavitamins Nutritional supplements Herbal Medicine Echinacea (purple coneflower) Ginger rhizome Ginkgo biloba extract Ginseng root Wild chrysanthemum flower Witch hazel Yellow wood
Manual Healing Acupressure Alexander technique Aromatherapy Biofield therapeutics Chiropractic medicine Feldenkrais method Massage therapy Osteopathy Reflexology Rolfing Therapeutic touch Trager method Zone therapy Mind-Body Control Art therapy Biofeedback Counseling Dance therapy Guided imagery Humor therapy Hypnotherapy Meditation Music therapy Prayer therapies Psychotherapy Relaxation techniques Support groups Virtual reality Yoga Pharmacologic and Biologic Treatments Antioxidizing agents Cell treatment Chelation therapy Metabolic therapy Oxidizing agents (ozone, hydrogen peroxide)
Office of Alternative Medicine Since its inception, the Office of Alternative Medicine has served certain important functions that have helped to legitimize some modalities of alternative medicine. Most notably, it has served as an institution that compiles data and serves as a granting agency for sponsoring some of those research projects. Other functions are outlined as follows8: 1. To provide and evaluate a research database. The research database program provides a framework for identifying and organizing scientific literature on alternative medical practices. This literature has grown to more than 100,000 specific citations on complementary and alternative medical topics. Currently, the program is involved in implementing a process of developing systematic reviews and meta-analyses of the alternative medicine scientific literature. 2. To serve as a clearinghouse of alternative medicine data. The agency disseminates information to the public, the media, and health care professionals to promote awareness and to provide education about alternative medical research. 3. To optimize media relations. The media relations section provides accurate coverage and subsequent follow-up of
4.
5.
6. 7.
relevant stories on alternative medicine to the news media and provides information about the Office of Alternative Medicine and its activities for mass media audiences. To facilitate sponsored research. Shortly after its inception, the agency provided 30 grants to fund research applications to study different aspects of complementary and alternative medicine. To create and fund alternative medicine specialty research centers. The agency has funded 10 specialty research centers designed to study complementary and alternative medicine treatments for specific health conditions. To facilitate an international and professional liaison program that participates in and promotes cooperative efforts in research and education. To organize intramural research training. This program allows scientists to conduct basic and clinical research in alternative medicine and supports postdoctoral training for appropriate candidates. The agency also evaluates specific alternative medical modalities by other institutes and centers within the NIH structure. Furthermore, several other governmental agencies interact with the Office of Alternative Medicine, including the Health Care Finance Agency, the Food and Drug Administration, the Agency for Health Care Policy and Research, and the Centers for Disease Control and Prevention.
Chapter 127—Alternative Pain Medicine
Scope In an attempt to determine prevalence, costs, and patterns of use of alternative medicine in the United States, Eisenberg et al3 demonstrated that alternative modalities are used not only for chronic pain but also for cancer, arthritis, acquired immunodeficiency syndrome (AIDS), gastrointestinal problems, chronic renal failure, and eating disorders. Among the commonly used therapies were the following: n n n n n n n
n n n n n n n n n n n
Relaxation techniques Chiropractic manipulation Massage Imagery Spiritual healing Promotional weight loss programs Lifestyle diets (e.g., macrobiotics, herbal medicine, megavitamin therapy) Self-help groups Energy healing Biofeedback Hypnosis Magnetic therapy Low-power laser therapy Homeopathy Acupuncture Folk remedies Exercise Prayer
More than 60% of the patients who used unconventional therapy did so without medical supervision and without active consultation with a provider of either conventional or unconventional therapy. The medical conditions for which most patients sought alternative therapy included back pain, allergies, arthritis, insomnia, sprains, strains, headaches, high blood pressure, digestive problems, anxiety, and depression. Most of the medical conditions listed here are associated with some form of chronic pain. Another criterion for considering the efficacy of alternative therapeutic modalities is based on reimbursement by either patients or third-party payers. Reimbursement for alternative therapy in 1990 was approximately $11.7 billion. Although this criterion is not a scientific index of efficacy, the magnitude of this sum of money does highlight the importance that patients placed on these modalities. Thus, unconventional or alternative medicine has a major presence in the health care system of the United States. The magnitude of this presence may be underestimated by conventional health care providers, but in 1990, approximately 22 million persons in the United States used alternative therapy modalities as a means of treating their health problems. Occasionally, these methods are used simultaneously with conventional medicine. A satisfying observation is that most users of alternative therapy do not replace conventional therapy with alternative techniques but rather use those alternative therapy modalities as adjuncts to conventional therapy. For example, few patients use alternative therapy modalities for the treatment of high blood pressure or digestive problems. This finding suggests that patients have been satisfied with the validity and efficacy of conventional therapy for these ailments. Yet many patients do use alternative medicine for the treatment of chronic back pain, headaches, arthritis, strains, or sprains.
937
As a part of the medical evaluation of patients with chronic pain, an attempt should be made to determine whether the patient is receiving alternative therapy and the frequency, amount (units), or intensity with which that particular modality is used. Currently, medical students are being taught very little about unconventional alternative therapy.9 Perhaps including some information about the subject in the medical school curriculum not only may broaden physicians' outlook on what patients are seeking but also may provide the sensitivity necessary to evaluate these modalities scientifically.
Alternative Therapy Modalities Many unorthodox modalities may be effective in patient care. The laws of consumerism may be influential in dictating not only the popularity but also the longevity of various medical modalities directly related to their therapeutic efficacy. Thus, patients seldom seek an alternative modality for a fractured bone because the conventional orthopedic maneuvers for treating a fractured bone are associated with satisfactory results. Many conditions do not respond to conventional therapy, and, in frustration, patients are prompted to seek alternative therapy even if the therapeutic efficacy of the alternative modality is not established. Some patients with cancer pain who receive satisfactory results and for whom death is imminent may seek not only unconventional treatments but also risky ones out of desperation. Many of the alternative and unconventional therapies do not fit the Western medical paradigm. More research is needed to evaluate the most widely used modalities. Although it is impossible to describe all the modalities used in alternative medicine, a few have been arbitrarily selected and are discussed here.
Music Therapy In a study of 30 women with chronic pain secondary to rheumatoid arthritis, Schorr10 demonstrated that chronic pain may be effectively controlled using music as a unitarytransformative intervention. Pain measurements used in the study were obtained from the Pain Rating Index rank (PRI-R) of the McGill Pain Questionnaire. Hanser11 also described the effective use of music as a distraction during lumbar punctures. Unfortunately, this study was a series of anecdotal reports and was not a scientifically conducted investigation. Nevertheless, it is reasonable to propose that for some patients with welldefined disorders, music therapy may not be effective by itself but can be a useful adjunct to conventional modalities for pain management.
Intercessionary Prayer and Spiritual Healing Several claims have been made regarding the effectiveness of intercessionary prayer, spiritual healing, divine intercessions, and meditation in controlling chronic pain.12 Certainly, it is not good medical practice for providers to be arbitrary about patients' respective spiritual or religious persuasions. In fact, those persuasions may be passively supported as long as they do not interfere with the delivery of medical care necessary for treatment. Many anecdotal reports regarding the efficacy of those modalities have been made, but few scientifically controlled studies have been done to determine efficacy.
938
Section V—Specific Treatment Modalities for Pain and Symptom Management
Sundblom et al,13 in a well-conducted clinical trial, demonstrated that spiritual healing was not only harmless but also subjectively helpful in managing patients with idiopathic chronic pain syndrome. In this study, 24 patients with idiopathic chronic pain were randomly assigned to 1 of 2 groups. One group received spiritual healing, and the other received no active treatment. All patients had passed a pretreatment psychological interview. The main outcome measures used included Visual Analog Scale, International Association for the Study of Pain (IASP) database outline, and various psychological measures. Patients were evaluated at baseline and 2 weeks after treatment and were studied over 11⁄2 years. A final assessment was performed at 1 year after treatment using a modified IASP database outline, and it revealed a minor decrease in analgesic drug intake and an improvement in the sleep pattern in patients treated by the spiritual healer. The group exposed to spiritual healing also experienced a decrease in the feeling of hopelessness and an increased acceptance of psychological factors as reasons for pain. One half of the treated patients believed that spiritual healing gave them satisfactory pain relief. Although this therapeutic approach is not effective for everyone, for selected patients, particularly those with terminal illness, spiritual healing may be used as an adjunct to conventional treatment if the patient or the family requests it.
Relaxation Therapy Relaxation therapy is a well-established psychogenic modality for managing chronic pain. Several variations of relaxation strategies have been used. Jacobson's progressive muscle relaxation techniques14 have been widely used to manage chronic pain syndromes, particularly myofascial pain syndromes, including low back pain. The use of relaxation to promote comfort and pain relief in patients suffering from advanced cancer pain was demonstrated to be effective by Sloman et al.15 Relaxation strategies, including deep breathing, muscle relaxation, and imagery, were tested as a nursing intervention for the promotion of comfort and pain relief in a group of hospitalized cancer patients. This intervention was implemented in accordance with Oren's self-care approach to nursing practice. Sixty-seven cancer patients were randomly assigned to 1 of 3 groups to receive relaxation training by audiotapes, live relaxation training by nurses, or no relaxation training at all. The relaxation training was administered twice a week over a 3-week period. All patients were tested before and after the study using the McGill Pain Questionnaire and the Visual Analog Scale for pain. Analgesic medication administered to the patients who received relaxation training led to significant reduction in subjective pain ratings, and nonopioid, as-needed (prn) analgesic intake also decreased significantly, a probable reflection of a reduced incidence of breakthrough pain. The study suggests that relaxation techniques can be effective in management of chronic cancer pain, especially when the techniques are used concurrently with conventional modalities.
Hypnosis Until recently, certain modalities were considered unconventional. With their widespread acceptance not only by the patient population but also by the medical establishment,
these formerly unconventional modalities have now become conventional. Unfortunately, at times they have not undergone the clinical trials necessary to be considered truly conventional. Hypnosis and acupuncture may fall into this category. Some well-established medical interventions, including surgical procedures, would not be used in clinical practice today if rigorous clinical trials had been instituted. A good example is the use of epidural steroids for chronic diskogenic back pain. The use of epidural steroids rapidly became widespread, although few well-conducted scientific studies were carried out to evaluate the efficacy of this approach.16 Hypnosis has been used with sufficient frequency to warrant investigation. Unfortunately, some providers of hypnotic therapy are not necessarily competent in the method's principles, applications, and nuances.17 This is precisely the danger of using a modality that has not been rigorously subjected to peer review evaluations. Hypnotherapy or hypnotic relaxation has been used as a sedative for medical procedures such as colonoscopy. Although colonoscopy is not exquisitely painful, it is associated with significant emotional and physical discomfort. Cadranel et al18 investigated the usefulness of hypnotic relaxation in 24 patients scheduled for colonoscopy in whom other forms of anesthesia were not available. Using hypnotic relaxation before the procedure resulted in moderate to deep sedation in 12 of the 24 patients. In the patients for whom hypnosis was successful, the pain and discomfort from the colonoscopy were less intense than in the patients for whom hypnosis was unsuccessful. All patients who received successful hypnotherapy were able to undergo colonoscopy uneventfully, whereas only 50% of the patients who did not receive hypnotic relaxation were able to undergo the procedure. All the patients in the successful group agreed to another examination under the same conditions using hypnotic relaxation, whereas only 2% of the patients in the unsuccessful group agreed to have hypnotic relaxation as the primary means of sedation after their experience. This study suggests that in a subgroup of hypnotizable patients, hypnotic relaxation may be a safe alternative to drug sedation for colonoscopy and related procedures.
Chiropractic Therapy The use of chiropractic therapy is widespread in the United States and is legal. No doubt it has a place in the management of musculoskeletal dysfunction and various myofascial pain syndromes. This modality has continued to develop, and, properly conducted, it can be effective. Although research into chiropractic therapy is not very widespread, the method is said to be much more effective than other conservative approaches, including bed rest, medication, physical therapy, and massage therapy. Unfortunately, in many instances chiropractic practitioners and medical practitioners have not been able to work together for the good of the patient with chronic musculoskeletal dysfunction. Indeed, inappropriately applied and incompetently administered, chiropractic therapy can be dangerous in some patients and may lead to a worsening of the patient's general condition. A classic case in point is the application of chiropractic measures for the management of back pain in a patient not recognized as having multiple myeloma or metastatic prostate cancer. By the time the
isdiagnosis is recognized, major and irreversible harm may m be done. In an ideal situation, chiropractic therapy would be administered to a patient in conjunction with and concurrent with conventional medical treatment.
Comfort Measures In addition to its being a science, medicine is also an art. In today's busy practice, physicians may appear to be uncaring, arrogant, and inattentive to a patient's real needs. The application of comfort measures goes a long way toward making patients feel comfortable and optimizing their immunosuppressant mechanisms to promote rapid healing and recuperation.19 Buchko et al20 demonstrated that comfort measures in breast-feeding primiparous women are very effective in treating postpartum nipple pain. This same principle may be applied to numerous relatively minor but uncomfortable procedures such as bone marrow biopsy, burn dressing changes, acquisition of vascular access, and cataract surgery. When properly applied, these comfort measures may obviate the need for pharmacologic intervention and may help to introduce a soft touch into a medical experience that may appear cold and uncaring.
Transcutaneous Electrical Nerve Stimulation Initially, transcutaneous electrical nerve stimulation (TENS)21 was thought of as a primitive alternative therapy modality. Its popularity increased after the publication of the gate control theory by Melzack and Wall.22 In fact, a proposed mechanism of action is that electrical stimulation of A-alpha and A-beta fibers suppresses nociception transmitted by A-delta and C fibers. Many published studies have shown the efficacy of TENS in the management of large numbers of pain syndromes,23 including myofascial, neuropathic, and cancer pain.24 Today, TENS is no longer considered an alternative modality and is, in fact, well established as a conventional medical modality for the treatment of chronic pain.25 Two other variants of TENS that have not been well studied are high-frequency external muscle stimulation (HF) and percutaneous electrical nerve stimulation (PENS).
Acupuncture Acupuncture has been used for more than 2000 years. It is based on various Chinese scientific principles that are not understood or taught in most Western medical systems, including the United States. Many publications have attested to the efficacy of acupuncture,26 and it is clear that acupuncture does control pain in selected patients. However, patient selection must be meticulous because some patients are more predisposed to benefit from acupuncture than are others. Many other intrinsic factors contribute to the success or failure of acupuncture.27 The tragedy of acupuncture in the United States or in a Western context is that very few practitioners are adequately trained to use this modality effectively.
Biostimulation Techniques Biostimulation techniques include the following: Acupressure Auriculotherapy n Vibration therapy n n
Chapter 127—Alternative Pain Medicine
939
Magnetic field therapy Low-power laser stimulation n Movement therapy n n
A major reason for the popularity of these modalities is that they are usually noninvasive and, in appropriate patients, may be beneficial adjuncts to conventional therapy. In a study of 24 patients with chronic pain, Guieu et al28 demonstrated that TENS therapy and vibration therapy, whether used singly or jointly, were more effective in providing long-lasting analgesia as compared with sham stimulation or placebo.
Magnetic Field Therapy First proposed by Franz Mesmer of Austria, magnetic stimuli and magnetic fields have been used medicinally since the 16th century. Mesmer's theories were investigated by a Royal Commission chaired by Lavoisier, whose recommendations were not favorable to the continued use of magnetic therapy. Since that time, magnetic field therapy has been practiced mainly by charlatans. In the early twentieth century, orthopedic surgeons often used magnetic therapy to correct malunion of long bone fractures. At that time, it was safer to use magnetic therapy than orthopedic surgery for long bone fractures, which were usually associated with osteomyelitis. Many claims have been made regarding the efficacy of magnetic field blocks and magnetic fields,29 but these have not been evaluated scientifically. To determine the efficacy of magnetic fields, Parris et al30 investigated the chronic pain animal model (rat) using the sciatic nerve ligation or chronic constriction injury. The objective was to determine whether repeated pulsating magnetic field therapy (PMFT) would affect hyperalgesia and spinal cord, brain, and plasma levels of substance P, met-enkephalin, and dynorphin after chronic constriction injury of the rat sciatic nerve. In this study, the rats were exposed daily to 180 g and 30 Hz for 1 hour. Control rats were exposed to a device in which the magnetic fields were not activated. The magnetic fields significantly increased the delay of hind paw withdrawal and decreased the duration of the evaluation on the side of the chronic constriction injury. Magnetic field therapy did not alter the behavioral pain response in sham rats. The findings also demonstrated that dynorphin levels were greatly elevated in the spinal cord on the side of the constriction injury as compared with the contralateral (unligated) side in animals with chronic constriction injury. No significant changes were noticed in met-enkephalin and substance P levels. The study showed that magnetic field therapy reduces hyperalgesia induced by chronic constriction injury of the sciatic nerve in the rat model of chronic pain. These basic science studies are important to help investigate purported mechanisms of analgesia in various alternative modalities. Furthermore, this study suggests that magnetic field therapy may be effective in various forms of neuropathic pain.
Low-Power Laser Therapy Parris et al,31 using the same animal model described for magnetic field therapy, investigated the effect of low-power laser on neuropathic pain. No biochemical or behavioral changes resulted. This finding illustrated that low-power laser therapy is not effective for neuropathic pain; however, this modality has been effective for myofascial pain.32
940
Section V—Specific Treatment Modalities for Pain and Symptom Management
Conclusion Conventional medicine teaches that it is reasonable and prudent to reexamine and reuse old techniques and old drugs for new applications. Examples of these principles include the use of aspirin not only for the prevention of heart disease but also for the management of myocardial infarction. The use of gabapentin, an anticonvulsant and antidepressant medication, to treat chronic neuropathic pain syndrome is another example of that principle. As investigators evaluate new techniques and new drugs, it is also appropriate to evaluate alternative medicine practices. This assessment must be done scientifically and fairly, however, not in response to commercial interests but in accordance with scientific principles. To accomplish that goal, the Office of Alternative Medicine has been invaluable, not only to the field of pain medicine but also to patients in general. Many aspects of conventional and traditional medicine possibly would be condemned if they were subjected to rigorous scientific scrutiny. The scientific evaluation of alternative medicine may reveal tremendous benefits to patients with chronic pain. It is hoped that just as regulations and safeguards exist for conventional medicine, similar governmental safeguards and regulations will govern alternative and complementary medicine. In this ideal scenario, the
appropriate federal, state, and local societies, the different medical organizations, the Food and Drug Administration, and the various agencies within the Department of Health and Human Services, the Drug Enforcement Agency, and the other centers and divisions of the NIH will help to support the burgeoning field of alternative medicine using their respective expertise, to ensure that patients are not exploited but, instead, are served with some degree of efficiency and integrity. Although practitioners of alternative medicine have no rigid guidelines to follow at present, ideally some regulation will be provided under the leadership of responsible clinical organizations and with direct, or indirect, governmental oversight. The future appears bright for alternative medicine. It is hoped that, with an unbiased, creative, and honest approach to evaluating alternative medicine modalities, beneficial agents and techniques will be promoted so that patients with chronic pain unresponsive to conventional therapeutic modalities may have the option of using approved alternative medicine modalities for pain control.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
128
V
Limitations of Pharmacologic Pain Management Richard B. Patt and Steven D. Waldman
C h ap t e r O u t lin e Risk-to-Benefit Ratio 941 Pharmacologic Dichotomy: Cancer Pain and Chronic Nonmalignant Pain 941 Cancer Pain 941 Chronic Pain 942
Role of Invasive Procedures 942 Cancer Pain 942 Chronic Pain 942
Advantages of Pharmacotherapy for Cancer Pain 942 Limitations of Pharmacotherapy for Cancer Pain 942
Risk-to-Benefit Ratio
All medical interventions are associated with risks and benefits that, when considered together, constitute that intervention's risk-to-benefit ratio. Alternatives exist for all interventions (including no intervention), and these alternatives also possess their own risk-to-benefit ratios. Clinical decision making involves comparing and contrasting the risk-to-benefit ratios of alternative interventions (relative risk-to-benefit ratio). The risk-to-benefit ratio is multiply determined and is usually inexact. It is, in part, intrinsic to a given therapy, and it also, in part, depends on the clinical situation for which treatment is under consideration. How the risk-to-benefit ratio is determined or interpreted is influenced by numerous factors, some of which are difficult to quantitate (e.g., provider bias, patient preference) or have an ambiguous value (e.g., cost, patient suffering). As a result, the perceived risk-to-benefit ratio may differ profoundly based on interrelated factors pertinent to the patient (e.g., age, overall health, functional status, ethnocultural and religious background), the physician (e.g., attitudes, beliefs, training, financial incentives), and the system (e.g., regulatory forces, facilities, economic factors). The risk-to-benefit ratio is not a fixed entity but instead varies as these factors and their relationships with each other change over time. This situation is further complicated when applied to the treatment of pain because as a result of the subjective nature of pain and the newness of pain management as a specialty, data regarding the outcomes of even accepted © 2011 Elsevier Inc. All rights reserved.
Limitations of Pharmacotherapy for Noncancer Pain 943 Specific Limitations 943 Dose-Limiting Side Effects 943
Specific Situations 943 Neuropathic Pain 943 Movement-Related Pain (Breakthrough or Incident Pain) 943 Narrow Therapeutic Window: Cachexia and Advanced Age 944 Suffering 945 Abdominopelvic Pain 945
Conclusion 945
i nterventions are scarce. In the past, this allowed for wide latitude in decision making. However, increased scrutiny of health care costs is likely to be associated with greater constraints on decision making.
Pharmacologic Dichotomy: Cancer Pain and Chronic Nonmalignant Pain Cultural and social forces have profound influences on therapeutic decision making regarding the treatment of pain with medications. A curious but contextually understandable dichotomy exists with respect to the treatment of pain of malignant versus nonmalignant origin with opioid analgesics.1
Cancer Pain Until relatively recently, opioids were avoided for all but the most desperate medical conditions. This stigmatization was based more on cultural bias than on medical fact. Initiatives emphasizing the concept of comprehensive cancer care mandate attention to symptom control throughout the course of a malignant illness.2 Contemporary approaches to managing pain in cancer patients emphasize earlier and more liberal use of opioids, and investigators cite a low potential for addiction and a generally favorable risk-to-benefit ratio.3,4 A review of the literature suggests that these principles are grounded firmly in science. 941
942
Section V—Specific Treatment Modalities for Pain and Symptom Management
Chronic Pain Opioids were long considered taboo as treatment for chronic nonmalignant pain.5,6 These concerns were mostly grounded in beliefs about the inevitability of addiction and typically reflected not just medical concerns but moral views as well. In light of data generated by opioid use in cancer pain, the prohibition of opioid therapy for noncancer pain has been called into question. A spectrum of opinion currently exists regarding the advisability and proper methodology for prescribing opioids in such patients. Although both proponents and detractors cite data that support opposing views, investigators agree that opioid therapy is more beneficial than harmful in a proportion of patients with chronic nonmalignant pain. Although reasonable scientific support exists for this general contention, support for guidelines to determine the risk-to-benefit ratio prospectively in individual cases remains empirical.7,8
Role of Invasive Procedures In the treatment of both cancer and noncancer pain, evidencebased support of the role of interventional pain-relieving modalities is less well defined than is support for the use of drugs. The situation is analogous to that of opioids for nonmalignant pain. Although fairly widespread agreement exists that procedures sometimes possess favorable risk-to-benefit ratios, a uniformly accepted, validated methodology is lacking for prospectively determining which settings are valuable for certain procedures.
Cancer Pain Although the use of interventional pain management modalities in the treatment of cancer pain has been well accepted in the clinical arena for decades, the more recent aggressive use of systemic opioids and adjuvant analgesics combined with the increased use of the spinal administration of opioids has reduced the frequency of neurodestructive procedures in the management of cancer pain.9,10 Certain procedures, such as celiac plexus neurolysis, radiofrequency lesioning of intercostals nerves, transsphenoidal pituitary neurolysis, and gasserian ganglion neurolysis continue to have a significant place in cancer pain management.11,12
Chronic Pain Debate over the role of interventional procedures for chronic nonmalignant pain is, if possible, even more contentious that the debate over the use of these modalities for cancer pain management. Evidence has been cited supporting diametrically opposed views, and the quality of such evidence has legitimately been questioned. Factors influencing this debate are as noted previously but also include bias (even rivalry) among specialists, third-party and governmental payers, financial stake, and opiophobia. Limited reasonable agreement remains among these parties regarding when, and in whom, certain procedures provide sufficiently meaningful and durable pain relief to justify their risks and costs. Agreement exists that the outcomes for procedures are most favorable when they are “properly” integrated within a multidisciplinary matrix, although the evidence for even this conventional wisdom is
questionable. Because of the subjective nature of pain and the difficulty in blinding subjects to the administration or withholding of local anesthetics in nerve blocks, evidence-based outcomes will continue to remain elusive, although downward pressure on health care spending may make the matter moot.
Advantages of Pharmacotherapy for Cancer Pain For various reasons, oral opioid therapy is considered the treatment of choice for uncomplicated cancer pain. These reasons include the induction of analgesia that is reversible, titratable, and suitable for different types of pain, including multiple topographically distinct pains, generalized pain, and lack of invasiveness. Furthermore, the risk-to-benefit ratio of properly administered opioid therapy in this clinical setting further promotes its use.13 The need for specialized training is modest, and efficacy is maintained when treatment is modified to apply to individuals across cultures and over a range of ages and medical fitness.14
Limitations of Pharmacotherapy for Cancer Pain In 70% or more of cancer patients, pain relief is known to be achieved with uncomplicated oral or transdermal administration of opioids, especially when combined with nonsteroidal antiinflammatory drugs (NSAIDs) and adjuvant analgesics (e.g., antidepressants, anticonvulsants). Up to 30% of all patients with cancer pain, however, require alternative interventions to achieve comfort. The construct that opioids should be administered in doses sufficient either to control cancer pain or to produce unacceptable side effects is widely accepted because this class of drugs has no ceiling effect, unlike the NSAIDs and most adjuvant analgeics.9,13,15 Although the end points of opioid therapy (i.e., comfort and unacceptable side effects) are difficult to quantify, this view recognizes unacceptable side effects as one possible consequence of drug therapy. These side effects constitute the most important limitations of drug therapy for cancer pain. Several investigators have attempted to identify specific clinical findings that, when identified prospectively, signal that pain relief will be difficult to achieve by pharmacologic means alone. The best validated schema, the Edmonton Staging System, suggests that the presence of a history of alcohol or drug abuse or recent tolerance, neuropathic pain, psychological distress, and movement-related pain predict a relatively poorer prognosis for controlling pain pharmacologically, whereas drug dose and the presence of delirium are not predictive.16–18 Other investigations suggest that incident and movement-related pain (kinesophobia) is the only consistent predictor of poor outcome for pharmacotherapy.19,20 This constitutes an extremely important area for further study, especially with methodologies that target specific clinical pain syndromes. Experience suggests that syndromes such as tumor-mediated brachial and lumbosacral plexopathy, abdominopelvic pain, and pain from the skin ulceration that accompanies fungating tumors are among other daunting syndromes in which pain often persists despite aggressive drug therapy. Although no single feature reliably predicts failure of
Chapter 128—Limitations of Pharmacologic Pain Management
pharmacotherapy, the presence of these features should alert the clinician that additional resources may be needed to help manage pain effectively.
Limitations of Pharmacotherapy for Noncancer Pain The historical view that the use of opioids was prima facie undesirable for the management of chronic pain allowed for a ready determination of risk-to-benefit ratio, no matter how unscientific. Contemporary views that opioid therapy for noncancer pain is justified in selected patients call for a general reappraisal of risk-to-benefit ratio and carefully individualized decision making.21 The baseline limitations of drug therapy for nonmalignant pain include the same potential side effects that restrict drug use in cancer patients. Additional limitations in this population depend on the degree to which a given patient is perceived as being at risk for addiction and the degree to which the practitioner perceives opioid therapy as being potentially effective and appropriate.22–25
Specific Limitations Dose-Limiting Side Effects One set of limitations relates to the various collateral (nonanalgesic) effects of the analgesics. The most prominent side effects of the opioids are constipation, nausea, vomiting, cognitive failure (ranging from drowsiness to hallucinations), dysphoria, myoclonus, and pruritus, although other side effects such as respiratory depression occasionally supervene.3,13,20 Similarly, treatment with the NSAIDs and other adjuvants is limited by undesirable pharmacologic side effects such as gastropathy, bleeding, renal insufficiency, masking of fever, sedation, constipation, dry mouth, dysrhythmias, cognitive failure, ataxia, hepatic insufficiency, and bone marrow depression.15 Drug side effects, especially opioid, can often be managed effectively.13,20,26 Strategies for managing opioid side effects in cancer patients are depicted in Table 128.1. Side effects of simple analgesics, NSAIDs, and adjuvant analgesics may be more problematic and are in many cases less readily reversible.15,27–30 Thus, an important distinction between the opioids and other analgesics is that opioids have few absolute contraindications, whereas the other analgesics often need to be avoided altogether lest complications occur (e.g., aspirin in the patient with an ulcer, hypersensitivity, or bone marrow depression).27 Paradoxically, for long-term use, the opioids are both the most stigmatized of all analgesics and, on a physiologic basis, arguably the safest.
Specific Situations Besides the general category of dose-limiting side effects, certain clinical situations impose specific limitations or increased risks from pharmacotherapy. Only a few such issues are cited here.
Neuropathic Pain Somatic and visceral nociceptive pain typically responds linearly to escalating doses of opioid analgesics. In contrast, the dose-response relationship for neuropathic pain is often
943
Table 128.1 Strategies for Limiting the Side Effects of Opioids Strategy
Comments
Prophylaxis
This approach is used especially for constipation and sometimes for nausea
Patient education
Informed of the potential for side effects, patients are less likely to assume they are allergic and more likely to cooperate with efforts at palliation
Patience
Nausea and sedation are usually transitory and remit with time Slower titration may reduce troublesome side effects
Symptomatic management
Treat with antiemetics, laxatives, psychostimulants, etc.
Trials of alternative (related) analgesics
Efficacy: side effect profile of opioids is often idiosyncratic Trials of alternative opioids are indicated because of incomplete cross-tolerance
Trials of adjuvant analgesics
Side effects may result from reliance on opioids for a pain syndrome that is relatively nonresponsive to opioids Successful therapy with adjuvants may allow for a reduction in opioid dose with fewer side effects
Alternate treatment modalities
Judicious application of antitumor therapy, procedures, psychotherapy, etc., may permit dose reductions with fewer attendant side effects
blunted. Treatment in higher dose ranges is required, as a result of which side effects are more likely to be problematic. Although neuropathic pain syndromes were once considered an opioid-nonresponsive set of disorders, the range of response observed for these syndromes forms the basis for the concept of relative responsivity to opioids.31,32 Increasingly, neuropathic pain syndromes are successfully treated by an approach that uses maintenance therapy with low-dose opioids for the induction of partial analgesia, after which sequential trials of adjuvant analgesics are conducted in an effort to gain more complete analgesia.27–32
Movement-Related Pain (Breakthrough or Incident Pain) The tempo of chronic pain is most often one of continuous, unrelenting, low-grade basal pain, punctuated by episodic exacerbations that can be unpredictable but that are most often related to activity. These superimposed flares are generally referred to as breakthrough pain.33 The basal component of pain is typically treated with a long-acting opioid administered on a time-contingent basis (by the clock), such as an oral controlled-release formulation of morphine or oxycodone administered every 12 hours, a transdermal preparation of fentanyl applied every 72 hours, or—less commonly—methadone. Breakthrough pain is then treated with the symptom-contingent administration of a second,
944
Section V—Specific Treatment Modalities for Pain and Symptom Management
short-acting oral opioid administered as needed (immediaterelease morphine sulfate, hydromorphone, oxycodone, or oral transmucosal fentanyl citrate [OMFC]). The dose of longacting medication is then titrated based on the frequency and urgency of the requirement for as-required treatment of breakthrough pain. Breakthrough pain that has a relatively consistent temporal relationship with specific activities has come to be referred to as incident pain.19,20 Breakthrough pain that occurs at predictable intervals just before the next scheduled dose of an analgesic drug is referred to as end-of-dose failure. Breakthrough pain that appears to be idiosyncratic and unrelated to either activity or scheduled doses of analgesics is typically referred to as either spontaneous breakthrough pain or idiopathic breakthrough pain, or simply as breakthrough pain. Pain that is exacerbated with movement is among the most difficult to control with analgesics.20 The pharmacokinetic properties of currently available drugs, even those administered intravenously, are not well matched to the often unpredictable, rapid, and wide fluctuations in severity of movement-related pain. When incident pain is relatively unpredictable, rescue doses are provided prophylactically, approximately 30 minutes in advance of the pain-provoking activity. When unanticipated breakthrough pain occurs, the rescue dose should be taken as soon after onset as possible, independent of the timing of the basal dose. If these strategies are unsuccessful, the clinician should consider a trial of an alternative short-acting opioid or a change in the route of administration. Breakthrough pain that is predictable, infrequent, of mild or moderate intensity, or slow to develop can often be managed effectively with oral analgesics such as immediate-release (IR) morphine, hydromorphone, or oxycodone. Breakthrough pain that is severe or that occurs unpredictably, frequently, or precipitously may not be adequately relieved with currently available oral agents. Although intravenous and subcutaneous opioids are pharmacokinetically well suited for labile or severe breakthrough pain, these advantages are offset by the invasiveness of the route of administration. OTFC, a newer formulation of the established opioid analgesic fentanyl, has been approved specifically for the treatment of breakthrough pain that arises in patients already using around-the-clock opioids.34 A sweetened fentanyl-impregnated lozenge mounted on a stick, it is a noninvasive means of delivering a potent lipophilic opioid through the oral mucosa, thus facilitating rapid absorption into the circulation and analgesia of relatively fast onset and short duration. Extensive controlled research was conducted on the use of OTFC as a specific remedy for breakthrough pain. This research confirmed the safety of this agent and demonstrated its superior efficacy to routine oral agents in cancer patients receiving concomitant therapy with immediate-release and controlled-release oral opioids for basal pain. The onset of meaningful analgesia typically occurs within 5 minutes of beginning consumption of a unit, peaks approximately 30 minutes later, and usually lasts approximately 4 hours. The duration of analgesia is slightly prolonged because approximately one half of each fentanyl dose is inevitably swallowed and is subjected to hepatic first-pass effect. The availability of fentanyl in a lozenge form allows for easy self-administration and permits patients to titrate the dose to an effective level of analgesia without the need for injections. An intranasal formulation of fentanyl may be a reasonable alternative that may have a faster onset of action.35
Even with this addition to the treatment armamentarium, prominent incident pain remains a treatment challenge because opioid requirements vary dramatically over short intervals. Doses of opioids required to treat pain during periods of rest are typically inadequate when activity increases, and, conversely, doses required to ease movement-related pain may produce sedation and other side effects when the provocative activity decreases.
Narrow Therapeutic Window: Cachexia and Advanced Age Although many patients with cancer are not candidates for curative therapy, palliative and supportive care may extend life. Pharmacologically based pain control is often more difficult to achieve in patients with advanced cancer because concomitant asthenia and cachexia increase the likelihood of side effects from opioids titrated to therapeutic effect (narrow therapeutic window). The sedative effects of opioids can often be countered by the judicious use of psychostimulants, such as methylphenidate, which are usually administered at starting doses of 10 mg on awakening and 10 mg at the noon meal and can be titrated to effect.36 Although dysrhythmias and anorexia are theoretical concerns, they are rarely problematic, although psychostimulants should be avoided in the presence of an anxiety disorder or brain metastases. Limited epidemiologic data suggest that chronic pain is about twice as common for geriatric individuals living in residential settings than in their younger counterparts; the incidence in older persons ranges from 25% to 50%.37 Although underrecognition and undertreatment of pain in nursing homes are so rampant that statistics are often misleading, targeted surveys reveal an incidence ranging from 45% to 80%. Degenerative arthritis and other musculoskeletal disorders are the most prominent sources of pain in older patients, although herpes zoster, decubitus ulcers, peripheral vascular disease, temporal arteritis, and polymyalgia rheumatica are disproportionately common with advanced age.38–40 Because the incidence of almost all malignant diseases increases with advancing age, oncologic pain is a particularly common problem in the geriatric population. It is an especially important problem because many of the factors that cause cancer pain to be undertreated in the general population are amplified in aging patients. Although some degree of age-associated changes in organ function (including the central nervous system) are ubiquitous, with a few exceptions these changes ordinarily exert little influence on pain threshold or pain tolerance, although pharmacodynamics or pharmacokinetics may be somewhat altered. Loss of neuronal tissue and proliferation of glial cells occur with advancing age, but no evidence indicates impairment in processing pain signals unless dementia or delirium is clinically evident. Clinical lore suggesting that older patients do not experience pain as keenly as their younger counterparts is unfounded and is often no more than a rationalization for an unwillingness to spend the added time often required in assessing the older patient. The hospice experience has demonstrated that, when appropriate time and effort are applied, pain can usually be managed effectively even in the frail, older patient. However, drug titration should be performed with considerable caution, and, when possible, polypharmacy should be avoided.41
Chapter 128—Limitations of Pharmacologic Pain Management
Suffering Pain is determined in multiple ways and often persists as a result of unidentified psychosocial causes. Analgesics themselves are unlikely to reduce complaints of pain that are rooted in more global suffering. Psychotropic drugs combined with psychotherapy may, however, be effective in this setting.
Abdominopelvic Pain Factors specific to patients with abdominopelvic pain that reduce the likelihood of attaining adequate pain control with systemic analgesics alone are listed in Table 128.2. NSAIDs, even of the cyclooxygenase-2–selective type, may be poorly tolerated or contraindicated owing to gastropathy and to general factors such as renal insufficiency, coagulopathy, bone marrow
Table 128.2 Potential Limitations of the Pharmacologic Management of Abdominopelvic Pain Treatment Modality
Limitations
Nonsteroidal antiinflammatory drugs
Gastropathy Renal dysfunction Bone marrow depletion Concerns about masking fever
Oral analgesics
Xerostomia Dysphagia Malabsorption Obstruction Nausea Vomiting Coma
Transdermal analgesics
Dose requirements for opioids possibly exceeding limitations of dose form
Parenteral analgesics
Inadequate household or community support to manage infusions
Opioids
Ileus Partial obstruction Intractable constipation Reduced responsivity resulting from neuropathic component of pain Dose-limiting side effects resulting from asthenia and cachexia
945
suppression, and masking of fever. The oral route may be unreliable in the presence of gastrointestinal dysfunction (e.g., dysphagia, malabsorption, intestinal obstruction, nausea and vomiting, xerostomia, coma). Reduced gastrointestinal motility is a common upshot of tumor encroachment or a sequela of surgery or radiation therapy. Even with a strict bowel protocol, opioids may exacerbate ileus or partial obstruction in patients with reduced motility. In such cases, the use of opioids, except in low doses, is undesirable. Although visceral pain is relatively opioid responsive, patients often present with pain of mixed causes. Typically, pain resulting from nerve injury (neuropathic pain) is less sensitive to opioids, and thus occult microscopic deposits of perineural tumor invasion may contribute to reduced opioid responsivity. Early use of alternative routes of administration (e.g., transdermal, intranasal) may help to avoid many of the problems associated with abdominopelvic pain.34,35 Splanchnic, celiac plexus, and hypogastric plexus blocks are especially useful in this patient population.12,42
Conclusion Notwithstanding the controversy on opioids for chronic pain, data support the primary role of pharmacotherapy for managing most pain syndromes. Some patients do not derive adequate comfort from systemic drug therapy alone, however, or are not candidates for liberal use of opioids. Even for cancer pain, when addiction is less of a concern and liberal prescribing is widely endorsed, physiologic and psychological features sometimes hinder achieving an adequate pharmacologic remedy. The most formidable limitations of drug treatment relate to their potential to produce pharmacologic side effects or complications. Careful monitoring and the use of strategies for preventing and managing drug side effects are often all that is required to maintain efficacy. Specific patient-related factors (e.g., neuropathic pain, movement-related pain, psychological distress, cachexia, alterations in gastrointestinal function) are associated with greater likelihood of limitations. The degree to which a selected drug's potential to induce habituation is an impediment to long-term use remains a topic of considerable and heated debate.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
129
Psychological Interventions Jennifer B. Levin and Jeffrey W. Janata
CHAPTER OUTLINE Psychological Aspects of Chronic Pain 948 Pain and Depression 948 Pain and Anxiety 949 Pain and Personality Disorders 949
Psychotherapeutic Approaches 949 Operant Conditioning 949 Cognitive-Behavioral Therapy 950 Comprehensive Multimodal Treatment 950 Component 1: Assessment and Initial Conceptualization 951 Component 2: Moving Toward a New Conceptualization 951
A review of the understanding of pain throughout history suggests that theorists have vacillated between definitions that emphasize emotional aspects of pain and definitions that promote a more sensory, physiologic view. Aristotle believed that pain is a “passion of the soul,” an affective experience. Aristotle's view was generally embraced until Descartes proposed that pain is a pure sensory phenomenon, a view that has persisted, aided by the rapid advances in medical understanding of sensory systems.1 Currently accepted definitions of pain recognize the emotional and sensory elements; it is almost impossible to read a pain text without being reminded that the International Association for the Study of Pain defined chronic pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage.”2 Current practice often fails to adequately address these psychological aspects of chronic pain. This chapter describes the emotional and behavioral components of chronic pain. It reviews the psychotherapeutic strategies that can be combined with rehabilitative, medical, and interventional procedures. It also describes patients' obstacles to engaging in treatment and presents evidence for the effectiveness of including psychotherapy as an integral part of a comprehensive approach to the management of chronic pain.
Psychological Aspects of Chronic Pain Pain and Depression Pain and depression are among the most common conditions seen by practitioners. At any given time, it is estimated that 17% of patients seen in primary care complain of 948
Component 3: Education and Skills Development 951 Component 4: Generalization and Relapse Prevention 951
Treatment Effectiveness 952 Obstacles to the Treatment of Chronic Pain 952 Primary Chemical Dependency 952 Primary Psychiatric Disorder 952 Ongoing Litigation 953 Lack of Motivation 953
Conclusion 953
ersistent pain.3 Furthermore, approximately 13% of adults p in the United States lose productive work time as a function of a pain problem; this problem has a $61 billion economic impact on productivity alone.4 Depression often goes undiagnosed or is inadequately treated in this large group of patients and can impede the effective treatment of pain.5 Experienced pain clinicians attest to the frequency with which patients with chronic pain present with concurrent depressive symptoms. Studies have shown prevalence rates for depression in chronic pain to range from 10% to 100%,6 but most find that coexisting depression is at the higher end of probability and is the most frequent psychiatric diagnosis to accompany chronic pain.7 Depression is more common than anxiety or personality disorders in patients who develop opioid dependency,8 and depression has been found to play an influential role in the development of chronic pain and disability.9 Criteria from the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision, for diagnosing depression10 include marked changes in mood, anhedonia, insomnia or hypersomnia, weight loss or gain, fatigue, psychomotor retardation or agitation, difficulty with concentration or indecisiveness, feelings of worthlessness and guilt, and thoughts of death and suicidal ideation. Anhedonia is the loss of interest in things or activities that previously were pleasurable. Anhedonia often is reported by patients with pain, who describe that the pairing of pleasurable activities with pain renders the activities far less pleasurable and, as a result, much less likely to be pursued. Lewinsohn and Gotlib11 suggested that symptoms of depression may be related to the loss of positive reinforcement that pleasurable activities provide. Loss of activities, of interests, and of the often social context in which the activities are enjoyed may contribute to the depression experienced © 2011 Elsevier Inc. All rights reserved.
by patients with pain. Research evidence supports this relationship; a path analysis in an older population showed that pain contributes to activity restriction, which contributes to the development of depressive symptoms.12 Insomnia is a common complaint in patients with chronic pain; studies suggest that insomnia accompanies pain in 50% to 88% of patients with various pain conditions.13,14 Patients with chronic pain often complain that their pain interferes with the quality of their sleep, and clinicians naturally may attribute sleep dysregulation solely to the painful condition and may overlook the possibility that sleep problems may be symptomatic of depression. Patients with depression and insomnia experience greater affective distress, reduced sense of control, and greater pain severity. Insomnia without concurrent depression was found to be associated with increased levels of pain,15 and evidence indicates that sleep deprivation produces hyperalgesic changes. Sleep deprivation may impede the analgesic effects of opioids and of the serotonin reuptake inhibitor class of antidepressants.16 Evidence suggests that although patients complain to clinicians most prominently about pain, often their less emphasized depressive issues are causing patients the greatest distress. A study of patients with facial pain found that depressive symptoms correlated more highly with psychosocial and physical functioning than did pain.17 This study highlights the concern that clinicians may focus on treating the pain complaints while overlooking the depressive issues. As a patient's distress persists, clinicians are at risk to escalate the use of analgesics, which are not notably effective in ameliorating depression. The correlation of pain and depressive symptoms begs the question of which comes first: Does depression increase one's vulnerability to developing chronic pain syndrome, or does the presence of chronic pain increase one's likelihood of becoming depressed? Gamsa,18 in a review of the literature and study of patients with chronic pain, provided support for the notion that pain is more likely to create than be created by emotional distress. Similarly, a systematic review of the literature yielded evidence that depression is more likely a consequence than an antecedent of chronic pain.19
Pain and Anxiety Studies generally have shown a high incidence of anxiety disorders in patients with chronic pain. Using a structured clinical interview, one study20 documented an overall prevalence rate of 16% to 28% in a sample of patients with various diagnoses. Dersh et al21 summarized research suggesting that studies that have examined the lifetime prevalence of anxiety in chronic pain found rates similar to those noted in the pain-free population. Current prevalence rates are found to be significantly higher, however, in individuals with chronic pain. Among the anxiety disorders, panic disorder and generalized anxiety disorder seem to be most commonly diagnosed. A theory of the situational specificity of anxiety in pain was developed by Lethem et al,22 who articulated the fearavoidance model, which has been the subject of increased research interest. The model proposes that two factors mediate pain and disability. Fear of pain and hypervigilance to painful stimuli develop as patients attach catastrophic thoughts to the experience of pain. Subsequent avoidance of activity is driven by fear that engaging in activity would worsen pain or cause physical harm. This avoidance of activity serves as negative
Chapter 129—Psychological Interventions
949
r einforcement of the patient's fear. Fear-avoidance beliefs and fear of movement and consequent injury have been shown to predict physical performance and disability from pain.23
Pain and Personality Disorders Clinicians often find that their pain populations include a disproportionate share of difficult patients and describe personality difficulties rather than medical complexities. Researchers have examined the prevalence of character disorders in patients who complain of chronic pain. In a study of 200 patients with chronic low back pain, 51% met the criteria for one or more personality disorders. Paranoid personality disorder was diagnosed in 33% of the sample; borderline (15%), avoidant (14%), and passive-aggressive traits (12%) also were identified.24 Gatchel et al25 reported that 24% of their sample met the criteria for a personality disorder. A study of primary care patients who presented with a range of pain problems found that 25% of the small sample (n = 17) met criteria for borderline personality disorder.26 These studies suggest that Axis II disease is considerably more prevalent in patients with chronic pain than in the population as a whole. Effective pain management in patients with comorbid personality disorders may be possible, but research into the necessary treatment adaptations is lacking.
Psychotherapeutic Approaches Evidence-based psychotherapeutic approaches that have been shown to be effective for increasing function and decreasing levels of pain and emotional distress include the following: operant conditioning (behavioral therapy), developed in the late 1960s27; cognitive-behavioral therapy (CBT), which emerged in the early 1980s; and a comprehensive multimodal treatment approach28 that integrates these treatments into interdisciplinary teams.
Operant Conditioning The operant conditioning model is based on the principles of Fordyce et al.29–31 These investigators noted that patients with pain exhibited numerous pain behaviors, such as guarding, pain complaints, and grimacing. They also observed that patients with chronic pain exhibited passive, maladaptive behaviors, such as excessive rest, inactivity, a reduction in family and work responsibilities, and an overreliance on pain medications. The operant model assumes that individuals behave in certain ways according to reinforcement patterns. It follows that for patients with chronic pain, maladaptive pain behaviors are positively and negatively reinforced, whereas adaptive, well behaviors are ignored and extinguished. An example of positive reinforcement is attention from a spouse or coworker; examples of negative reinforcement are avoidance of household or work responsibilities and relief from pain by reliance on as-needed pain medication. As such, the treatment for such maladaptive patterns is to identify the environmental contingencies and restructure them such that the emphasis is on reinforcing active, adaptive coping skills and ignoring maladaptive behaviors until they extinguish or remit. Therapies that rely on the operant conditioning model use graded activity, social reinforcement, time-contingent medication management, and self-control skills training including self-monitoring, self-reinforcement, and relaxation training.32
950
Section V—Specific Treatment Modalities for Pain and Symptom Management
Studies have confirmed that operant conditioning is effective for increasing activity levels, exercise, and tolerance and for reducing the intake of pain medications. The direct effects on pain are less dramatic, however.33 Some researchers have noted that the efficacy of operant conditioning may have an alternate explanation—that cognition may be an active ingredient in the change process. Specifically, these investigators have suggested that the changes in environmental contingencies themselves may not be accounting for the improvement, but rather the way in which the patient perceives and interprets the changes may lead to progress.34 The reconceptualization of the operant conditioning model relies to a large degree on a broader paradigmatic shift in clinical psychology—the shift toward CBT.
Cognitive-Behavioral Therapy Similar to behavioral therapy, CBT uses numerous procedures to modify behavior, such as graded practice, relaxation training, homework assignments, and self-reinforcement. In contrast to behavioral therapy, CBT acknowledges the relationships among behavior, thoughts, and feelings and places an emphasis on modifying maladaptive thoughts and beliefs to alleviate emotional distress and reinforce behavior change. Although both behavioral therapy and CBT manipulate environmental contingencies, the purpose and path toward change differ. In CBT, the goal of these manipulations is to provide the patient with an opportunity to identify, question, reappraise, and restructure thoughts, feelings, behaviors, and physical sensations on which their belief system is built. CBT for chronic pain management draws to a large degree from the treatment and research literature for depression and anxiety disorders. This affinity stems from the observation that the emotional sequelae of chronic pain often include depressive symptoms related to loss of function, sleep disturbance, and a reduction in pleasurable activities. As such, the treatment of these aspects of pain symptoms employs the same techniques as those used by classic forms of CBT that have been found to be highly efficacious. These techniques include the use of pleasure schedules and identification of negative thought patterns in conjunction with cognitive restructuring. Parallels also may be drawn between the somatic focus, fear-avoidance paradigms, and attention to danger signals central to the development and maintenance of anxiety disorders and those seen in chronic pain–based disorders. As such, the behavioral interventions, such as graded exposure and relaxation training, and the cognitive components, such as behavioral experiments, cognitive restructuring, and coping self-statements, that have been found to be efficacious in the treatment of anxiety disorders34 can be applied effectively in the management of chronic pain.
Comprehensive Multimodal Treatment The specific procedures and interventions used in CBT should be separated from the theory behind the cognitivebehavioral approach. The theoretical underpinnings of the approach advocate an active, structured, problem-focused, time-limited, educationally based, scientific methodology that involves collaboration between the patient and the therapist. The specific CBT multidisciplinary model for pain management as outlined by Turk and Stacey28 includes an important
team rehabilitation approach. Although only the psychological components of the treatment are reviewed here, in the multimodal approach, CBT treatment goals are addressed and reinforced across disciplines. Fear of reinjury is addressed simultaneously in CBT, physical therapy, and occupational therapy and by the treating physician. In CBT, the focus is on identifying fear beliefs and understanding the relationships among the beliefs, behavior, and emotions and developing a hierarchy of fears for graded exposure. In physical therapy and occupational therapy, the patient has the opportunity to carry out the graded exposure. Finally, in the physicianpatient treatment relationship, the physician (1) reinforces the patient's active approach to pain management, (2) deemphasizes the role of narcotic and other analgesic medications, (3) eliminates as-needed medication, (4) works to stabilize the patient's sleep patterns, and (5) provides information that would contribute to more evidence-based thoughts and expectancies regarding reinjury. In this model, the consistency across modalities accounts for the added efficacy above and beyond that of single modalities.35 Keeping this idea in mind, this chapter addresses the process of CBT as it relates to pain management. The main objective of pain management is not to reduce pain, but rather to assist patients to learn to live healthier and more satisfying lives, despite the presence of pain and discomfort. Some pain reduction is a natural byproduct of the treatment and stems from increased conditioning and a reduction in focused attention on pain. As such, secondary goals are likely to include the following: taking more responsibility for one's health care, depending less on analgesic medication, and functioning better in occupational, familial, and social settings. The primary CBT objectives in pain management as outlined by Turk and Okifuji36 include the following: (1) facilitating a change in approach to pain and suffering from being overwhelming and “out of my control” to manageable and “within my control”; (2) teaching coping skills for the pain and problems stemming from the pain; (3) moving from a passive, helpless role to an active, resourceful role; (4) facilitating the understanding of the relationships among thoughts, feelings, and behaviors and being able to identify and modify maladaptive patterns; (5) strengthening self-confidence and taking credit for successes; and (6) facilitating the identification of problems and proactive problem solving to bring about maintenance of gains. The dominant theme of CBT to be reinforced across disciplines is the paradigm shift from taking a passive role, which leads to negative emotional, behavioral, and physical consequences, to taking an active role in finding the wherewithal to confront the pain and in doing so to “take back their lives.” The focus is on the following: (1) developing a more internal rather than external locus of control, as defined by the perception that the individual (internal management or selfmanagement), as opposed to outside sources (external or “fix me” approach), has control over the outcomes of his or her actions37; and (2) increasing self-efficacy, or an individual's belief in his or her ability to influence behavior, thoughts, and feelings38 as they relate to pain management. These two concepts, although related, are not equivalent. To be successful, patients must maintain the belief that they hold the responsibility for their pain outcomes (internal locus of control) and develop a belief in their ability to carry out what is needed to reach the desired outcomes (self-efficacy).
Although no two CBT protocols look exactly alike, the overall conceptualization of pain and of appropriate treatment interventions has some consistency. Turk and Okifuji36 outlined six phases of CBT, including (1) assessment, (2) reconceptualization, (3) skills acquisition and consolidation, (4) rehearsal and application training, (5) generalization and maintenance, and (6) treatment follow-up. Similarly, Bradley39 and Johansson et al40 identified four essential components of CBT: (1) education, (2) skills acquisition, (3) behavioral rehearsal, and (4) generalization. Given that assessment, conceptualization, and skills development are part of an ongoing process in the management of chronic pain, in this chapter four fundamental treatment components are discussed: (1) assessment and initial conceptualization, (2) moving toward a new conceptualization, (3) education and skills development, and (4) generalization and relapse prevention.
Component 1: Assessment and Initial Conceptualization The initial assessment incorporates information collected from the patient interview, medical records, family interview when available, and validated assessment measures. Areas for assessment include the following: (1) a complete history of the pain, including its location, severity, and duration, what has and has not been effective for the relief of pain, and patterns of pain and well behaviors including activity level and medication intake; (2) the degree and type of psychological distress, including depression, anxiety, and the relationship between pain and psychological distress; (3) behavioral patterns at home, work, and in social and recreational activities; (4) specific information regarding beliefs surrounding the pain, expectations for recovery, and functional goals; (5) a detailed work history; (6) the degree and character of social support, including the possible role of significant others in the maintenance of maladaptive behavior patterns and how to integrate these significant others into the paradigm shift; (7) addiction patterns and risk for addiction; and (8) incentives and disincentives for work, pain, and treatment, including financial consequences of long-standing pain, disability incentives for work-related injury, pending litigation, drugseeking behavior, and legitimate release from responsibilities. From the information gathered in the assessment phase, the patient-therapist team can begin to develop a conceptualization of the role of the pain for this individual, of the way in which pain affects his or her thoughts, feelings, and behavior, and of the elements that may be maintaining the system.
Component 2: Moving Toward a New Conceptualization This stage, comparable to Turk and Ofikuji's36 collaborative reconceptualization of pain, flows directly from the evidence gathered during the assessment phase. During this phase, the focus is on gradually moving the patient from a passive, helpless role in search of pain relief to an active, empowered role of increasing function and satisfaction. This paradigm shift is reinforced throughout the treatment process, starting as a concept that is discussed to one that is practiced and leads to a change in underlying beliefs about pain and the patient's role in managing it. This reconceptualization is most likely to be gradually internalized by the patient when it is adopted and reinforced by the entire treatment team, including the
Chapter 129—Psychological Interventions
951
sychologist, physician, and rehabilitation staff. This attip tude can be a particular challenge given that the physician and rehabilitation staff traditionally have approached pain management from a medical and physical perspective. To accomplish this challenging task, the CBT model first must gain acceptance from the team and requires ongoing communication among health care providers. This communication is essential because the patient naturally may fall back on the long-standing belief that pain results from purely medical causes whose management must be primarily medical. This conclusion is natural, given that the patient experiences the pain physically, but it must be disproved through the sense of efficacy and control that develops from the mastery of selfmanagement strategies introduced early in treatment.
Component 3: Education and Skills Development After developing a new conceptualization of pain management, one that places the patient in the driver's seat, it is important to provide the patient with the skills to manage pain successfully. The education and skills development focus on the continuous process of providing information and a forum for the learning and practicing of new skills for pain management. The emphasis is on skills to manage, rather than decrease, pain. These skills fall into the behavioral and cognitive realms. In the behavioral category, elements are likely to include positive coping skills, relaxation training exercises, pacing, graded exposure to feared situations, attention diversion techniques, and pleasant activity scheduling. In the cognitive category, elements are likely to include cognitive restructuring, or the identification and challenging of negative thought patterns that perpetuate negative emotions and subsequent self-defeating behaviors, coping skills such as positive coping self-statements, and behavioral experiments with the goal of gathering evidence to negate unfounded cognitions. Other skills that may be the focus of attention include assertiveness training, development of communication and social skills, and problem solving. These skills are individualized according to the strengths and deficits of each individual patient. Some of these skills may be best introduced and practiced in group settings because role playing and group feedback are likely to enhance the learning experience.
Component 4: Generalization and Relapse Prevention During the generalization phase, the focus is on practicing the skills developed and reinforced in session and across disciplines in the home and work environments. This practice is essential to the maintenance of treatment gains. Additionally, during this phase, relapse prevention is introduced. Essential elements in this phase include the following: reviewing and integrating material covered during treatment; evaluating and reinforcing treatment gains; identifying areas in need of strengthening; discussing ways to incorporate skills into one's daily routine and how to apply them to unexpected situations, stressors, and flare-ups; and addressing potential pitfalls and how to handle them should they occur. Follow-up booster sessions are carried out with increasingly longer periods between sessions. The goal of these sessions is to let the patients practice their new skills independently between sessions and selfreinforce for their efforts, yet have a place to continue to
952
Section V—Specific Treatment Modalities for Pain and Symptom Management
hone their skills and receive outside feedback and reinforcement. This stage is often a major factor in relapse prevention. Frequently, the more the patient improves, the more obstacles he or she must face. Return to work may require more advanced skills than increasing functionality at home. It may be only after taking “a break from treatment” that the patient can really test out how well his or her new skills work in the real world. The application of skills in a real-life situation with limited structure is in stark contrast to the highly structured rehabilitation environment.
Treatment Effectiveness How effective are these treatments and for whom? This discussion provides a brief overview of the efficacy research in this area. For a more comprehensive review of treatment outcomes, the reader is referred to McCracken and Turk.41 When reviewing the efficacy data, one should take into consideration the literature's limitations, which include the heterogeneity of pain syndromes studied and variable inclusion criteria, levels of specificity with regard to treatment components, and outcome measures. Studies also differ in their control of the complexity and variability of medical treatment. Much of the early efficacy research consisted of studies of patients with back pain; these investigators reported that operant conditioning was successful in increasing activity levels and in decreasing medication use in this population.42–45 In an attempt to tease out which aspects of operant conditioning were effective, Lindstrom and associates33 reported that graded activity led to a quicker return to work than did traditional medical treatment. Similarly, Turner et al46 found that graded activity was an effective component that contributed significantly to the positive outcomes of behavioral therapy. In a review of the literature, McCracken and Turk41 identified five different studies reporting a reduction in pain levels as a function of relaxation training. More recently, Vlaeyen et al23 studied the effectiveness of graded exposure to feared stimuli (in this case, exposure to particular physical movements previously avoided because of fear of pain), as opposed to an activation intervention. The results indicated that the graded in vivo exposure protocol was more effective in reducing pain-related fear and disability and increasing activity level than was the activation intervention. Keefe et al47,48 provided evidence for the efficacy of spouse-assisted treatment for improvement in pain, self-efficacy, psychological disability, and marital satisfaction. The clinical efficacy of CBT for the management of chronic pain has been supported in numerous studies with patient populations having headache, arthritis, temporomandibular pain disorders, fibromyalgia, irritable bowel syndrome, low back pain, complex regional pain syndrome, and heterogeneous chronic pain samples, among others.36 In an early metaanalysis, Malone et al49 reviewed nonmedical treatments, including 4 studies on cognitive therapy for various chronic pain conditions, and reported effect sizes ranging from 0.55 to 2.74. In a meta-analysis of 25 studies that met inclusion criteria, Morely et al50 found significant effect sizes on all outcome measures compared with waitlist controls. Compared with other active treatments, CBT produced significantly greater changes on measures of the pain experience, coping, and behavioral expression of pain. Overall, strong supporting evidence indicates that CBT is effective in reducing pain behavior
and coping. Results are less clear, however, with regard to work status, medication, or health care use, given that fewer studies have evaluated these variables.41 A meta-analysis of 65 studies of multidisciplinary treatment for chronic pain indicated that such treatments are more efficacious than no treatment, than a waitlist control, or than componential treatments made up of an isolated discipline such as medical treatment, physical therapy, psychological treatment, or occupational therapy alone.51 In Turk's52 more recent review of the work in this area, he concluded that multimodal rehabilitation programs are comparable to other pain treatments with regard to pain reduction. These programs have significantly better outcomes, however, for decreasing medication and health care use and for increasing function and activity level, return to work, and closure of disability claims and with significantly fewer adverse events. Turk52 indicated that such treatment is more cost effective than some of the more invasive medication interventions, such as spinal cord stimulation and surgery. Despite these positive outcome data, none of the existing treatments are efficacious for all patients. The following questions remain: What are the obstacles to treatment for patients who are not benefiting? Ultimately, how can treatment options for these patients be improved?
Obstacles to the Treatment of Chronic Pain Despite the demonstrated effectiveness of these psychological and behavioral approaches to chronic pain treatment, behavioral issues that may interfere with treatment require attention. Careful clinical assessment can identify the following challenges to successful outcomes and can allow clinicians to make informed judgments before proceeding with chronic pain management.
Primary Chemical Dependency Chronic pain complaints can mask a primary chemical dependency. Addiction affects approximately 10% of the population, and it may be overrepresented in populations with chronic pain. Although substance use disorders are beyond the scope of this chapter, clinicians should be aware that pain and addiction have many symptoms in common. Depression, sleep disturbance, anxiety, and disability in work, relationships, and activity are symptoms that are separately typical of pain and addiction.53 As such, careful addiction assessment should be an integral part of pain management, particularly in patients with a personal or family history of addiction. Although evidence suggests that addiction does not preclude effective pain treatment, practitioners should consider suspending treatment pending a thorough evaluation of any patient whose agenda may include the acquisition of pharmaceutical-grade substances. In a study of patients who were otherwise adherent to prescribed controlled substances in a carefully controlled pain practice, 16% were identified through random urine testing to be using illicit drugs.54
Primary Psychiatric Disorder Significant psychological and psychiatric issues accompany chronic pain. Patients with psychotic disorders, with significant dementia, with severe affective disorders, and, particularly, with
active suicidal intent are not good candidates for aggressive pain management. Although it is true that “even schizophrenics have bad backs” and should not be cavalierly dismissed from pain treatment, severe psychopathologic conditions should be addressed psychiatrically before pain management is reconsidered. Similarly, patients experiencing overwhelming life stresses other than pain are at risk to be emotionally or pragmatically unavailable to take an active role in their treatment.
Ongoing Litigation It has been axiomatic in chronic pain treatment that practitioners delay treating patients who have ongoing litigation or pending disability until the legal issue is resolved. Although specialty programs and clinics may have the luxury of postponing treatment, most primary care physicians do not. The concern is that patients recognize (or are told) that improvement in pain or in physical function may reduce or eliminate the monetary benefit that drives litigation and disability seeking. Many, if not most, patients who are pursuing legal remedies have honorable and conscientious motives and may cease their legal pursuits if the ability to function is restored. The difficulty the practitioner faces is in determining the motives of any particular patient. The research suggests caution. Blyth et al55 studied the effect of litigation on pain-related disability and found that past or present pain-related litigation was correlated significantly with higher levels of disability. Long-term follow-up of patients treated with a radiofrequency procedure showed a negative correlation between outcome and litigation status.56 Factors that mediate the relationship between pain complaints and litigation or pursuit of disability deserve considerable research attention.
Lack of Motivation A vexing issue for practitioners is to define for individuals experiencing pain the specific behavior changes that would lead to improvement in function and decreases in pain only to have the patient resist making the suggested changes. Despite the evidence supporting the effectiveness of cognition modification, exposure to feared stimuli, and increased productive
Chapter 129—Psychological Interventions
953
activity, some patients experiencing chronic pain do not engage successfully with treatment.57 Prominent among the approaches to addressing this apparent lack of motivation is the application of Prochaska and DiClemente's58 stages of change model to chronic pain. At its essence, the model proposes that individuals vary in their readiness to engage in behavior change, and that series of stages of readiness exist. In a typical variant of the model, the stages include precontemplation (in which no change is considered), contemplation (in which change is considered, but is not likely to occur in the near future), preparation (in which steps are being taken to make changes), action (in which behavior change is attempted), and maintenance (in which one works to sustain change). In addition to developing instruments to quantify readiness to change, researchers have begun to examine the utility of tailoring interventions to match specific stages.59–61
Conclusion Chronic pain is maintained by biologic, psychological, and social factors. Conceptual models and treatment strategies that solely emphasize sensory and organic aspects of pain are inadequate in addressing the complex problems presented by many patients with chronic pain. Evidence-based interventions require the inclusion of behavioral approaches as a component of a comprehensive interdisciplinary strategy. As treatment strategies have demonstrably become more effective, research efforts are needed to determine which specific interventions tailored to which patients for what particular problems in what social and environmental context are most efficacious. The research efforts designed to enhance treatment effectiveness for patients who fail to engage are particularly noteworthy. These studies represent important attempts to understand behavioral and psychosocial subgroups of patients within given physical diagnoses.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
V
130
Biofeedback Frank Andrasik and Carla Rime
CHAPTER OUTLINE Historical Considerations 955 Indications 955 Techniques 957 General Approach 957 Electromyography-Assisted Relaxation 957 Skin Conductance–Assisted Relaxation 957 Skin Temperature–Assisted Relaxation 958 Specific Approach 959 Adaptation 959
Biofeedback is a process that involves receiving information (feedback) about the body or self (bio). Applied biofeedback consists of monitoring and exerting influence to produce a change in the incoming information. Combing one's hair is an everyday example of applied biofeedback.1 An individual receives biofeedback on his or her physical appearance by looking in a mirror. Applied biofeedback, then, would be altering one's physical appearance and reflection in the mirror. In a clinical setting, biofeedback is accomplished through specialized equipment that provides information about physiologic responses occurring within the body (e.g., muscle activity, body temperature, sweat gland activity, heart rate). Obtaining accurate information about these processes would be difficult by simply looking in the mirror. The available feedback provided by proper instrumentation would then allow an individual to monitor and influence these physiologic responses. The term applied biofeedback, as it is used in a clinical setting, was introduced by Olson2 and encompasses the procedural operations and goals of biofeedback. Schwartz and Schwartz3 made some minor revisions to Olson's definition (indicated by the italic words in the following list). As a process, applied biofeedback is 1. a group of therapeutic procedures that 2. uses electronic or electromechanical instruments 3. to measure, process, and feed back accurately, to persons and their therapists, 4. information with educational and reinforcing properties 5. about their neuromuscular and autonomic activity, both normal and abnormal, 6. in the form of analogue or binary, auditory, or visual feedback signals. 7. Best achieved with a competent biofeedback profes sional, 954
Baseline 959 Reactivity 959 Recovery 960 Muscle Scanning 960 Muscle Discrimination 960 Practitioner and Patient Considerations 960
Side Effects and Complications 961 Conclusion 962
8. the objectives are to help persons develop greater awareness of, confidence in, and an increase in voluntary control over their physiologic processes that are otherwise outside awareness or under less voluntary control, 9. by first controlling the external signal 10. and then by using “cognitions, sensations, or other cues to prevent, stop, or reduce symptoms.”3 Components 1 through 7 of this comprehensive definition depict the key procedures of biofeedback, whereas elements 8 through 10 depict the key goals of biofeedback. The primary goal of biofeedback is self-management of physiologic responses. This type of treatment emphasizes an active approach on the part of the patient to cope more effectively with pain and its associated symptoms.4 This active involvement can reduce pain-related disability by increasing a patient's confidence in the ability to prevent, manage, and cope with pain.5,6 In fact, patients who attribute improvements in therapy to their own efforts demonstrate better long-term maintenance than do patients who attribute their improvements to others, such as the interventions of health care providers.7 Dr. Bruno Kappes, who has specialized in applied psychophysiology and biofeedback since the 1970s, stated, “The self-efficacy created by learning to influence our psychophysiologic self-validates our mind's ability to direct our personal healing of the body.”1 This chapter on biofeedback outlines historical considerations of pioneers, research, and other growing fields that contributed to the development of biofeedback. Treatment indications and the efficacy of biofeedback are then addressed. The techniques section delineates three approaches of biofeedback, practitioner and patient considerations, and typical treatment procedures. Possible complications and side effects are also discussed. Biofeedback is often used in conjunction with a host of other self-regulation approaches (e.g., guided imagery, © 2011 Elsevier Inc. All rights reserved.
regulated breathing, autogenic training, and progressive muscle relaxation training, which are discussed in Chapter 132).
Historical Considerations Although yogis and other individuals from Eastern cultures have long been exerting voluntary control over their internal states, it was not considered possible in Western science until the 1960s. Before then, investigators had believed that organisms could not self-regulate visceral functions of internal organs of the digestive, respiratory, endocrine, and vascular systems because these functions were considered automatic and involuntary. In the 1960s, Dr. Neal E. Miller et al of Yale University in Connecticut countered this idea by pursuing research on this topic in the animal laboratory.8 Skeptics believed that so-called volitional control of an involuntary response could well be mediated by slight skeletal movements. To rule out skeletal movements as an alternative explanation for visceral reactions, much of the research was conducted on curarized rats. Curare is a paralyzing agent that prevents skeletal movement, and it was considered too dangerous for human research. Nonetheless, in the name of science, a courageous individual offered to be curarized. As recounted in Andrasik and Lords,1 Lee Birk, who was working with David Shapiro and Bernard Tursky at Harvard University in Massachusetts, volunteered for the risky experiment of being curarized in 1967. The outcome of such an experiment would determine whether autonomic activity could be operantly conditioned without skeletal muscle movement. The research was conducted safely, and the results were successful in indicating that human voluntary control over visceral organs was possible in the absence of skeletal movement. Later, Birk wrote, edited, and published Biofeedback: Behavioral Medicine (1973), the first medical book on biofeedback.1 The aforementioned pioneers conducted research that was considered unpopular at the time, but they were responsible for a paradigm shift regarding potential voluntary control in human physiology. While these individuals were paving the way for biofeedback, other areas of study such as psychophysiology, behavioral therapy, biomedical engineering, and cybernetics also contributed to the development of biofeedback. Psychophysiology is the study of the interdependent relationships between cognitive and physiologic variables. In 1965, David Shapiro offered the first class in psychophysiology, just 2 years before the pivotal research he conducted with Lee Birk. Clinical biofeedback is often considered a form of applied psychophysiology.9 In the twentieth century, behavior therapy was a growing field in psychology. This area of study was based on principles of learning, and investigators contended that a learned maladaptive behavior could be unlearned. Behavioral medicine was a specialized area within behavioral therapy that emerged in light of work on stress management and the physiologic stress response. The emphasis of behavioral medicine is on health behaviors associated with medical disorders.1,9 Many behavioral therapy techniques, such as shaping and reinforcement, are used in biofeedback. Biomedical engineering and cybernetics are two other fields that have contributed to biofeedback. Biomedical engineering supplied instruments that made monitoring physiologic responses possible. With the proper instrumentation, one could detect and monitor muscle activity, cardiac activity,
Chapter 130—Biofeedback
955
peripheral blood flow, blood pressure, sweat gland activity, and brain electrical activity. Cybernetics involves providing physiologic information, which is otherwise unavailable, to an individual in such a way that learning voluntary control of these responses can be achieved.1,9 Miller, Shapiro, and Birk among many others were early pioneers in biofeedback. The scientific approaches of psychophysiology, behavioral therapy, biomedical engineering, and cybernetics also assisted in the development of applied biofeedback. The Biofeedback Society of America was formed in 1968 by researchers dedicated to seeking empirical evidence for applied biofeedback. This organization is now called the Association for Applied Psychophysiology and Biofeedback (AAPB). It cosponsors the journal Applied Psychophysiology and Biofeedback (previously entitled Biofeedback and SelfRegulation), in which many studies on biofeedback can be found. The following section addresses the efficacy of biofeedback in terms of medical disorders.
Indications The AAPB organized two broad reviews of evidence-based research for biofeedback applications in general. The most recent10 used five efficacy levels, formulated by La Vaque et al,11 to evaluate and categorize the available research support. Level 1 findings are not empirically supported. Level 2 indicates biofeedback as possibly efficacious. Level 3 findings are probably efficacious. Level 4 signifies efficacious results, and level 5 represents efficacious and specific findings. Table 130.1 describes the criteria for each level of efficacy. Approximately 40 conditions were examined and sorted into one of the five levels according to these criteria. In some cases, the disorders were not sufficiently investigated, whereas in others, research was conducted but some negative results were reported. Among the disorders investigated in the latest broad review, some relate to pain. Table 130.2 summarizes the levels of efficacy for the pain disorders reviewed in Yucha and Montgomery10 and discussed in more detail in this chapter. Here, those applications accorded level 3 and higher are briefly reviewed. The AAPB, in conjunction with the International Society for Neurofeedback and Research (ISNR), commissioned a series of “white paper” evidence-based reviews that are being assembled by area experts and then sent out for peer review and eventual publication. These reviews are focusing on specific disorders and thus are more comprehensive. Three such reviews have appeared to date for pain: Crider et al12 for temporomandibular disorders (TMDs), Karavidas et al13 for Raynaud's disease, and Nestoriuc et al14 for r ecurrent headache. Thermal biofeedback and electromyography (EMG) biofeedback have been used for the treatment of chronic arthritis. Bradley15 and Bradley et al16 found a reduction in rheumatoid factor titer, pain behaviors, and self-reports of pain intensity with a treatment consisting of thermal biofeedback in conjunction with cognitive-behavioral therapy. This treatment was compared with participants assigned to a control condition and those who received social support only. Furthermore, another study found that EMG biofeedback decreased the duration, intensity, and quality of arthritis pain.17 A 2.5-year follow-up of the same participants found that these beneficial effects were maintained.18 A meta-analysis of 25 randomized controlled trials revealed similar support across several dimensions.19
956
Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 130.1 Criteria for Levels of Efficacy Level 1: Not Empirically Supported The reports supporting this level are anecdotal or non–peer-reviewed case studies. Level 2: Possibly Efficacious The reports supporting this level include at least one statistically sound study, but without random assignment for a control condition. Level 3: Probably Efficacious The reports supporting this level consist of multiple observations, clinical studies, controlled/wait list conditions, and within-subject replication. Level 4: Efficacious The reports supporting this level include studies in which the treatment under examination is statistically significant and superior in comparison with a randomly assigned no-treatment control group, a different-treatment group, or a placebo group. The inclusion criteria for a special population are reliable and operationally defined. Outcome measures associated with the problem are valid. The procedures in the study are described in such a way that other independent investigators are able to replicate the study. The superiority of the treatment under examination has been indicated in at least two independent studies. Level 5: Efficacious and Specific The reports supporting this level include all the criteria for level 4 in addition to indicating superior statistical significance for the treatment under examination when compared with credible placebo treatment, medication, or a different treatment in at least two independent studies. From La Vaque TJ, et al: Template for developing guidelines for the evaluation of the clinical efficacy of psychophysiological interventions, Appl Psychophysiol Biofeedback 27:273, 2002.
Table 130.2 Efficacy Levels for Biofeedback Treatment in Pain Disorders Level 3 Arthritis Headache: pediatric Vulvar vestibulitis Level 4 Chronic pain Headache: adult Temporomandibular disorders
A randomized controlled investigation examined whether EMG biofeedback and cognitive-behavioral therapy were equivalent to vestibulectomy.20 All three interventions led to significant improvements in pain, sexual function, and psychological adjustment. Although the magnitude of improvement was greatest for the surgical procedure, several patients assigned to this condition refused to participate. Two less wellcontrolled investigations provided similar levels of support for EMG biofeedback combined with pelvic floor exercises (with regard to pain and discomfort during sexual activity).21,22 Biofeedback, either alone or in combination with other procedures, has been investigated for a wide range of chronic pain conditions, including endometriosis, recurrent abdominal pain, systemic lupus erythematosus, complex regional pain syndrome, osteoarthritis, phantom limb pain, advanced cancer, whiplash, and pain of the face, head, neck, and lumbar spine. The greatest focus has been on back pain, by using EMG biofeedback to treat muscle dysfunction and resultant reflexive muscle spasms that can develop and exacerbate pain. A metaanalysis of single and combined treatments found moderate evidence for EMG biofeedback as a separate therapy.23 EMG biofeedback has also shown equivalent benefits when compared with cognitive therapy.24,25 Additionally, Flor and
Birbaumer26 found that EMG biofeedback had better effects on different aspects of back pain and TMD when compared with cognitive therapy. These results remained consistent at a 2-year follow-up. Biofeedback combined with relaxation has been found to be of value in treating chronic pain in children and adolescents as well.27 Biofeedback as a treatment for headache, both tension-type and migraine, appears to be well validated,14,28 with an efficacy level of 4. The white paper review by Nestoriuc et al14 found blood volume pulse (BVP) biofeedback to be the most efficacious biofeedback procedure for remediating migraine headaches. BVP biofeedback involves monitoring blood flow in the temporal artery and providing feedback to teach patients how to decrease or constrict blood flow. This approach, as first envisioned by Friar and Beatty,29 can be thought of as the nonpharmacologic counterpart to an abortive agent. A review by the American Academy of Neurology U.S. Consortium, consisting of a panel of experts composed of representatives of the American Academy of Family Physicians, the American Academy of Neurology, the American Headache Society, the American College of Emergency Physicians, the American College of Physicians–American Society of Internal Medicine, the American Osteopathic Association, and the National Headache Foundation, accorded grade A to thermal biofeedback combined with relaxation training and EMG biofeedback in the treatment of migraine headache (and cognitive-behavioral therapy as well).30 Thermal biofeedback has been classified as a level 3 treatment for pediatric headache. After a review of the literature, Hermann and Blanchard31 concluded that thermal biofeedback produces clinically significant (≥50% reduction in headache) effects in approximately two thirds of the young participants. Thermal biofeedback is the modality most studied for Raynaud's disease (a primary condition) and Raynaud's phenomenon (a secondary condition). The most recent and largest study to date, comparing medication (nifedipine) with thermal biofeedback, EMG biofeedback, and placebo, found medication
to have the greatest effect.32 However, a close inspection of patients assigned to thermal biofeedback revealed that many patients did not acquire the necessary abilities to regulate their peripheral temperature.33 A white paper evidence-based review, selecting studies wherein patients were adequately trained to regulate hand temperature, provided sufficient support for assigning this treatment a rating of level 4.13 Finally, biofeedback as a treatment for TMDs has been classified as a level 4. Efficacy has been established through research with biofeedback, either alone34 or in combination with other treatments.35,36 Treatment reduces pain and pain-related disability while increasing mandibular functioning. A meta-analysis conducted by Crider and Glaros37 found that EMG biofeedback was better than no treatment or placebo control for selfreported pain. The mean improvement rate for the 13 trials in this literature review was 68.6% for biofeedback treatments compared with 34.7% for the control conditions. Another meta-analysis, included in a white paper review, analyzed 14 trials for biofeedback interventions for TMDs. This review concluded that EMG treatment and biofeedback-assisted relaxation are probably efficacious, whereas EMG in combination with cognitive-behavioral therapy is efficacious.12 The following section outlines the different approaches of biofeedback and addresses some of the detailed treatments discussed for the conditions in this section.
Techniques Biofeedback, as a self-management therapy, allows an individual to exert voluntary control over physiologic responses with the use of equipment that provides accurate measures. The emphasis is on active involvement. In fact, Yucha and Montgomery10 advised using the term biofeedback training in place of biofeedback treatment, to emphasize the active participation necessary for biofeedback therapy. This term also stresses the importance of patient education. A biofeedback practitioner (certified or appropriately trained) needs to coach the patient on what to expect and to assist the patient in reaching his or her goals with biofeedback. The two approaches to biofeedback are general and specific.4
General Approach The objectives of the general approach to biofeedback are to decrease overall arousal and to enhance a state of general relaxation. Three ideas underlie the association between generalized relaxation and pain reduction, as described by Andrasik and Thorn.38 The first idea is that a decrease in general arousal reduces peripheral sensory inputs in central processing. The second is that relaxation can reduce negative affect, which is linked to an increase in pain reports and a decrease in pain tolerance.39 The last idea is based on the observation of the relationship between stress and prolonged cortisol levels, in which activation of the stress response can increase the subjective nature of pain.40 A decrease in arousal thus would be beneficial for those experiencing pain. The general approach to biofeedback aims to reduce this overall arousal through the three “workhorses” of biofeedback.1 The three most commonly used methods are EMG-assisted relaxation, skin conductance–assisted relaxation, and skin temperature–assisted relaxation. Figure 130.1 shows a therapist explaining biofeedback-assisted relaxation to a child.
Chapter 130—Biofeedback
957
Electromyography-Assisted Relaxation Sensor placement for EMG is generally on the forehead, neck, or trapezius. A series of sensors, two active and one ground electrodes, is placed on any of these areas along the muscle fibers. The two separate circuits identify electrical activity. The resultant signal is the difference between each of the two active circuits, in which the amount subtracted out is regarded as noise. When a muscle contracts, electrochemical changes occur. The electrodes detect and process the ion exchange across the muscle membrane where the muscle action potential takes place. The raw EMG signal is transformed into an audible or visual presentation with a microvolt value. The modification of the raw signal into average time periods is necessary because EMG activity is too low in its original form, thus making the small detection difficult to discriminate. To interpret and learn how to influence the muscle activity, the signals must be represented in an understandable manner. The power spectrum of surface EMG can range from 20 to 10,000 Hz. Some of the commercially available biofeedback equipment may have a more limited range, however. This characteristic can result in lower readings overall, and clinicians need to be aware of the band pass of their machine. Similarly, a practitioner should know that measures from one machine may not be equivalent to measures from another machine. Measurements can also be affected by sensor size and type, sensor placement, distance between sensors, and the patient's adiposity because fat can dampen the signal.41 Practitioners should follow consistent procedures for accurate EMG readings. The goals are to reduce muscle activity and to achieve a more relaxed state overall.
Skin Conductance–Assisted Relaxation Historically, measures of skin resistance were obtained to aid in the understanding of hysterical anesthesias. Romain Virouroux used this method of measurement in the late 1880s.42,43 In the 1900s, Carl Jung measured electrical activity of the skin because he believed it was a technique that could be used to in reading the mind during word association experiments.1 Electrodermal activity, or sweating, has been long regarded as a measure associated with arousal. Biofeedback sensors are typically positioned on the palm of the hand or the fingers, which are areas of the body densely populated with eccrine sweat glands. Perspiration is made up of salts that are conductive to electricity, more so than dry skin. The biofeedback machine sends low, undetectable voltage to the skin and records changes in skin conductivity. The sweat glands are primarily responsive to psychological variables and are associated with the sympathetic division of the autonomic nervous system.43,44 Changes in autonomic arousal produce changes in dermal activity. Conductance measures are favored over resistance measures (measured in micro-ohms or microsiemens) because the conductance activity has a linear relation to the amount of activated sweat glands. In clinical applications, conductivity measures are more understandable. Skin conductance increases as arousal increases, and as arousal decreases so does skin conductance. The goal of skin conductance–assisted biofeedback is to promote relaxation by means of reducing skin conductance and arousal.
958
Section V—Specific Treatment Modalities for Pain and Symptom Management
Fig. 130.1 Child receiving thermal- and electromyography (EMG)–assisted biofeedback training. In the top panel, the therapist is explaining the feedback modalities to the child. The vertical bars on either side of the computer monitor display EMG activity (the one to the left presents EMG activity from the forehead, whereas the one to the right is monitoring forearm muscle activity). The circle in the middle and the bar on the bottom of the monitor are providing temperature feedback (in a relative sense). Actual temperature values are provided digitally in the middle of the circle. The bottom panel on the left shows a typical EMG electrode array for promoting generalized relaxation. The bottom panel on the right shows a typical thermistor placement for monitoring surface skin temperature.
Skin Temperature–Assisted Relaxation Skin temperature–assisted relaxation was discovered unexpectedly. During a standard evaluation at Menninger Clinic in Houston, Texas, an individual's migraine attack abruptly subsided with a flushing in the hands and a rapid increase in hand temperature.45 Consequently, the clinicians who observed this event tested a hand-warming treatment for migraineurs. Increasing hand temperatures became a method in regulating
stress and headache activity. Skin temperature is believed to provide an indirect measure of activity in the sympathetic nervous system. A reduction in arousal, or sympathetic outflow, leads to an increase in vasodilation and blood flow to the peripheral areas of the body, which is indicated by an increase in skin temperature. Conversely, an increase in arousal and sympathetic outflow constricts peripheral blood flood and results in a lower skin temperature.
Thermistors containing semiconductors, and occasionally thermocouples, are used to monitor temperature change in the skin. These temperature-sensitive sensors are placed on the fingers. Thermal-assisted biofeedback generally employs aspects of autogenic training,46 in an effort to achieve an increase in peripheral skin temperature. When combined in this manner, the procedure has been termed autogenic feedback. While recording an individual's skin temperature activity, the practitioner needs to keep in mind that measurements may be influenced by the clinic, laboratory, outdoor temperatures, or humidity. Heat buildup on the conductive leads and sensors can also affect the accuracy of the measurements. These three most common techniques of biofeedback— EMG, skin conductance, and skin temperature–assisted relaxation—are all designed to promote a decrease in sympathetic arousal and an overall state of relaxation. A common feature of relaxation is distraction, which has been illustrated by functional magnetic resonance imaging research to activate areas within the periaqueductal gray region.47 This brain region has been associated with higher cortical control of pain. General relaxation-assisted biofeedback may be influencing these central mechanisms of pain.48 For a more detailed description of relaxation therapies, including autogenic training, see Chapter 132. In many instances, a brief psychophysiologic assessment, or a psychophysiologic stress profile, is used for biofeedback-assisted relaxation. In fact, this type of assessment is prudent to include in routine practice because it helps determine psychophysiologic targets for treatment and provides another way to gauge response to subsequent treatment. A more thorough psychophysiologic assessment is used in the specific approach to biofeedback, as described in the next section. (For more information on biofeedback instrumentation, see Peek41).
Specific Approach Many of the conditions listed in the section of this chapter on indications are treated through a specific approach to biofeedback. To obtain initial information about a patient's condition, a psychophysiologic assessment is conducted. This preliminary evaluation is designed to identify response modalities and physiologic dysfunction relevant to the pain disorder. Various stimulus conditions, both psychological and physical, are examined that simulate work and rest. These situations may include, for example, reclining, bending, stooping, lifting, and working a keyboard. The information gathered in this assessment guides treatment and gauges progress. Flor48 outlined the utility and advantages of collecting psychophysiologic data in the treatment of chronic pain: (1) it provides support for the role of psychological factors in dysfunctional physiologic functioning; (2) it justifies the use of biofeedback treatment; (3) it facilitates customized therapy for patients; (4) it makes it possible to record the efficacy, generalization, and transfer of therapy; (5) it assists in predicting treatment response; and (6) it serves as a source of motivation for the patient. This profile can help to foster self-efficacy in the patient, who comes to realize that he or she is capable of voluntarily controlling physiologic responses with his or her own cognitions and emotions. Typical phases of the psychophysiologic stress profile consist of adaptation, resting
Chapter 130—Biofeedback
959
baseline, self-control baseline, reactivity, recovery, muscle scanning, and muscle discrimination.49,50
Adaptation Three objectives for the adaptation phase are as follows: (1) to allow patients to become accustomed with the setting, clinician, and monitoring procedure; (2) to minimize presession effects, such as rushing to the appointment, temperature and humidity differences, and differences between the setting and areas outside of the setting; and (3) to permit habituation of the orienting response and for response stability. During the adaptation phase, patients are instructed to sit quietly while refraining from any conscious efforts of relaxing. Even though a prebaseline period is widely accepted, the key parameters and amount of time for stability are not well researched. Generally, individuals adapt to a stable response within 5 to 20 minutes; however, some individuals do not achieve adaptation even after a 60-minute session. Practitioners are advised to extend the adaptation phase until some stability is achieved for the physiologic response of interest. This is defined as a minimal response or fluctuation in response for a specified period of time or a response that is going in a direction opposite to that desired. Without an appropriate amount of time for adaptation, a clinician may mistake a habituation effect for a training effect.
Baseline After the adaptation phase, the baseline phase begins. Data collected from the baseline phase are used for the basis of comparisons with later phases. Baseline data collection also allows the therapist or researcher to gauge progress within and across subsequent treatment sessions. Again, the parameters and amount of time for collecting information in this phase are not definitive. Decisions, such as whether eyes should be open or closed, whether the patient should recline or sit upright, or whether conditions should be neutral or promote relaxation, are at the practitioner's discretion. The baseline duration generally ranges from 1 to 5 minutes, which should provide an adequate, representative sample of the patient's ordinary responses during resting states. Often, a clinician obtains a second type of baseline. This is a particularly valuable measure for assessing biofeedback acquired skills. The practitioner instructs the patient to relax with a statement such as the following: “I would now like to see what happens when you try to relax as deeply as you can. Use whatever means you believe will be helpful. Please let me know when you are as relaxed as possible.” The purpose of the second baseline is to evaluate the patient's preexisting abilities to relax and can be used to compare with future training effects.
Reactivity The third phase of the psychophysiologic assessment examines simulated stressors that pertain to the patient's condition or similar real-world situations in which pain onset, exacerbation, and perpetuation are associated with the pain. No procedure has been empirically validated, but some common examples include the following: Negative imagery, wherein a patient focuses on a personally relevant unpleasant situation (these details are usually obtained during an intake interview)
n
960
Section V—Specific Treatment Modalities for Pain and Symptom Management
Cold exposure (e.g., for Raynaud's disease or phenomenon) or a cold pressor test (as a general physical stressor) n Movement (e.g., sitting, walking, rising, bending, stooping) n Load bearing (e.g., lifting or carrying an object) n Operation of a keyboard or other office equipment n
Even though baseline differences for EMG have not been reliable in distinguishing pain disorders, certain symptom responses have been found to be more consistent for specific pain conditions (for further discussion, see Flor48). Travell and Simons51 introduced a psychophysiologic model for assessing muscle reactivity. They contended that a large percentage of chronic muscle pain is an effect of trigger points. Hubbard52 extended this view, based on the following rationale: (1) muscle tension and pain are sympathetically mediated hyperactivity of muscle spindles, or muscle stretch receptors; (2) muscle spindles are encapsulated organs that are composed of their own muscle fibers and are scattered throughout the muscle belly (hundreds of these muscle spindles are within the trapezius muscle); (3) even though muscle spindles are traditionally thought of as stretch sensors, they are now recognized as organs that can be activated by sympathetic activation and sense pain and pressure; and (4) therefore, the pain associated with trigger points actually arises in the spindle capsule. This model is supported by research in which careful electrode placements detected high levels of EMG activity in the trigger point but minimal activity in nontender sites just adjacent (only 1 cm away) to the trigger point.53 Additionally, when an individual is exposed to a stressful stimulus, EMG activity increases at the trigger point but not at any of the nearby sites.54 These studies demonstrate an association between behavioral and emotional influences on muscle pain. Gervitz, Hubbard, and Harpin55 designed a treatment program that uses EMG biofeedback to foster muscle tension awareness in sessions and in daily life activities. This treatment also identifies stressors generating increased EMG activity and assists patients in coping with situations producing tension.
Recovery Following the reactivity phase is the recovery phase, in which time is allotted for the patient's physiology to return to a value close to the baseline measure. Most often, the responses do not fully return to the values before the reactivity to stress phase. Therefore, a response is labeled as recovered if it returns to within a certain percentage of its initial value. If several stressful stimuli are presented to a patient, then a recovery period is suggested after each stimulus presentation. The foregoing phases characterize the progression of a typical psychophysiologic assessment. Although used less frequently, muscle scanning and muscle discrimination are two other approaches that may be useful.
Muscle Scanning Cram56 designed an approach that allows a practitioner to evaluate EMG activity quickly from multiple sites and that requires only two channels. Two hand-held “post” electrodes are used to acquire brief (∼2 seconds per site) sequential bilateral recordings while the patient is sitting, standing, or moving. A normative database aids the clinician in determining
whether any of the measures are abnormally high or low. It also determines whether any asymmetries (right versus left side differences) exist, which may suggest bracing or favoring of a particular position or posture. The objective of biofeedback, then, is to return the aberrant recordings to a more normal state.57 Even though this procedure may seem clear-cut, it is actually more complex, because several factors may affect the measures obtained. For example, the angle and force of the applied sensors, the sensor locations used for the norming sample, and the other variables previously discussed may influence EMG readings.
Muscle Discrimination Flor et al58 found that individuals with chronic pain misperceive muscle tension, both in affected and nonaffected muscles. When patients were presented with tasks that required the production of muscle tension, they would overestimate physical symptoms, report greater pain, and rate the task as more aversive. Heightened sensitivity may account for the inability to perceive bodily states accurately. To assess muscle discrimination abilities in a clinical setting, Flor48 recommended the following: Present the patient with a bar of varying height on a monitor. Instruct the patient to tense a muscle to the level in the height of the presented bar. n Vary the bar height from low to high. n Correlate the EMG measures with the actual heights of the bars. n Define as “good” discrimination abilities with correlation coefficients greater than or equal to .80. n Define as “bad” discrimination abilities with correlation coefficients less than or equal to .50. n n
The psychophysiologic assessment techniques for the specific approach to biofeedback allow a practitioner and the patient to monitor and record progress for areas associated with pain. These techniques may also be used in a more abbreviated manner for the general approach to biofeedback. Another style of biofeedback is the indirect approach. The general and specific approaches have their own unique techniques and objectives. The general approach promotes overall relaxation typically through EMG, thermal, or skin conductance biofeedback, which can reduce stress, tension, and pain. The specific approach can be used for precise pain sites, such as specific muscles and trigger points. A psychophysiologic assessment, or stress profile, is employed for evaluating the pain symptoms and physiologic responses. Responses to treatment may vary among individual patients. Patient considerations are discussed next.
Practitioner and Patient Considerations The emphasis on patient education and treatment progress can establish therapy that is successful. The professional relationship between the clinician and the patient is of great importance. In fact, Taub and School59 reviewed several experimental variables and reported that the behavior of the practitioner, as well as his or her confidence in the treatment, has the greatest effect on a patient's progress in biofeedback therapy. In addition to the clinician's expectations, the patient's expectations are also very important. Holroyd et al60 found that the number one predictor of significant improvement for
t ension-type headache with EMG biofeedback is the patient's expectation about his or her ability to control the onset and course of the condition voluntarily. Similarly, beneficial treatment outcomes for headache are affected by the individual's perceived self-control.61 Individuals referred for biofeedback treatment may be confused about the nature of their pain condition and uncertain about their chances for improvement. Patient education offered by the practitioner is crucial in alleviating a patient's apprehension regarding biofeedback treatment. Identifying variables that may be controlled by the patient that are affecting his or her condition is often helpful for the patient's initial feelings about the therapy. Additionally, a detailed description of the treatment and a live demonstration can give the patient an idea of what to anticipate in therapy (a typical session of biofeedback is described later). The biofeedback practitioner is regarded as a coach guiding patients in treatment. The patient is the active player learning skills of self-management. Coaching involves sharing observations for discussion (“I noticed that your EMG signal suddenly increased. It seemed you might have been clenching your teeth then. How about dropping your lower jaw and moving it a bit forward? I wonder if anything in particular was on your mind then?”) The clinician also determines when breaks and encouragement may be needed. Initial attempts to lower EMG activity and skin conductance and to increase hand temperature are frequently met with the opposite effect, and this may paradoxically worsen as patients try harder and harder. These situations can be valuable in demonstrating the interaction between psychological and physiologic functioning and can illustrate how the patient's current coping strategies are actually backfiring. The coach explains how and why this happens and can alleviate the patient's frustration and get him or her back on track. The therapist also helps the patient articulate, understand, and consolidate the learning of skills. Other self-management techniques are also imparted to the patient. The discretion of the clinician is important in facilitating progress, because an overbearing coach can negatively affect treatment.62 The U.S. Headache Consortium29 has summarized individuals who may be especially good candidates for biofeedback or other behavioral treatments. One or more of the following factors must be present: The patient prefers the approach. Pharmacologic treatment cannot be tolerated or is medically contraindicated. n Pharmacologic treatment response is absent or minimal n The patient is pregnant, plans to become pregnant, or is nursing. n The patient has a history of frequent or excessive use of analgesic or acute care medications. n The patient is faced with several stressors or has deficient stress-coping skills.
Chapter 130—Biofeedback
961
“Self-control” baseline determination (the patient's ability to regulate the target response in the desired direction in the absence of feedback, to provide a comparison with the ability to perform skills outside the treatment setting67) n 20 to 30 minutes of actual feedback (continuous or with breaks) n Final resting or self-control baseline determination (assess learning within the session) n Final progress review and assigned homework n
No firm standard exists for the number of treatment sessions necessary for reaching the appropriate goals of therapy. The duration of treatment depends on the clinical response of symptom relief or the patient's adequate control of the target measure. When treatment reaches a point of diminishing returns, such as response plateaus, then the practitioner should begin to consider changing course or terminating treatment. Research on biofeedback-assisted relaxation has shown that desired goals are typically accomplished in 8 to 12 sessions. Haddock et al68 found that patients with headache respond more quickly to treatment when homework assignments consist of detailed manuals and relaxation tapes. The treatment duration is subject to individual differences in treatment response. Lynn and Freedman69 outlined the following methods to increase generalization and maintenance of beneficial biofeedback skills: (1) overlearning the response and continuing to practice learned skills; (2) incorporating booster treatments; (3) fading or gradually removing feedback during treatment; (4) training under stressful situations such as during noise, distractions, and physical or mental tasks; (5) using multiple practitioners, which is possible with group treatment; (6) varying the physical setting; (7) providing portable biofeedback devices for homework assignments; and (8) supplementing biofeedback with other procedures such as cognitive and behavioral techniques. Many of these suggestions are based on learning principles of behavior therapy. This section delineates the two approaches of biofeedback, patient considerations, coach or practitioner considerations, a typical treatment session, treatment duration, and procedures for improving the durability of the skills learned from biofeedback therapy. The next section addresses some of the side effects and complications of biofeedback treatment.
n n
Children often respond especially well to biofeedback.63,64 Older patients usually need more time to master self-regulation skills.65,66 A typical biofeedback session consists of the following components: Sensor attachment and time for adaptation Initial progress review n Resting baseline determination n n
Side Effects and Complications Even though biofeedback treatments commonly have positive outcomes, a few difficulties have been reported. A few of patients may experience initial negative outcomes such as muscle cramps or disturbing sensory, cognitive, or emotional reactions. Other problems may arise that can affect adherence and practice. A few individuals may experience an abrupt increase in anxiety as they become deeply relaxed because a deep state of relaxation may be foreign to them. This condition is termed relaxation-induced anxiety, and symptoms can range from mild to moderate in intensity and may come close to a minor panic attack.70 If this situation occurs, the practitioner must remain calm and reassure the patient that the episode will soon pass. Having the patient sit up or walk around the office usually helps. When patients are at risk for relaxationinduced anxiety, the clinician may instruct them to concentrate on the somatic aspects rather than the cognitive aspects
962
Section V—Specific Treatment Modalities for Pain and Symptom Management
of training.71 See Schwartz, Schwartz, and Monastra72 for a discussion of other problems and solutions. A more detailed description of complications for relaxation therapies can be found in Chapter 132. Some medications may act on the central and autonomic nervous system and may thereby complicate biofeedback therapy. For example, muscle relaxants may relax target muscle groups and elicit inaccurate measures for the process of biofeedback training. Other medications, such as asthma inhalers, act on the autonomic nervous system and cause blood vessels to constrict. This may impede thermal biofeedback training by decreasing blood flow to the peripheral areas of the body. In some instances, improvement attained in biofeedback therapy may require medication adjustments. This is one of the many reasons that biofeedback clinicians should maintain a collaborative working relationship with medical associates.
Conclusion Biofeedback treatment is a viable option for many pain disorders and accompanying symptoms. This chapter summarizes historical considerations such as early pioneers, research, and other related fields contributing to the development of biofeedback. A comprehensive AAPB evidence-based review of treatment options for arthritis, chronic pain, headache in adults and children or adolescents, vulvar vestibulitis, Raynaud's
isease and phenomenon, and TMDs is analyzed. Efficacy d levels for these conditions vary, and some areas merit more research to examine outcomes with biofeedback therapy. The section on techniques addresses the general and specific approaches of biofeedback including the components of a psychophysiologic assessment. Furthermore, this section discusses practitioner and patient considerations, a typical biofeedback session, and treatment duration. Side effects and complications for biofeedback therapy are minimal. Relaxation-induced anxiety and medication complications are identified as infrequent occurrences. Throughout the chapter, the patient's active role and education in the therapy process are emphasized. For more information regarding research, credential programs, or biofeedback in general, the reader may visit the following websites: Association of Applied Psychophysiology and Biofeedback http://www.aapb.org Biofeedback Certification International Alliance http:// www.bcia.org Biofeedback Foundation of Europe http://www.bfe.org International Society for Neurofeedback and Research http://www.snr-jnt.org
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
131
V
Hypnosis Howard Hall
CHAPTER OUTLINE Historical Considerations 963 Indications 964 Hypnosis for Preoperative and Postoperative Pain Management 964 Hypnosis for Management of Acute Pain 964 Hypnosis for Cancer Pain Management 964 Hypnosis for Obstetric Pain 965 Hypnosis for Emergency Treatment of Burns 965 Hypnosis for Chronic Pain Conditions: Headaches, Fibromyalgia, Gastrointestinal Disorders, and Sickle Cell Disease 965
Clinically Relevant Anatomy 965
Historical Considerations Perhaps one of the first written descriptions of surgery on a patient under what appears to be a hypnotic trance can be found in the Bible in Genesis 2:21-22 with the creation of Eve from Adam's rib: “And the Lord God caused a deep sleep to fall upon Adam and he slept: and he took one his ribs, and closed up the flesh instead thereof; And the rib, which the Lord God had taken from man, made he a woman, and brought her unto the man.” The origin of hypnosis is associated with an 18th century Viennese physician, Franz Anton Mesmer (1734-1815; Fig. 131.1). Mesmer became famous in Paris for inducing a type of convulsive seizure he called a “crisis,” which was apparently linked to therapeutic effects on the body. The setting for Mesmer's treatments included soft background music and a draped room in which patients would hold onto metal bars that extended from a wooden tub filled with water, ground glass, and iron filings. Mesmer developed a theory of animal magnetism that used the iron filings and magnets for healing purposes; his method later became known as “mesmerism.” His theory of disease and healing involved “balancing magnetic fluids,”1 an approach that today might be termed “energy medicine.” Many of the conditions he treated with mesmerism might now be considered functional disorders, with a psychologic, rather than physical, basis. These include conversion symptoms of paralyses, seizures, and deafness and stress-related conditions, such as headaches.2 Mesmerism generated so much attention that in 1784 Louis XVI of France formed a commission, headed by Benjamin Franklin, to examine the theory of animal magnetism. After running a series of controlled experiments to test the phenomenon, the commission concluded © 2011 Elsevier Inc. All rights reserved.
Technique 965 Hypnosis Technique for Preoperative and Postoperative Pain Management 965 Hypnosis Technique for Management of Acute Pain 965 Hypnosis Technique for Cancer Pain Management 965 Hypnosis Technique for Obstetric Pain 966 Hypnosis Technique for Emergency Treatment of Burns 966 Hypnosis Technique for Chronic Pain 966
Side Effects and Complications 966 Conclusion 966 Acknowledgments 966
that Mesmer's cures were produced by the patient's imagination and not magnetism.1 It should be noted that the commission did not find that Mesmer's results were invalid, just that they were not the results of magnetism. However, during this era of reason and enlightenment, a pronouncement of this kind was equivalent to saying that the results of magnetism therapy were not real. One of the most important applications of mesmerism in the early 1800s in France, England, and later, the United States was as an anesthetic agent for surgical patients. Mesmerism anesthesia was used for mastectomies, amputations of legs, removal of glands and jaw tumors, and tooth extractions. In one case of tooth extraction, the patient was described as showing no apparent discomfort or reaction to the pain.2 Around 1840, English surgeon James Braid (1795-1860) recognized that some mesmeric phenomena were genuine but argued against the doctrine of animal magnetism. Braid put forward his own view that the phenomenon of mesmerism was related to subjective or psychologic factors.3 He used an eye-fixation induction that he learned from a mesmerist and coined the term “hypnosis” to describe the observed trance phenomenon that he believed was an artificially induced state of sleep (Hypnos is the Greek god of sleep). Today, of course, we know hypnosis is unrelated to sleep because the two have divergent electroencephalographic (EEG) patterns. An especially dramatic historical example of the application of hypnosis is the achievement of painless surgery in procedures performed by James Esdaile between 1845 and 1851. Esdaile, a Scottish surgeon, practiced medicine in India and performed hundreds of operations with hypnosis as the sole analgesic technique.2 Even more impressive, more than 300 of these operations involved major surgery and 963
964
Section V—Specific Treatment Modalities for Pain and Symptom Management and anxiety, and reduced opioid use.9 Other reports that indicate efficacy for hypnosis cite decreased postoperative orthopedic pain, faster surgeon-rated recovery, and in one study, no postoperative complications, versus eight instances in customary care conditions without hypnosis intervention.10
Hypnosis for Management of Acute Pain
Fig. 131.1 Franz Anton Mesmer with patient.
Esdaile's mortality rate was only about 5%, as compared with the 40% to 50% death rate for conventional surgical procedures at that time. Nevertheless, the role of hypnosis as an anesthetic technique declined by the third quarter of the 19th century for several reasons. First, hypnosis provided variable and unpredictable results. A report actually cited a patient who sued for assault when she emerged from hypnotic analgesia in the middle of an operation. Second, after Liston performed the first operation with ether in England in 1846, use of chemical anesthetic agents increased.4 Further, unprofessional and fringe practices entered the field of hypnosis, tarnishing its reputation and leading to a decline in its use.2 Hypnosis for the treatment of children goes back more than 200 years, but it was not until the 20th century that it emerged as a subspecialty area with novel training opportunities that emphasized pain management.5–8 Children are generally believed to be relatively more responsive to hypnosis than adults because they have such active powers of imagination, which has important implications for successful pain management. Hypnotic induction with children also tends to be more permissive, playful, imaginative, and less structured and authoritative than the approaches used with adults. One has to be mindful of a child's developmental level with use of hypnotic approaches because techniques vary widely and must fit those developmental milestones and abilities to be effective.
Indications Hypnosis can be used in an integrative manner as an adjunctive treatment along with traditional medical and pharmacologic approaches to pain management or as an alternative nonpharmacologic treatment. A hypnotic intervention can be used before, during, or after painful procedures or operations.
Hypnosis for Preoperative and Postoperative Pain Management Hypnosis and other psychologic interventions applied before surgery have been associated with faster postoperative recovery, shorter hospital stays, relatively less postoperative pain
Controlled trials for acute pain reduction provide good evidence that hypnosis is superior to standard care, attention controls, or other viable pain-reduction interventions.11 Anxiety is a major contributor to distress during painful medical procedures, which becomes patently clear when children begin crying as soon as a doctor approaches them with a needle or when adults become distressed at the sound of the drill in the dentist chair. However, and more dramatically, anxiety can rise to the same level in the parking lot, before the doctor visit even begins, or in the dentist's waiting room. Hypnosis has been used within dentistry and has been helpful to reduce anxiety and pain perception during a host of medical procedures.12 Response to hypnotic interventions for children and adolescents with cancer who undergo bone marrow aspirations varied as a function of the child's age, gender, and hypnotic susceptibility.13 However, the relative benefit of hypnosis versus other cognitive approaches to pain management in children requires further research.14 Hypnosis has also provided added benefit to local anesthetics, such as eutectic mixture of local anesthetics (EMLA) cream, for lumbar punctures and bone marrow aspirations with young cancer patients. This procedure has an impact on management of both pain and anticipatory anxiety.15 An updated review of randomized controlled trials of psychologic interventions for needle-related procedural pain and distress in children and adolescents provided some insight into this issue.16 These authors found sufficient evidence to support the efficacy of hypnosis, distraction, and combined cognitive behavioral interventions for the management of procedural pain and distress in children. The effect sizes of these psychologic interventions showed an average of more than 20% reduction of pain, compared with meta-analytic results for topical anesthetics that ranged from 20% to 50%. A recent randomized clinical trial showed that a combined multifaceted distraction intervention that included hypnotic suggestions of diminished sensation without a formal induction resulted in a significant reduction in discomfort from immunizations in children 4 to 6 years old compared with routine control conditions.17 As these authors noted, hypnosis with young children does not necessitate a formal hypnotic induction because children easily go into natural trance states during stressful and anxiety-provoking situations such as injection.
Hypnosis for Cancer Pain Management Hypnosis is used for the management not only of pain and anxiety of medical procedures associated with cancer, as noted previously, but also for the neuropathic pain associated with the disease itself. Often hypnosis can provide added benefits for conditions such as neuropathic cancer pain where opioids and other medical treatments have not been found to be totally effective when used alone. Emphasis is now placed on integrating hypnosis along with traditional medical treatments for chronic pain conditions.18
Hypnosis for Obstetric Pain
Chapter 131—Hypnosis
965
Hypnosis has been used during pregnancy for the management of nausea and vomiting, for prevention of premature labor, as an adjunctive treatment for pregnancy-induced hypertension, and as an intervention for pain and discomfort during labor and delivery.19,20 About 20% to 35% of women are estimated to use hypnosis as the sole anesthesia during labor or delivery.19 For other women, hypnosis can be used as adjunctive nonpharmacologic analgesia along with standard care.
score very low on these scales show comparable response levels to pain reduction for hypnosis and placebo conditions.31 In highly hypnotizable individuals, hypnotic analgesia does appear to be associated with a complex ability to cognitively restructure or dissociate conscious overt pain sensation from covert experiences. In a novel set of experiments, hypnotically talented subjects who reported no overt pain to painful stimuli under hypnosis did indicate perception of pain when a covert or “hidden observer” part of their consciousness was asked about the experience.18
Hypnosis for Emergency Treatment of Burns
Technique
Case histories of hypnotic interventions for burn victims have reported dramatic attenuation of the inflammatory response burn injury, if hypnosis is conducted during the first 2 hours after the burn.22 However, controlled studies provide less dramatic outcomes.23
Hypnosis for Chronic Pain Conditions: Headaches, Fibromyalgia, Gastrointestinal Disorders, and Sickle Cell Disease Evidence from controlled trials of chronic pain shows hypnosis to be superior to no treatment but equivalent to relaxation and autogenic training.11 Chronic pain is a complex phenomenon and does not respond as robustly to hypnotic interventions as acute pain conditions.11 Self-hypnosis training, however, has been associated with a reduction in pain days, disrupted or inadequate sleep, and pain medication for patients with sickle cell disease.24 Hypnosis is also associated with a substantial reduction of the symptoms of irritable bowel syndrome in adults25 and in children, and it is considered a well-established and efficacious treatment for recurrent headaches in children.26 Self-hypnosis training is also associated with reduced frequency, duration, and intensity of headache symptoms in children and adolescents.27
Clinically Relevant Anatomy Although views differ as to what hypnosis is and how it works for pain control,11 hypnosis is often described in terms of an altered state of consciousness or awareness.6 However, some consensus seems to exist as to what hypnotic pain control is not. The pain reduction effectiveness of hypnosis is not the result of simple relaxation because it does not necessarily bring about a relaxed state.28 On the other hand, clinical hypnosis has been associated with profound relaxation effects accompanied by decreased measures of psychologic symptoms of distress and somatization scores in patients with chronic pain conditions such as irritable bowel syndrome.29 Hypnosis does not appear to function as an opiate receptor-based analgesic because the opiate antagonist naloxone has no effect on hypnosis-induced analgesia.11,30 The adult literature has observed that hypnotic responsiveness can be measured and predicted reliably such that individuals who score very high on these hypnotizability scales achieve robust hypnotic analgesia responses in the laboratory.20 Hypnotic analgesia is not a placebo effect for those individuals who score very high on responsiveness scales because they show a higher pain threshold and pain tolerance under hypnotic analgesia conditions than under placebo conditions. By contrast, those who
Hypnosis Technique for Preoperative and Postoperative Pain Management The use of language plays an important role in hypnotic work and in clinical practice in general. For children in particular, and adults as well, the use of permissive and indirect language is generally preferred to authoritative approaches. For example, direct suggestions that “You will feel no pain” are avoided (especially with adults who are not highly hypnotizable). Instead, the wording to follow might be, “You may be surprised how comfortable you might feel during and after the procedure.” Also, permissive suggestions can be given for the preoperative and postoperative periods. For example, the point at which the medication is administered can be a signal for the person to have a pleasant daydream; also, the area being operated on can remain soft, comfortable, and loose during the operation. A suggestion can be offered in advance that when the patients awaken in the recovery room the operation will be over, their condition relieved, and healing already under way. In addition, suggestions can be given stating how surprised they can be at how quickly recovery is likely to occur and how much easier the whole procedure was than anticipated.32 Hypnosis for postsurgical pain management and recovery has included relaxation methods and suggestions for a smooth recovery, comfort, improved limb mobility, and success with o ccupational or physical therapy.10
Hypnosis Technique for Management of Acute Pain Hypnoanalgesia techniques for young patients may include suggestions for feelings of numbness and glove anesthesia and numbing other body parts with that “magic” glove. Also effective are distancing suggestions such as moving pain away from self, or transferring it to another body part, or moving the self away from the pain. Yet another approach offers suggestions for feelings antithetical to pain, such as comfort, laughter, or relaxation. Distraction techniques directing attention away from the pain, adding time distortion, reframing, and suggesting amnesia are documented and effective.6
Hypnosis Technique for Cancer Pain Management Hypnotic suggestions for cancer pain management may involve dissociative imagery of going to a favorite place, hypnotic analgesia suggestions of numbness or pain on-off switches (i.e., blocking pain), and sensory transformation experiences that either explore the pain or transform its intensity, color, or temperature.18
966
Section V—Specific Treatment Modalities for Pain and Symptom Management
Hypnosis Technique for Obstetric Pain A range of hypnotic processes and posthypnotic suggestions has been suggested for management of labor and delivery. These include simple relaxation, trance states, time distortion, redirection of attention, glove anesthesia, and transferring of numbness. A reframing approach suggests a reinterpretation of potentially negative sensations to familiar and pleasant ones (e.g., “Each contraction can be considered as a pleasing occurrence, drawing you nearer to your goal, bringing a new love for your enjoyment.”).32
Hypnosis Technique for Emergency Treatment of Burns Emergency situations are often traumatic and result in trance states as a natural defense against pain and fear. Thus, a formal hypnotic induction is not generally needed. When a burn patient is in a natural trance state, he or she can be told to “go to your laughing place” or be given a similar initial suggestion. Then, as the health team takes care of the injury, a hypnotic suggestion is given, alluding to a state of being “cool and comfortable.”22 This intervention is best carried out within 2 hours of the injury to reduce the inflammatory response.
Hypnosis Technique for Chronic Pain Chronic pain is a complex phenomenon that does not respond as robustly to hypnotic interventions as acute pain conditions.11 Thus, work with hypnosis needs to be done in an integrative fashion. Self-hypnosis practice may also facilitate clinical relaxation effects and reduce symptoms of psychologic distress for many chronic pain conditions. Attention to lifestyle factors and behavioral sleep issues may be helpful in sickle cell disease and other chronic pain conditions.24
Side Effects and Complications In the hands of a practitioner with appropriate background, training, and licensure, hypnosis is generally a safe intervention. In management of pain, however, a good history and physical examination are critical to success. Karen Olness and Patricia Libbey,33 pioneers in the field of child hypnotherapy, observed that 25% of children referred for hypnotherapy were later found to have some unrecognized organic condition that accounted for their symptoms. Of course, the most important intervention in those cases was not hypnosis but appropriate medical treatment. The author's only negative experience with hypnosis and pain management involved a teenage boy with functional abdominal pain. This case was very early in the author's career. The author made a direct suggestion for the pain to go away (now, the author's approach is more permissive and cautious). After the induction had ended, the boy said that his pain was gone but that everything seemed upside down (i.e., he was disoriented). The author had him close his eyes and suggested that when he opened his eyes the room would be back to how it was. This approach was unsuccessful, and the patient was becoming somewhat alarmed about how he was feeling (the author was becoming concerned as well). Then, the author had him close his eyes and go back into hypnosis; the author had him “bring the pain back.” He opened his eyes and said everything was back to normal, but his stomach was hurting again. Follow-up work involved weekly traditional psychotherapy and learning how to get in contact with the feelings he was somaticizing.
The patient did well and eventually learned to express his feelings in words instead of somatic symptoms. The author saw the patient again about a decade later for a different problem related to the demise of his marriage. The author and patient did a lot of talk therapy and some hypnosis with no direct suggestions of symptom removal and no complications. The author's first-line approach to chronic pain is a thorough medical, psychologic, and lifestyle assessment, followed by permissive relaxation type of hypnotic induction with no direct suggestion for pain to go away. If the pain remains despite the lack of obvious physiologic cause and active selfhypnotic practice, hypnosis may be used to explore the meaning of the pain. A patient under hypnosis might be asked to describe the pain and ask the pain why it is there and what the pain is attempting to teach the patient. Some colleagues have children draw pictures to obtain some of this information. Another colleague encourages children to use the computer word processor to help them gain insight into psychologic factors underlying their medical symptoms.34
Conclusion As noted previously, a discrepancy often exists between modest findings from experimental trials and statistically significant clinical reports for hypnotic pain control. Although this discrepancy might cast doubts on the clinical trials and case reports, one must keep in mind that clinical and experimental settings are different. Standardized protocols are often used within laboratory settings that would be of limited use in clinical situations, where one would be inclined and able to capitalize on the patient's unique interests, strengths, and preferences, especially when working with children. Some practitioners caution against the use of hypnosis in adolescents who score low on a standard scale of hypnotizability. The author finds these scales useful in the laboratory but not as useful in a clinical setting because clinically significant improvement can be accomplished if hypnosis is used not as an isolated treatment but rather in an integrative manner. Pediatric neurologists often refer children with recurrent headaches to the author because they believe that pharmacologic treatments have limited benefit. The author's approach, after obtaining careful medical, psychologic, sleep, diet, and other lifestyle assessment, is to teach self hypnosis as a “skill and not a pill” for headache prophylaxis.35 For hospitalized children with chronic pain, self hypnosis can be of great benefit if introduced before the administration of daily opioids with their undesirable side effects. The author's clinical success rates have been excellent, but he looks forward to more conventional analyses. In conclusion, it is the author's opinion that hypnosis can be a valuable component of a comprehensive and integrative program for pain management.
Acknowledgments The author thanks Kenneth Spencer and Tracie Williams of the Cuyahoga County Community College Bridges to Success in the Sciences for their help in research and preparation of the manuscript for this chapter.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
132
V
Relaxation Techniques and Guided Imagery Carla Rime and Frank Andrasik
CHAPTER OUTLINE Historical Considerations 968 Progressive Muscle Relaxation 968 Autogenic Training 968 Meditation 968 Yoga 969 Guided Imagery 969
Indications 969 Techniques 971
Autogenic Training 971 Progressive Muscle Relaxation 972 Relaxation Treatment Regimen 972 Mindfulness-Based Stress Reduction 973
Side Effects 975 Conclusion 975
Relaxed Breathing 971 Guided Imagery 971
Relaxation interventions are self-management approaches underscoring the active involvement of the patient. Relaxed breathing, progressive muscle relaxation (PMR), autogenic training (AT), meditation, yoga, and guided imagery (GI) are all forms of relaxation treatments that are reviewed in this chapter. The National Center for Complementary and Alternative Medicine, a division of the National Institutes of Health, classifies these therapies as mind-body medicine defined as “techniques designed to enhance the mind's capa city to affect bodily function and symptoms.”1 According to a 2007 survey, approximately 4 in 10 adults and 1 in 9 children in the United States had used some form of complementary or alternative medicine in that previous year.2 The use of deep breathing exercises, meditation, and yoga had increased since the earlier survey in 2002. The actual mechanisms contributing to the effects of relaxation techniques are unclear.3 Theories have been put forth to account for these effects. One theory, proposed by Benson et al,4 contends that relaxation therapies elicit a generalized relaxation response whereby the body undergoes a series of physiologic changes initiated by the autonomic nervous system. These changes include a decrease in respiration, oxygen consumption, carbon dioxide elimination, heart rate, and arterial blood lactate concentration. Moreover, an increase in slow alpha brain waves with intermittent theta brain waves occurs and indicates a hypometabolic, wakeful state. The relaxation response, which is a general increase in parasympathetic nervous system activity, competes with Cannon's fight-or-flight response, which is a general increase in sympathetic nervous system activity. Although Benson et al4 asserted that relaxation © 2011 Elsevier Inc. All rights reserved.
procedures are equivalent, Davidson and Schwartz5 proposed that relaxation techniques have distinctive, specific effects classified primarily as cognitive, autonomic, or muscular. Despite this debate, both theories may be accurate in that many of the physiologic responses of relaxation are interconnected. Several factors may explain the beneficial outcomes of relaxation for individuals with pain. First of all, a general decrease in arousal also diminishes the central processing of sensory stimulation.6 Additionally, reducing the frequent activation of the autonomic stress system can decrease the pain associated with this prolonged and heightened physiologic state, which is marked by an increase in cortisol levels.7 Distraction may also play a role in the effects of relaxation. Tracey et al8 found, through functional magnetic resonance imaging (MRI), that distraction activates the periaqueductal gray region, a cortical area related to pain control. The anterior cingulate cortex, a structure in the limbic system, is another region of the brain implicated in pain. This region is believed to be associated with the affective and cognitive evaluation of pain.9,10 Relaxation may result in changes of activation in the anterior cingulate cortex that reduce pain perception.11,12 Depression, anxiety, and fear are often a result of pain and are intricately involved in the pain–negative affect cycle.13 A reduction in these secondary symptoms through relaxation can increase pain tolerance.6,14,15 Relaxation may be effective in reducing symptoms by “uncoupling” pain with its affective evaluation and thus leading to better coping.16,17 Finally, feelings of helplessness can be a consequence of an ongoing pain condition.15,18,19 Acquiring relaxation skills may provide a sense of control through active coping of the pain. Thus, 967
968
Section V—Specific Treatment Modalities for Pain and Symptom Management
mechanisms of relaxation therapies for pain may operate on the basis of decreased sensory input, competition of the stress response, distraction, and changes in pain perception associated with the cognitive and affective evaluation of pain that may lead to a sense of control and better coping. This chapter on relaxation techniques starts with a discussion of historical considerations of PMR, AT, meditation, yoga, and GI. The section that follows considers indications for these therapies for several pain disorders and their accompanying symptoms. Next, techniques for each of these procedures are reviewed. This chapter closes with possible side effects and precautions for relaxation procedures.
Historical Considerations Progressive Muscle Relaxation In the early 1900s, Edmund Jacobson studied reactions to unexpected loud noises known as the startle response. Participants who were deeply relaxed did not display this typical startle response to sudden noises. This finding prompted Jacobson to continue researching the effects of relaxation. He found that the strength, or amplitude, of knee-jerk reflexes was related to the individual's tension levels. Those who exhibited sustained chronic muscular tension had less latency and more amplitude in their knee-jerk responses. Those who practiced relaxation displayed a decrease in the amplitude of knee-jerk reflexes.20 Consequently, Jacobson developed PMR to aid individuals in gaining an awareness of muscle tension and muscle relaxation through physiologic introspection. He did not believe in intentionally tensing muscles to perceive the differences between relaxed and tense muscles.21,22 Later variations of Jacobson's original PMR added the tension and release cycles and the use of suggestion for relaxation. To create slight tension, Jacobson did instruct clients to raise the arm or bend the hand. The purpose of PMR is to learn physiologic control of increasingly more subtle muscle tension. Jacobson's PMR program involves more than 100 sessions, each usually an hour in length, while focusing on specified muscle groups. It could take months or years to obtain the skill to relax through the original version of PMR. Because of the extensive time commitment for completing Jacobson's PMR program, others developed and tested shortened versions. Joseph Wolpe23 adapted an abbreviated version of Jacobson's PMR, called systematic desensitization, for the counterconditioning of fear. This therapy usually takes 10 or fewer training sessions to complete. Wolpe combined more muscle groups and included suggestions and specific instructions. Others modified Jacobson's prescribed PMR program and Wolpe's abbreviated form to fit their patients' needs. Examples of these contemporary methods are described in the section of this chapter on techniques.
Autogenic Training Johann Schultz was a German neurologist and psychiatrist who is credited as the founder of AT. The prominent school of thought at the time was psychoanalysis. Schultz was disenchanted with this approach, and in 1924 he began implementing AT in his private practice as a therapeutic method. Schultz created formulas for AT based on brain research
conducted by Oskar Vogt. Vogt had observed that his participants, through deliberate mental concentration, could selfhypnotically produce sensations of warmth and heaviness. In 1932, Schultz published a book entitled Das Autogene Training that described the six formulas of the AT method.24 Wolfgang Luthe, a physician and follower of Schultz, began translating the AT formulas into English in the 1960s. Luthe, with the assistance of Schultz, wrote the six-volume Autogenic Therapy, which details the AT formulas. Thus began the propagation of AT in English-speaking regions.24
Meditation The English word meditation is derived from the Latin word meditari, which means “to heal.”25 This implies a restoration of physical, mental, and spiritual well-being. Transcendental and mindfulness are common types of meditation.26 Transcendental meditation involves quietly or silently repeating a mantra, which can be a syllable, word, or phrase. Mindfulness meditation requires a passive, nonjudgmental attitude while experiencing sensations and perceptions in the moment. Table 132.1 provides guidelines for practicing meditation. Meditative practices are often found in religious contexts. Merkabolism, an early form of Judaism dating back to the first century bc, has literature describing transcendental prayer sequences.4 In Eastern cultures, Shintoism, Taoism, and Sufism use meditation. Christian writers St. Augustine and Martin Luther also applied meditation to prayers as contemplative exercises.4 Mindfulness meditation, in contrast, has origins in Buddhist traditions dating back more than 2500 years and has become more popular in the West since the 1960s.27 Adiswarananda25 explained that meditation can facilitate achieving self-knowledge and self-control by obtaining mastery over the mind through direct perception. A 12-second period of sustained focus is said to equal 1 unit of concentration. Twelve units of concentration are equal to 1 unit of meditation, and, in turn, 12 units of meditation lead to total absorption. Suffering is believed to be self-created, and meditation can awaken the mind's ability to heal. Sleep rejuvenates the body, whereas meditation rejuvenates the mind. A fatigued mind has a tendency to repeat habitual thoughts and behaviors. In contrast, a fresh mind uncovers innovative ways of meeting life's challenges, such as pain.
Table 132.1 Guidelines for Meditation Quiet place
When starting, a quiet place with few distractions is ideal.
Specific posture
This could include sitting, standing, lying down, or walking.
Focused attention
The object of attention could be a mantra, breath, image, or sensations.
Open/passive attitude
This allows for distractions to come and go without engaging in them.
Data from Benson H, Kotch JB, Crassweller KD, et al: Historical and clinical considerations of the relaxation response, Am Sci 65:441, 1977; and Sood A: Mind-body medicine. Mayo Clinic book of alternative medicine: the new approach to using the best of natural therapies and conventional medicine, New York, 2007, Time Inc Home Entertainment, pp 87–103.
Chapter 132—Relaxation Techniques and Guided Imagery
Yoga The English word yoke is related to the term yoga, which is derived from the Sanskrit root yuj, meaning “to unite.”14,28 The earliest documentation of the practice of yoga dates back to 3000 bc in India.14 Vedic science is an Indian philosophy with traditions developed in the Indus Valley by sages known as Vedas.28 In 200 bc, sage Maharishi Patanjali expanded on this science through his writings. He wrote about the eight branches, or limbs, of yoga,25,28 which are summarized in Table 132.2. In the ninth century, sage Adi Shankara revived the Vedic science of yoga.28 Hatha yoga is the most commonly used form in North America, and it is based on the third branch of yoga, asana.14,29 Mindfulness meditation and Hatha yoga are key features of the Mindfulness-Based Stress Reduction (MBSR) program. This intervention draws from similar but distinct philosophies; mindfulness meditation has roots in Buddhism, and yoga has roots in Indian Ayurvedic science.30 Dr. Kabat-Zinn27 designed the MBSR program in 1979 at the University of Massachusetts Medical Center. The program was created to relieve suffering for medical patients, and the yoga segments were originally included to prevent disuse atrophy. It is described in more detail in the section on techniques.
Guided Imagery It is difficult to determine who may have been the founder of GI techniques. Imagery can be traced back to Ancient Greece, however, where dreams and visions were evaluated in the Asclepian temples for medical purposes. Aristotle, Hippocrates, and Galen were all trained in this method of imagery-based healing.31 During the behaviorist movement in the mid-1900s, imagery as a mental process was considered irrelevant for research, let alone for therapeutic purposes. When the cognitive revolution in psychology took place, imagery was reintroduced as a topic for research and treatment.
Table 132.2 The Eight Branches, or Limbs, of Yoga Branch
Meaning/Translation
1. Yama
“Rules of social behavior” or restraint
2. Niyama
“Rules of personal behavior” or discipline
3. Asana
“Seat/position” or posture
4. Pranayama
Based on prana, which stands for “life force” or control of breath
5. Pratyahara
Based on prati, which means “away,” and ahara, which means “food” and encompasses the withdrawal of the mind
6. Dharana
“Concentration” or the mastery of attention and intention
7. Dhyana
“Meditation” or the development of awareness
8. Samadhi
“Total absorption” or pure awareness
Data from Adiswarananda S: Meditation and its practices, Woodstock, Vt, 2003, Skylight Paths Publishing; and Chopra D, Simon D: The seven spiritual laws of yoga: a practical guide to healing body, mind, and spirit, Hoboken, NJ, 2004, John Wiley & Sons.
969
In the early 1900s, Edmund Jacobson and Johann Schultz discovered the therapeutic value of PMR and AT, respectively, Meditation, yoga, and imagery have a much longer history. The following section discusses the effectiveness of these techniques as they relate to pain management.
Indications The National Institutes of Health Technology Assessment Panel3 concluded that “…the evidence is strong for the effectiveness of [relaxation] techniques in reducing chronic pain in a variety of medical conditions.” The panel further stated that “…the data are insufficient to conclude that one technique is usually more effective than another for a given condition.” Baer32 examined research on the MBSR program and acknowledged that this intervention is “probably efficacious,” where the preliminary studies are promising, but more rigorous research is still needed. Relaxation techniques are often combined into a treatment package. Various investigations have been conducted in order to determine the effectiveness of these isolated or combined interventions. Relaxation procedures and GI have been applied to a wide array of acute and chronic pain conditions and their secondary symptoms. The following represents an assortment of the research regarding these procedures as treatments for arthritis, back pain, headache, carpal tunnel syndrome, cancer, ulcers, irritable bowel syndrome, and phantom limb pain. The Arthritis Self-Management Program is a patient education intervention for the treatment of rheumatoid arthritis, osteoarthritis, and fibromyalgia. It incorporates relaxed breathing, PMR, GI, mindfulness meditation, body scan, and yoga postures, along with cognitive restructuring, problem solving, and communication skills.33 The intervention consists of six sessions, each approximately 2 hours in length. An evaluation of the program found an average of 15% to 20% reduction from baseline in arthritis-related pain and disability.34 A study of a modified version of the Arthritis SelfManagement Program, highlighting self-efficacy, reported that reductions in pain were maintained after 4 years and that physician visits decreased by 43%; these findings suggest the long-term effectiveness of the program and a reduction in health care costs.35 Results of a 12-week study for rheumatic pain indicated that PMR significantly improved muscle function of the lower extremities compared with strength training.36 Another 12-week intervention of PMR and GI for osteoarthritis led to significant decreases in pain and mobility difficulties when compared with a control group.37 Yoga was also applied to treat osteoarthritis of the knee and resulted in enhanced flexibility, strength, and quality of life.38 Kolasinski et al39 found that yoga reduced pain symptoms and disability for individuals with osteoarthritis of the knee. Furthermore, they concluded that yoga is a feasible treatment for obese individuals who are more than 50 years old, because most of the participants in their study met these criteria. Fibromyalgia, another form of arthritis, has symptoms that are difficult to treat through conventional methods.40 A withinsubjects study design found significant reductions in skin conductance levels during and after the body scan technique of the MBSR program for participants with fibromyalgia.41 The decrease in skin conductance signifies a reduction in sympathetic nervous system activation. Another study of MBSR for
970
Section V—Specific Treatment Modalities for Pain and Symptom Management
fibromyalgia revealed significant improvements in pain perception, quality of life, and coping with pain for those receiving the intervention compared with patients who had an active social support condition.42 These outcomes were sustained at a 3-year follow-up. Relaxation procedures have also been used for the prevention and treatment of other musculoskeletal disorders, such as back pain, headache, and carpal tunnel syndrome. Yoga43 and PMR44 trainings have been used in corporate settings to decrease stress and the risk of injury. Chronic back pain is another disorder that is challenging to treat with conventional care.45 In a study of MBSR, older individuals with low back pain were assessed after completing the intervention.46 A significant increase in physical function and pain acceptance was reported for the MBSR group compared with the control group after the intervention. Approximately three fourths of the participants from the MBSR group reported a continuation of their meditation practices 3 months later. Nearly three fourths of participants reported that they had recommended the program to others, and almost half reported a reduction in pain and sleep medications. This particular study omitted the yoga and all-day retreat characteristic of the MBSR program. A pilot study examining the effects of yoga for the treatment of chronic low back pain found that balance and flexibility improved, whereas disability and depression scores decreased for the yoga group compared with the control group. Even though the results were not statistically significant, which could be the result of the small sample size, the outcomes were in the desired direction, a finding warranting further research. Yoga, exercise, and a self-care book were compared in a study for individuals with chronic low back pain.47 After 12 weeks, both the yoga and exercise groups were superior to the book group in terms of functional status. An analysis at the 3-month follow-up indicated that symptoms continued to improve for the yoga group only. The yoga group also reported more reductions in medication use. Similarly, a study comparing yoga and an educational control group for low back pain found a significant decrease in functional disability and medication use for the yoga group compared with the control group after the 16-week intervention.48 Yoga has also been used to prevent and treat carpal tunnel syndrome. Results from a study employing this method indicate that those in the yoga group had a significant increase in grip strength and a significant decrease in pain ratings compared with the control group.49 Meta-analytic reviews found that behavioral interventions are effective in preventing and treating tension-type and migraine headaches in both adults50–52 and children.53,54 These therapies include relaxation training, biofeedback, cognitivebehavioral therapy, and stress management training, either in isolation or combined. A study assessing yoga for the treatment of tension-type headache found a significant decrease in pain perception for the yoga group compared with the control group.55 In another yoga study for tension-type headache and migraine, the yoga group displayed a significant decrease in headache activity and medication use with an improvement in coping behaviors compared with the control group.56 Medication intake actually increased for participants in the control condition. Similarly, John et al57 found that a yoga intervention for those with migraine significantly decreased headache frequency, intensity, duration, and medication use, in addition to reducing anxiety, depression, and pain perception
compared with the control group. Participants in the control group had an increase in all these measures except for headache duration. Relaxation procedures have been applied to cancer pain and the side effects of chemotherapy. Syrjala et al58 examined the following interventions for patients undergoing bone marrow transplants: (1) relaxation and imagery; (2) cognitive-behavioral treatment combined with relaxation and imagery; (3) therapist support; and (4) treatment as usual, which served as the control condition. The relaxation/imagery and cognitive-behavioral/ relaxation/imagery interventions resulted in significant pain reductions on self-report measures compared with the therapist support group and treatment as usual group. Combining the cognitive-behavioral treatment to the relaxation and imagery intervention did not add incremental value. A pilot study on yoga therapy for women with metastatic breast cancer found that, on the day of yoga practice, these women had a significant increase in invigoration and acceptance.59 Measures taken the day after yoga practice indicated that the outcomes of increased invigoration and acceptance were still experienced, as well as an increase in relaxation and a reduction in pain and fatigue. It appears as though yoga may have immediate and long-lasting outcomes, as well as delayed effects. Burish et al60 investigated the utility of PMR and GI for cancer patients undergoing chemotherapy. These investigators found that patients in the treatment group had significantly less nausea and vomiting compared with the control group. Moreover, the intervention group had lower blood pressures, pulse rates, and anxiety. Campos de Carvalho et al61 researched the use of PMR in isolation to treat the unwanted side effects of chemotherapy and found similar results. Relaxation techniques have also been used in alleviating pain from both ulcerative colitis and irritable bowel syndrome. Shaw and Ehrlich62 compared the pain ratings of a relaxation intervention group with an attention control group for patients with ulcers. Following the 6-week intervention, patients in the relaxation group had significant reductions in pain ratings. These results were maintained at a 6-week follow-up. Brooks and Richardson63 found a decrease in recurrences of ulcerative symptoms over 3 years after individuals received relaxation and assertiveness training when compared with individuals in a control group. In a yoga study of adolescents with irritable bowel syndrome, investigators found that the intervention group reported significantly lower levels of gastrointestinal symptoms than the control group.64 Participants in the experimental group found yoga therapy to be helpful for their condition. GI has been used in the treatment of phantom limb pain. This phenomenon is believed to be caused by a remapping of the brain in the sensory and motor cortexes after amputation.65,66 Certain pain centers in the brain may become entangled during this rewiring, and the result is pain in a nonexistent limb. MacIver et al11 explored the use of GI in treating individuals with phantom arm pain. After participants underwent a body scan technique to induce relaxation, they were instructed to imagine movements and sensations of the phantom limb. Over the course of the seven-session intervention plus home practice, participants reported significant pain relief. Functional MRI scans denoted a reduction in cortical reorganization from the sensory, motor, and anterior cingulate cortex. Ramachandran and Blakeslee66 noted: “It seems
Chapter 132—Relaxation Techniques and Guided Imagery
extraordinary to contemplate the possibility that you could use a visual illusion to eliminate pain, but bear in mind that pain itself is an illusion—constructed entirely in your brain like any other sensory experience.” The aforementioned studies in this section are just a sampling of the well-documented research in which relaxation techniques and GI had favorable outcomes. These therapies can be applied to treat various medical conditions and in some cases serve as a preventive measure for recurrent pain (e.g. headache, ulcer) or musculoskeletal pain caused by poor posture or overuse.
Techniques This section reviews procedures for relaxed breathing, GI, AT, PMR, mindfulness meditation, and yoga. Therapists often begin with methods of deep breathing, and this topic is addressed first in this section. Next, GI techniques of pleasant imagery and pain-transforming imagery are discussed. The six formulas comprising AT are summarized. Then, an abbreviated version of Jacobson's PMR is described because the less time consuming PMR variations are more widely used in clinical settings. A relaxation treatment program usually involves more than one of these techniques, by combining and tailoring the procedures based on individual needs. An example of a treatment regimen incorporating deep breathing, GI, AT, and PMR is examined. Finally, the MBSR intervention, consisting of relaxed breathing, mindfulness meditation, and yoga, is outlined.
Relaxed Breathing Slow diaphragmatic breathing is a commonly used technique. To minimize shallow chest breathing, the patient is directed to draw air deeply into the lungs by pushing the diaphragm downward. On average, people take 12 to 15 breaths per minute. The goal of slow diaphragmatic breathing is usually 6 to 8 breaths per minute.67 Decelerated breathing may feel strange to an individual who has a high respiration rate (30 or more breaths per minute). Clients should be assured that these unfamiliar feelings of slow, deep breathing will soon pass.6 The following methods demonstrate deep breathing by using the diaphragm: (1) while breathing, place one hand on the chest and the other on the upper abdomen, maximize the movement of the lower hand, and minimize movement of the upper hand; (2) hold hands straight overhead while breathing; and (3) while lying on the floor, place a moderate-weight book on the abdomen and lift and lower the book while breathing in and out.6 Paced respiration breathing and pursed-lip breathing are other breathing therapy techniques.67 Paced respiration is breathing at a predetermined rate. It usually involves a metronome, an external pacing device, to coordinate the rate of respiration. Pursed-lip breathing consists of exhaling slowly while the lips are partially pursed, as if whistling. This type of therapy has been used with patients who have chronic obstructive pulmonary disease. Slow, deep breathing is often an element of all relaxation procedures. It can be quickly and easily brought under voluntary control at any time. Patients are encouraged to use diaphragmatic breathing frequently throughout the day, especially in response to stress.68
971
Guided Imagery Imagery sends messages from the cerebral cortex to the limbic system, an area of the brain associated with emotion.26 Information is then relayed to the autonomic nervous system, thus influencing the immune, endocrine, nervous, cardiovascular, respiratory, and gastrointestinal systems of the body.69 If the images are vivid enough, the body undergoes physiologic changes as if the event is actually happening.69 The physiologic and biochemical changes that occur with imagery have been used to explain the placebo effect in untreated individuals.31,69 The purpose of GI is to generate the healing systems of the body to reduce pain sensation and perception. GI therapies either distract from the pain or focus on it in an attempt to modulate it.17 Imagery with relaxing scenes is a way to distract from pain. Clients are instructed to conjure a relaxing image in the “mind's eye.” Examples of pleasant imagery may include a favorite vacation spot, lying on the beach, or walking in a meadow. Images that may cause arousal (e.g., sexual content, vigorous activity) should be avoided. Other sensory modalities (auditory, olfactory, tactile, and gustatory) are included to enhance the vividness of the image.19,70 Associating a word, such as “relax” or “calm,” engages both hemispheres of the brain and can facilitate recall.26 After practicing a relaxing image, it can be quickly and vividly evoked. Clients are encouraged to apply their personally relevant relaxing scenes in stressful situations.6 Imagery is also used to focus on the pain to suppress or transform it.69 One example of symptom suppression involves a two-step approach. The first step involves inducing feelings of numbness in the hand to initiate “glove anesthesia.” Patients are then instructed to place the “anesthetized” hand on painful areas in the body and to transfer this numbness where it hurts. Symptom suppression is helpful for patients who are experiencing intense discomfort and are having trouble concentrating otherwise. Transforming the pain through symptom substitution imagery consists of mentally moving pain in the body to another area of the body where it is more tolerable. This technique is not intended to suppress the pain, but instead to move the discomfort to a less threatening area of the body.69 For instance, a patient may be guided to move pain to his or her little finger. Another method to transform symptoms is by visualizing the pain as the color red and then imagining the color as becoming less bright, corresponding to a decrease in pain intensity.17 Bresler69 contended that GI draws from an individual's inner resources for coping.
Autogenic Training Schultz created a series of six formulas for AT: (1) the heaviness experience (muscular relaxation), (2) the warmth experience (vascular dilation), (3) the regulation of the heart, (4) the regulation of breathing, (5) the regulation of visceral organs, and (6) the regulation of the head.71 Self-suggestion is used for each stage to produce the ideal effect. Key statements are passively focused on, such as, “heavy arm,” or “warm arm.”71 A patient is instructed to focus on feelings of heaviness and warmth, especially in the extremities. This peripheral warming is believed to increase blood flow, decrease arousal, and promote relaxation. It is recommended that patients personalize their own phrases for heaviness and warmth and to repeat these phrases 50 to 100 times.72
972
Section V—Specific Treatment Modalities for Pain and Symptom Management
Progressive Muscle Relaxation Jacobson's method was adapted by Bernstein and Borkovec to provide a much abbreviated version of PMR for research and clinical application. Andrasik74 delineated a treatment therapy for PMR based on this shortened approach. Major muscle groups are systematically tensed and relaxed. Later in the therapy, muscle groups are combined for more rapid effects. The tensing and releasing of the specified muscles aid in discriminating between levels of tension. With the development of this discrimination, patients can become more aware of their tension levels during the day and can implement PMR to counteract it. Regular practice is emphasized throughout the therapy. The patient acts out a few tension-release cycles of a specified target group. The practitioner observes these practice cycles for complete, but not excessive, tension levels of the target group only. Table 132.3 outlines the 18 steps for the sequential tensing and relaxing of 14 target muscle groups. The tensionrelease cycle for each target muscle group consists of 5 to 7 seconds of tensing and 20 to 30 seconds of relaxing. Each step is repeated twice, with additional practice if needed. It is important to have the previous muscle group fully relaxed before moving on to the next step. The patient is instructed to focus on the sensations of both tension and relaxation of the muscles. Muscles that are tender or causing pain are omitted from the procedure. After the patient becomes more skilled with the 18 steps of tensing and relaxing, then the muscle groups are combined into an even more abbreviated form (Table 132.4). 20
73
Relaxation Treatment Regimen Table 132.5 describes elements of an 8-week relaxation treatment program.74 Over the course of 10 sessions, patients are trained in diaphragmatic breathing, PMR, AT, and GI. The first session consists of an introduction and rationale for the relaxation regimen. Relaxed breathing and PMR are practiced in the first session and during every subsequent session. The specified muscle groups start with the 18 steps and progress to the combined 8 and 4 steps later in therapy (see Tables 132.3 and 132.4). Deepening exercises, such as suggestive self-statements
of warmth and heaviness that are principles of AT, are used to enhance relaxation. Another deepening exercise is having the patient count backward from 5 to 1 while imagining descending stairs or floors in an elevator and becoming more relaxed. These deepening exercises are implemented during the 20 to 30 seconds of the relaxation segment of the tense-and-release cycles. Pleasant imagery is added to treatment in the second session. Discrimination muscle training is implemented in the third session for specific muscle groups. The patient completes a tension-release cycle for a target group and then is instructed to tense only half as much, followed by one fourth, and alternations between these values. The patient continues tensing with decreased force to learn to discriminate more subtle sensations of tension. The patient is advised to use this differential muscle tensing for problem areas. For instance, an individual who has tension-type headaches may want to focus on the forehead and neck areas.
Table 132.4 Abbreviated Target Muscle Groups Eight Muscle Groups
1. Both hands and lower arms 2. Both legs and thighs 3. Abdomen 4. Chest 5. Shoulders 6. Back of neck 7. Eyes 8. Forehead Four Muscle Groups
1. Arms 2. Chest 3. Neck 4. Face (with focus on eyes and forehead) From Andrasik F: Relaxation and biofeedback for chronic headaches. In Holzman AD, Turk DC, editors: A handbook of psychological treatment approaches, New York, 1986, Pergamon, p 228.
Table 132.3 The 18 Steps for Tensing the Initial 14 Targeted Muscle Groups 1. Right hand and lower arm (by having the patient make a fist and simultaneously tense the lower arm) 2. Left hand and lower arm 3. Both hands and lower arms 4. Right upper arm (by having the client bring his or her hand to the shoulder and tense the biceps) 5. Left upper arm 6. Both upper arms 7. Right lower leg and foot (by having the client point his or her toe and tense the calf muscle) 8. Left lower leg and foot 9. Both lower legs and feet 10. Both thighs (by pressing the knees and thighs tightly together) 11. Abdomen (by drawing the abdominal muscles in tightly) 12. Chest (by having the client take a deep breath and hold it) 13. Shoulders and lower neck (by having the client “hunch” his or her shoulders or draw the shoulders toward the ears) 14. Back of the neck (have the client push the head backward against a headrest or chair) 15. Lips (by pressing them together very tightly but not clenching the teeth) 16. Eyes (by closing the eyes tightly) 17. Lower forehead (by having the patient frown and draw the eyebrows together) 18. Upper forehead (by having the patient wrinkle the forehead area) From Andrasik F: Relaxation and biofeedback for chronic headaches. In Holzman AD, Turk DC, editors: A handbook of psychological treatment approaches, New York, 1986, Pergamon, pp 225–226.
Chapter 132—Relaxation Techniques and Guided Imagery
More advanced techniques, such as relaxation by recall and cue-controlled relaxation, are introduced in the sixth and eighth sessions, respectively. Relaxation by recall involves having the patient focus on the sensations of relaxation that were created during PMR practice. The patient is then directed to reproduce these sensations without the tension and release cycles. Cue-controlled relaxation associates a word with a state of relaxation. The cue may be as simple as the word relax, and with the skills that have been acquired throughout the training, the body can respond to the cue accordingly. When the focus is on deep breathing, cues can be stated quietly or silently with each exhalation. It is suggested that patients use breathing, imagery, self-suggestion, and cues that are personalized. The remaining sessions further refine the learned relaxation techniques. Patients should to discover what techniques and variations are most suitable for facilitating their own relaxation. From the beginning of the program, patients are instructed to practice at home once or twice a day for 20 minutes. An audiotape recorded during an early session can assist the patient in pacing his or her home practice. Supplementing live instruction with either commercially available or tailored audiotapes seems to promote a generalization of skills learned from the clinic to daily routines.22 The patient is advised to use the audiotape daily until the fourth week of treatment, at which point the patient is instructed to practice both with and without the audiotape. By week 8, and the last session, the patient should be able to practice without an audiotape at all. Furthermore, patients are advised to continue practice after the treatment has been completed. The methods are designed to aid an individual in coping with daily stress and tension.
Mindfulness-Based Stress Reduction The 8-week MBSR treatment program incorporates both meditation and yoga.75 Mindfulness meditation is introduced in the early sessions, whereas yoga is employed later.
973
Kabat-Zinn75 delineated certain attitudes that facilitate mindfulness. These include (1) nonjudging, (2) patience, (3) a beginner's mind, (4) nonstriving, (5) acceptance, and (6) letting go. Participants meet once a week for 2.5 to 3 hours and once for a full day (7 hours) of mindfulness. The first four sessions involve a 45-minute body scan meditation technique, integrating deep breathing. Lying down, an individual focuses his or her mind from the toes, slowly to the top of the head. This fosters the development of calm, sustained attention. If pain draws attention away from the focused body region, then it is suggested that the person start again at the toes and slowly move up toward the pain and then past it. The patient is instructed to experience fully every sensation in the body, including the painful areas, in a detached manner. Patients are directed to practice the body scan 6 days a week for 45 minutes in the initial 2 weeks of treatment. The second session of the MBSR program consists of the body scan technique and sitting meditation. During sitting meditation, the focus is generally on relaxed breathing. When distracting thoughts occur, patients are encouraged to take note and return their attention to their breath. Home practice begins at 10 minutes daily and later progresses to 45 minutes at a time. In addition to an awareness of breathing, sounds, thoughts, or feelings can be the focus of meditation with the aforementioned nonjudging approach. Two mindful yoga sequences are introduced in the third and fifth session of the MBSR program. The first yoga sequence entails postures that are all floor exercises, including the corpse, wind relieving, and locust poses. The corpse pose is similar to the position of the body during the body scan technique. The sequence begins and ends with the copse pose. The second yoga sequence consists predominantly of standing postures with a mix of floor exercises. It includes sky reaching, tree, and bent knee forward bend poses. This sequence also closes with the corpse pose. During the various postures, individuals are instructed to pay attention to their breathing and subtle sensations in the body. This attention brings awareness
Table 132.5 Relaxation Training Regimen
Week 1
Session
Introduction and Treatment Rationale
Number of Muscle Groups
Deepening Exercises
Breathing Exercises
1
X
14
X
X
14
X
X
2 2
Relaxing Imagery
Muscle Discrimination Training
Relaxation by Recall
CueControlled Recall
X
3
14
X
X
X
X
4
14
X
X
X
X
5
8
X
X
X
X
6
8
X
X
X
X
X
4
7
4
X
X
X
X
X
5
8
4
X
X
X
X
X
X
6
9
4
X
X
X
X
X
X
7
None
8
10
4
X
X
X
X
X
X
3
From Andrasik F: Relaxation and biofeedback for chronic headaches. In Holzman AD, Turk DC, editors: A handbook of psychological treatment approaches, New York, 1986, Pergamon, p 225.
974
Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 132.6 Yoga Asanas/Postures Sanskrit Name
English Name
Brief Description
*Savasana
Corpse pose
Lying on the back with arms and legs extended, palms up
*Pavanamuktasana
Wind relieving pose
Starting with a corpse pose, place hands below right knee, bend and bring toward the chin, release, then repeat with the left leg, release, and then bring both legs up and gently rock forward and backward, side to side
Pranamasana
Salutation pose
Standing with feet together, bring palms together in front of chest in prayerlike fashion
*Hasta Uttanasana
Sky reaching
Starting with a salutation pose, raise arms straight above the head, palms facing forward
*Vrksasana
Tree pose
Standing with feet together, arms at sides, bring the sole of right foot up to the left thigh, then raise arms above head, palms together, release, and then repeat on left side
*Janu Sirsasana
Bent knee forward bend
Sitting upright with both legs extended in front, pull bottom of right foot into inner thigh of left leg, stretch toward left foot, release, and then repeat on other side
Bhujangasana
Cobra pose
Lying on the stomach, with palms planted under shoulders, raise chest and head up, leaving lower abdomen on floor
Parvatasana
Mountain pose
Standing with legs slightly apart and straight, place palms on the floor above the head, and lift buttocks upward, creating a triangular space below the body
Matsyendrasana
Spinal twist
Sitting upright with both legs extended in front, bend left leg with the bottom of left foot on floor next to the right thigh, place right arm around left knee and gently twist spine to the left, release, and then repeat on other side
*Salabhasana
Locust pose
Lying on the stomach with arms at sides or under abdomen, lift right leg straight up, release, then repeat with the left leg, release, and then bring both legs up, keeping knees together, release
*Yoga postures featured in the Mindfulness-Based Stress Reduction Program.75 From Chopra D, Simon D: The seven spiritual laws of yoga: a practical guide to healing body, mind, and spirit, Hoboken, NJ, 2004, John Wiley & Sons.
and acceptance of an individual's physical capabilities and limitations. Each sequence takes approximately 45 minutes to complete. In addition to the yoga group training, patients are given audiotapes to guide them through the sequences for home practice. See Table 132.6 for a list of common yoga postures and brief descriptions. Walking meditation is practiced in the fourth session of the MBSR intervention. It can be done at any walking pace. Again, individuals are instructed to concentrate on their bodies' movements and any sensation that may arise. This technique allows one to apply meditation to a regular, daily activity. Mindfulness can also be expanded to other routine activities, such as household chores. Some patients prefer the movements of yoga and walking meditation as opposed to the stillness of the body scan and sitting meditation. Home practice is still suggested to be at least 45 minutes per day for 6 days a week, using any combination of the learned techniques. The sixth session of the MBSR program is an all-day retreat, lasting 7 hours. The group is silent and avoids eye contact for the first 6 hours, with only the instructors talking and guiding the practices. The retreat begins with a sitting breath mediation followed by yoga. Sitting and walking meditation are alternated throughout the day. In the last hour of the retreat, participants talk about their experiences from the previous 6 hours of silence. The day of mindfulness closes with 15 minutes of sitting meditation. The remaining weeks of the intervention involve practicing and trying variations of the techniques taught in the early sessions. Research on the effectiveness of the MBSR program typically followed this protocol, although some studies excluded
the yoga segments or the all-day retreat.12,46 Yoga, however, appears to have an important role in decreasing symptoms, increasing mindfulness, and increasing well-being when compared with the body scan and sitting meditation techniques. One study found that practice time for yoga, more than the other techniques, was significantly correlated with these outcome measures, even though yoga was practiced for fewer days and fewer minutes overall.76 In addition to the rationale of using relaxation in the treatment of pain, meditation and yoga techniques may also offer beneficial outcomes by enhancing mood and acceptance of the pain condition. Results from an electroencephalographic study found a significant increase in activation of the left anterior region of the brain immediately after 8 weeks of the MBSR program for the meditators compared with the control group of nonmeditators.77 This area of the brain is believed to be associated with positive affect.78 The changes in electroencephalographic activation endured at a 4-month follow-up, a finding signifying lasting effects of the MBSR program.77 The attitude of acceptance that is cultivated through the MBSR program may also apply to a level of acceptance of the pain syndrome.32 This acceptance is not considered resignation, but rather a willingness to live in spite of the pain.79 The perception of pain is transformed from a negative experience to just an experience. Regular home practice is crucial in developing the techniques outlined in both the relaxation treatment regimen, using PMR, and the MBSR program. This practice requires active involvement and a commitment to treatment to acquire the skills and
Chapter 132—Relaxation Techniques and Guided Imagery
maximize the benefits. Individuals may respond differently to the relaxation techniques. For example, those who have migraine headaches may find peripheral warming characteristic of AT the most effective in preventing migraine attacks, whereas those who have tension-type headaches may find better results with PMR.80 Yoga may be especially effective for those with musculoskeletal disorders, in which pain is a result of poor posture or spinal misalignment. Relaxation techniques can be used in isolation or combined with other compatible approaches. Several options are available, and no one procedure has been found to be more effective than another in inducing relaxation.3,19 Moreover, these methods appear to be feasible and applicable for all ages including pediatric81 and elderly12,29,46,82 populations.
Side Effects Relaxation techniques and GI are generally considered safe. Unwanted side effects have been reported, however. A negative phenomenon, known as relaxation-induced anxiety (RIA), describes a group of musculoskeletal, sensory, and cognitive effects that can result from relaxation procedures.83 Negative musculoskeletal activity reactions include tics, spasms, restlessness; negative sensory experiences include unusual sensations, feelings of floating, and other disturbing sensations; negative cognitive and affective responses include sadness, fear, and intrusive thoughts.84 Heide and Borkovec83 proposed possible explanations for these paradoxical effects of RIA. First, individuals who are unfamiliar with relaxation may find the novel sensations strange or bothersome. Second, relaxation procedures emphasize a passive component, and an individual may have a fear of losing control. The fear of inactivity is another possible explanation for RIA, in which individuals have a difficult time sitting still and quietly. Other persons may find self-focused attention aversive. Finally, individuals undergoing relaxation training commonly report interfering thoughts. RIA is uncommon and can usually be alleviated within a training session. One remedy is to change to an alternate relaxation technique.83 For instance, if pleasant imagery is causing symptoms of RIA, then switching to PMR may be appropriate. Another remedy is to implement relaxation procedures gradually, with shorter sessions.83 Although RIA occurs infrequently, practitioners should be aware of it and offer solutions. Even mild symptoms of RIA can influence adherence and attrition to relaxation training programs. Individuals who have pervasive or generalized anxiety seem to be more susceptible to RIA. Investigators have also found that relaxation procedures may not be beneficial for individuals with clinical depression. Support exists, however, for using relaxation techniques in individuals who have secondary depressive symptoms resulting from pain.80
975
Freeman31 discussed certain conditions that can be exacerbated by GI. For instance, patients who have chronic severe depression may not respond favorably to GI. Individuals who have epilepsy should be carefully monitored because imagery can alter brain wave activity. Moreover, glucose levels can be affected by imagery, and patients who have unstable diabetes should also be carefully monitored. Even though no adverse events were reported for yoga in the studies reviewed in the section on indications, certain precautions must be taken. Some yoga postures may put unneeded strain on the joints or the back. Yoga treatment for lower back pain should omit postures that involve back bending.48 Sood26 suggested checking with a physician before beginning a yoga regimen for individuals with neck or back pain. He also advised individuals who have high blood pressure that is difficult to treat, blood clots, certain eye conditions (i.e., glaucoma), or osteoporosis to seek a physician's approval before starting yoga. Women who are pregnant should check with their obstetrician before performing yoga. Some yoga postures that involve twisting at the waist can put pressure on the uterus. Yoga classes designed specifically for pregnant women are available.26
Conclusion Relaxation techniques may generate a general relaxation response,4 with a reduction in activation of the sympathetic nervous system. Additionally, specific effects may account for the beneficial outcomes of relaxation through cognitive and affective mechanisms.5 This chapter begins with the rationale for the use of relaxation techniques and GI for pain conditions. Both PMR and AT were developed in the early 1900s by Jacobson and Shultz, respectively. Meditation, yoga, and GI have a much longer history, as discussed in the section on historical considerations. The section on indications discusses the way in which relaxation techniques and imagery have been successfully applied to various conditions, including arthritis, back pain, headache, carpal tunnel syndrome, cancer, ulcers, irritable bowel syndrome, and phantom limb pain. Procedures for breathing therapies, GI, AT, and PMR are outlined in the section on techniques. A treatment regimen consisting of relaxed breathing, PMR, AT, and GI and the MBSR program, consisting of deep breathing, mindfulness meditation, and yoga, is summarized. This chapter closes with the potential side effect of RIA and other patient precautions.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
133
Therapeutic Heat and Cold in the Management of Pain Steven D. Waldman, Katherine A. Kidder, and Howard J. Waldman
CHAPTER OUTLINE The Physiologic Effects of Therapeutic Heat 978 Choosing a Therapeutic Heat Modality 978
Superficial Heating Modalities 979 Modalities That Deliver Heat via Conduction 979 Hydrocollator Packs 979 Circulating Water Heating Pads (K-Pads) 980 Chemical Heating Packs 980 Reusable Microwavable Heating Pads 980 Paraffin Baths 981 Modalities That Deliver Heat via Convection 982 Hydrotherapy 982 Fluidotherapy 982
Deep Heating Modalities 982
Ultrasound 983 Shortwave Diathermy 983 Microwave Diathermy 984
Therapeutic Cold Modalities 984 The Physiologic Effects of Therapeutic Cold 984 Choosing a Therapeutic Cold Modality 984 Ice Packs and Slushes 984 Iced Whirlpools 985 Ice Rubs 985 Evaporative Cooling Spays 985 Chemical Ice Packs 986
Contrast Baths 986 Conclusion 986
Modalities That Deliver Heat via Conversion 982
Heat and cold have been used in the treatment of pain since the time of Hippocrates. In spite of their widespread use for centuries, a search for the scientific justification for these universally accepted modalities was not undertaken until the birth of the specialty of physical medicine and rehabilitation after World War II. The knowledge that was derived from this search forms much of our rationale for the use of heat and cold in the treatment of pain. This chapter reviews common therapeutic heat and cold modalities and provides the clinician with a roadmap for their safe application.
The Physiologic Effects of Therapeutic Heat The mechanisms by which heat exerts its analgesic effect extend beyond the simple effects of local heat on the target tissue. Locally, heat elicits the following physiologic responses: (1) increased blood flow; (2) decreased muscle spasm; (3) increased extensibility of connective tissue; (4) decreased joint stiffness; (5) reduction of edema; and most importantly, (6) analgesia (Table 133.1).1 Because the sensations of temperature and pain are carried to the higher centers via the same neural pathways, imagining that heat exerts a modulating effect at the spinal and supraspinal levels is not unreasonable. In addition, the feeling of well-being associated with therapeutic heat most likely causes the release of endorphins and other neurotransmitters, further modifying the pain response. However, although the beneficial nature of therapeutic heat 978
cannot be denied, this treatment modality is not without side effects. The relative contraindications to the use of therapeutic heat are summarized in Table 133.2. Although these precautions are not absolute, special care should be taken with the decision to use therapeutic heat in these clinical settings.
Choosing a Therapeutic Heat Modality The clinician who is considering therapeutic heat as an adjunct in the treatment of a patient's pain can choose from a variety of heating modalities (Table 133.3). Although the indications for the use of therapeutic heat apply to all therapeutic heating modalities discussed in this chapter, each modality has its own distinct advantages and disadvantages that can not only influence the success or failure of the therapeutic intervention but can also determine the incidence of side effects and complications if the wrong modality is chosen or if a modality is used in the incorrect clinical situation (Table 133.4). As a practical consideration, the failure to match the modality to the patient usually results in a less than optimal outcome. When matching the modality to the patient, an understanding of the underlying physics of each therapeutic heat modality is essential. Each heat modality accomplishes the delivery of heat to the target tissue via a specific physical mechanism of heat transfer. For sake of organization, these mechanisms can be divided into the categories of conduction, convection, and conversion. Whereas conduction and convection provide © 2011 Elsevier Inc. All rights reserved.
Chapter 133—Therapeutic Heat and Cold in the Management of Pain
Table 133.1 Physiologic Effects of Therapeutic Heat
Table 133.4 Indications for the Use of Therapeutic Heat Modalities
Increased blood flow
Pain
Decreased muscle spasm
Muscle spasm
Increased extensibility of connective tissue
Bursitis
Decreased joint stiffness
Tenosynovitis
Reduction of edema
Collagen vascular diseases
Analgesia (most important)
Contracture
979
Fibromyalgia Induction of hyperemia
Table 133.2 Relative Contraindications to Therapeutic Heat
Hematoma resolution Superficial thrombophlebitis Reflex sympathetic dystrophy
Lack of or reduced sensation Demyelinating diseases Acute inflammation Bleeding disorders Hemorrhage Malignant disease Inability to communicate or respond to pain Atrophic skin Ischemia Scar tissue
Table 133.5 Indications for Therapeutic Ultrasound Tendinitis Bursitis Nonacutely inflamed arthritis Frozen joints Contractures Degenerative arthritis Fractures
Table 133.3 Therapeutic Heat Modalities Superficial heat modalities
Modalities That Rely on Conduction Hydrocollator packs Circulating water heating pads Chemical heating pads Reusable microwavable heating pads Paraffin baths Modalities That Rely on Convection Hydrotherapy Fluidotherapy Deep heat modalities
Modalities That Rely on Conversion Ultrasound Shortwave diathermy Microwave diathermy
primarily superficial heating, conversion has the ability to heat deep tissues. Therefore, the first question in choosing a therapeutic heat modality is whether superficial or deep heat is the desired goal. The next step in matching the modality to the patient is an understanding of which modalities transfer heat via which mechanism (Table 133.5). Hot packs, the most commonly used heat modality in clinical practice, transfer superficial heat via
Plantar fasciitis
conduction, as do heating pads, circulating water heating pads, chemical heating packs, reusable microwave heating pads, and paraffin baths. Hydrotherapy and fluidotherapy deliver superficial heat to the target tissue via convection. The deep heating modalities of ultrasound, radiant heat, shortwave diathermy, and microwave diathermy deliver heat to the target tissues via conversion. With an understanding of how each heat modality delivers heat, the clinician can use the unique characteristics of that modality to best meet patient needs. Specific heat modalities are discussed subsequently.
Superficial Heating Modalities Modalities That Deliver Heat via Conduction Hydrocollator Packs As mentioned previously, the mechanism by which the various types of hot packs deliver heat to the target tissue is conduction. The amount of heat delivered via conduction is directly proportional to the following variables: (1) the area of heat delivery; (2) the length of time the heat is delivered; (3) the temperature gradient between the hot pack and the target tissue; and (4) the thermal conductivity of the surfaces.2 The amount of heat delivered via conduction is inversely proportional to the thickness of the layers of materials and tissue through which the heat must be conducted. With alterations
980
Section V—Specific Treatment Modalities for Pain and Symptom Management
of any of these variables, the amount of heat delivered to the target tissue can be increased or decreased as the clinical situation and patient comfort dictate. Hydrocollator packs are flexible packs that contain a silicate gel product and are heated in a water bath to approximately 77°C (170°F) (Fig. 133.1). The large surface area and flexible nature make this modality ideally suited for treatment of low back and dorsal spine pain. Smaller hydrocollator packs are useful in the treatment of neck pain. The packs do not absorb significant amounts of water, but the surface is wet, which increases conduction. A terrycloth towel is placed between the patient and the hydrocollator pack, with the thickness of towels being the easiest way to control the dosimetry and allow titration of the temperature to patient comfort. The packs maintain a therapeutic temperature for approximately 20 to 30 minutes to allow for superficial heating of large surface areas. To avoid burning the patient, care must be taken to allow excess water to drain from the pack before use. The hydrocollator pack should always be placed on rather than under the patient for easy removal should the patient find the pad is too hot.
Circulating Water Heating Pads (K-Pads) Like the hydrocollator pack, the circulating water heating pad is ideally suited for treatment of low back and dorsal spine pain. More flexible than the hydrocollator pack, the circulating water heating pad can also be used on shoulders and extremities. The circulating water pad is thermostatically controlled so that the water temperature remains constant, which allows for superficial heating of relatively large surface areas. This confers two additional benefits to this heat delivery device: (1) unlike hydrocollator packs, hot water bottles, and microwave heating pads that cool over time, the circulating water heating pads can deliver a constant temperature to the target tissue over time; and (2) the thermostatically controlled circulation system greatly decreases the risk of thermal injuries associated with traditional electric pads (Fig. 133.2). In spite of the increased safety of circulating water pads relative to electric heating pads, because they do not cool spontaneously, their use should be closely monitored and carefully timed.
nally segregated chemicals. These chemicals, when mixed with squeezing or kneading of the package, cause an exothermic reaction that releases heat capable of producing superficial heating of the affected body part. Other chemical heating pads produce heat via oxidation when the chemical heating pack is exposed to air. Most chemical heating packs that rely on oxidation contain iron powder, activated charcoal, sodium chloride, and water. Although inexpensive and convenient to use, the chemical heating packs produce varying degrees of heat and have the potential to cause severe burns even when used properly.3 The chemicals contained in the packs can cause irritation to the skin if the outer package integrity is compromised. Chemical heating packs have the advantage of being portable and not needing electricity or external heating.
Reusable Microwavable Heating Pads The widespread use of microwave ovens has spawned a variety of new reusable heating pad products that are designed to be quickly heated in the microwave oven. These products consist of an outer bag, which may be made of cloth or plastic, and a sealed inner bag that contains gel or grains (including rice, corn, or wheat) and delivers heat via conduction to provide superficial heating of the affected tissues (Figs. 133.3 and 133.4). Some products add aromatic substances to provide the added theoretic benefit of aromatherapy. Although convenient and easy to use, these products have some serious drawbacks. First, as with microwave popcorn, variations in the heating abilities of microwave ovens can cause overheating or underheating. In addition, there is no simple way to verify the actual temperature of the product; and because of the nature of microwave ovens, significant inconsistencies of
Chemical Heating Packs Chemical heating packs are readily available in most pharmacies. They consist of a flexible outer layer that contains inter-
Fig. 133.1 Hydrocollator packs are flexible silicate gel packs that are heated in a water bath to approximately 77°C (170°F).
Fig. 133.2 Thermal injury of the type associated with traditional electric pads.
Chapter 133—Therapeutic Heat and Cold in the Management of Pain
surface temperatures with “hot spots” may result in serious burns. Like hydrocollator packs and other heat delivery modalities that do not deliver a constant source of heat, cooling can be inconsistent.
Paraffin Baths Used primarily for the treatment of hand abnormalities associated with rheumatoid arthritis, degenerative arthritis, and other collagen vascular diseases such as scleroderma, paraffin baths are a useful form of conduction-type heat therapy capable of providing superficial heating of the affected tissues.4,5 Paraffin baths are reasonably safe as long as the temperature of the liquid paraffin is checked before extremity immersion or application. The paraffin is generally mixed with mineral oil (7 parts paraffin to 1 part of mineral oil) and placed in a thermostatically controlled heater (Fig. 133.5). The affected body part is dipped into the
Fig. 133.3 The widespread use of microwave ovens has spawned a variety of new reusable heating pad products that are designed to be quickly heated in the microwave oven.
981
paraffin bath and then removed to allow the paraffin to solidify. This procedure is repeated up to 10 times. The affected body parts are placed under an insulating sheet for approximately 20 minutes, and then the paraffin is stripped off and returned to the thermostatically controlled heater to melt and use again. This technique is usually not undertaken with acutely inflamed joints and can be used only after anti-inflammatory drugs have begun to treat the acute inflammation.
Fig. 133.5 Paraffin baths are a useful form of conduction-type heat therapy capable of providing superficial heating of the affected tissues.
Fig. 133.4 Reusable microwavable heating pads consist of an outer bag that may be made of cloth or plastic and a sealed inner bag that contains gel or grains (rice, corn, or wheat). They deliver their heat via conduction to provide superficial heating of the affected tissues.
982
Section V—Specific Treatment Modalities for Pain and Symptom Management
Modalities That Deliver Heat via Convection Hydrotherapy
Deep Heating Modalities
Water is an ideal medium for delivery of heat to affected tissues because of its high specific heat. Hydrotherapy uses this physical property to advantage with the agitation of a whirlpool to constantly move the layer of heated water that has cooled after contact with the skin and replace it with water heated to the correct temperature. In addition to the superficial heat delivery properties of hydrotherapy, immersion of the affected body part, or entire body in the case of Hubbard tank therapy, allows the high specific gravity of water to partially eliminate the effect of gravity, adding another potentially therapeutic sensation to the analgesic milieu (Fig. 133.6). The massaging effect of water can also help reduce muscle spasm and provide gentle débridement of wounds. For treatment of single limbs, immersion in waters with temperatures of 115°F (46°C) is generally well tolerated if careful monitoring is carried out. Temperatures above 102°F (39°C) should be avoided with use of total body immersion to avoid overheating. Total body immersion should not be used in patients with multiple sclerosis to avoid the triggering of neurologic deficits that may sometimes become permanent.
The heat delivery modalities previously discussed have in common their ability to produce superficial heating of affected tissues. When heating of the deep tissues is desired, clinicians have several modalities at their disposal. These include three modalities in common clinical use: (1) ultrasound; (2) shortwave diathermy; and (3) microwave diathermy. These modalities all have the ability to safely heat deep tissues via the physical property of conversion of physical energy into heat when properly used. Variables that affect the amount of heat ultimately delivered to deep tissues for each of these modalities include: (1) the pattern of relative heating; (2) the specific heat of the tissue being heated; and (3) the physiologic factors that affect the tissues being heated. Each of these variables is discussed individually. Relative heating is the relative amount of energy that is converted into heat at any point in the tissue being heated. For sake of consistency, common reference points for the pattern of relative heating include the subcutaneous fat/muscle interface, the muscle/bone interface, and so on. The pattern of relative heating is different for each of the deep heat modalities currently in common clinical use. The specific heat of the tissue also influences how deep heat is distributed through affected tissues. Each type of tissue being heated has its own specific heat. As each of these tissues is heated, the thermal conductivity of the tissue changes as the relative temperatures of each type of tissue reach equilibrium, thus affecting the heat exchange between warmer and cooler tissues.
Fluidotherapy Fluidotherapy uses convection as its mechanism of heat transfer. In contrast with hydrotherapy, which relies on the high specific heat of water delivered at lower temperatures, fluidotherapy relies on substances with a low affinity for heat (e.g., glass beads, pulverized corn cobs, etc) and high heat temperatures of 116°F (47°C) (Fig. 133.7). The result is a dry semifluid mixture that is heated with thermostatically controlled hot air. The patient is able to immerse the affected hand, foot, or portion of an extremity into the mixture. As the affected body part is heated, sweating enhances heat transfer, producing superficial heating. This treatment modality is useful in the treatment of reflex sympathetic dystrophy in that the medium used (e.g., glass beads) provides gentile tactile desensitization.
Fig. 133.6 Immersion of the affected body part, or entire body in the case of Hubbard tank therapy, allows the high specific gravity of water to partially eliminate the effect of gravity, adding another potentially therapeutic sensation to the analgesic milieu.
Modalities That Deliver Heat via Conversion
Fig. 133.7 Fluidotherapy relies on substances with a low affinity for heat (e.g., glass beads, pulverized corn cobs) and high temperatures of 47°C (116°F).
Chapter 133—Therapeutic Heat and Cold in the Management of Pain
The physiologic changes induced with deep heating also influence the heat distribution by modifying the physiologic factors that existed before the deep heat was applied. For example, in normal conditions, the skin temperature is generally lower that the deeper muscle tissues. The application of a deep heating modality further raises the core temperature of the muscle being heated, thereby increasing the temperature gradient between skin and deep muscle. However, as the deep heat is applied to muscle, an increase in blood flow to the heated muscle occurs. The incoming blood is cooler than the heated muscle, so the blood with its relatively high specific heat acts as a cooling agent, carrying off excess heat and cooling the muscle.6 The interplay of these and other physiologic factors ultimately affects the pattern of temperature distribution.
Ultrasound Ultrasound uses sound waves to deliver energy to affected tissue. These sound waves occur at a frequency well above the upper level of human hearing (which occurs at approximately 20,000 Hz) and are produced with the use of a piezoelectric crystal that converts electrical energy into sound waves. These sound waves produce both thermal and nonthermal therapeutic effects on tissue, and manipulation of the physical properties of these effects can tailor the therapeutic response delivered—for example, high-temperature destruction of malignant liver tumors, phonophoresis (the forcing of steroids and anti-inflammatory drugs into tissues with sound), lithotripsy, and deep heating of tissues. Although an extensive discussion of the physics involved in the therapeutic use of ultrasound is beyond the purpose of this chapter, a few general comments are useful for the clinician to understand how the modalities are used to produce deep heat for the treatment of pain and the other conditions listed in Table 133.3. For the purposes of our discussion, it is sufficient to note that the two major variables at play that determine the propagation of ultrasonic energy are: (1) the absorption characteristics of the tissues being exposed to the sound waves; and (2) the reflection of these sound waves as they impinge on tissue interfaces (e.g., muscle, bone). These two variables give ultrasound the unique characteristic of being able to heat deep tissues such as joints with little heating of overlying skin and subcutaneous tissues.7 Each variable can dramatically affect the amount of sound energy that is converted to heat. One example is absorption: bone absorbs almost 10 times more energy than does skeletal muscle and almost 20 times more energy than subcutaneous fat, which means that much more of the ultrasonic energy is converted into heat at the bone interface relative to the muscle or subcutaneous fat interface. Likewise, reflection of the ultrasonic energy occurs primarily at the bone interface, with very little reflection occurring at the subcutaneous fat or muscle interface. Thus, most of the sound energy delivered is able to penetrate the subcutaneous tissues and muscle, with the reflected sound waves producing much of their heating effect at the muscle-bone interface. This physical property of reflection can produce extremely high temperatures if ultrasound is accidentally used in patients with metal prosthetics or large metal surgical clips because reflection from these artificial interfaces can produce an intense increase in reflected ultrasonic energy that can cause disastrous deep thermal injury.
983
The admonition that ultrasound is contraindicated over metal implants should be heeded.8 If sound waves are to be effectively delivered to the intended tissues, coupling between the skin overlying the tissue and the ultrasound wand must be accomplished. This is accomplished with introduction of a medium called a coupling agent. Gel and degassed water are commonly used coupling agents. Ultrasound is usually delivered with the ultrasound wand, which has been liberally covered with coupling agent, being moved slowly over the affected area for 5 to 10 minutes. For body parts with irregular surfaces, such as the ankle, ultrasound can be delivered indirectly with immersion of the affected body part in degassed water and placement of the ultrasound wand in close proximity to the skin but not actually touching it and then slowly moved over the affected areas. This technique is known as indirect ultrasound and necessitates higher energy levels to offset the absorption of sound waves by the water to achieve similar deep heating effects when compared with direct ultrasound. Indications for ultrasound are summarized in Table 133.5. Tendinitis and bursitis generally respond well to treatment with ultrasound, as does degenerative arthritis.9 Although the use of ultrasound is generally avoided when a joint is acutely inflamed, it can be beneficial as the joint inflammation is resolving after intra-articular injection of steroids or the implementation of anti-inflammatory drugs. Ultrasound can be used in concert to enhance the effects of active and passive range of motion and stretching of joints that have lost normal range of motion—and in the treatment of plantar fasciitis.10,11
Shortwave Diathermy Shortwave diathermy uses electromagnetic radio waves to convert energy to deep heat. As with ultrasound, shortwave diathermy is thought to exert its therapeutic effects via both thermal and nonthermal mechanisms. The primary nonthermal mechanism associated with the use of therapeutic shortwave diathermy is vibration induction of tissue molecules with exposure to radio waves. By changing the characteristics of the shortwave applicator, clinicians can target the specific type of tissue they want to heat. With use of an inductive applicator that generates a magnetically induced eddy of radio wave currents in the tissues, selective heating of water-rich tissues, such as muscle, can be obtained (Fig. 133.8). With use of a capacity-coupled applicator that generates heat via generation of an electrical field, selective heating of water-poor t issues, such as subcutaneous fat and adjacent soft tissues, can be accomplished.12 With either type of shortwave diathermy, metal must be avoided; the patient must remove all jewelry, and treatment must be carried out on a nonconductive (e.g., wooden) treatment table. Implanted pacemakers, spinal cord stimulators, surgical implants, and copper-containing intrauterine devices (IUDs) should never be exposed to shortwave diathermy to avoid excessive heating and thermal injury. Indications for shortwave diathermy mirror those listed for ultrasound, although the ability to heat subcutaneous fat and adjacent soft tissues not reached with superficial heat modalities and less well heated with ultrasound may lead the clinician to choose shortwave diathermy for treatment of painful conditions and other pathologic processes that are thought to find their nidus in more superficial tissues.13
984
Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 133.6 Indications for Therapeutic Cold Pain Muscle spasm Acute musculoskeletal injury Bursitis Tendinitis Adjunct to muscle re-education
Table 133.7 Precautions and Contraindications with Use of Therapeutic Cold Lack of or reduced sensation Ischemia Raynaud's phenomenon Cold intolerance
Fig. 133.8 Shortwave diathermy uses electromagnetic radio waves to convert energy to deep heat.
Microwave Diathermy Microwave diathermy uses electromagnetic radio waves with frequencies of 915 and 2456 MHz.14 On the basis of the physical properties of these waves and the corresponding dimensions of the microwave antennae, microwave diathermy has two unique properties that can be used to clinical advantage. The first is that microwaves are selectively absorbed in tissues with high water content, such as muscle.15 This makes microwave diathermy ideally suited to treatment of pathologic processes that occur in the muscles and adjacent fat.16 The second is that microwaves are more easily focused than the short waves used in shortwave diathermy, thereby decreasing energy leakage and making heating more efficient. Microwave diathermy also has several unique side effects of which the clinician must be aware. First, microwaves can cause cataract formation, so protective eyewear must be worn whenever microwave diathermy is used.17 Second, in addition to the precautions and contraindications to the use of shortwave diathermy listed previously, because microwave diathermy has a selective affinity to heat water, this technique should not be used in patients with edema or blisters or in patients with hyperhidrosis because the sweat beads may become heated and cause burns to the skin.
Therapeutic Cold Modalities The Physiologic Effects of Therapeutic Cold The application of therapeutic cold exerts both local and remote physiologic effects.2 Locally, the application of therapeutic cold causes vasoconstriction, which is ultimately followed by a reflex vasodilation after the vascular smooth muscles are paralyzed from the cold. Therapeutic cold decreases the metabolic activity of the treated part and
decreases muscle tone. As cooling progresses, spasticity is also decreased.18 As cooling slows nerve conduction, analgesia occurs. Indications for the use of therapeutic cold are summarized in Table 133.6.
Choosing a Therapeutic Cold Modality As with the choice of heat modalities, matching of the therapeutic cold modality to the patient is paramount to the success of the treatment and to minimization of the side effects and complications associated with its use. The major determinants in the choice of therapeutic cold modalities are primarily based on two categories: (1) the body part being treated; and (2) whether the modality is administered by a qualified health care professional. As with therapeutic heat, improper use of therapeutic cold modalities can cause serious complications (Table 133.7).
Ice Packs and Slushes The high specific heat capacities of ice packs and slushes allow rapid cooling of affected areas. Ice packs can be simply made with placement of melting ice and cold water in a Ziploc plastic bag. With use of crushed ice and more cold water, a slush pack can be made. Commercially available plastic gel packs, often covered with a soft fabric, may be stored in the refrigerator or freezer and are also a convenient way of therapeutic cold delivery (Fig. 133.9). The flexible nature of both these therapeutic cold modalities allows them to be used over joints or to cool larger areas such as the low back. The rate of cooling of the skin is rapid, and the rate of the cooling of deeper tissues is largely a function of the thickness of fat interposed between skin and muscle. When used for periods of 20 minutes or less, they packs are usually safe. The use of a towel between the ice pack or slush and the affected body part increases tolerance and compliance and decreases the incidence of thermal injury. For home use, a package of frozen peas or corn can serve as an effective and inexpensive ice pack for many painful conditions.
Chapter 133—Therapeutic Heat and Cold in the Management of Pain
985
Fig. 133.9 Commercially available plastic packs, often covered with a soft fabric, that contain gel and may be stored in the refrigerator or freezer until use are a convenient way of therapeutic cold delivery. Fig. 133.10 Chemical ice packs are made of a flexible outer layer and a two-compartment inner layer.
Hot water
Cold water
Fig. 133.11 Contrast baths consist of a hot and a cold bath with temperatures of 43°C (110°F) and 16°C, (60°F), respectively.
Iced Whirlpools Used primarily for athletic injuries, the iced whirlpool can rapidly cool an injured extremity by constantly moving water that is warmed by contact with the patient's skin away and replacing it with colder water. Many patients find that the temperatures needed to adequately cool muscle are too uncomfortable to tolerate for the time necessary to achieve the intended therapeutic effect. However, some patients find the iced whirlpool more beneficial than similar heated whirlpool treatments.
Ice Rubs Useful for application of therapeutic cold to larger surface areas such as the low back, ice rubs that use water frozen in a plastic or styrofoam cup can rapidly achieve therapeutic
temperatures, with cutaneous anesthesia being achieved within 8 to 10 minutes. In addition, the rubbing action can produce a relaxing effect and aids in tactile desensitization. In healthy patients, ice rubs for periods of 20 minutes or less are usually safe.
Evaporative Cooling Spays Useful in the treatment of trigger points associated with fibromyalgia and as an adjunct to stretching, the application of evaporative cooling sprays can be quite effective.19 In the past, ethyl chloride spray was the agent of choice; however, the flammability and potential toxicity of the agent has led to the use of the chlorofluormethane compounds. Although effective, these compounds have been criticized as having a negative
986
Section V—Specific Treatment Modalities for Pain and Symptom Management
effect on the environment. For use of the evaporative sprays, the trigger point or affected muscle is identified and the agent is aimed at the target area from a distance of approximately 1 meter and applied for approximately 10 seconds. Prolonged cooling of a single point with the evaporative agents can result in thermal injury.
Chemical Ice Packs A large number of disposable ice packs are available for home use and for clinical applications. Chemical ice packs are made of a flexible outer layer and a two-compartment inner layer (Fig. 133.10). One inner compartment contains water, and the other contains ammonium nitrate that, when combined with squeezing or kneading of the package, creates cooling via an endothermic reaction. These products have the advantage of needing no refrigeration, being easily moldable to joints given their flexibility, and being relatively inexpensive. As with chemical heat packs, the temperature of chemical ice packs is poorly controlled and thermal injuries or inadequate or uneven cooling may occur.20 Exposure of the skin to the chemicals contained in the pack may cause chemical irritation.
Contrast Baths As a combination of therapeutic heat and cold, contrast baths are useful in the treatment of reflex sympathetic dystrophy and other sympathetically maintained pain syndromes and
rheumatoid arthritis.21 Their efficacy is thought to be the result of desensitization of nerves with alternating exposure of the affected extremity to heat and cold. Contrast baths consist of a hot and a cold bath with temperatures of 43°C (110°F) and 16°C (60°F), respectively (Fig. 133.11). Therapeutic contrast baths begin with the soaking of the affected extremity in the warm bath for 10 minutes. The extremity is then rapidly transferred to the cold bath for a period of 3 minutes, followed by rapid transfer back to the warm bath for 5 minutes. The cycle is repeated four times. For patients with extreme allodynia, less extreme temperatures may be necessary during initiation of therapy. Contrast baths should be combined with tactile desensitization techniques if optimal results are to be obtained.
Conclusion The use of therapeutic heat and cold represents a useful adjunct in the treatment of a variety of painful conditions. Although the modalities are relatively safe if used properly, severe injury can occur if risk factors are ignored or a specific modality is misused. The correct matching of the modality to the patient is paramount if optimal results are to be achieved and side effects and complications are to be avoided.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
134
V
Hydrotherapy David A. Soto-Quijano and Martin Grabois
CHAPTER OUTLINE Historical Considerations 987 Principles of Hydrotherapy 988 Physical Effects 988 Therapeutic Effects 989 Techniques 989 Water-Based Exercises 989 Indications 989 Equipment 990 Prescription 991 Contraindications 993
Hydrotherapy is the use of a water environment for therapeutic effects. Aquatic rehabilitation or aquatic therapy refers to the combination of healing and rehabilitation modalities in water.1 The use of the aquatic environment to help in managing pain and increasing function through rehabilitation is rapidly increasing because of the proven physiologic and biodynamic properties of water that allow the patient with pain to rehabilitate more rapidly and safely.2 More than 7.2 million people participated in nonswimming aquatic exercise in 2007, according to a 2008 superstudy of sports participation.3 When used in a comprehensive therapeutic approach, aquatic exercises are designed to aid in the management and rehabilitation of patients with pain. Aquatic therapy not only promotes modification of pain and increases function but also accomplishes this in a costeffective environment.
Historical Considerations The use of water as a healing medium dates back many centuries, although its original use does not coincide exactly with the present perception of its use for rehabilitation purposes. The original use of water (dating back to 2400 bc) was closely connected to the mystical and religious worship of water and its perceived power of healing.4 The Greek civilization in 500 bc began to use water more logically for specific physical treatments, and the Romans expanded the bath system. The Romans added a system of baths at various temperatures and used them not only for rest and recreational activities but also for health and exercise to heal and treat injuries.5 By the early Middle Ages, religious influences had led to the decline of the use of water for its healing power because this use was considered a pagan act.6 The period from 1600 to 1800 saw a resurgence of water healing, but not for hygienic © 2011 Elsevier Inc. All rights reserved.
Whirlpool and Hubbard Tank 993 Indications 993 Equipment 993 Prescription 993 Contraindications 994 Contrast Baths 994 Indications 994 Equipment 994 Prescription 994 Contraindications 994
Conclusion 994
purposes, and the term hydrotherapy started to take hold.7 The use of hydrotherapy continued to be primarily passive, although at about this time, spas, built around a natural spring and usually surrounded by natural beauty, were developed in Europe and then in the United States.4 During the early to middle 1900s, the property of buoyancy began to be used to exercise patients in water, with the development of the Bad Ragaz technique and the Hallwich method in Europe.4 During the poliomyelitis epidemics of the early 1900s, medically supervised exercises in water began to gain popularity in the United States.4 Finnerty and Corbitt6 related that a young person with poliomyelitis fell from his wheelchair into a pool. While attempting to keep himself afloat, the young man discovered that he could move his paralyzed legs. This movement was not possible on land. He continued with a pool exercise program to strengthen his lower extremities and was able to progress from being wheelchair bound to ambulating independently without braces and using only a cane. Many European rehabilitation facilities continued to maintain some type of aquatic therapy as part of an integrated rehabilitation program that was largely publicly funded. This was not the case in the United States.4 Through the 1950s and 1960s,7 the use of this technique declined in the United States as a result of the control of poliomyelitis, limited insurance reimbursement, and a lack of education regarding water as a therapeutic exercise medium. In the 1980s, the use of hydrotherapy increased in the United States, but it still lagged behind Europe because of reimbursement issues, as well as lack of evidence-based efficacy studies, accepted treatment protocols, and education of practitioners.4 This is also true of other therapeutic techniques that have withstood the test of time but lack significant evidence bases of cost effectiveness and efficacy. Morris8 pointed out a shortage of efficacy research in aquatic physical therapy and other 987
988
Section V—Specific Treatment Modalities for Pain and Symptom Management
therapies that address patient outcomes. Currently, aquatic therapy is increasingly used in the United States. Its continued acceptance as a common modality will depend on research on cost effectiveness and efficacy, protocols of treatment, insurance coverage, and education of health care personnel.
Principles of Hydrotherapy The practitioner must understand numerous principles of hydrotherapy to appreciate the beneficial effects of this modality in pain relief and improvement of function and to prescribe hydrotherapy in a safe, comprehensive, and effective rehabilitation program. All aquatic exercise therapy routines must address two important factors: the body's physiologic response to immersion in water and the physical properties of water.1 Nearly all the biologic effects of immersion are related to fundamental principles of hydrodynamics, including buoyancy, hydrostatic pressure, and temperature 2 Table 134.1 lists the principles of hydrotherapy. Buoyancy is explained by the finding that a body submerged in water is supported by a counterforce that supports the submerged object against the downward pull of gravity. The submerged body seems to lose weight equal to the weight of the water displaced, and the results are less stress and less pressure on muscle and connective tissue.9 Patients exercising in water feel lighter, move more easily, and feel less weight on their joints because of this buoyancy property.10 On land, the center of gravity of a body is just in front of the sacrum at the S2 level. In the water, the center of gravity is located at the level of the lungs. The degree of partial weight bearing varies with pool depth, with buoyancy of 90% when the body is immersed up to the neck.11 Buoyancy can be used in an assistive, resistive, or supportive manner. This force assists any movement toward the surface of the water and resists any movement away from the surface of water. These attributes of buoyancy can be enhanced through the use of flotation devices. Hydrostatic pressure is pressure exerted by water on a submerged body. The pressure opposes the tendency of blood to pool in lower portions of the body and thus helps to increase venous return to reduce lower extremity swelling and stabilize unstable joints. Because of the property of hydrostatic pressure, patients with chronic obstructive pulmonary disease may have difficulty breathing, given that the pressure of water resists chest wall expansion of 85% immersion.2 Specific heat is the amount of energy necessary to increase the temperature of a substance by 1°C (34°F). Because the specific heat of water is several times that of air, heat loss is 25 times that of air at a given temperature.12 When more heat is lost to water than is produced by muscle, the patient feels cold.2 Vigorous exercise performed in warm water (33°C [91°F]) results in an increased core temperature (39.4°C [103°F]) and
premature fatigue.12 The ideal temperature for vigorous exercise is 28°C (82°F) to 30°C (86°F), but for patients with pain, who perform less intense exercise, a higher pool temperature is allowed.2 Other properties of water to be considered in the use of hydrotherapy are viscosity and refraction. Viscosity is defined as the frictional resistance presented to a body moving through a fluid. Although resistance in air is negligible, in water several factors can lead to resistance proportional to effort exerted, and this property allows for the use of water for strengthening. As water temperature increases, however, the viscosity decreases and can be beneficial for stabilizing small, weak muscle.2 Refraction is the deflection of light as it passes through air into water. Refraction can affect visual feedback and requires appropriate guidance for patients acquiring new skills and for coordination of movements.1
Physical Effects Many profound physiologic effects are produced by immersion of the human body in water (Table 134.2). Additionally, the physiologic effects experienced by patients immersed in warm water depend on the posture, with the greatest physiologic changes observed in the upright posture.13 These effects can be a problem in patients with medical conditions that limit responses to these changes. The physiologic responses experienced by the body during warm water immersion are similar to the responses of localized heat application, although they are less concentrated.14 Wilder et al2 summarized the physiologic effects of immersion in water. The cardiac effects produced through immersion are profound and are probably salutary for overall health and for the rehabilitating heart. Prominent among these effects are the increases in stroke volume and cardiac output. The effects of immersion on the respiratory apparatus and the pulmonary system have been found to increase respiratory effort and work. A program of regular aquatic exercise should produce a significant training effect and should increase pulmonary functioning.
Table 134.2 Physiologic Changes during Warm Water Exercise Increased respiratory rate Decreased blood pressure Increased blood supply to muscle Increased muscle metabolism Increased superficial circulation Increased heart rate
Table 134.1 Principles of Hydrotherapy Buoyancy Hydrostatic pressure Specific heat Viscosity Refraction
Increased amount of blood returned to heart Increased metabolic rate Decreased edema of submerged body parts* Reduced sensitivity of sensory nerve endings General muscular relaxation *Because of the hydrostatic pressure at the water surface, 14.7 psi plus an increase of 0.43 psi for every 1-ft increase in depth.
Chapter 134—Hydrotherapy
The effects on the circulatory system and the autonomic nervous system and the compressive effect of water pressure dramatically alter muscle blood flow and thus increase oxygen delivery and metabolic waste product removal. These effects are salutary on healing, normal exercising muscle and ligament structures. The aquatic environment produces renal system changes that promote removal of metabolic waste products and produce diuresis, lower the blood pressure, and assist the body in regulation of sodium and potassium. These effects persist longer than the period of immersion and may have general applicability in the management of some forms of hypertension.2
Therapeutic Effects The various physiologic changes noted during warm water immersion also can offer therapeutic effects in numerous medical conditions, including chronic pain (Table 134.3). The relaxation response of muscles depends on how comfortable the patient is in the water. The warmth of the therapeutic pool reduces muscular tension and helps to prevent restricted joint movement.1 Warm water also helps patients with pain to relax and feel more comfortable. The water provides support for injured limbs that allows comfortable positioning without increased pain. The stimulatory effects of warm water promote the relaxation of “tight” spastic muscles and thereby reduce muscle guarding. During warm water immersion, the sensory inputs are competing with the pain input; as a result, the patient's pain perception is blocked out or “gated.” This reduction in pain is perhaps the most significant advantage of aquatic therapy. Additionally, body parts immersed in water warmer than 35°C (95°F) begin to increase in temperature toward the temperature of the core.14 This warmth reduces abnormal muscular tone and spasticity. The physical properties and the warmth of the water play important roles in improving or maintaining joint range of motion. The buoyancy of water decreases the compression forces on painful joints and assists movement. The water also provides support and decreases the need for splinting or guarding. The warmth of the water reduces spasticity, promotes relaxation, and helps to prepare the connective tissue for stretching. Elongated tissue has a lower risk of injury and
Table 134.3 Therapeutic Benefits of Warm Water Exercise Promotes muscular relaxation Reduces pain sensitivity Decreases muscle spasm Increases ease of joint movement Increases muscular strength and endurance in cases of excessive weakness Reduces gravitational forces (early ambulation) Increases peripheral circulation (skin condition) Improves respiratory muscles Improves body awareness, balance, and proximal trunk stability Improves patient morale and confidence (psychological)
989
of muscle soreness after exercise.13 The water also provides greater resistance to movement than air and thus allows the joint to move more freely. In the water, movements are more consistent and are more easily graded using the principles of buoyancy without the pain of active movement. Warm water promotes relaxation of the spastic antagonists of a weak, exercising muscle. Strength training often can begin in the water before it is possible on land.14 Similarly, because of the reduction of gravitational forces, an injured patient can stand and begin gait training and strengthening exercises earlier on water than on land without being concerned about causing further damage to the healing structures.15,16 Walking earlier helps to improve balance and increase muscle tone. As time goes on, a gradual reduction in the water level can help the patient retrain for the weightbearing aspect of gait. Circulation increases in water temperatures higher than 34°C (>93°F). The redistribution of blood during immersion augments flow to the periphery that causes an increase in the blood supply to the muscles and helps in increasing venous return.14 Exercising injured limbs in deep water further increases circulation, and as water depth increases, so does the hydrostatic pressure exerted on the submerged body part.14,16 In chest-deep water, the hydrostatic pressure exerted on the walls of the chest and abdominal muscles increases during breathing. The neutral warmth provided by the water relaxes spastic respiratory muscles. Aquatic activities that require an increase in respiration (e.g., swimming, aerobic exercise) or help to train the breathing component (e.g., blowing bubbles) are beneficial to patients who have respiratory problems.17 Warm water stimulates awareness of the moving body parts and provides an ideal medium for muscle reeducation. The supportive properties of the water give patients with poor balance time to react during falling by slowing the movement. Stabilization during exercise also can be obtained through the use of railings, parallel bars, underwater benches, submerged chairs, tubes, and other devices in water.17 Finally, for patients with pain and patients who cannot yet exercise on land, water provides a positive medium in which to move and relax. The ease of movement allows the patient to achieve much more in water than on land and provides the patient with confidence to aid rehabilitation. In water, patients have less fear of falling or of hurting the injured or painful sites.
Techniques As previously stated, the term hydrotherapy includes any use of water for healing purposes. Under that definition, hydrotherapy includes hot or cold compresses, sitz baths, steam baths, colonic irrigation, douches, enemas, shower carts, swimming, and saunas. This chapter discusses the hydrotherapy techniques most commonly used for pain management: water-based exercise, Hubbard tank, whirlpool baths, and contrast baths.
Water-Based Exercises Indications Water-based exercises are commonly used in the treatment of musculoskeletal ailments. The previously discussed properties of water and the physiologic effects of the water on the body allow patients with pain to enjoy the benefits of exercises in a
990
Section V—Specific Treatment Modalities for Pain and Symptom Management
safe and controlled environment. Water-based exercises potentially can be used in the treatment and rehabilitation of almost any musculoskeletal problem. However, most published studies are related to the treatment of knee and hip osteoarthritis, rehabilitation after joint replacement, and low back pain. Interest has also increased in the use of water-based exercise program in patients with fibromyalgia.18,19 Other diagnoses for which water-based exercises are used include stroke,20 lymphedema,21 rotator cuff repair surgery,22 and rheumatoid arthritis.23 Different water-based exercise programs are used for knee, hip, and back pain, depending on the severity, body characteristics, overall health status, and needs of the patient. Each patient must be evaluated by the rehabilitation team before a specific protocol is prescribed. As with land-based physical therapies, different centers and clinicians specialize in different types of programs. In addition, books of aquatic exercises for the different muscle groups can help to delineate an appropriate exercise prescription.24 For the treatment of joint pain, the goals of the aquatic rehabilitation program are to relieve pain, decrease muscle spasm, maintain or restore muscle strength, maintain or restore range of motion, prevent deformities, promote relaxation, and enforce a normal pattern of movement. Despite the rising popularity of aquatic rehabilitation for joint pain, more scientific studies must be published to validate its efficacy. In one study, patients awaiting joint replacement surgery of the hip or knee were enrolled in a multidimensional land-based or pool-based exercise programs for 6 weeks. When clinical outcomes were compared, both interventions were found effective in reducing pain and improving function, but the pool-based group had less pain immediately after the exercise classes.25 The effects of gym versus hydrotherapy exercises for patients with knee or hip osteoarthritis were compared, and a similar beneficial effect on physical function was noted in both groups compared with control subjects, although the gym group gained more leg strength.26 A review of published articles on aquatic exercises for the treatment of osteoarthritis concluded that although high-quality studies are lacking, aquatic exercises appear to have some beneficial short-term effects for patients with hip or knee osteoarthritis.27 Studies comparing land-based and water-based exercise programs after joint replacement found comparable outcomes, with a positive effect on early recovery of hip strength in patients who received hydrotherapy.28,29 For patients with total knee replacements, the benefits of hydrotherapy were still present 6 months after discharge.30 Patients with rheumatoid arthritis can also receive benefits from exercises in water. A randomized controlled trial comparing patients with rheumatoid arthritis who received hydrotherapy with patients with the same disease who received exercises on land found that the hydrotherapy group reported feeling much better or very much better more frequently than did the land exercise group.23 A systematic review examining the effectiveness of therapeutic aquatic exercise in the treatment of low back pain found that, although most published studies on the subject are of low methodologic quality, therapeutic aquatic exercise is potentially beneficial to patients suffering from chronic low back pain and pregnancy-related low back pain.31 One study compared hydrotherapy with land treatment in patients with low back pain and found that both groups improved significantly in functional ability and pain levels. Overall, no significant difference
was noted between the two types of treatment.32 Based on experience with many patients, the consensus of musculoskeletal rehabilitation therapists is that water-based exercises are very helpful in the treatment of low back pain, especially in patients with severe pain that precludes any other exercise program. Water-based exercises also have been used as part of a comprehensive treatment program for pain syndromes. Fibromyalgia is a very challenging condition to treat, and some centers use hydrotherapy as part of their multidisciplinary approach to the disease. One group of patients with fibromyalgia received group pool exercises once a week for 6 weeks, combined with an educational program. After 6 weeks, the patients showed improvements in symptom severity, walking ability, and quality of life compared with an untreated control group. A follow-up study found that improvements in symptom severity, physical function, and social function were still present 6 and 24 months after completion of the program.18,33 A review of randomized controlled clinical trials on the efficacy of hydrotherapy in fibromyalgia syndrome found moderate evidence that hydrotherapy has short-term beneficial effects on pain and health-related quality of life in this population.34 Obesity is a very common health problem that is difficult to treat, especially in patients with chronic pain. Aquatic exercise programs have been used with success as a way to increase activity levels in obese patients. No good studies have been conducted to confirm the long-term effect of aquatic exercise in this population, but many patients and therapists have used this technique with success. Because of all the previously stated characteristics of the aquatic environment, obese patients are able to exercise in water without stressing their joints or exacerbating their pain. Therefore, obese patients who cannot safely tolerate physical activity on dry land can participate in exercises as part of a weight loss program. However, the longterm goal in these patients to transfer them, once they build tolerance to exercise, to a regular weight loss exercise program at home or in a gym, because studies of nonobese populations suggested that exercise in water causes less decrease in fat than does exercise on dry land.35,36 Patients who have had a stroke comprise another population that is sometimes difficult to enroll in an exercise program because of residual motor deficits. A relatively short program of water-based exercises, three times a week for 8 weeks, proved beneficial for the cardiovascular fitness of a group of patients with stroke who had mild to moderate residual motor deficits. The experimental group also improved in maximal workload, gait speed, and paretic lower extremity muscle strength.20
Equipment Water-based exercises can be performed in any standard pool. Large rehabilitation facilities usually have an indoor, temperature-controlled pool accessible to handicapped patients. The pool at its deepest point should be deep enough to cover standard-sized patients up to their necks, although that much water is not needed to obtain the benefits of the water environment. Other features, such as ramps, grab bars, seats, or underwater treadmills, are also available. Smaller tanks can be used for water-based exercises. These special tanks can include all the features of a larger pool in a smaller space. Some tanks even include an artificial water flow system that allows the patient to swim without the need of a long pool, similar to running on a treadmill. A hydraulic motor produces an adjustable current that is used for resistance.
Chapter 134—Hydrotherapy
Special equipment can be used to enhance the effect of water-based exercises. Some aids include floating balls, web gloves, flippers, and flotation devices of different shapes. Delta bells and barbells are made of foam and are consequently weightless outside the pool. When these devices are used in water, their shape creates resistance that is used in exercise programs. An aqua jogging belt allows running-like motion and is commonly used in sports rehabilitation to keep an athlete fit while protecting weight-bearing joints.
Prescription As previously stated, a water-based exercise prescription follows an evaluation by the physician and the therapist. Strengthening exercises are prescribed for weak muscles, and stretching and mobilization exercises are recommended for stiff joints, muscles, or segments. Exercises in water are not the same as similar exercises done on land. A complete discussion of the different exercises is beyond the scope of this chapter. Books and manuals are available that describe the different types of exercises and techniques. It is impossible to recommend a standard program that fits the needs of every patient, but the following paragraph contains a description of some aquatic exercises recommended for diskogenic pain, a common diagnosis in pain clinics. Water walking forward (Fig. 134.1) helps strengthen abdominal and ambulatory muscles and promotes proper posture. Water walking backward (Fig. 134.2) helps the same muscles but emphasizes the paraspinal muscles. The wall sit (Fig. 134.3) is used to strengthen the quadriceps and hamstring
Fig. 134.1 Water walking forward.
Fig. 134.2 Water walking backward.
Fig. 134.3 Wall sit.
991
992
Section V—Specific Treatment Modalities for Pain and Symptom Management
Fig. 134.6 Wall crunch.
Fig. 134.4 Modified superman.
Fig. 134.5 Supine sculling.
muscles isometrically. The patient is supported by the pool wall in the vertical position while the hips and knees are kept at 90 degrees. The modified superman (Fig. 134.4) exercise requires the patient to stand vertically and hold the edge of the pool with both hands. One leg is then flexed 45 degrees at the knee. That same leg is extended to 20 degrees at the hip and is brought back to neutral repeatedly. To add difficulty, the knee is flexed to 90 degrees, or a weight or resistance is added to the ankle. This movement trains the ipsilateral hip flexor and extensor muscles, the contralateral gluteus medius, and all abdominal and paraspinal muscles. Supine sculling (Fig. 134.5) is a more complex exercise that requires the use of a flotation jacket, a flotation collar, and direct assistance from a therapist for the patient to maintain a supine position in the water. The upper extremities perform a sculling motion at the hip level, while the lower extremities execute a flutter kick. This is a good overall exercise that strengthens upper and lower extremities and paraspinal muscles. In the wall crunch
(Fig. 134.6), the patient stands with his or her back against the pool wall and attempts to flex the hip to 90 degrees with the knee flexed while the ipsilateral hand isometrically resists the movement, to maintain an isometric contraction for 5 seconds at a time. This exercise requires the use of the quadriceps, hamstring, gluteal, ipsilateral hip flexor, rotational abdominal, and paraspinal muscles. The log roll swim (Fig. 134.7) is another complex exercise, requiring the use of a mask, a snorkel, a flotation belt, and support from the therapist to keep the body in a prone position. The neck is flexed 20 degrees, the knees are flexed 25 degrees, and the patient begins a small rotatory movement of the arms under the chest. With the hips in 25 degrees of flexion, the knees initiate a small flexion-extension propulsion movement. The patient is taught a lateral rocking movement to minimize the segmental stress of the lumbar spine. The whole purpose of the exercise is to promote appropriate spine movement on ambulation while strengthening the upper and lower extremities.
Chapter 134—Hydrotherapy
993
Fig. 134.7 Log roll swim.
Contraindications When prescribing water-based exercises, the clinician must practice common sense and remember that a pool and its surroundings can be a dangerous place. Aquatic therapy should not be ordered for a patient who cannot follow basic safety rules. Difficult cases always should be discussed with the therapist before the referral. Contraindications to water-based exercises include fear of water, open wounds, bladder or bowel disorders, skin disease, and high fever. Patients with unstable angina, congestive heart failure with symptomatic low ejection fraction, frequent high-grade ectopy, or significant aortic or mitral valve problems should not participate in water programs. A cardiology evaluation and clearance usually are recommended for patients with cardiac conditions before they begin an exercise program.
Whirlpool and Hubbard Tank Indications The most important uses of whirlpools and Hubbard tank baths are for adjunctive treatment of degenerative arthritis and acute musculoskeletal injuries and for cleansing and débridement of burns or skin ulcerations. Patients with musculoskeletal pain (arthritis, diffuse myalgias, muscle spasm, muscle strains) can benefit from the massage created by water turbulence, the therapeutic effect of water temperature, and the decreased stress on bones and joints that the aquatic environment provides. The massage and heat effects created by the turbulence are particularly helpful for muscle pain and spasm. The agitated water causes localized and controlled joint movement that helps to improve the function of patients with arthralgias or joint stiffness. In some cases, patients are advised to move the joint actively while receiving the treatment to maximize the effect on range of motion. The movement and hydrostatic pressure of the water in whirlpool help in the mobilization of fluids and cause the resolution of edema and swelling in chronic or acute musculoskeletal injuries. The relaxation effect and the decrease in pain perception of water immersion are also beneficial. Whirlpools and Hubbard tanks are commonly used for pressure ulcers and for wound and burn treatment. Unfortunately, little trial evidence exists to support these indications.37 The warm, gently agitated water of the whirlpool permits comfortable solvent action and gentle débridement and aids in bandage removal. A study of patients with stage III or IV pressure ulcers compared conservative treatment with conservative treatment plus whirlpool 20 minutes per day. Conservative treatment included pressure relief
measures and wound care with wet-to-wet dressings using normal saline solution. When followed up for 2 or more weeks, patients who received whirlpool treatments improved at a significantly faster rate than did patients who received conservative treatment alone.38 Use of a whirlpool has been mentioned as part of a multiple-intervention approach to patients with nonspecific chronic pain.18 One study examined the effects of whirlpool therapy on pain and surgical wound healing in adults who had undergone major abdominal surgery. Measures of pain were repeated over a 3-day period. The experimental group response to verbal pain was not significant, but it did reveal an improvement in observable pain behaviors using the Pain Rating Scale. The investigators concluded that the intervention of whirlpool therapy promoted some degree of comfort and positive signs of wound healing.39
Equipment Whirlpool baths and Hubbard tanks possess water pumps or turbines that agitate water and provide connective heating or cooling, massage, and gentle débridement. Whirlpool baths come in different sizes and shapes. Small, 120-L tanks are used for treatments to a single extremity or area, whereas large Hubbard tanks are used when the entire body must be immersed. The large tanks usually are equipped with a stretcher that may be fitted into an adjustable support bracket. Normally, the tank is butterfly shaped, so that the patient can move the extremities through abduction if indicated.
Prescription Whirlpool or Hubbard tank treatments may be given daily or twice daily for acute problems and less often for more chronic problems. Treatments usually take 20 to 25 minutes. The water turbulence is directed to the involved area, unless it exacerbates pain. Depending on the affected area, a small whirlpool or a Hubbard tank is recommended. Water temperature is regulated depending on the patient's needs. Temperatures of 33°C (91°F) to 36°C (97°F) are considered neutral. If heat is indicated, water temperature can be increased to 43°C (109°F) to 46°C (115°F) in healthy patients receiving localized or single limb treatment. In full body submersion, the temperature is limited to 38°C (100°F) or less if the patient is going to exercise in the tank. Because of the water's constant motion, no insulating layer of cooling water is formed around the patient, and more vigorous heating is attained. On burns or infected areas, antiseptic conditions are preferred. Although truly sterile conditions are difficult to achieve, antibacterial solutions, such as
994
Section V—Specific Treatment Modalities for Pain and Symptom Management
sodium hypochlorite or povidone-iodine, may be added to the water. When large wounds or exposed organs are present, sodium chloride should be added to the water to approximate normal saline solution and to minimize fluid shift. Cases of severe hyponatremia, hyperkalemia, and prerenal uremia have been described in burn patients after they received hydrotherapy in tap water.40
Contraindications A chance of drowning in a whirlpool or Hubbard tank always exists. Care should be taken with patients at risk, such as weak patients, cognitively impaired patients, and children.41 Extreme temperatures should be avoided in patients with sensory problems, small vessel disease, affected cognition, or an inability to communicate. Hot water should not be used in patients with systemic fever or acute inflammatory conditions. Caution should be exercised when using a whirlpool in patients with motion sickness because the water movement may cause dizziness. Epidemiologic studies suggest that the use of a hot tub or whirlpool bath during pregnancy doubles the risk of miscarriage. This risk increases with the frequency of use and with use during early gestation. This potential complication should be considered when clinicians prescribe aquatic therapy to women of childbearing age.42,43
Contrast Baths Indications Contrast baths are indicated for subacute or chronic traumatic and inflammatory conditions, impaired venous circulation, and indolent ulcers. Contrast baths also have been used for neuropathic pain, rheumatoid arthritis, chronic pain syndromes, and complex regional pain syndrome. The purpose of this technique is to cause cyclic vasodilation and vasoconstriction that produces neurologic desensitization.44
Equipment Contrast baths use alternate immersion of body parts in baths. Warm water and cold water baths are used, thus causing alternate dilation and constriction of the local blood vessel. No special equipment is required for this technique. Whirlpool tanks and any other safe water container that can hold water at the required temperatures can be employed.
Prescription After the patient has been positioned comfortably, two pails of water of a depth that covers the treated area are prepared. The cold bath is usually 13°C to 18°C (55°F to 64°F), and the hot bath is 38°C to 43°C (100°F to 109°F). The affected area is immersed in the hot bath for approximately 6 minutes and then in the cold bath for 4 minutes, or at least 1 minute if the patient cannot tolerate the cold bath. This process is repeated for approximately 30 minutes. As in the whirlpool or Hubbard tank, povidone-iodine or sodium hypochlorite can be added to the water to prevent infections.
Contraindications Contraindications to contrast baths are the same that the contraindications to the use of whirlpools and Hubbard tanks. Extreme temperatures should be avoided in patients with sensory problems, small vessel disease, affected cognition,
or an inability to communicate. Hot water should not be used in patients with systemic fever or acute inflammatory conditions.
Conclusion Hydrotherapy has been used in the management of pain since ancient times, and more recently its use has increased again. Reduction of pain and increase in function are accomplished by using the physiologic and biodynamic properties of water. This chapter presents a basic understanding of different techniques of hydrotherapy. In addition, the physical properties of water are reviewed, including buoyancy, hydrostatic pressure, viscosity, refraction, and specific heat. The use of water has many physiologic effects. These effects are seen in the cardiopulmonary, circulatory, autonomic, and renal systems. Most appropriate to patients with pain are the physiologic and therapeutic effects seen in patients with musculoskeletal pain. The primary therapeutic effects of hydrotherapy are the promotion of muscle relaxation with decreased muscle spasm and the increased ease of joint motion. Additionally, decreased pain sensitivity, reduced gravitational forces, increased circulation, increased muscular strength, and improved balance can be helpful in the rehabilitation of patients with chronic pain. Water-based exercises can be used for the treatment and rehabilitation of almost any musculoskeletal problem. For patients with pain who cannot exercise on land, water provides a positive medium in which to move and relax. The ease of movement allows the patient to achieve much more benefit than on land and provides the patient with confidence to aid rehabilitation because he or she has less fear of falling or of hurting the injured or painful sites. The different water-based exercise programs are prescribed, depending on the severity, body characteristics, overall health status, and needs of the patient. Aquatic exercise programs have been proposed for the treatment of knee and hip osteoarthritis, rehabilitation after joint replacement, low back pain, fibromyalgia, stroke, lymphedema, rotator cuff repair surgery, and rheumatoid arthritis. As with other therapeutic treatment techniques, more clinical studies are needed to validate efficacy. Whirlpool and Hubbard tank baths are used for adjunctive treatment of degenerative arthritis and acute musculoskeletal injuries, as well as for cleansing and débridement of burns or skin ulcerations. Patients with musculoskeletal pain and spasm can benefit from the massage created by water turbulence, the therapeutic effect of water temperature, and the decreased stress on bones and joints that the aquatic environment provides. This technique also is useful for resolution of edema and swelling. Antibacterial solutions such as sodium hypochlorite or povidone-iodine may be added to the water when concerns about infection exist. Contrast baths produce neurologic desensitization by alternating heat and cold cyclic vasodilation and vasoconstriction. Contrast baths have been used for subacute or chronic traumatic and inflammatory conditions, impaired venous circulation, indolent ulcers, neuropathic pain, rheumatoid arthritis, chronic pain syndromes, and complex regional pain syndrome.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
135
V
Transcutaneous Electrical Nerve Stimulation Steven D. Waldman
C ha p te r O ut l ine Scientific Basis of Transcutaneous Electrical Nerve Stimulation 995 Indications for Transcutaneous Electrical Nerve Stimulation 996 Acute Pain 996 Musculoskeletal Pain 996 Peripheral Vascular Insufficiency 996 Abdominal and Visceral Pain 996 Neuropathic Pain 996
Long before the gate control theory of Melzack and Wall, the use of sensory stimulation for pain relief had gained widespread acceptance. The modalities of heat and cold, massage, burning, scarification, moxibustion, cupping, and the like were the mainstays of nonpharmacologic pain relief. Reports from ancient Egypt tell of the use of electric catfish applied to the area of pain as one means of pain control. Given that these electric fish could produce a discharge of up to 400 V, one must wonder whether the patient experienced a miraculous cure just to avoid another treatment.1 The explanation by Melzack and Wall of how a stimulus could theoretically provide pain relief by modulating or closing a presynaptic gate that allows transmission of pain impulses to the higher centers finally gave a scientific basis for the use of what heretofore had been highly accepted but largely discounted techniques. This impetus led to renewed interest in the use of electricity as a “counter-irritant,” or stimulus that could close the gate on pain. The early work by Shealy in dorsal column stimulation spurred a search for less invasive ways to deliver electricity to nerves. One of the results was transcutaneous electrical nerve stimulation (TENS), which was used initially as a noninvasive screening tool to determine whether a patient would experience pain relief with implantation of a dorsal column stimulator. The ease of use and noninvasive nature of TENS made it an instant success. These same attributes led to its overuse and, to a certain extent, to its mediocre reputation as a pain-relieving modality. This chapter discusses the scientific rationale behind TENS and provides the clinician with a practical guide to its use.
© 2011 Elsevier Inc. All rights reserved.
Cancer Pain 996 Behavioral Pain 996
Transcutaneous Electrical Nerve Stimulation Apparatus 996 How to Use Transcutaneous Electrical Nerve Stimulation 997 Contraindications to Transcutaneous Electrical Nerve Stimulation 997 Conclusion 997
Scientific Basis of Transcutaneous Electrical Nerve Stimulation As mentioned previously, the gate control theory was, in essence, the first unified theory of pain. Earlier theories that were largely based on the Cartesian view of peripheral nociception carried to the central nervous system could not explain how a peripheral stimulus for counter-irritative techniques (e.g., acupuncture, moxibustion, electric shock) could produce pain relief. The gate control theory changed everything. For the first time, scientists, psychologists, and physicians were presented with an elegantly simple explanation of how pain could be produced or blocked in the periphery. The theory stated that small-fiber afferent stimuli, particularly pain, entering the substantia gelatinosa can be modulated by largefiber afferent stimuli and descending spinal pathways so that their transmission to ascending spinal pathways is blocked or gated.2 That the gate control theory could not explain many of the clinical observations associated with the use of TENS soon became apparent. Among these observations were the frequently seen phenomenon of anesthesia persisting hours after stimulation and the delayed onset of analgesia experienced by some patients in pain. The neurophysiologic basis of these clinical observations remains the source of much debate— with alternative explanations such as endorphin or enkephalin release currently the most popular in spite of the fact that TENS analgesia is not reversed with naloxone. This lack of a scientific rationale has not deterred TENS enthusiasts, nor has
995
996
Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 135.1 Clinical Indications for Transcutaneous Electrical Nerve Stimulation Acute post-traumatic pain Acute postoperative pain Musculoskeletal pain
Abdominal and Visceral Pain Most clinicians believe that TENS is not particularly useful in the treatment of chronic abdominal and visceral pain. Some investigators believe that, in spite of less than optimal pain relief, TENS may exert a salutary effect on bowel function and may also improve the obstipation and postoperative nausea and vomiting associated with opioid analgesics.9,10
Peripheral vascular insufficiency Functional abdominal pain (?) Neuropathic pain (?)
it been lost on TENS critics, mainly insurance companies that do not want to pay for this popular pain-relieving technique.
Indications for Transcutaneous Electrical Nerve Stimulation Practically every known pain syndrome has been treated with TENS because of its ease of use and lack of side effects. The true efficacy of TENS for the painful conditions discussed subsequently is complicated to ascertain because true doubleblind placebo-controlled trials are difficult to conduct because of the patient's ability to perceive whether the TENS unit is delivering stimulation or not. Despite this fact, the following indications fall within the broad category of conditions in which TENS is, at least, worth considering. Table 135.1 summarizes the current clinical applications for TENS.
Acute Pain TENS has been shown to reduce pain and, in some cases, to reduce the need for opioid analgesics and improve pulmonary function after upper abdominal, thoracic, or orthopedic surgery and total hip or knee arthroplasty.3,4 TENS may also be useful after traumatic rib fracture and other acute trauma.5 Sterile electrodes allow placement of electrodes adjacent to lacerations or surgical incisions, theoretically enhancing efficacy.
Musculoskeletal Pain TENS has been successfully used to reduce pain associated with osteoporosis-induced vertebral compression fractures, arthritis pain, and strains and sprains.6,7 Anecdotal reports regarding the efficacy of TENS in the management of carpal tunnel syndrome suggest a positive response in some patients with failed conservative and surgical management of this entrapment neuropathy. Its benign nature and flexibility make the modality suitable for these more chronic pain reports.
Peripheral Vascular Insufficiency Early reports suggested that TENS had the ability not only to reduce pain associated with peripheral vascular insufficiency but also to improve blood flow. Further studies have cast doubt on these claims, although many anecdotal reports are found of improvement in ulcer size and healing with the use of TENS.8 Given the lack of treatment options for these difficult cases, TENS represents a reasonable treatment option if nothing else is working.
Neuropathic Pain In general, TENS has been shown to be ineffective in the treatment of most neuropathic pain states. Whether this is from lack of sensory afferent nerve function to carry the TENS impulses to the spinal cord or from other changes in the nervous system is unclear. Anecdotal reports of efficacy continue to be found in a variety of neuropathic pain states, including postherpetic neuralgia and diabetic polyneuropathy.11
Cancer Pain TENS has not been a first-line treatment for pain of malig nant origin. However, given the favorable side effect profile for this noninvasive, nonpharmacologic modality, it may be a reasonable option, especially in patients who experience significant side effects from pharmacologic interventions and who refuse more invasive treatments. A recent reports suggests that TENS may provide pain relief in selected patients with cancerrelated bone pain.12
Behavioral Pain Beyond the placebo effect, very little is found to recommend TENS in the treatment of pain without an organic basis. Initial patient enthusiasm may be quickly replaced with confounding behavior surrounding the use of TENS in this clinical setting. The use of TENS without a clear clinical indication is in most cases a fruitless endeavor.
Transcutaneous Electrical Nerve Stimulation Apparatus The TENS unit consists of a battery-powered pulse generator that is capable of delivering a variety of different pulse characteristics and stimulation frequencies, leads, and a set of electrodes to deliver the stimulus to the affected area (Fig. 135.1). Most investigators prefer a monophasic square wave that is delivered by a pulse generator capable of automatically sensing and compensating for the variation in impedance caused by normal and diseased skin and less than optimal electrode contact. Stimulation frequencies between 30 and 100 Hz are most comfortable for patients. Lower frequencies, which are designed to produce what is thought to be an effect more analogous to acupuncture, are recommended by some clinicians, although many patients find this stimulation frequency too uncomfortable. This discomfort may be decreased with use of a pulse generator capable of producing a series of 8 to 10 rapid pulses of a lower frequency stimulus. Reusable electrodes that require the use of conductive gel and tape have been replaced with disposable pregelled self-sticking electrodes.
Chapter 135—Transcutaneous Electrical Nerve Stimulation
997
Table 135.2 Contraindications to Transcutaneous Electrical Nerve Stimulation Patients with pacemakers Patients with implantable drug delivery systems Patients with spinal cord stimulators Patients with significant impairment of sensation Patients who are pregnant
most efficacious for a variety of painful conditions. A stimulus frequency of 90 to 100 Hz is generally a good starting place, and the frequency can be adjusted by the patient to comfort and efficacy, thereby giving the patient some control over one portion of the treatment. The clinician should demonstrate to the patient what TENS-induced muscle contractions look like and how adjusting the unit can make them stop.
Contraindications to Transcutaneous Electrical Nerve Stimulation
Fig. 135.1 The transcutaneous electrical nerve stimulation apparatus.
How to Use Transcutaneous Electrical Nerve Stimulation If efficacy is to be achieved, the patient must be thoroughly familiar with the basic operation of the TENS unit and clear on how electrodes are to be placed. Although the placement of electrodes is certainly more of an art than a science, the author's experience has been that giving the patient specific parameters for electrode placement works better than telling the patient to experiment with electrode placement. The clinician should generally place the electrodes in the painful area and in most instances place the electrodes within the same dermatome whenever possible. Dual-channel units are currently the norm and allow large painful areas to be treated. A form with an anatomic outline that shows where the electrodes should be placed is helpful when instructing the patient on the use of the TENS unit. Because electricity is involved, it may be useful for the clinician to first demonstrate the TENS unit by having the patient apply the electrodes to the clinician's forearm and then turning on the unit before placing electrodes on the patient. This increases patient confidence and lowers the anxiety regarding getting “shocked.” After proper electrode placement, the patient should be instructed to turn all settings on the pulse generator to zero before turning on the unit. This helps avoid any sudden shock sensation and allows the patient to slowly determine the sensation threshold necessary to feel the first sign of stimulation. In general, a level of 2.5 to 3 times the sensation threshold is
TENS is a remarkably safe treatment modality. Without the risk of thermal injury associated with heat and cold and without the side effects associated with pharmacologic, nerve block, and surgical interventions, the perception among many clinicians and third-party payers that TENS is overused is not surprising. A small group of patients remains in whom TENS may produce risk (Table 135.2). These patients include: (1) patients with pacemakers; (2) patients with significant sensory impairment (e.g., patients with quadriplegia, because of risk of skin breakdown; patients with implantable drug delivery systems); (3) patients with spinal cord stimulators; and (4) patients who are pregnant, because of risk of inducement of labor. Some clinicians caution against placement of TENS electrodes near the carotid sinuses or laryngeal nerves because of the risk of vasovagal syncope and laryngospasm, although this admonition may be more theoretic than real.
Conclusion TENS as a pain-relieving modality has appeared to stand the test of time. In spite of the apparent disconnect between the enthusiastic anecdotal clinical reports and lack of demonstrable long-term efficacy of controlled studies, TENS represents a viable alternative for a variety of painful conditions. Given the favorable risk-benefit ratio and cost-benefit ratio of TENS when compared with other pain-relieving options, TENS remains a part of our armamentarium in the treatment of pain.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
136
Osteopathic Manipulative Treatment of the Chronic Pain Patient Kevin D. Treffer
CHAPTER OUTLINE Historical Considerations 998 Somatic Dysfunction and the Nociceptive Model 999 Structural Examination of the Patient with Chronic Pain 1000 Osteopathic Manipulative Treatment and Choosing the Treatment Modality 1004 Manipulative Medicine Modalities 1005 Post–Patient Encounter Recommendations 1005
Historical Considerations The beginnings of what is now known as osteopathic medicine were first developed by Andrew Taylor Still, MD/DO, in the mid 1800s (Fig. 136.1). A son of an itinerant preacher/ physician, Dr. Still was trained in medicine on the prairies of Kansas by his father. This path of medical education was not unusual for the time. As Dr. Still began treating patients with the available tools of his day, he began to lose confidence in their effectiveness, believing that other options could be used to help the body help itself. In 1864, three of Dr. Still's children died of meningitis and one of pneumonia, which significantly altered his thoughts on the practice of medicine. These events caused him to be dissatisfied with the treatment methods of the day and their failures, and he began looking for a better way to approach treatment of the human body. He was a student of anatomy and had studied cadaveric specimens thoroughly, looking for the ways in which the musculoskeletal system was integrated into the body and how it could be treated to improve health. As he farmed and practiced medicine over several years, he developed his ideas of how the patient should be treated. On June 22, 1874, he first expressed his views publicly, effectively flinging the banner of osteopathy to the breeze.1 The Kirksville consensus report in 1953 perhaps best delineates Dr. Still's ideas for our profession; these ideas have been the standard for the tenets of osteopathic medicine (Table 136.1).2 Health to Dr. Still was an optimal interaction 998
Clinical Applications 1006 Low Back Pain 1006 Whiplash 1007 Migraine Cephalgia 1007 Ankle Sprains 1007 Scoliosis 1007 Fibromyalgia 1007 Obstetric Application 1008
Conclusion 1008
of all body systems, communicating via neurologic, vascular, lymphatic, and hormonal means and resulting in a homeostasis (balance) between each, allowing the individual to function at an optimal capacity.3 With this functioning, the body is able to resist environmental noxious influences and compensate for any effects of these. Disease then represents the breakdown of this homeostasis between systems, allowing symptoms to be expressed in varied patterns. Dysfunction within the musculoskeletal system is part of the expression of disease and involves the concepts of viscerosomatic and somatovisceral reflexes. These neural reflexes involve afferent activity from either the somatic structure or a visceral structure with resulting inhibitory or excitatory effects on motor neurons (somatic or autonomic).4 The ability to treat the musculoskeletal system effects change throughout the systems of the body by helping resolve these inappropriate neural reflexes and aiding in improving neural function to viscera associated with the spinal level in question.5 Osteopathic manipulative medicine then is the ultimate expression of the osteopathic philosophy. With diagnosis and treatment of dysfunction within the musculoskeletal system, abnormal function of the neurologic, vascular, hormonal, and lymphatic tissues is removed and the body is able to develop a better balance (i.e., homeostasis) between all systems. The result is a reduction of the presenting symptoms and an improvement in function of all systems: a stable state of health for the patient. © 2011 Elsevier Inc. All rights reserved.
Chapter 136—Osteopathic Manipulative Treatment of the Chronic Pain Patient
Today, osteopathic medicine consists of an integration of the original tenets along with the modern usage of all aspects of medicine (basic sciences and clinical sciences). The patient with chronic pain can be effectively treated with osteopathic manipulative treatment (OMT) within the context of the etiology of the pain, to develop an optimal balance of the patient's musculoskeletal mobility and thereby improve functional integration with all body systems.6,7 This chapter describes this author's osteopathic approach to the examination and treatment of the patient with chronic pain. The comprehensive evaluation and treatment presented is a unique idea that has evolved out of the osteopathic philosophy. This examination is not one that all osteopathic physicians will do for their patients. The idea of a complete evaluation is first introduced in principle in osteopathic medical schools. Although many osteopathic physicians perform manipulation, few perform an extensive approach for a variety of reasons. After several hundred patient visits, the author was not having great success with chronic pain cases. After much discussion and work with William Brooks, DO, the author modified his approach to include the grading of motion patterns and developed his version of this type of examination.8–10 The author's personal observations have shown a better response in this patient population. A growing segment of the population is actively seeking out complementary and
alternative medical treatment. The osteopathic philosophy with its use of manipulative treatment is on its way to becoming an expected standard of care within the chronic pain population.11 This paradigm of evaluation and treatment is still evolving as further evidence-based literature is published. The physiologic basis for this paradigm, treatment modalities, and clinical problems that respond to the application of OMT are the focus of this chapter.
Somatic Dysfunction and the Nociceptive Model In evaluation of the musculoskeletal system, the osteopathic physician looks for what is diagnosed as somatic dysfunction. It is defined as “the impaired or altered function of related components of the musculoskeletal system: skeletal, arthrodial, and myofascial structures, and related vascular, lymphatic, and neural elements.”12 The physician evaluates first for tissue texture changes in all aspects of the musculoskeletal system (Table 136.2). The next aspect is asymmetry of position and motion with palpation of bony landmarks for static position and evaluation of dynamics of motion (both active and passive motion). The physician assesses for symmetry of the joint's motion pattern, noting any restricted motion in one direction and ease of motion in the other. Palpation may also elicit tenderness at the site (tenderness, asymmetry, restricted range of motion, tissue texture [TART] changes; Table 136.3).13 With finding of TART changes in the musculoskeletal palpatory examination, somatic dysfunction can be diagnosed.
Table 136.2 Evaluation of Tissue Texture Changes
Fig. 136.1 A. T. Still, MD, DO.
Table 136.1 Principles Emphasized by the Philosophy of Osteopathic Medicine The human is a dynamic unit of function The body possesses self-regulatory mechanisms that are self healing in nature
999
Tissue Texture Changes
Acute
Chronic
Texture
Bogginess
Smooth
Temperature
Increased
Decreased (coolness)
Moisture
Increased
Decreased
Tension
Increased
Ropiness, tissue contraction
Tenderness
Present
Present
Edema
Present
Not generally present
Erythema
Vasodilation in tissues
Minimal
(From the Educational Council on Osteopathic Principles: Glossary of osteopathic terminology, Washington, DC, 2001, American Association of Osteopathic Colleges.)
Table 136.3 TART Examination T: Tissue texture changes A: Asymmetry of position
Structure and function are interrelated at all levels
R: Restriction of motion
Rational treatment is based on these principles
T: Tenderness
1000 Section V—Specific Treatment Modalities for Pain and Symptom Management An understanding of how the body develops these TART findings and how they relate to the patient with chronic pain is important. Currently, the model for the etiology of somatic dysfunction is via nociceptive pathways. The source of the stimulation of the nociceptor varies with the variety of injuries and disease processes our patients present with. The stimulus of a peripheral nociceptor must be of sufficient strength and remain for a sufficient time to activate a cascade of events that results in the musculoskeletal effects of somatic dysfunction.14 As the stimulus (e.g., inflammatory process) persists, the continual afferent activity into the spinal cord level affects interneurons within the cord, lowering their activation thresholds. This facilitates more efferent activity to the motor pathways, including somatic and visceral motor neurons. This is the basis of the facilitated segment concept of Korr and Denslow, developed during the mid 1900s.15,16 These effects not only reach the somatic structures, as evidenced by the TART findings, but have consequences for visceral function (viscerosomatic and somatovisceral reflexes). The result is disruption of the body's homeostasis or system integration. The osteopathic physician recognizes this alteration in integration as a predisposition for disease processes to occur. The facilitation changes at the spinal cord level can produce short-term effects in neuronal activity that resolve if the stimulus is short lived. If the stimulus is allowed to remain, the effects can become long term or sometimes permanent and are associated with chronic pain states and central (spinal) sensitization.17 The nociceptive information (cause of facilitation) is then processed within the cord, brainstem, thalamus, and cortex. Spinal facilitation processes activate the brainstem arousal system that is coupled to two efferent pathways: the sympathetic nervous system (SNS) and the hypothalamic-pituitaryadrenal axis (HPA).18 These efferent pathways are driven by norepinephrine in the SNS and cortisol in the HPA and alter bodily function (immune and neuroendocrine) to respond appropriately to a noxious stimulus. This process is referred to as allostasis and is a normal response by the body. However, if the stimulus is allowed to remain, the result is an increase in the allostatic load, which is detrimental to reestablishment of homeostasis. Gene expression changes allow receptors to become active at the spinal cord level, adding the modulation of central facilitation.11 The result is the beginning of the process of allodynia (generalized lower thresholds to pain). The continual exposure to an increased allostatic load decreases the function of feedback loops meant to restore homeostasis, leaving the body “in a chronic compensatory state.”19 Osteopathic manipulative medicine as a part of the overall management plan helps to modulate the hypersympathetic tone and has been linked to pain reduction.11 With a chronic increased allostatic load, the response of the musculoskeletal system is continual motor output to the soma, which results in the maintenance of somatic dysfunction.20 From a physical examination standpoint, this means maintenance of restricted ranges of motions within fascial planes, extremity joints, and spinal segments. Allostatic load also affects visceral function by altering the outflows to the SNS and thereby affects the function of viscera innervated from the spinal segments involved in the somatic dysfunction.19 The resulting effects do not just involve musculoskeletal tissues but potentially affect multiple organ systems and the integration of their functions.
The limbic system of the brain is responsible for the emotional component of the patient and has connections to the brainstem arousal system (SNS and HPA). The spinoreticular tracts of the brainstem arousal system can be affected by limbic system function, and emotional feelings become an important part of dealing with chronic somatic dysfunction and its resolution.21 This reticular system also has connections to postural controls, which may explain persistent postural strain patterns observed in evaluation of patients with chronic pain.22,23 How the patient deals emotionally with the pain or the disease process may play a role in the perpetuation of the severity of the pain and the chronicity of somatic dysfunction. As a stimulus starts the cascade of effects within the neuroendocrine-immune axis and the spinal cord, palpable changes in the tissue textures and the decreased range of motion within the patient's musculoskeletal system can be noted. The longer this remains, the more detrimental it becomes for the patient by affecting other bodily systems, causing breakdown in function and the possibility of the disease processes to flourish. The osteopathic physician's approach to the patient with chronic pain begins with a look at the patient as a whole (all systems) and then with use of OMT to resolve somatic dysfunction. The result is a reduction in the somatic portion of inappropriate reflexes within the central nervous system (CNS) involving the SNS and HPA systems, aiding the body to reestablish a homeostasis (decreased allostatic load). The patient with chronic pain always has some form of afferent activity, and with periodic evaluation and treatment, the osteopathic physician helps the patient find health by maintaining the best homeostatic state possible, given the condition and its course.
Structural Examination of the Patient with Chronic Pain The beginning of all patient interaction is the history and physical examination. A thorough history of the presenting symptoms, review of systems, medical history, social history, and surgical history is vital to appropriately guiding the physical examination. From an osteopathic approach, this process is no different from procedures of our other medical colleagues. The osteopathic physician does emphasize musculoskeletal, neurologic, psychosocial, and trauma histories in the approach to a patient with chronic pain but not to the exclusion of any other aspect of the history and physical examination. Because a large percentage of patients have had multiple other evaluations and treatment plans before coming for manipulative evaluation and treatment, the history of these specific evaluations and treatments and their successes and failures is important. Examination of the musculoskeletal (MS) system is of great importance to the osteopathic physician. As the MS system is evaluated, the areas of greatest restriction (the primary dysfunctions) are of particular clinical significance. The examination begins with a postural evaluation followed by both active and passive motion patterns. How the patient's body responds to gravity may provide clues regarding the regions of the MS system that may have somatic dysfunction. A center of gravity is established to enhance ideal postural alignment because the body responds to forces from within and from without itself (Table 136.4). A failure of establishment of ideal posture places a strain on the myofascial and arthrodial tissues, generating inappropriate stresses to tissues that are not typically weightbearing.23 Because the
Chapter 136—Osteopathic Manipulative Treatment of the Chronic Pain Patient 1001
t issues respond to changing forces, the body is observed for symmetry verses asymmetry in the sagittal, coronal, and transverse planes. Surface anatomic landmarks are used to evaluate for asymmetry (Fig. 136.2). Some landmarks need only observation, whereas others need palpation for comparison of left versus right and anterior versus posterior. The patient is then put through ranges of motion that involve the entire MS system. As we observe motions actively and passively, we watch for smooth and sequential motion within the myofascial and arthrodial aspects of the MS system (quantity and quality). Can the patient exhibit full range
Table 136.4 Landmarks for the Sagittal Plane Ideal Postural Line External auditory meatus Shoulders Center of the body of L3 Greater trochanter Lateral condyle of the femur Just anterior to the lateral malleolus
A
B
C
Fig. 136.2 Evaluation of posture is done in three planes. A, Transverse plane. B, Sagittal plane with ideal postural line. C, Coronal plane (anterior and posterior).
1002 Section V—Specific Treatment Modalities for Pain and Symptom Management of motion actively and passively? It is important during passive evaluation to first observe where linkage to other regions of the MS system exists. For example, with the patient in the supine position with the knee and hip flexed to 90 degrees, adduction at the hip joint links into the pelvis and trunk and results in rotation of the pelvis and trunk within the transverse plane (Fig. 136.3). For the best assessment of the available hip joint range of motion, the physician should block this linkage with one hand while assessing the pattern of motion in question, thereby giving the clinician a truer picture of the available motion. With a restricted pattern of motion, this linkage is expected to occur early in the range of motion; how much restriction depends on this motion's significance to the overall MS system dysfunction. As the idea of linkage is applied to each motion pattern, a grade is given for each one. The grading is done during passive motion testing. As one is passively moving part of the MS system in its range of motion, the physician can note the quality of the motion and the quantity. A patient may be able to attain the full range of motion (FROM) without causing tissue disruption but may be using a great amount of force to get to FROM. The grade should be applied when the quality of motion changes at the point in which greater force is needed to attain the FROM or linkage occurs. The grading system also provides objective evidence of the available motion within the MS system. If the motion pattern goes from 0 to 25% beyond the FROM, then the grade assigned is a +1. If the motion pattern tested achieves 100% of the expected range of motion, then FROM is documented. If the motion attained is between 75% and 100%, the grade assigned is −1. If the motion attained is between 50% and 75%, the grade is −2. If the motion is between 25% and 50%, the grade is −3; and if the motion is between starting position and 25% of expected motion, the grade is −4 (Fig. 136.4 [online only]).8 This system differs slightly from the American Osteopathic Association standardized outpatient OMT form in which a 0 to 3 grading system is used. Because different postures related to the trunk and the extremities affect symptom expression, repeating the grading of motion patterns in multiple contexts is recommended.20 The idea is to evaluate motion in the standing,
A
seated, supine, and prone contexts to determine whether the greatest restrictions are context dependent. This becomes relevant in the planning phase of management because the area of greatest restriction should be treated in the context in which it was found to be the most restricted.19 After all motion patterns are graded, the physician identifies the motion pattern that has the greatest restriction. This motion pattern then should be approached by evaluating for functional pathology (i.e., somatic dysfunction) within the joints and myofascial tissues involved with that motion pattern. Once dysfunction is identified, a manipulative treatment plan can be developed and carried out to remove the restriction as much as possible given the chronicity of the cause. Another piece of information available from the grading of motion patterns is total body mobility. If the patient has a large number of −2s or −3s and very few FROM, then the patient's system is noted to be a very tight system. Contrast this with the patient with a large number of FROM and +1s; this system is considered a loose system. Most patients fall into the range of mostly FROM and a few −1s or a few +1s. Patients with a loose MS system may have pain despite a “normal” range of motion of a joint. These patients may be used to a greater than normal amount of motion and therefore may need treatment to restore them back to that range they are used to. All motion patterns are reevaluated at each visit, and the grades are compared with earlier data. This information can be used at each subsequent visit to evaluate the patient's progress and to demonstrate the success of the treatment plan. If the patient was assigned stretching exercises, then the information could be used to show the patient the benefit of the exercises. If the patient is not compliant, then the information can be used to encourage the patient to do the exercises that are essential to recovery. The patient's symptoms may not be associated with those motion patterns with the greatest restriction. If one applies the ideas of biotensegrity, which suggests that the spinal column is not simply a stack of blocks but a structured system of continuous tension and discontinuous compression, forces are displaced throughout the MS system to find a balance of tension and force.24 Levin explains the body as a layer of tensegrity
B
Fig. 136.3 A, With the hip and knee at 90 degrees, linkage within the trunk occurs with abduction at the hip. B, With blocking of the linkage, the true degree of available motion within the pattern is determined.
Chapter 136—Osteopathic Manipulative Treatment of the Chronic Pain Patient 1003
systems within tensegrity systems, thus allowing for the displacement and compensation of gravitational forces without crushing the body's tissues. The myofascial tissues are analogous to tension trusses, and the bony structures are analogous to compression structures. The icosahedral design in this system allows for instantaneous increasing or decreasing tensions and compression as loads are placed on the structure without changing overall shape.24 The loading forces placed on the body are instantaneously displaced through all tissues and allow the body to maintain a posture in relationship to gravity, ideal or not. As disease processes and injury patterns occur in the body, a change in the distribution of force is expected, thereby changing tension within the MS system to establish a new or stable (although abnormal) posture. This is represented by somatic dysfunction and all its elements that have been discussed so far. Restriction in one motion pattern has to be compensated by another for the posture to balance. The symptomatic expression of this may be in the areas of increased mobility (prolonged functional strain) and not in the areas of greatest restriction.11 For example, McConnell25 notes that lack of external rotation and extension within the hip causes an increase in lumbar spine transverse plane mobility to accommodate for this restriction of motion during the gait cycle. Over time, this causes torsional strain in the annulus fibrosus portion of the intervertebral disks. Because nociceptors are found in the outer layers of the annulus fibrosus, this repetitive trauma can cause low back pain. One expects symptoms to be expressed sooner in patients with preexisting chronic dysfunction and structural pathology in the lumbar spine. The root of the problem exists within the hip muscle restriction and not in the lumbar disks. Manipulative treatment then provides a way to remove the hip rotation restriction and allow for a release in the tension/compression forces and reestablish a more normal balance in postural control and relief of low back symptoms. After posture and motion evaluation, evaluation of the patient's gait is helpful. The patient must be observed for several full-gait cycles, with observation for symmetry in the stance and swing phases of gait. The patient's postural center of gravity is one of the determinants of how efficient the cycle is. The determinants of gait as noted by Saunders and coworkers are pelvic rotation in the transverse plane toward the stance phase side; downward pelvic tilt in the coronal plane toward the swing phase side; knee flexion during the swing phase side; combined action of the foot, ankle, and knee on the stance phase side; and the constant displacement of the center of gravity during the gait cycle.26 Optimal mechanics of these determinants result in an efficient use of energy during the gait cycle. Evaluation of the cycle should be split into the stance and swing phases. Each phase has motions within the MS system that rely on neuromuscular and biomechanical processes to accomplish a normal cycle. Swing phase begins with toe-off from the stance leg and ends with heel strike of the same leg. During this phase, the pelvis rotates toward the stance leg, the hip and knee are flexing, and the ankle is dorsiflexing. During the latter half of the swing phase, the knee extends; and at the end of swing phase, the foot is supinated, which combined with the remaining amount of knee flexion acts as a shock absorption during the heel strike portion of stance phase.25,26 If dysfunction is seen within the knee (e.g., hyperextension) or the subtalar joint, an increase in pelvic rotation or coronal plane tilt is noted, resulting
in excessive motion within the lumbar spine.25 Over time, this could lead to strain in the spine and its myofascial structures and further musculoskeletal pain. In individuals who already have significant pathology in the lumbar spine, the added strain can cause exacerbations of their pain (increased allostatic load). Manipulation of the dysfunctions to improve motion acts to decrease the allostatic load and decrease nociceptive input into the system. Stance phase begins with heel strike and ends with toe-off. During this phase, the hip goes into extension, the knee fully extends, and the ankle and foot plantar flex and pronate to allow for toe-off at the end of the cycle.26 The subtalar joint has great clinical significance during stance phase because dysfunction here results in a disturbance in the shock absorption on heel strike and affects lumbopelvic motion as well.25 Physical findings are represented by abnormal areas of callus formation on the plantar surface of the foot, indicating abnormal weightbearing.26 Again, manipulative treatment to dysfunctional tissues involved in gait restores the necessary motions to allow a more efficient gait cycle and lessen nociceptive input. The gait efficiency shows in the stamina of patients with chronic pain in the activities of their daily lives as they try to function with a chronic problem. The gait cycle is a total body phenomenon. To counterbalance some of the lower extremity and pelvic motions, the upper body rotates toward the swing leg side and the upper extremities swing anterior on the stance leg side. This also helps minimize head rotation, keeping the head forward. The physician should be mindful of mobility within the trunk and upper extremities that may have effects on restricting mobility within the gait cycle. Patients with chronic pain who have significant musculoskeletal structural abnormalities need to have an efficient use of energy during their gait cycle. Addressing joint function and dysfunction aids in their conservation of energy for use in other activities of daily living. The context in which the patient is evaluated includes standing, seated, supine, and prone. Standing context includes the postural examination in three planes. Seated examination begins with simultaneous evaluation of passive right and left upper extremity flexion, extension, adduction, and abduction, blocking any linkage noted. All of these motions are done with the elbow in full extension (a so-called straight upper extremity). For all of these motions, the FROM is based on the practitioner's favorite reference text for motion mechanics. Hoppenfeld's Physical Examination of the Spine and Extremities is an excellent resource for the expected ranges of motion (Tables 136.5 and 136.6). Each of these patterns should be graded for available motion and documented as discussed previously. The scapulothoracic motion is an important component of total shoulder motion, and therefore, the amount of gapping between the scapula and the thoracic cage is noted. With passive retraction of the ipsilateral shoulder girdle, the tension around the medial aspect of the scapula is loosened. The free hand then attempts to slide the fingers between the scapula and the thoracic cage. The expectation is that the fingers are able to slide up to the proximal interphalangeal joint. This is graded in the same fashion as noted before and documented. This author's experience in practice reveals that tension within the pectoralis minor muscle and subscapularis muscle commonly restricts this gapping motion, effectively locking the scapula onto the chest cage. This tension within these muscles
1004 Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 136.5 Expected Full Range of Motion for Upper Extremity Seated context
Abduction = 180 degrees Adduction = 45 degrees Flexion = 90 degrees Extension = 45 degrees Supine and seated context
Internal rotation = 55 degrees External rotation = 40 to 45 degrees From Hoppenfeld S: Physical examination of the spine and extremities, Norwalk, CT, 1976, Appleton and Lange, p 1.
Table 136.6 Expected Full Range of Motion for Lower Extremity Supine context
Flexion at the hip with knee flexed = 120 degrees Flexion at the hip with the knee extended = 90 degrees Abduction at the hip with the knee/hip flexed = 45 to 50 degrees Adduction at the hip with the knee/hip flexed = 20 to 30 degrees Internal rotation at the hip with the knee/hip flexed = 35 degrees External rotation at the hip with the knee/hip flexed = 45 degrees Prone context
Extension at the hip with the knee flexed = 30 degrees External rotation at the hip with the knee flexed = 45 degrees Internal rotation at the hip with the knee flexed = 35 degrees Flexion at the knee = 135 degrees From Hoppenfeld S: Physical examination of the spine and extremities, Norwalk, CT, 1976, Appleton and Lange, pp 143,171.
and restriction of motion of the scapulothoracic joint have been associated with atypical shoulder pain. Supine evaluation involves motion of the upper and lower extremity motion patterns, with any linkage noted and blocked appropriately. The lower extremity flexion at the hip is noted with the knee in full extension and then in full flexion. Abduction and adduction at the hip are evaluated with the knee extended and also with the hip and knee flexed to 90 degrees. Internal and external rotation is evaluated with the hip and knee flexed to 90 degrees. The upper extremity is evaluated for internal and external rotation at the shoulder with the elbow flexed 90 degrees and glenohumeral joint abducted 90 degrees. It is important to appreciate the scapulothoracic component of internal rotation at the shoulder, which is a major portion of the normal internal rotation. Restriction within the periscapular muscles decreases this pattern of motion in combination with a decreased scapular gapping evaluation. Other muscles that cross this region may also produce restriction. The latissimus dorsi muscle takes its origin
from the lumbar aponeurosis and inserts into the shoulder, directly linking the shoulder region to the low back. Therefore, restrictions in the shoulder motions may be affected by fascial restrictions within the lumbar spine or may be from the pelvis or lower extremity because the fascial tissue is contiguous through the gluteus medius, into the posterior sacroiliac capsule, into the sacrotuberous ligament, and into the origin of the posterior thigh muscles off the ischial tuberosity. This anatomic knowledge lends credence to the idea that the area of greatest restriction may not be in the area of pain expression. Significant dysfunction from the lumbar spine or down into the feet that may manifest with upper extremity symptoms from fascial tethers within the system is entirely possible. For this reason, a thorough and comprehensive examination is the best approach to MS system chronic pain issues. For all of these motions, the FROM is based on the examiner's favorite reference text for motion mechanics. Prone evaluation of the patient does involve both upper and lower extremity motion patterns. The lower extremity is evaluated for flexion at the knee, external rotation at the hip with the knee flexed, internal rotation with the knee flexed, and extension at the hip with the knee flexed. The upper extremity is evaluated for horizontal extension at the shoulder with the elbow fully extended. Tension with the pectoral muscles of the chest restricts this motion pattern and is associated with patients with protracted shoulder girdles (rounded shoulders) or slumping postures in today's sedentary society. After all motion patterns are evaluated, the primary restricted patterns are noted. The muscles, fascia, and joints involved within the primary pattern are evaluated specifically for somatic dysfunction. The sequence for evaluation is variable with this approach. It may necessitate starting in the foot and ankle or in the head and neck. As the MS system is more specifically evaluated, the areas of greatest restriction are again of high clinical significance. For example, as one palpates for dysfunction of the forefoot, mid foot, and hind foot, the degree of restriction is noted and documented. This is repeated for the fibula and tibia, hip, innominates, sacrum, lumbar spine, thoracic spine, cervical spine, ribs, shoulders, clavicles, radius, ulna, carpals, and phalanges. Many osteopathic physicians practice osteopathy in the cranial field and include this portion of the examination as part of the comprehensive examination of the entire musculoskeletal system. The region with the greatest restriction should be addressed manipulatively first. The American Osteopathic Association's textbook entitled Foundations for Osteopathic Medicine explains how to diagnose somatic dysfunction in all of the aforementioned areas. This is by no means the only text written on this subject, and indeed, many fine texts are available to choose from.
Osteopathic Manipulative Treatment and Choosing the Treatment Modality Once a diagnosis of somatic dysfunction is made, then a plan to relieve the restriction and restore motion is produced. The art of practicing manipulative medicine includes knowing when and where to apply a certain modality of manipulation for any given patient. First, one must be confident in the diagnosis made and that osteopathic manipulative treatment is indicated for this patient.
Chapter 136—Osteopathic Manipulative Treatment of the Chronic Pain Patient 1005
During the examination process, one should determine whether the source of the problem is structural pathology or functional pathology. Structural pathology generally means instability within anatomic structures that need stabilization before application of an OMT modality. Treatment of unstable structures with manipulation may cause injury and add an acute problem onto a chronic one. Most structural instabilities are associated with a hypermobility of the MS segment in question, although not all are hypermobile. For example, degenerative processes such as osteoarthritis and its associated sclerotic changes can give hypomobility to any given segment and still be unstable enough to contraindicate the use of OMT to that segment. However, this may not contraindicate the use of OMT to other MS segments within the same individual. OMT is best suited for tissues with hypomobility that are capable of responding to treatment. One caveat should be noted: although an individual may have structural pathology, he or she possesses functional pathology in compensation for the abnormal structure. Somatic dysfunction is a component of functional pathology and is associated with hypomobility within patients with chronic pain. If OMT is appropriate for the patient, then a decision of whether to use a direct or indirect technique needs to be addressed. With evaluation for segmental somatic dysfunction and TART findings, the physician notes the quality of the range of motion end-feel. Does it feel as if a brick wall is being encountered as the segment is being moved into the extremes of motion in one direction or another? If the range of motion for the segment is asymmetrical in one direction versus another, then a restrictive barrier is said to be present, limiting the motion. The quality of the end-feel may determine what modality is best to use for that dysfunction. A hard end-feel may be better suited for a high-velocity low-amplitude (i.e., thrusting) technique, indicating the problem is more arthrodial; a softer or tethered end-feel may respond better to muscle energy or myofascial release modality, indicating the problem is more myofascial. Patient preference of modality may make the decision easier. If a patient does not want a certain modality used, then the physician is well advised not to proceed. Comorbid diagnoses may preclude the use of some modalities. No absolute rules have been developed for the frequency of manipulative treatments.27 Therefore, an individualized program should be designed for each patient. Patients with very tight MS systems may need more frequent treatments at first, followed by longer periods of time between treatments. Severely affected patients may need evaluation and treatment on a weekly basis, whereas others may need only quarterly treatments. As with all patients, the ideal situation would be treatment of the patient for a short period of time, then release from care to a productive life. At times, this is a scenario that plays itself out. Given the chronicity of many MS diseases and injuries, these patients need periodic treatment to maintain the homeostasis they have achieved with their disease or injury process. OMT is not a cure for structural changes but is effective for the functional changes related to structural pathology. This author prefers to give the body a chance to adjust to changes made in the MS system and sees the patient every 4 to 6 weeks if schedules allow. Few patients need weekly treatment over extended periods of time, although there are always those small percentages that function better with weekly or biweekly treatments.
Manipulative Medicine Modalities Multiple treatment modalities are available for the osteopathic physician in approaching the patient with chronic pain. Each has its pros and cons, and the physician must weigh the risk versus the benefit of using the modality. As discussed previously, the decision of whether the etiology of restriction originates in the arthrodial or the myofascial tissue is important. At times, the problem lies within both aspects, and multiple modalities are needed to restore motion. Sometimes, the patient may have too much tension to allow techniques to be applied to the joints, and the clinician must work on the soft tissues to ultimately treat joint motion. Osteopathic texts, such as Foundations for Osteopathic Medicine, describe each modality well. Myofascial tissue modalities are effective at restoring motion restricted by soft tissue strain patterns. These modalities include soft tissue massage, myofascial release (both directly into the restrictive barrier and indirectly or away from the barrier), strain-counterstrain techniques, facilitated positional release, and spray and stretch techniques. These modalities require physicians to concentrate on tissue reaction occurring under their hands, such as palpating for tissue relaxation or stretch (tissue creep). The physician must have good proprioception skills to be successful with these modalities and be able to respond to changes within the myofascial tissues, as the treatment is applied. Arthrodial modalities affect joint restriction more than soft tissue restriction. The realization that tissue texture changes occur with all dysfunctions is important; however, some end-feel of motion is harder, requiring different types of treatment modalities. These modalities include muscle energy, high-velocity—low-amplitude (HVLA) (i.e., thrusting techniques), articulatory, and Still's techniques. Osteopathy in the cranial field is another modality in that much of the work is done on the sutures, cranial membranes, the sphenobasilar junction, and cranial rhythmic impulse. Manipulative medicine modalities carry some risk in performance. Most injuries come from the more forceful modalities. Thrusting techniques are popular and easy to use; however, they do have some limitations. Some patients do not care for the techniques because of fear of the popping sound or of injury. Vick et al28 noted that HVLA techniques are safe, given several hundred million treatments done each year and only 185 reported injuries over 68 years. The reporting of injuries is probably low during the time frame of the study. The recent study from Haldeman et al29 did not identify factors in the history and physical that accurately predict cerebral ischemia after cervical manipulation and, therefore, declared it a rare complication of this treatment approach. Although a crystal ball would be nice, the reasonable conclusion is to examine our patients thoroughly before thrusting and know that possible complications may occur. We must be aware of conditions that carry more risk than benefit from the modality. This then should be communicated to our patients before use of a thrusting technique and documented in the record.
Post–Patient Encounter Recommendations After the examination and the treatment procedures are completed, the patient encounter is not finished without educating the patient about his or her condition. A few
1006 Section V—Specific Treatment Modalities for Pain and Symptom Management inutes spent explaining in simple terms the clinical findm ings and the plan to manage them involve the patient in the treatment plan. Recall that the grading of the motion patterns identifies restriction within patterns of motion and is useful in demonstrating the need to work on stretching exercises. The best method is to actually demonstrate the exercise and then give the patient something in writing. For the patient with chronic low back pain, exercises for the abdominal and lumbar multifidus muscles have been noted to decrease pain and increase function.30,31 As patients return for reevaluation, the same motion patterns can be reassessed and used to show patients the success of doing the exercises; or they may be used to educate and encourage patients to perform the exercises if they are not complying. If patients report ache in the muscles for an extended time after the stretch, they potentially are using too much force in the stretch. You may want them to demonstrate how they are doing the exercise. This allows you to modify the exercise as you see fit. With stretching exercises, more can be better in this situation. Length of time in a stretch and how often patients perform the stretch are important in overcoming any myofascial recoil that may occur after stretching. Pharmaceuticals may help the patient tolerate any pain experienced. Medications used with each patient should be individualized. Some patients may need muscle relaxants and pain medication, whereas some may just need a nonsteroidal anti-inflammatory drug. There are those who need short-term opioids, and others who need chronic opioid usage, including contracts between the doctor and patient with management of their usage. Some patients may benefit from localized epidural injections by a pain management specialist. A multidisciplinary approach is useful in the complicated chronic pain case. However, one physician coordinating the plan and prescribing the opioids is best. This physician should keep in contact with other members of the team regarding the response from the patient. As long as the manipulative evaluations and treatments are helping the patient, they can be continued. If the patient's condition is getting worse, then the manipulative treatments should be stopped and the patient's history and physical examination should be reevaluated. Use the motion pattern grading system to evaluate progress and regression and the history. If a plateau is reached and the patient's condition is stable and comfortable, then seeing the patient every 4 to 6 months is appropriate. If a flare in symptoms or a new trauma occurs, the patient should be reevaluated sooner. Because chronic pain generally does not go away, expect the patient to return for repeat treatments. Some patients do better if they are seen on a more frequent basis. Each patient is an individual, and the frequency of treatment should be tailored to the point the patient is most functional for the longest amount of time between treatments.
Clinical Applications Many etiologies may produce chronic pain in our patients. OMT is designed to help treat the functional pathologies that are related to the structural pathologies. Indeed, at times, only a functional pathology exists, and OMT is appropriate for treatment in this case.32 The general principles presented in this chapter may be applied to any chronic pain case. Choice of treatment modality should be made in the
context of the extent of structural pathologies present and considering the risk versus benefit ratio with each patient individually.
Low Back Pain Low back pain is one of the most common, if not the most common, problem our patients face. Furlan and associates33 note that 75% to 85% of the population will experience low back pain during their lives, with 10% of those with development of chronic low back pain, accounting for greater than 90% of the costs for back incapacity. Many dollars are spent in this country for low back pain, ranging from $20 billion to $50 billion annually.34,35 Many differing approaches to the treatment of chronic low back pain are found. The approach that encompasses both structural and functional problems is the most comprehensive management plan. OMT provides an additional therapeutic option with a low risk-to-benefit ratio and a growing evidence base in the literature.11 Chronic postural responses, as a result of structural or functional pathology, result in repetitive overuse injuries, with low back pain occurring from an abnormal increase of spinal segmental motion.36 With the spine resembling a tensegrity tower, a response to treatment is associated with changes in motion and force displacement, thereby integrating this reaction with the rest of the extremities, head, and viscera.37 Therefore, to use the osteopathic approach, you must be thorough in your evaluation of the musculoskeletal system to find the primary dysfunction. A broader response within the patient's musculoskeletal system is expected with this treatment approach. On the basis of a review of manipulative treatment in the literature, Mein postulates that patients with low back pain benefit most from manipulation rather than other chronic pain treatment modalities.11 The patient with chronic pain has increased motor output from nociceptive input that maintains the pain-spasm cycle via facilitated segments, thereby sustaining pain.11 With central descending inhibitory pathways overwhelmed and the convergence of nociceptive and mechanoreceptor stimuli on common spinal pathways, motion can be perceived as pain.32 Manipulative treatment is designed to decrease the facilitated segments within the cord, allowing a decrease in the motor output. The result is less muscle spasm, less pain, and more mobility to a segment and motion pattern. Management of the patient with chronic low back pain is not complete without a psychiatric evaluation for anxiety and depression. Patients with neuropathic pain have been shown via positron emission tomography to shift acute pain activity from the sensory cortex to areas of affective/motivational control, indicating a need to evaluate for pain's impact on the mental, emotional, and spiritual functions of the patient.11 Depression can affect the function of the descending nociceptive inhibitory pathways in the brainstem, allowing an increase in transmission of nociception.32 With the central nociceptive connection with the limbic system, an exacerbation of the pain level can fluctuate with the mental state of the patient. Adequate treatment of depression or anxiety can go a long way in helping the patient attain homeostasis in all systems so the patient can find a state of health as defined previously. Early research in the manipulative treatment of psychiatric conditions is not detailed as to specific conditions. However, current research is pending for the role of manipulative treatment in depression. Studies show
Chapter 136—Osteopathic Manipulative Treatment of the Chronic Pain Patient 1007
r esolution of psychosomatic back pain after the patient's psychiatric issues have been resolved.38 Specific regions to treat depend on the findings of the examination and the associated grade applied to the dysfunctions found. The patient with routine low back pain benefits from manipulation with less medication and physical therapy.39 Choice of manipulative treatment modality depends on the patient's structural status and personal preference. In the patient with chronic low back pain, McConnell25 advocates restoring motion to the hips and thoracic spine and treatment of the subtalar joint motion to help decrease the lumbar compensation. This should not be understood as the only regimen for treatment. The patient with chronic needs requires a more thorough evaluation, increased frequency of treatments, medication, and counseling as needed. Addressing the stabilizing muscles (core strength), such as the multifidus, abdominal muscles, and gluteus medius, with endurance exercises aids in appropriate recruitment of muscles during desired motion patterns and helps the patient rehabilitate to the best possible homeostatic state, given the chronicity of the problem.25
Whiplash Another chronic pain presentation is the whiplash injury. The symptoms associated are varied, as is the extent of injury. The typical flexion/extension inertial injury causes an S-shaped curvature in the cervical spine (flexion of upper segments and extension of lower), leading to injury. The soft tissue injury that occurs leads to changes in the mechanical function of the myofascial tissues, which may lead to a significant lowering of the thresholds of nociceptors and mechanoreceptors, resulting in the increased allostatic load and all of its effects over time.40 If rotation of the cervical spine occurs at the time of impact, the tissue trauma may be more extensive, with involvement with the scalene muscles and the pectoralis minor muscle, resulting in a thoracic outlet syndrome presentation. The associated headache could be from the upper cervical spine because of common pathways between nociceptive inputs from C1-C3 and the spinal nucleus of the trigeminal nerve.32 Attention to dysfunctions within the cervical spine may alleviate headache symptoms. Because of the tissue trauma that has occurred, use of modalities that may further traumatize tissue during the early stages of recovery is not recommended. For example, thrusting techniques may cause further injury to the tissues and direct muscle energy may be more painful to the patient. Indirect myofascial techniques, soft tissue massage, and articulatory, facilitated positional release, and Still's techniques are all good choices for treatment in the early stages. Giles and Muller41 found in their comparison study that acupuncture was superior to manipulation for chronic neck pain but spinal manipulation was better for all other chronic spine pain, indicating that consideration should be given to alternative modalities in the early course of treatment. As the patient's rehabilitation progresses, other modalities may be added. Muscle strengthening exercises, along with manipulative treatment, are beneficial to helping the patient decrease pain and improve neck range of motion and muscle function.42,43
headaches 6 months after injury, 20% after 1 year.44 The trauma is the stimulus that starts the depolarization of neurons that allows a significant potassium efflux. This leads to the release of glutamate, which subsequently activates N-methyl-d-aspartate and d-amino-3-hydorxy-5-methyl-4-isoxasolepropionic acid receptors, allowing a further efflux of potassium and calcium. These changes result in protease activation with cell damage or death, neurofilament dysfunction, increased dependence on glycolysis-generated adenosine triphosphate, and an intracellular decrease of magnesium. The culmination of these steps leads to the development of central sensitization and neuropathic pain.45 Bronfort et al's review article found studies that show a positive effect for manipulation in tension-type headaches and for the management of migraine cephalgia.46 By addressing the entire musculoskeletal system for dysfunction, this author has seen a decrease in severity and frequency of headache in this patient population. Use of cranial manipulation in addition to other treatment modalities, within the context of the described diagnostic approach, has been central in observation of this change. The connections of the spinal nucleus of the trigeminal nerve and the upper cervical segments may play a role in success seen.
Ankle Sprains Many patients with chronic pain suffer falls and other MS injuries that may cause further problems for their overall homeostasis. Ankle sprains respond to manipulative treatment as long as the modality chosen does not exacerbate tissue trauma. Higher grade sprains are not effectively treated with thrusting techniques. Early intervention helps restore lymphatic flow, decrease edema, and decrease the inflammatory process.47,48 Pellow and Brantingham47 looked at a separation thrusting technique for the treatment of lower grade sprains with positive results. Because of compensatory changes, treatment should include a thorough evaluation and treatment of the entire extremity (attention to cuboid and fibular head), pelvis, and lumbar spine. Use the motions of gait with respect to the extremity and low back as a guide for treatment.49 Low-grade ankle sprains are very common, and addition of manipulative treatment to the management can decrease healing time for many patients.
Scoliosis The approach to evaluation and treatment as presented has been applied to patients with scoliosis as well. Both direct and indirect modalities can be used effectively in the management of the chronic musculoskeletal pain associated with the curvatures. With use of this comprehensive evaluation and treatment approach, Hawes and Brooks50 showed a decrease in chest circumference inequity by more than 10 cm, an improvement in the rib cage deformity, and a 40% reduction in the Cobb angle in an idiopathic scoliotic curve that was stable for 30 years. With improvement in chest wall compliance, the respiratory function and exercise capacity improve, allowing the patient better overall body function. This may be enough change for the patient to become more active and have improved quality of life.
Migraine Cephalgia
Fibromyalgia
A brief mention of migraine cephalgia and manipulation is appropriate. Head and neck injuries account for 15% of chronic daily headaches. Also, 45% of these patients have
Patients with fibromyalgia benefit from manipulative treatment. Soft tissue massage, myofascial release, muscle energy techniques, and counterstrain techniques are beneficial modalities
1008 Section V—Specific Treatment Modalities for Pain and Symptom Management to use in these patients. Manipulative treatments have been shown to reduce pain at the tender point sites, improve sleep, improve activities of daily living, and decrease depressive symptoms.51–53 Increased physical activity increases the nociceptive threshold; therefore, with educating the patient to remain active, the long-term effect is a decrease in pain.54
Obstetric Application Although pregnancy is not necessarily considered a chronic pain condition, a significant amount of postural strain contributes to multiple musculoskeletal changes over the 40 weeks. If chronic pain is defined as pain for greater than 6 months, then most of this pain by definition is chronic. Studies in the past have shown positive effects for treatment of low back pain with OMT in the pregnant patient. A recent study of 144 women was completed as a randomized, placebo-controlled trial conducted to compare usual obstetric care and osteopathic manipulative treatment, usual obstetric care and sham ultrasound treatment, and usual obstetric care only. The end point of the study included the average pain levels and the Roland-Morris Disability Questionnaire to assess backspecific functioning. The study showed that the group using OMT plus routine obstetric care had significantly less deterioration in back-specific functioning compared with the sham treatment plus routine obstetric care and routine obstetric care only. The pain of pregnancy was not shown to be significantly decreased; however, the subjects maintained better function throughout the pregnancy (effect size, 0.72; 95% confidence interval, 0.31 to 1.14; P = .001 versus usual obstetric care only; and effect size, 0.35; 95% confidence interval, −0.06 to 0.76; P = .09 versus usual obstetric care and sham ultrasound treatment).55 The evaluation method described can be modified for the patient based on the term of the pregnancy. The study cited used a set protocol for treatment and can used as an example of a comprehensive treatment plan. The follow-up study is underway with a larger n value, and further questions are being investigated. Postpartum dysfunctions within the innominates (pubic shears or compressions) are associated with sacroiliac pain and dysfunction.11 Multiple modalities of treatment can be used in this patient population to treat the dysfunctions safely. The effect of the pregnancy on the lumbar spine and pelvis is exaggeration of the lumbar lordosis and an anterior pelvic tilt. The thoracic spine then compensates by increasing kyphosis curvature. Because of the stress of the postural strain through the lumbar spine, pelvis, and into the lower extremity, ankle, and foot, dysfunctions can be noted.56 The result of these dysfunctions leads to the back pain of pregnancy. Manipulative treatment did not prevent the postural changes of the developing pregnancy, but it did show an effect on how well the patient is able to compensate in a more homeostatic manner and thus maintain a higher level of function.
Conclusion Dr. Still developed a new approach to patient care, to alleviate pain by treating the entire body and helping with function at an optimal level. His legacy and philosophy of treatment have grown over the last century. Research shows the benefits of the addition of manipulative treatment in the management of patients with chronic pain. The practitioner must be thorough in the evaluation of the MS system and be mindful of structural and functional pathology. This requires an extended amount of time during the patient encounter; however, the results are well worth the time spent. The patient must be a part of the overall management plan; the success of the treatment plan may hinge on the patient's acceptance of the plan and following through with the postevaluation instructions and exercises. If medications are used, then close monitoring of usage and effectiveness is required. If narcotics are used, a contract with the patient is recommended. As the management plan is carried out, the physician should periodically reevaluate the entire patient presentation to see whether the patient is responding to treatment and whether there is compliance with the plan. The motion patterns observed for grading can be numerous, especially if all are done in multiple contexts. This author does a more abbreviated version of this examination, saving time in the examination room. Dr. Brooks uses a much more comprehensive evaluation for his patients. The author has found that with use of a select few motion patterns, mobility has been effectively improved in a majority of patients with chronic pain. In those individuals whose conditions do not respond, the full evaluation then becomes a better option to guide treatment. Many patients with chronic pain have gone through multiple evaluations over the timeline of their disease process. As a result, many of them have been offered relief from the pain, but many do not get relief. For those who do not have response to medical treatment, the comprehensive evaluation and treatment plan set forth can help these patients with chronic pain find health, despite the chronicity of their problems. The emphasis in treatment of chronic pain with OMT should therefore be on removing restrictions to motion, thus decreasing nociception and central sensitization pathways. This allows our patients to return to more normal activities of daily living.11 Much research is ongoing in this field, and the reader should be on the watch for the results of the OSTEOPATHIC Trial, which will be ending soon. This trial is a phase III randomized controlled trial of 488 subjects assessing the efficacy of OMT and ultrasound physical therapy.57 This study, when completed in 2010, will be the largest randomized control trial involving OMT, adding much needed primary data for OMT and chronic low back pain. We welcome the addition to the evidence base so that we can find the best practice that will help our patients find “Health.”
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
137
V
Nociceptors, Pain, and Spinal Manipulation Rand S. Swenson and Geoffrey M. Bove
CHAPTER OUTLINE Introduction 1009 Innervation of the Spine 1010 Nociceptors 1011 Nociceptor Function 1011 Neurogenic Inflammation 1012 Differences Between Deep and Cutaneous Nociceptors 1013 Central Transmission and Regulation of Nociceptive Signals 1013 Spinal Cord Terminations of Nociceptors 1013 Central Neural Mechanisms for Amplification of Nociception 1013
Introduction Spinal manipulative therapy (SMT) is among the most common of the complementary and alternative medicine therapies.1,2 The first written description of SMT was by Hippocrates, who was quoted as saying that it was an ancient art.3 Annually, at least 7.5% of the adult population visits a chiropractor, for a total of approximately 120 million treatments each year.4 Most treatments are for pain in the back and neck,5–9 but nonmusculoskeletal conditions are also treated.10,11 The former conditions are extremely common, with approximately 18% of the population experiencing back pain that lasts more than 1 month in any given year12 and many having significant disability.13 Almost 95% of SMT is performed by chiropractors14; the remainder is performed by osteopaths, physical therapists, practitioners of Oriental Medicine, and other bodyworkers. The philosophic approach to SMT by chiropractors and osteopaths is historically similar15,16 and seems to be based, at least in part, on observations published in the early 19th century,17–21 although a similar philosophy was also expressed by Hippocrates. Most of the scientific support for SMT has come from randomized clinical trials (RCTs). With the large numbers of RCTs, several efforts have been made to conduct systematic reviews and meta-analyses of this extensive literature. Most,14,22–27 but not all,28,29 of these evaluations have concluded some beneficial effect of SMT for low back pain when compared with no intervention or “treatment as usual.” However, few studies have directly compared SMT with other treatments, and no studies have rigorously compared the many types of SMT with each other. In addition, true placebo-controlled trials, despite their © 2011 Elsevier Inc. All rights reserved.
Neural Mechanisms for Suppression of Nociception 1015 Psychology and Nociception 1016
Spinal Manipulation and Pain 1016 Mechanism One: Direct Effect on Pain Generation 1016 Mechanism Two: Activation of Pain Suppression Mechanisms 1017 Mechanism Three: Effect on Motor Output 1017 Mechanism Four: Effect on Higher Centers of Processing 1018 Summary of Spinal Manipulative Mechanisms 1018
Conclusion 1018
importance in validation of pain therapies,30 have proven difficult because of challenges validating of appropriate placebos for physical interventions.31–35 Short of general anesthesia,36 it is not clear whether completely satisfactory blinding is possible in studies of SMT. Despite extensive clinical use of SMT, the mechanisms of effect remain elusive. Two dominant theories are used to explain these effects: the first implicates a direct effect of the manipulation on spinal biomechanics, and the second considers direct and indirect effects on neural tissue. The effects on the nervous system could be via direct alleviation of neuropathology36 or via activation of spinal and paraspinal receptors. This latter theory implicates various central nervous system (CNS) mechanisms in the ultimate effect. In that regard, several studies have shown a short-duration (1.5 to 2 mA) may result in a failed block. ■ Not only the dermatomes but also the myotomes and osteotomes for the surgical procedures to be performed must be remembered. ■
■
The local anesthetic chosen must last the duration of the procedure, and enough time must be allowed for the block to function fully before surgical intervention.
As stated earlier, peripheral blockade of the lower extremity is not a new technique. For more than a century, physicians have been anesthetizing the nerves of the lower extremity. Differences have occurred in technology and pharmacology through the years, both of which have only been improving the results of our predecessors.
Acknowledgment Gordin et al. would like acknowledge Shinichi Sakura, MD, for permitting the use of pictures from his articles for publication.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
173
Peripheral Nerve Stimulation Matthew P. Rupert, Gabor B. Racz, and Miles R. Day
CHAPTER OUTLINE Historical Considerations 1300 Indications 1300 Clinically Relevant Anatomy 1301
Historical Considerations Electricity has been used to treat pain for thousands of years. In ancient times, Egyptians and Greeks were known to place electrogenic torpedo fish over painful areas in hopes of eliciting a cure. In modern times, peripheral nerve stimulation has been used to treat pain since the 1960s, in parallel with the introduction of the gate-control theory of pain, in which stimulation of larger afferent fibers diminishes the sensation from smaller pain fibers. Peripheral nerve stimulation was implemented initially with the placement of cuffed electrodes around the affected nerve.1,2 Cuffed electrodes soon gave way to flat, paddle electrodes.3 These electrodes were believed to be less constrictive and thereby, have potentially less risk of scarring or nerve injury.4 This has given way to use of percutaneous cylindrical leads that can allow singlestage trialing.5,6 This application has been broadened to include subcutaneous lead placement in proximity to a target nerve and just within the field area of pain. This chapter focuses on treatment of patients with identifiable nerve injuries who have failure with conservative and less invasive interventional therapies. The mechanism of action of peripheral nerve stimulation is not entirely understood; both peripheral and central theories have been proposed. Campbell and Taub7 showed a sensory loss in human subjects in the distribution of a peripherally stimulated nerve that was associated with a loss in the A-delta component of the afferent action potential. Wall and Gutnick8 showed a reduction in the rate of spontaneous neuroma firing that outlasted a peripherally applied electrical stimulus. On the basis of a central gate-control theory, Chung et al9 showed inhibition of spinothalamic tract transmission in primates after application of a peripheral electrical stimulation. This central response also was shown to outlast the initiating peripheral stimulus. Buonocore et al10 have shown antidromic activation of peripheral nerves with dorsal column stimulation. Hanai11 showed inhibition of pain pathways with peripheral stimulation of A-fiber afferents (beta and delta) in a different nerve. Advancements in the understanding 1300
Technique 1301 Side Effects and Complications 1302 Conclusion 1302
of multicontact electrodes and improvements in solid-state components have allowed increasing control of the applied electrical field.12
Indications Peripheral nerve stimulation is indicated for neuropathic pain in a single nerve distribution, with failed less invasive treatments. This technology was traditionally used to treat painful conditions of the median, radial, ulnar, sciatic, posterior tibial, and common peroneal nerves. It also has been used to treat neuralgias of the intercostal, ilioinguinal, occipital, superior cluneal, supraorbital, and supratrochlear nerves.5,13 Other indications include complex regional pain syndromes, plexus avulsions, and electrical injuries.14 Cancer pain, idiopathic pain, and nerve root injury pain have generally been found unresponsive to peripheral stimulation.15 Treatment of mononeuropathy is more effective with peripheral nerve stimulation than with spinal cord stimulation.16 As with any implantable technology, patient selection is multifactorial. Ruling out correctable pathology, such as nerve entrapment, is important; however, a peripheral nerve stimulation trial might be weighed in comparison with a repeat surgery. A complete patient evaluation should include psychologic assessment, and no evidence of drug abuse should be found. A transcutaneous electrical nerve stimulation trial is suggested, although not required.17 A positive diagnostic block of the suspected nerve with local anesthetic is likewise suggested. Temporary relief with such a block does not guarantee peripheral nerve stimulation will work, but a negative diagnostic block suggests that peripheral nerve stimulation is unlikely to help.2 Adherence to these criteria may improve success rates. Additional interim steps before implantable trials have been suggested. Some investigators have advocated a trial of targeted needle stimulation with evidence of neuromodulation effects as an interval step.18 Others have recommended durational failures of neurolytic procedures.13 © 2011 Elsevier Inc. All rights reserved.
Chapter 173—Peripheral Nerve Stimulation 1301
Clinically Relevant Anatomy
Peripheral nerve stimulator placement continues to change as lead design and implant techniques advance. In general, the use of the implantable devices consists of a two-stage procedure after a positive block with local anesthetic. The trial can be performed via a surgical incision or percutaneously. Both can be implanted with an extension lead for immediate conversion to a permanent lead if the trial is positive. An externalized percutaneous trial lead also can be performed so that a negative trial can be removed without a second surgery. The surgical trial and permanent pulse generator placement are described first (Figs. 173.1 and 173.2).
The site for electrode placement is usually proximal to the site of injury, but placement should respect surgical approach and surrounding structures. An intimate understanding of the surgical anatomy is imperative. The surgical incision and dissection are taken down to the neurovascular bundle. A 2-inch section of the nerve is freed from surrounding tissues, with care taken not to disrupt any blood supply. The selected electrode is secured with sutures immediately below the nerve, with the active leads facing the nerve. Next, a piece of fascia is sutured directly to the electrode covering the active leads (Fig. 173.3). This step is recommended to minimize irritation and scarring of the nerve to the electrode. The nerve is allowed to rest in its normal position, and overlying tissue is loosely secured to maintain proximity of the nerve to the electrode. The lead is connected to an extension set and secured below the skin. The limb is taken through a full range of motion to rule out impingement or increased tension before the primary incision is closed. The extension lead is externalized for trial with a temporary screening device, usually for 2 to 3 days. If the trial is positive, the patient returns to the operating room for implantation of the permanent pulse generator. Upper extremity and occipital nerve generators can be placed on the upper chest wall. Lower extremity generators can be placed over the medial thigh or the lateral buttocks. The generator is secured to the underlying fascia with suture. A new extension set is connected from the lead to the generator through a new subcutaneous tunnel. The old extension is then removed, either by preparing and cutting it at the skin and pulling inward or by cutting at the connection and
Fig. 173.1 Left sciatic peripheral nerve stimulator with 1 × 4 array On-Point lead. (Medtronic, Minneapolis, MN).
Fig. 173.2 Right ulnar peripheral nerve stimulator with 2 × 4 array lead.
The key to peripheral nerve stimulation implantation is correct identification of the offending peripheral nerve through history, physical examination, and diagnostic blockade. No specific limitation exists as to what nerves can be targeted for stimulation. When identified, exposure and electrode placement can be performed by a qualified physician. Physical constraints include size of electrode, anatomic restrictions, and proximity of other nerves. Hardware placement should not impinge on surrounding structures through ranges of motion. Stimulation of nontargeted nerves or surrounding musculature is undesirable. Some superficial nerves can be approached via percutaneous placement of cylindrical leads. Examples include occipital, supraorbital, supratrochlear, and superior cluneal nerves.
Technique
1302 Section V— Specific Treatment Modalities for Pain and Symptom Management ulling outward. If the trial is ineffective or uncomfortable, p the patient needs a second surgery for hardware removal. Percutaneous cylindrical leads can be placed as well. Initially, this placement was recommended for terminal branches of peripheral nerves. However, the increasing use of ultrasound scan guidance for peripheral nerve blocks and catheter placement has provided a natural advancement for peripheral stimulation trials.6 The percutaneous lead can now be placed with direct visualization (Fig. 173.4). It can be placed with an extension as above or by itself. The advantage of a single lead wire is the ease of removal if the trial is negative. If positive, either mode necessitates a second surgery for the generator placement. Lead placement done in this fashion can be confirmed with on-table stimulation and patient affirmation.
Side Effects and Complications Potential complications associated with peripheral nerve stimulators are similar to complications associated with other implantable technology. Infection and bioincompatibility are possible. Nerve injury, scarring, and associated
Fig. 173.3 Peripheral nerve stimulating electrode applied to the sciatic nerve above the bifurcation. Two On-Point Medtronic electrodes are sutured together in a saddle shape with nonabsorbable sutures. The active electrodes are covered with a thin layer of harvested fascia and the polytetrafluoroethylene skirt of the electrode loosely stitched around the nerve with an absorbable suture. The appropriate location of the electrodes is verified with motor or tetanic stimulation to cover the targeted tibialis or peroneal nerves. High-frequency linear array
ischemia have occurred. The use of longitudinal rather than cuffed electrodes, the placement of an overlying fascial flap, and eliminating nerve skeletalization are believed to minimize these risks. Whether percutaneous lead placement should be parallel, perpendicular, or oblique to the target nerve is unknown. Stimulation of surrounding musculature may be a concern for nonparallel placement. The patient may have no response, an uncomfortable response, or aberrant sensory or motor stimulation. The use of multicontact electrodes allows some titration of effect. Mechanical problems, such as lead fractures, electrode shorts, lead migration, and battery depletion, are possible. Implanted batteries can interfere with pacemakers and can channel electrical and magnetic fields. The units should be turned off when electrocautery or electrocardiogram is to be performed. An implanted generator is generally a c ontraindication for magnetic resonance imaging.
Conclusion Peripheral nerve stimulators have shown efficacy in many clinical settings of chronic neuropathic pain in a single nerve distribution. Implantable technology is invasive and expensive; adequate conservative and less invasive methods should be tried first. Peripheral and central mechanisms of action have been postulated. Patient selection is multifactorial and should include a psychologic assessment and absence of correctable pathology. Patients should have positive screening procedures such as diagnostic nerve blockade and a period of trial stimulation before placement of permanent equipment. The use of transcutaneous nerve stimulation can be helpful but is not diagnostic or prognostic for the use of peripheral nerve stimulation. Electrode implantation is dictated by the specific nerve anatomy, which may necessitate surgical exposure or may be amenable to percutaneous placement. Advances in clinical strategies, electrode design, and neuroscience research continue to pave the road for future changes. In the modern treatment of chronic regional pain syndrome, the earlier use of neuromodulation techniques is recommended.19,20
References Full references for this chapter can be found on www.expertconsult.com.
Extensor digitorum longus
Tibialis ant. Superficial peroneal n. Deep peroneal n. Tibialis post.
Peroneal longus Peroneal brevis Fig. 173.4 Lateral needle access between peroneal muscles and soleus muscle to access corridor for superficial and deep peroneal nerves. Ultrasound scan visualization with high-frequency linear array probe placed anterior. Fascial separation with needle and saline solution followed by advancement of cylindrical catheter electrode.
Tibial n.
Tibia Popliteus
Fibula Soleus Gastrocnemius lateral head
Gastrocnemius medial head
Chapter
174
V
Spinal Cord Stimulation Danesh Mazloomdoost, Marco R. Perez-Toro, and Allen W. Burton
CHAPTER OUTLINE History 1303 Mechanism of Action 1303 Technical Considerations 1304 Anatomic Considerations 1304 Devices and Components 1304
Patient Selection 1306 Surgical Technique 1306 Trial 1306 Permanent Implantation 1307
Programming 1307
Spinal cord stimulation (SCS) describes the use of pulsed electrical energy near the spinal cord for control of pain.1,2 This technique was first applied in the intrathecal space and finally in the epidural space as described by Shealy, Mortimer, and Reswick2 in 1967. In the present day, most commonly, SCS involves the implantation of leads in the epidural space to transmit this pulsed energy across the spinal cord or near the desired nerve roots. This technique has notable analgesic properties for neuropathic pain states, anginal pain, and peripheral ischemic pain. The same technology can be applied in deep brain stimulation, cortical brain stimulation, and peripheral nerve stimulation (PNS).3–6
History A bump on the head often feels better when it is vigorously rubbed. In a similar fashion, the theories on neurostimulation began when this observation was analyzed physiologically. Neurostimulation began when Melzack and Wall's6 published the gate control theory in 1965. This theory proposed that nonpainful stimulation of large myelinated A-beta fibers could impede painful peripheral stimuli carried by C-fibers and lightly myelinated A-delta fibers. Shealy, Mortimer, and Reswick2 designed the first spinal cord stimulator device for the treatment of chronic pain. Although this technique was noted to control pain, early devices did not garner interest for clinical application because of the impracticality of the required external power supply, which transmitted power transdermally via an internal coiled antenna.7 In the 1980s, implantable batteries were developed and spinal cord stimulators became a clinical option.8 Early indications included persistent neuropathic pain, spasticity,9 ischemic limb,10,11 and facial pain.12 The first rechargeable © 2011 Elsevier Inc. All rights reserved.
Complications 1308 Outcomes 1308 Failed Back Surgery Syndrome 1308 Complex Regional Pain Syndrome 1309 Peripheral Ischemia and Angina 1309
Cost Effectiveness 1309 Peripheral, Cortical, and Deep Brain Stimulation 1310 Future 1310 Conclusion 1310
implantable pulse generators (IPGs) became available in 2004, which dramatically increased the stimulator lifespan.8 Deep brain stimulation was developed during the same time frame. In 2006, 14,000 new spinal cord stimulators were reported to be implanted annually.13 The market continues to grow rapidly.14 Although the gate theory was initially proposed as the mechanism of action, the underlying neurophysiologic mechanisms are not clearly understood.
Mechanism of Action Although SCS devices have existed for more than 40 years, the understanding behind the mechanism of action remains somewhat elusive. The limitations stem from the challenges of an effective model. Unlike other organ systems that can be studied on a cellular level, pain pathways depend on multicellular neural interactions; in vivo models are limited by ethical standards, and animal models can be costly or difficult to extrapolate from simple neuroanatomy because of the complexity found within humans.15 Current evidence suggests that an inhibitory process takes place at the dorsal horn with SCS.15,16 As nociceptive and somatic sensory fibers enter the dorsal horn of the spinal cord, they synapse with second order neurons of the substantia gelatinosa. With SCS, the nociceptive signal is inhibited from further propagation to the sensory cortex, but the mechanism is still elusive. Some of the theories behind the mechanisms of action are listed in Table 174.1 and include signal inhibition via interneurons or descending central fibers, modulation of neuroactive mediators, and limiting pathologic processes like antidromic inflammatory release in ischemic pain and downregulation of wind up at wide-dynamic range neurons.13 1303
1304 Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 174.1 Proposed Mechanisms of Action Suppression of antidromic active mediators in ischemic pain Substance P CGRP Closing gate: Blocking transmission to the spinothalamic tract at the dorsal horn Inhibitory effect of collateral or interneurons Limiting the upregulated signaling that provokes WDR neurons
Ligamentum flavum Dura
Epidural fat CSF DORSAL COLUMN
Dorsal root entry zone (DREZ)
Feedback loop: Activation of central inhibitory mechanisms influencing: Thalamocortical system Anterior pretectal nucleus WDR neurons Autonomic: Sympathetic afferent stimulation Neurotransmitters: Inactivation of putative neurotransmitters (e.g., glutamate, adenosine, serotonin) and activation of protective/depressant neurotransmitters (glutamate)
Fig. 174.1 Green area represents the area of desired stimulation. The red represents the DREZ, where the dorsal roots enter. Because of anatomic location, the DREZ has a lower threshold of stimulation than does the dorsal column. For ideal stimulation, the green area must be activated and the red area inhibited.
CGRP, calcitonin gene-related peptide; WDR, wide dynamic range.
Technical Considerations Anatomic Considerations Understanding the neuroanatomic pathways involved in sensory afferents can help direct the placement, control, and modulation of SCS. Afferent fibers that relay both nociceptive and somatic sensations enter the spinal cord via the dorsal root entry zone (DREZ). After synapsing at second order neurons of the dorsal horn, nociceptive and somatic afferents respectively separate to the spinothalamic tract and the dorsal column (DC). At a single vertebral level, the DC may carry fibers from many dermatomes, whereas the DREZ holds fibers from a single dermatome.17 Depending on the electric field, stimulation of the DC at a single level can result in paresthesia and analgesia of a wide area. Stimulation of the DREZ limits the paresthesia to a single dermatome because it relays nerves from a single dorsal root ganglion (DRG) (Fig. 174.1). Furthermore, because it carries somatosensory fibers and has more synaptic interactions with the musculoskeletal system, it may also induce pain or motor deficits if is set at stimulation levels intended for the DC.8 Because of its geometry in entering the spinal canal and the impedance of the surrounding tissue, the DREZ has a lower threshold of stimulation than the DC.17,18 Clinical evidence corroborates mathematic modeling in showing that as the electric field is moved laterally the perception threshold is reduced and area of coverage decreases.19 Shaping of electric fields has become a critical area of research in SCS. The tissue within the spinal column has variable conductivity: cerebrospinal fluid (CSF) > spinal cord > epidural fat.20 This influences the electric field generated. When the distance between electrode and spinal cord is large, such as in the midthoracic level, stimulation of DC becomes challenging because the necessary electric field tends to incorporate the DREZ.21 The electrode itself has specific influences on the tissue. Negative leads, for instance, hyperpolarize the surrounding tissue, thus inhibiting action potentials, and positive leads depolarize and propagate it. Used in combination, the resultant electric field can be maximally evoked over a designated area.22
Table 174.2 Locations and Lead Type Versus Dermatopic Effect23 C4
Unipolar Midline: The hand, forearm, and upperarm Lateral: The anterior shoulder, forearm, upper arm, and hand Bipolar Midline: The hand and forearm Lateral: The hand, forearm, and upper arm T10 Unipolar Midline: The anterior and posterior of thigh, leg, knee, ankle, and foot Lateral: The abdomen, anterior leg, knee, and anterior thigh Bipolar Midline: The abdomen, anterior leg, knee, and anterior thigh Lateral: The anterior thigh, anterior leg, knee, and foot
The topographic placement of leads depends on the location of pain (Table 174.2).23 Clinical data are limited, but Barolat et al24 have provided mapping data of coverage patterns based on lead location in 106 patients.
Devices and Components Two types of leads are used in spinal cord stimulators: paddle and percutaneous (Fig. 174.2). Paddle leads are flat and wide, with insulation on one side and electrical pads on the other. This has the advantage of directing current in one direction. Paddles leads must be surgically placed via laminotomy or laminectomy.25 Percutaneous leads are cylindrical catheters placed via spinal needle. Because contacts are cylindrical, they generate an electric field circumferentially around the catheter.8 Percutaneous leads are less efficient in power usage because they induce an electric field 360 degrees around the electrode, whereas, because of electrode insulation, paddle leads direct the charge toward the DC. This translates into longer battery life for a paddle lead, which creates an equivalent electric field
Chapter 174—Spinal Cord Stimulation 1305
Fig. 174.2 Neurostimulator leads (left to right): percutaneous type to paddle type. (Courtesy of St. Jude Medical, Inc.).
C Fig. 174.3 C, Implantable pulse generator neurostimulation units with leads. (C, Courtesy of St. Jude Medical, Inc.)
as a percutaneous lead. Fostering a relationship between pain physician and neurosurgeon is valuable because collaboration is necessary in situations where one of these types is better suited. Electrode selection is a complex topic with a significant amount of research on ideal lead configuration. Mathematic modeling has been used calculate electric field potentials in an effort to identify ideal lead configurations. Unipolar leads are theoretically less favorable than bipolar and tripolar leads because they provide less control over the laterality of field generation8 and require higher pulse charges for similar field generation.26 In clinical studies, however, these advantages are controversial, and some studies have even shown statistical disadvantage in bipolar leads.27 The clinical data may be difficult to extrapolate generally, however, because dual-lead placement was staggered and parallel lead alignment has been shown to provide larger DC stimulation than staggered.21 As discussed previously, tripolar lead placement theoretically stimulates the DC more selectively and shields the DREZ,18,28 which allows for wider control of the paresthesia because the DC contains fibers from several dermatomes. Tripolar paddle leads use this property, and recently, tripolar percutaneous leads have been used in a similar fashion.29 Electrodes are connected to a power source, which are of two general types: an IPG or a radiofrequency unit (RF; see Fig. 174.2). RF units work by transmitting power transdermally with an external source and internal coiled wire loop. Because RFs are not limited by battery life, they can outlast IPGs and be programmed with high stimulation amplitude, rate, or pulse width, which is necessary for some patients.30 They require an external power system with an antenna worn over the RF receiver, which is inconvenient and may irritate the skin.8 They are generally outdated because improvements in battery technology allow for high-capacity and rechargeable systems that are internally placed. IPGs are of two types: primary cell and rechargeable (Fig. 174.3 A, B [online], and C). 1. Primary cell devices have an average lifespan of 4 years, versus 9 years for rechargeable devices,8 but the lifespan
is heavily dependent on usage. Primary cell devices tend to be larger but are useful for patients who need low outputs or do not recharge consistently. Small primary cell generators are available for pediatric or petite patients, but they are limited to low or infrequent currents. 2. Rechargeable IPGs contain Li-ion cells, which have a fixed number of charge-discharge cycles, with a degradation in the battery capacity over the span of multiple cycles. Most systems have a safeguard against full discharge because chemical changes can result in permanent battery failure. When patients fail to recharge the IPG, the generator fail safes to deep-discharge mode during which the device is disabled until reprogrammed. Overall, battery life depends on the stimulation energy necessary (voltage/amplitude, number of active leads, pulse width, frequency), hours of usage (all day, during waking hours, intermittent doses), depth of discharge (interval and consistency of recharging), and battery degradation. Physicians need to understand how patients plan to use the stimulator to plan for the best generator option. Currently, three companies produce neurostimulation equipment: Medtronic, Inc; American Neuromodulation Systems, Inc; and Advanced Bionics, Inc (Table 174.3). Variability is found in how the devices work, but no study has suggested superiority of one device over another. The two main differences are in how the electric field is generated. Some other differences include the following: Control over individual electrode versus an array of electrodes n Fixed-current versus fixed-voltage to control the generated electric field n Generator size and options for rechargeable or primary cell n• Options for leads n
1306 Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 174.3 Manufacturers of Neurostimulation Equipment Medtronic Neuromodulation Patient Services: Mail Stop RCW115, 7000 Central Ave NE, Minneapolis, MN 55432-3576. (888) 638-7627. www.medtronic.com/patient-services/. St. Jude Medical, Inc., 6901 Preston Road, Plano, TX 75024. (972) 309-8000. http://www.sjm.com/. Boston Scientific, 25155 Rye Canyon Loop, Valencia, CA 91355. (888) 272-1001. www.bostonscientific.com/.
Patient Selection Patient selection is an integral factor in the overall success of neurostimulation. Failure in selection can not only yield poor outcomes from disease management but can also have numerous detrimental effects31: n n n n n n
Increase physician demand Influence negative emotional outcomes for patient Increase cost of care Increase demand for medications Increase risk of litigation Contribute to disease progress
Appropriate cases for neurostimulation implant must meet the following criteria: the patient has a diagnosis amenable to this therapy; the patient has had failed conservative therapy; significant psychologic issues have been ruled out; and a trial has shown pain relief.32 Whereas implantable devices show improvements in pain, they lack evidence for improvements in functional outcomes.33 Although, the reasons for this require further quantification, lack of motivation and demoralization from chronic pain may play a role. An interesting study by Olson et al32 revealed a high correlation between many items on a complex psychologic testing battery and favorable response to trial stimulation. Few studies, however, have evaluated outcomes in combined interventional and psychobehavioral therapies on both pain and functional recovery. Early studies indicate that combining psychotherapy with implantable devices results in improved outcomes.34 Thus, as part of the workup for an implantable neuromodulatory device, such as a stimulator or intrathecal infusion pump, psychologic testing is recommended. A variety of testing tools are available depending on the physicians' practice; some are listed in Table 174.4. To maximize the probability of improvements in functional outcomes and pain, part of the preoperative evaluation is establishment of functional goals. This evaluation reinforces to the patient that improvement in pain is not the primary endpoint; rather, the endpoint should be return to functional activity.35 Patients are often fearful that pain is indicative of damage and that behavior may limit their rehabilitation even after pain improves.36 A careful trial period is advocated to avoid a failed implant. Trials of different lengths have been advocated. The main risk of a longer trial is infection, whereas the risk of too short a trial is misreading success. Mazloomdoost, Perez-Toro, and Burton use a 5-day to 7-day trial and encourage the patient to be as active as possible in the usual environment, with the exception of limiting bending and twisting movements to avoid stimulator lead migration.
Table 174.4 Psychologic Testing Tools Minnesota Multiphasic Personality Inventory–2 (MMPI-2) 567 questions (60–90 minutes) Gold standard Millon Clinical Multiaxial Inventory–III (MCMI-III) 175 items (25–30 minutes) Correlates with DSM-IV diagnosis Millon Behavioral Medicine Diagnostic (MBMD) 165 questions (20–25 minutes) Defined outcomes: no/relative/absolute contraindications Oswestry Disability Index (ODI) 10 questions (10–15 minutes) Primarily for low back pain disability assessment Pain disability index67 Similar to ODI except applicable to any pain state DSM-IV, Diagnostic and statistical manual of mental disorders, 4th ed.
Surgical Technique The workup leading to SCS implantation takes place in two stages: (1) trial with external stimulator; and (2) internal implantation. Before implantation of a device, a trial is warranted in which leads are externally connected to a pulse generator. Trial stimulation is undertaken to attempt to “cover” the painful area with an electrically induced paresthesia. This is to avoid surgery and its associate side effects and complications in cases of poor outcome or intolerable effects from the SCS. On proven efficacy, the patient may proceed to device implantation. The procedures involved in both trial and implantation are similar except that in a trial, leads are left external, whereas for permanent implantation, leads are anchored to the supraspinous fascia and tunneled to an internal generator. Both procedures take place with fluoroscopy and with sterile conditions. Trials can be done in a sterile office-based setting, but permanent implantation requires an operative environment.
Trial Fluoroscopic guidance is used to place stimulation leads in the posterior epidural space at the dermatome corresponding to the painful area. Insertion site for the lead is distal to the final destination of the lead to allow for steering and lead adjustment. Steering is facilitated by minimizing the catheter's angle of entry into the epidural space because it reduces the number of pivot points in the path of the catheter (Fig. 174.4). Thus, the second or third vertebral body caudal to the desired entry site into the epidural space is chosen for initial insertion point of the needle. Some researchers advocate making an incision before needle entry both to reduce the angle of entry and to minimize the risk of introducing skin flora into the epidural space. A stimulator trial may be accomplished in two ways: straight percutaneous or implanted lead. In the straight percutaneous trial, the needle is withdrawn, an anchoring suture is placed into the skin, and a sterile dressing is applied. After completion of the trial, the leads must be removed and discarded regardless of the success of the trial. When the patient returns for implant, a new lead is placed in the location of the trial lead and connected to an implanted IPG. In the implanted lead trial, after
Chapter 174—Spinal Cord Stimulation 1307 Generators are sometimes also placed anteriorly in the lower abdominal quadrants for ease of patient access during recharging. This, however, increases the risk of lead migration because twisting motions can torque the leads. Paddle electrode implantation requires the addition of a laminotomy to slip the flat plate electrode into the epidural space. Some physicians trial the patient with the straight percutaneous approach and, if successful, send the patient to a spine surgeon for a paddle electrode implant.
Programming Fig. 174.4 Angle of needle entry. Reducing the angle of entry for the intrathecal (IT) needle eases steering of the catheter by reducing pivot points around which the catheter rotates.
successful positioning of the trial lead, the lead is secured, similar to a permanent placement, except a temporary extension piece is tunneled away from the back incision and out through the skin. If the trial is successful at the time of implant, the permanent lead is hooked to new extension and tunneled to an IPG. This method has the advantage of retaining the same lead position in a successful trial, reducing the probability of successful trial but failed permanent implant from new lead positioning. On the other hand, it adds an incision, which increases postoperative pain, confounding trial interpretation. Furthermore, implanted leads may have a greater risk for infection than straight percutaneous method.37 Most clinicians consider 50% or more pain relief to be indicative of a successful trial, although the ultimate decision should include other factors, such as activity level and medication intake. To paraphrase, some combination of pain relief, increased activity level, and decreased medication intake is indicative of a favorable trial.
Permanent Implantation The technical challenges of permanent lead placement depend on: (1) proper fixation; and (2) lead redundancy. Consistent and reliable stimulation depends on fixing an electric field over a small area of the spinal cord. Leads have a limited capacity for stretch, and certain body movements can stretch leads significantly and prompt lead migration. Whereas sclerotic changes in the tissue surrounding the implanted system stabilize the leads over the long run, during the acute phase, proper anchoring is a major factor in successful lead placement. In the event of minor lead migration, electrode redundancy is used to accommodate for minor shifts by using alternative leads to accommodate the desired electric field. After a successful trial, system implantation requires both reinsertion of sterile leads (because the externalize leads from trial are no longer sterile) and placement of an IPG or radiofrequency receiver. Placement of the generator requires preoperative planning because generator location, patient's operative positioning, skin preparation, and lead tunneling depend on the final destination of the generator. Sites commonly used for the generator depend on the location of the lead to minimize torque imposed by body movements. Cervical or occipital generators, for instance, may be placed between the shoulder blades lateral to spinous processes and facets. Thoracic and lumbar leads can be placed in the anterior gluteal area.
Several parameters in neurostimulation may be adjusted to create stimulation paresthesias in the painful areas, thereby mitigating the patient's pain. These include amplitude, pulse width, rate, and electrode selection.38 Amplitude is the intensity or strength of each individual pulse and can be controlled by voltage (V) or current (ohms). As discussed previously, various systems use either voltage or current to control the pulse charge and no evidence is found of superiority of one system over another. From a theoretic standpoint, current-control systems are more immune to changes in electrical resistance in the tissue because of sclerosis and patient positional changes. As such, mathematic modeling predicts more even paresthesia.39 Amplitudes are variable even for an individual patient, but typical initial settings are 60% to 90% of motor threshold.13 n Pulse width is the duration of a pulse measured in microseconds (μsec). It is usually set between 100 and 400 μsec. Similar to increasing the amplitude, a larger pulse width delivers more energy per pulse and typically broader coverage. Common initial settings are 0.2 ms.13 n Rate is measured in hertz (Hz) or cycles per second, between 20 and 120 Hz. At lower rates, the patient feels more of a thumping, whereas at higher rates, the feeling is more of a buzzing. Higher frequencies (>500 Hz) are suggested to increase blood flow and decrease vascular resistance.40 n Electrode selection depends on the desired electrical field distribution and the breadth of dermatomes stimulated. Because much variability is seen in individual dermatomal distribution at the level of the DC, availability of more leads for future programming is advisable. Furthermore, if inadvertent lead migration is to occur, lead redundancy cephalad and caudad to the area of desired stimulation allows for compensatory programming adjustments rather than surgical revision. n•
The primary target is the negative cathode, from which electrons flow to the positive anode. Most patient stimulators are programmed with electrode selection changed until the patient obtains anatomic coverage; then, the pulse width and rate are adjusted for maximal comfort. The patient is left with full control of turning the stimulation off and on and the voltage up and down to comfort. The lowest acceptable settings on all parameters are generally used to conserve battery life. Other programming modes that save battery life include a cycling mode during which the stimulator cycles full on/off at patient-determined intervals (minutes, seconds, or hours). The patient's programming may change over time, and reprogramming needs are common.
1308 Section V—Specific Treatment Modalities for Pain and Symptom Management Neurostimulator manufacturing companies are helpful for clinicians with patient reprogramming assistance. Many busy pain practices designate a nurse who specializes in stimulators to handle patient reprogramming needs.
Complications Complications with SCS range from simple problems, such as lack of appropriate paresthesia coverage, to devastating complications, such as paralysis, nerve injury, and death. Before the implantation of the trial lead, an educational session should occur with the patient and significant family members. This meeting should include a discussion of possible risks and complications. In the postoperative period, the caregiver should be involved in identifying problems and alerting the health care team. After more than 20 years of use, overall complication rates from SCS range from 28% to 42%.33,41 In a recent systemic review, the most common complication was found to be lead migration or breakage, which occurred in 22% of implanted cases.42 Studies by May and Barolat reported lead revision rates from lead migration of 4.5% and 13.6% and breakage of 0% and 13.6%, respectively.37,44 The generator can also be a source of revision if changes in body habitus affect the source position. Three studies showed infectious rates to range from 2.5% to 7.5%,43–45 but these infections rarely progressed into more serious infections, for an incidence rate of less than 0.1%.33 To avoid infectious complications, the patient should be instructed on wound care and recognition of signs and symptoms indicative of infection. Many superficial infections can be treated with oral antibiotics or simple surgical exploration and irrigation. At the center of Mazloomdoost, Perez-Toro, and Burton, to avoid infection, the standard includes prophylactic intraoperative antibiotics. Although controversial, patients are commonly placed on oral antibiotics for 3 to 5 days after surgery. If infection reaches the tissues involving the devices, in most cases, the implant should be removed. In such cases, one should have a high index of suspicion for an epidural abscess. Abscess of the epidural space can lead to paralysis and death if not identified quickly and treated aggressively. In the case of temporary epidural catheters (somewhat analogous to a percutaneous stimulator trial), Sarubbi and Vasquez43 discovered only 22 well-described cases of complications. The mean age was 49.9 years, the median duration of epidural catheter use was 3 days, and the median time to onset of clinical symptoms after catheter placement was 5 days. Most patients (63.6%) had major neurologic deficits; 22.7% also had concomitant meningitis. Staphylococcus aureus was the predominant pathogen. Despite antibiotic therapy and drainage procedures, 38% of the patients continued to have neurologic deficits. These unusual but serious complications of temporary epidural catheter use necessitate efficient and accurate diagnostic evaluation and treatment because the consequences of delayed therapy can be substantial. Schuchard and Clauson46 reported an infection with Pasteurella during an implanted lead trial, which necessitated explanting the system.
Outcomes The most common use for SCS in the United States is failed back surgery syndrome (FBSS), whereas in Europe, peripheral ischemia is the predominant indication. Subdivision of clinical outcomes based on diagnosis makes sense. In a review
of the available SCS literature, most evidence falls within the level IV (limited) or level V (indeterminate) category because of the invasiveness of the modality and the inability to provide blinded treatment. Recognition must also be given to the time frame within which a study was performed because of rapidly evolving SCS technology. Basic science knowledge, implantation techniques, lead placement locations, contact array designs, and programming capabilities have changed dramatically from the time of the first implants. These improvements have led to decreased morbidity and much greater probability of obtaining adequate paresthesia coverage with subsequent improved outcomes.44 Thus, even a level II review study, such as the one on patients with FBSS from 1966 to 1994 by Turner, Loeser, and Bell,47 reported fewer positive outcomes than Barolat et al's44 level IV FBSS study in 2001. The authors believe this represents the effect of improving technology.
Failed Back Surgery Syndrome A recent systematic review that evaluated the cost efficacy of SCS found only two randomized controlled trials (RCTs) on SCS for failed back surgery.48 North et al49 selected 50 patients as candidates for repeat laminectomy. All the patients had undergone previous surgery and were excluded from randomization if they presented with severe spinal canal stenosis, extremely large disk fragments, a major neurologic deficit such as foot drop, or radiographic evidence of gross instability. In addition, patients were excluded for untreated dependency on opioid analgesics or benzodiazepines, major psychiatric comorbidity, the presence of any significant or disabling chronic pain problem, or a chief symptom of low back pain exceeding lower extremity pain. Crossover between groups was permitted after the 6-month follow-up interval. Of the 26 patients who had undergone reoperation, 54% (14 patients) crossed over to SCS. Of the 24 who had undergone SCS, 21% (5 patients) opted for crossover to reoperation. For 90% of the patients, long-term (3-year) follow-up evaluation has shown that SCS continues to be more effective than reoperation, with significantly better outcomes with standard measures and significantly lower rates of crossover to the alternate procedure. In addition, patients randomized to reoperation used significantly more opioids than those randomized to SCS. Other measures for assessment of activities of daily living and work status did not differ significantly. The second RCT50 was a multicenter international study that randomized 100 patients with FBSS and neuropathic radicular leg pain to SCS plus conventional medical management (SCS group) or conventional medical management (CMM group) for 6 months. Primary outcome was 50% or greater reduction in pain, with secondary outcome measures of quality-of-life indicators, functional capacity, pain medication use, satisfaction, and complications. Crossover was permitted at the 6-month interval with an intentionto-treat model, and patients were followed for an entire year. The results showed a statistically significant advantage of SCS over CMM for the primary (P < 0.001) and secondary (P ≤ 0.05%) outcomes. After the study midpoint, 5 of 50 patients in the SCS froup crossed over to the CMM group versus 32 of 50 patients from CMM to SCS. At the study conclusion, however, 32% of patients in the SCS group had experienced device-related complications.
Three systematic review articles are found on neurostimulation.47,48,51 Turner completed a meta-analysis from the articles related to the treatment of FBSS by SCS from 1966 to 1994.33 Pain relief exceeding 50% was experienced by 59% of patients, with a range of 15% to 100%. On the basis of this review, however, the authors concluded that insufficient evidence was found in the literature for drawing conclusions about the effectiveness of SCS relative to no treatment or other treatments. North and Wetzel's51 review consisted of case-control studies and two prospective control studies. They concluded that if a patient reports a reduction in pain of at least 50% during a trial, as determined with standard rating methods, and shows improved or stable analgesic requirements and activity levels, significant benefit may be realized from a permanent implant. The authors conclude the bulk of the literature appears to support a role for SCS (in neuropathic pain syndromes) but caution that the quality of the existing literature is marginal—largely case series. The review from Bala et al48 focused more on cost efficacy and reviewed one RCT, one retrospective cohort study, and 13 case series. The conclusion was that SCS is effective for treatment of FBSS and less costly over the long term.
Complex Regional Pain Syndrome Research of high quality regarding SCS and complex regional pain syndrome (CRPS) is limited, but existing data are overwhelmingly positive in terms of pain reduction, quality of life, analgesic usage, and function. Kemler et al52 published a prospective, randomized, comparative trial of SCS versus conservative therapy for CRPS. Patients with a 6-month history of CRPS of the upper extremities were randomized to undergo trial SCS (and implant if successful) plus physiotherapy versus physiotherapy alone. At a 6-month follow-up assessment, the patients in the SCS group had a significantly greater reduction in pain, and a significantly higher percentage was graded as much improved for the global perceived effect. However, no clinically significant improvements were seen in functional status. The authors concluded that in the short term, SCS reduces pain and improves the quality of life for patients with CRPS involving the upper extremities. Several important case series have been published on the use of neurostimulation in the treatment of CRPS. Calvillo et al53 reported a series in which patients with advanced CRPS were treated with either SCS, PNS, or both. After a 3-year period, patients with SCS had a statistically significant reduction in pain score and improvement in return to work. The authors concluded that in late stages of CRPS, neurostimulation (with SCS or PNS) is a reasonable option when alternative therapies have failed. Another case series reported by Oakley and Weiner54 is remarkable in that it used a sophisticated battery of outcomes tools to evaluate treatment response in CRPS with SCS. The study followed 19 patients and analyzed the results from the McGill Pain Rating Index, Sickness Impact Profile, Oswestry Disability Profile, Beck Depression Inventory, and Visual Analog Scale. After an average of 8 months, all scales showed statistical benefits after SCS and all patients received at least partial relief, with 30% receiving full relief. A literature review by StantonHicks55 of SCS for CRPS consisted of seven case series. These studies ranged in size from 6 to 24 patients. Results were noted as “good to excellent” in greater than 72% of patients
Chapter 174—Spinal Cord Stimulation 1309 over a time period of 8 to 40 months. The review concluded that SCS proved to be a powerful tool in the management of patients with CRPS.55 Even in failed, cases, evidence shows that more aggressive stimulation, only possible with RF generators, can still have a benefit. A retrospective, 3-year, multicenter study of 101 patients by Bennett et al30 evaluated the effectiveness of SCS applied to CRPS I and compared the effectiveness of octapolar with quadripolar systems, and high-frequency and multiprogram parameters. The authors concluded that SCS is effective in the management of chronic pain associated with CRPS I. For 15% of patients, pain control was attainable only with use of dual-octapolar systems with multiple-array programming capabilities, and high-frequency stimulation (>250 Hz). These settings are not available with standard implantable devices.
Peripheral Ischemia and Angina Cook et al11 reported in 1976 that SCS effectively relieved pain associated with peripheral ischemia. This result has been repeated and noted to have particular efficacy in conditions associated with vasospasm, such as Raynaud disease.56 Many studies have shown impressive efficacy of SCS in treatment of intractable angina.57 Reported success rates are consistently greater than 80%, and these indications, already widely used outside of the United States, are certain to expand within the United States. This is an active area of research with a quickly expanding body of literature. Interested readers are encouraged to evaluate the literature because it is beyond the scope of this chapter.
Cost Effectiveness Cost effectiveness of SCS (in the treatment of chronic back pain) was evaluated by Kumar, Malik, and Demeria58 in 2002 and again by Bala et al48 in 2008. Kumar, Malik, and Demeria prospectively followed 104 patients with FBSS. Of the 104 patients, 60 were implanted with an SCS with use of a standard selection criterion. Both groups were monitored over a period of 5 years. The stimulation group's annual cost was $29,000 versus $38,000 in the control group. The authors found 15% of subjects returned to work in the stimulation group versus 0% in the control group. The higher costs in the nonstimulator group were in the categories of medications, emergency center visits, radiographs, and ongoing physician visits. As discussed previously, Bala et al's group conducted a systemic review of the literature to identify RCTs (two studies found), controlled observation studies (one retrospective cohort study found), and case series with more than 50 patients and at least 1-year follow-up periods (13 qualifying case series). The beneficial effects of SCS were consistent in all studies. Of the three studies that fulfilled inclusion criteria for cost-effectiveness evaluation, all consistently showed higher initial costs, but overall long-term cost efficacy was greater than conventional medical management. Bell, Kidd, and North59 performed an analysis of the medical costs of SCS therapy in the treatment of patients with FBSS. The medical costs of SCS therapy were compared with an alternative regimen of surgeries and other interventions. Externally powered (external) and fully internalized (internal) SCS systems were considered separately. No value was placed
1310 Section V—Specific Treatment Modalities for Pain and Symptom Management on pain relief or improvements in the quality of life that successful SCS therapy can generate. The authors concluded that by reducing the demand for medical care by patients with FBSS, SCS therapy can lower medical costs and found that, on average, SCS therapy pays for itself within 5.5 years. For those patients for whom SCS therapy is clinically efficacious, the therapy pays for itself within 2.1 years. Kemler and Furnee60 performed a similar study by looking at “chronic reflex sympathetic dystrophy (RSD)” using outcomes and costs of care before and after the start of treatment. This essentially is an economic analysis of the Kemler et al RSD outcomes paper discussed previously. During a 12-month followup period, costs (routine RSD costs, SCS costs, out-of-pocket costs), and effects (pain relief with visual analog scale, healthrelated quality-of-life60 improvement with a validated qualityof-life instrument) were assessed in both groups. SCS was both more effective and less costly than the standard treatment protocol. As a result of high initial costs of SCS in the first year, the treatment per patient was $4,000 more than control therapy. However, in the lifetime analysis, SCS per patient was $60,000 cheaper than control therapy. In addition, at 12 months, SCS resulted in pain relief and improved health-related quality of life (HRQL). The authors found SCS to be more effective and less expensive when compared with the standard treatment protocol for chronic RSD.
Peripheral, Cortical, and Deep Brain Stimulation Besides stimulation of the spinal cord, neurostimulation can successfully be used at other locations in the peripheral and central nervous systems to provide analgesia. PNS was introduced by Wall and Sweet61 in the mid 1960s. This technique has shown efficacy for peripheral nerve injury pain syndromes and CRPS, with use of a carefully implanted paddle lead with a fascial graft to help anchor the lead without traumatizing the nerve.62 Motor cortex and deep brain stimulation are techniques that have been explored for treatment of highly refractory neuropathic pain syndromes, including central pain, deafferentation syndromes, trigeminal neuralgia, and others.63 Deep brain stimulation has become a widely used technique for movement disorders, and much less so for painful indications, although many case reports of utility in treatment of highly refractory central pain syndromes are found.64
Future Many projected innovations will continue to make SCS an attractive option for treatment of pain. Modern implants have a lifespan of 2 to 10 years,8 but battery capacity and microprocessor power consumption have improved rapidly, which will eventually prolong the lifespan, decrease the maintenance requirements, and reduce costs of future implantable devices. Current stimulators are contraindicated for use within magnetic resonance imaging (MRI) because of the risk of magnetically generated currents heating the leads and causing neural injury; manufacturers are developing MRI-compatible leads. Research is evolving that demonstrates synergistic effects of intrathecal medications with SCS
Table 174.5 Principles of Spinal Cord Stimulation 1. SCS mechanism of action is not completely understood but influences multiple components and levels within the central nervous system (CNS) with both interneuron and neurochemical mechanisms. 2. SCS therapy is effective for many neuropathic pain conditions. Stimulation-evoked paresthesia must be experienced in the entire painful area. No consistent evidence exists for the efficacy of neurostimulation in primary nociceptive pain conditions. 3. Stimulation should be applied with low intensity, just suprathreshold for the activation of the low-threshold, large-diameter fibers, and should be of nonpainful intensity. To be effective, SCS must be applied continuously (or in cycles) for at least 20 minutes before the onset of analgesia. This analgesia develops slowly and typically lasts several hours after cessation of the stimulation. 4. SCS has shown clinical and cost effectiveness in FBSS and CRPS. Clinical effectiveness has also been shown in peripheral ischemia and angina. 5. Multicontact, multiprogram systems improve outcomes and reduce the incidence of surgical revisions. Insulated paddletype electrodes probably decrease the incidence of lead breakage, prolong battery life, and show early superiority in quality of paresthesia coverage and analgesia in FBSS as compared with permanent percutaneous electrodes. 6. Serious complications are exceedingly rare but can be devastating. Meticulous care must be taken during implantation to minimize procedural complications. The most frequent complications are wound infections (approximately 5%) and lead breakage or migration (approximately 13% each for permanent percutaneous leads and 3% to 6% each for paddle leads). Adapted from Linderoth B, Meyerson BA: Spinal cord stimulation: mechanisms of action. In Burchiel K, editor: Surgical management of pain, New York, 2002, Thieme, p 505.
compatible leads, combined pump-stimulators. As the physiologic understanding of DC stimulation improves, newer modes of pulse waveforms and neuroanatomic distribution of currents can substantiate novel therapeutic roles. Closed-loop biofeedback innovations that record neural responses to SCS could play a role in improving the effects of SCS.65
Conclusion SCS is an invasive, interventional surgical procedure. Linderoth and Meyerson66 wrote some principles of neurostimulation that are cornerstones of SCS theory and practice (Table 174.5). The difficulty of randomized clinical trials in such situations is well recognized. On the basis of the present evidence with two randomized trials, one prospective trial, and multiple retrospective trials, the evidence for SCS in properly selected populations with neuropathic pain states is moderate. Clearly, this technique should be reserved for patients who have failure with more conservative therapies. With appropriate patient selection and careful attention to technical issues, the clinical results are overwhelmingly positive.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
175
V
Implantable Drug Delivery Systems: Practical Considerations Steven D. Waldman
CHAPTER OUTLINE History 1311 The Role of Patient Selection in Consideration of Implantable Drug Delivery Systems 1311 Does a Spinally Administered Drug Relieve the Symptoms Being Treated? 1311 The Preimplantation Trial 1312 Side Effects 1312 The Patient's Ability to Assess the Results of the Preimplantation Trial 1312 The Patient's Support System 1313 Unique Problems in Management of Patients with Cancer Pain 1313
Cost of the Implantable Drug Delivery System, Drugs, and Supplies 1313
Classification of Implantable Drug Delivery Systems 1313 Type I: Percutaneous Catheter 1314 Type II: Subcutaneous Tunneled Catheter 1314 Type III: Totally Implantable Reservoir/Port 1314 Type IV: Totally Implantable Infusion Pump 1315 Type V: Totally Implantable Programmable Infusion Pump 1315
Conclusion 1315
Spinal opioids have dramatically changed the way acute, obstetric, nonmalignant chronic pain and pain of malignant origin are managed. The development of various implantable drug delivery systems (IDDSs) has complemented and facilitated the growth of this treatment modality. With interfacing of appropriate patient selection with the unique advantages and disadvantages of each type of IDDS, improved results in terms of both pain relief and patient satisfaction can be achieved.
This experimentation has not been without its critics, but by and large, the use of spinal opioids for acute pain has been a great advance. Clinicians have successfully adapted this technique to relieve postoperative and other acute pain syndromes, obstetric pain, nonmalignant chronic pain, and cancer pain in thousands of patients. In tandem, the development of various IDDSs has occurred and facilitated this expanded role of spinal drugs in the palliation of pain and, more recently, spasticity.4
History
The Role of Patient Selection in Consideration of Implantable Drug Delivery Systems
In the late 1970s, a group of cancer patients at the Mayo Clinic underwent spinal administration of morphine in the hope of finding an alternative to neurodestructive procedures for relief of intractable pain of malignant origin. This brilliant clinical application by Wang, Nauss, and Thomas1 of the basic research of Yaksh2 heralded a new era in the specialty of pain management. This development not only dramatically changed the management of cancer pain but also triggered an entirely new way of looking at the route of drug administration. The years since this landmark event have yielded vast clinical experience with this powerful new modality, which in turn has resulted in the publication of an extensive literature describing the use of spinal opioids in a variety of clinical situations.3 As clinicians gained more experience in the use of spinal opioids for the management of cancer pain, they began to apply this modality to nonmalignant acute pain and experiment with the spinal administration of drugs other than opioids. © 2011 Elsevier Inc. All rights reserved.
Does a Spinally Administered Drug Relieve the Symptoms Being Treated? The first factor to consider in determination of whether a patient is an appropriate candidate for implantation of an IDDS is whether spinal opioids adequately relieve the patient's pain and whether spinal administration of baclofen adequately relieves the patient's spasticity. Not all pain is relieved with spinal opioids, and not all spasticity is relieved with spinally administered baclofen.5,6 For this reason, an IDDS should never be implanted without verification first of the ability of the intended drug to relieve the patient's pain or spasticity on at least two occasions. Failure to do so could subject the patient to implantation of a delivery system that fails to achieve the desired result—namely, pain relief. 1311
1312 Section V— Specific Treatment Modalities for Pain and Symptom Management
The Preimplantation Trial Table 175.1 outlines a suggested protocol for the preimplantation trial for spinal opioids. The expected result of the preimplantation trial of spinal opioids is adequate pain relief as perceived by the patient. This relief should be of appropriate duration for the narcotic analgesic injected.7 Other variables that should be quantified include the level of activity, the use of narcotics via other routes, and the amount and quality of sleep. This same approach should be used to verify that spinally administered baclofen adequately relieves the patient's spasticity.
Side Effects Side effects from spinal opioids, including pruritus, urinary retention, and respiratory depression, must be noted. Side effects from spinally administered baclofen, including weakness and sedation, must also be noted. These side effects must be acceptable to the patient before implantation can be considered. Any inconsistency in the expected versus the observed results should alert the clinician to strongly consider delaying implantation of the delivery system. Careful evaluation of the patient's ability to assess pain relief, and reevaluation of other behavioral or psychosocial factors at play, should be undertaken before implantation of an IDDS.
The Patient's Ability to Assess the Results of the Preimplantation Trial The ability of the patient to accurately assess the adequacy of pain relief or relief of spasticity is essential to avoid the implantation of an IDDS that will be deemed useless. Impairment of this ability may be either physiologic or behavioral in origin. Physiologic abnormalities that may impair the patient's ability to assess the adequacy of pain relief or relief of spasticity are listed in Table 175.2. Most occur in patients with significant multisystem disease, but occasionally, seemingly otherwise healthy patients may have significant impairment of mentation that is not obvious to the clinician. Many of these abnormalities are reversible, and every attempt should be made to correct them before a trial of spinal opioids is undertaken. Remember that the central nervous system symptoms caused by these abnormalities may be incorrectly interpreted as uncontrolled pain by the patient and clinician alike.
Table 175.1 Protocol for Preimplantation Trials of Spinal Opioids 1. Explain the procedure, expected goals, and potential side effects to the patient and family. 2. Select an appropriate narcotic for intraspinal administration. 3. Determine the appropriate dosage and volume of diluent expected to relieve the pain. 4. Administer the intraspinal narcotic and diluent via the intended route of delivery (i.e., epidural or subarachnoid). 5. Quantify on a flow sheet the duration of pain relief, level of activity, amount of sleep, and need for additional narcotic analgesics. 6. Quantify the side effects of intraspinal narcotics. 7. Repeat the trial to quantify the results. 8. Observe 24 hours after intraspinal narcotics and requantify the variables listed in item 5 before proceeding with an implantable drug delivery system.
Behavioral factors that may affect the patient's ability to assess the adequacy of pain relief or relief of spasticity (Table 175.3) are often difficult to identify. They may coexist with physiologic factors, but care must be taken to not attribute inadequate pain relief solely to behavioral factors until all other reasons have been explored. A patient who received adequate pain relief during the preimplantation trial may be a candidate for implantation of an IDDS. Adequacy of patient motivation, the patient's support system, concurrent therapy,
Table 175.2 Common Physiologic Abnormalities That May Interfere with the Patient's Ability to Assess Pain Relief Metabolic encephalopathy Hypercalcemia Hyponatremia Hypoxemia Hypercapnia Azotemia Hepatic encephalopathy Paraneoplastic syndrome Drug-induced organic brain syndrome Narcotics Minor tranquilizers Barbiturates Phenothiazine reactions Cimetidine Structural brain disease Metastatic tumor Increased intracranial pressure Preexisting structural abnormality Cerebral infarction Cerebral hemorrhage Abscess Preexisting neurodegenerative disorders Alzheimer's disease
Table 175.3 Common Behavioral Abnormalities That May Interfere with the Patient's Ability to Assess Symptom Relief Preexisting psychiatric illness Preexisting chemical dependence Use of pain as a controlling device Use of pain to obtain more medication to alter the sensorium Use of pain as an attention-seeking device Patient's refusal to accept the person designated as caregiver Patient's use of pain to punish certain caregivers within the support system
Chapter 175—Implantable Drug Delivery Systems: Practical Considerations 1313
s ystemic infection, life expectancy, and the cost of spinal opioids must also, however, be evaluated before referring a patient for implantation.
The Patient's Support System An IDDS requires a baseline level of commitment not only from the patient but also from the support system. The person or persons designated as the patient's support system must be acceptable to the patient in the role of care provider. If such is not the case, problems may arise. This person must be available night and day to care for and, if a type I to III delivery system is used, be available to inject medication into the delivery system should the patient be unable to do so. Patients who inject narcotics into their own delivery system initially may be unable to do so later in the course of the disease. If the support system is unable or unwilling to care for the delivery system, a continuous infusion pump may be a better option; however, someone must be available to bring the patient to the pain center to have the pump refilled. Also, consider the possibility that family members may divert the patient's drugs for illicit purposes.
Unique Problems in Management of Patients with Cancer Pain Before proceeding with implantation of an IDDS, a review of concurrent primary therapy and its potential to relieve the pain is indicated. In this author's opinion, long-term administration of spinal opioids should be reserved for patients with pain of malignant origin. Our experience with the use of spinal opioids for nonmalignant chronic pain has been disappointing. However, other clinicians have reported more satisfactory results with this group of patients. Currently, this author reserves implantation of an IDDS for the following groups of patients: (1) cancer patients in whom primary modes of tumor eradication (surgery, chemotherapy, and radiation therapy) did not relieve the pain; (2) patients with spasticity uncontrolled with aggressive oral drug therapy; and (3) rare patients with nonmalignant chronic pain whose disease process is so devastating that it is analogous to cancer pain, such as those with end-stage connective tissue disease or advanced demyelinating disease. The author's opinion is that one of two things is necessary before the use of spinal opioids for nonmalignant chronic pain can be routinely recommended: (1) a better way to identify patients who will experience long-term satisfactory results with this modality; or (2) release of new drugs suitable for spinal administration that do not cause tolerance or the myriad behavioral issues associated with the long-term use of opioids administered spinally or systemically for nonmalignant chronic pain. In determination of whether a specific patient is suitable for the implantation of an IDDS, it should be recognized that patients with pain of malignant origin present some specific challenges. A cancer patient may have quantitative and qualitative problems with clotting that may be further compromised by chemotherapy and radiation therapy.8 In the author's experience, this rarely presents any practical problems as long as the patient's clotting parameters are brought into acceptable range before implantation takes place. However, in a cancer patient undergoing systemic anticoagulation therapy, the risk for epidural hematoma is an ever-present possibility. In these
patients, the risk-to-benefit ratio of the anticoagulants must be weighed carefully. In a cancer patient with immunocompromise, ongoing infection is not uncommon. Epidural abscess formation, and spondylitis and diskitis, has been reported in some cases when percutaneous catheters were advanced into the epidural space without subcutaneous tunneling and left in place for as little as 6 days.9,10 For long-term use, an IDDS that is totally implanted or subcutaneously tunneled appears to be superior to a percutaneous indwelling epidural catheter. Common sense dictates against placement of an indwelling foreign body in a patient with sepsis. A realistic appraisal of life expectancy is necessary to determine the appropriateness of an invasive and relatively expensive procedure for pain relief. For cancer patients with limited life expectancy, simple percutaneous placement of an epidural or subarachnoid catheter with subcutaneous tunneling may be more reasonable than a more expensive type III to V system.
Cost of the Implantable Drug Delivery System, Drugs, and Supplies In evaluation of the cost of an IDDS, consideration of the cost of both the system and the drugs to be administered through it is necessary. The hardware for an IDDS can amount to more than $10,000 for a totally implantable infusion pump, exclusive of professional fees and hospital charges. The cost of the narcotics or adjuvant drugs, or both, is not insubstantial, nor is the cost of antiseptic solutions, sterile preparation swabs, gauze, and so forth needed for patients who are self administering opioids via a type I to III system. Some patients simply cannot afford the daily expense. Cost must be considered before implantation of a delivery system that will ultimately not be used.
Classification of Implantable Drug Delivery Systems Table 175.4 describes the five basic types of IDDS. The type I system, a simple percutaneous catheter analogous to those used for obstetric pain control, is one with which clinicians are most familiar. The type II system is simply a catheter suitable for percutaneous placement and tunneling. The type III system consists of a totally implantable injection port that is attached to a type II tunneled catheter. The type IV system is a totally implantable continuous infusion pump that is connected to a type II tunneled catheter. The type V system is
Table 175.4 Spinal Drug Delivery Systems Type I: Percutaneous epidural or subarachnoid catheter Type II: Percutaneous epidural or subarachnoid catheter with subcutaneous tunneling Type III: Totally implanted epidural or subarachnoid catheter with a subcutaneous injection port Type IV: Totally implanted epidural or subarachnoid catheter with an implanted infusion pump Type V: Totally implanted epidural or subarachnoid catheter with an implanted programmable infusion pump
1314 Section V— Specific Treatment Modalities for Pain and Symptom Management a totally implantable programmable infusion pump attached to a type II tunneled catheter. The programmable feature of a type V IDDS allows a broad spectrum of delivery rates and modes, including occasional bolus injections. Each of these drug delivery systems has its own unique profile of advantages and disadvantages. The clinician must be familiar with the particular merits of each system if optimal selection is to be made. In this time of increasing pressure to control the cost of health care, economic factors must also play a role in the selection of an IDDS. The cost of both the intended delivery system and the drugs to be administered through the delivery system must be considered before implantation of an IDDS. A perfectly functioning IDDS is of no value to a patient who is unable to pay for the drugs, special needles, and supplies needed to use the delivery system. Similarly, implanted systems may superimpose financial hardship on a difficult terminal course. With prior planning, the financial issues can be individualized and resolved.
Type I: Percutaneous Catheter The type I percutaneous catheter has gained wide acceptance for the short-term administration of spinal opioids or local anesthetics, or both, for the palliation of acute pain, including obstetric and postoperative pain (Fig. 175.1). The type I system also has three applications in cancer pain management. The first is in the acute setting, in which the delivery of opioids into the epidural or subarachnoid space can provide temporary palliation of pain after surgery or until other concurrent treatments, such as radiotherapy, become effective. The second is in imminently dying patients too ill for more invasive procedures. The third is the use of a percutaneous catheter to administer test doses of spinal opioids before placement of a more permanent IDDS. In many centers, the use of a percutaneous catheter for the delivery of epidural and especially subarachnoid opioids is limited because of the ease with which catheters can be tunneled. The improved catheter fixation and
Fig. 175.1 Type I percutaneous catheter.
reduced risk for infection associated with subcutaneous tunneling, combined with the relative ease of tunneling, have led many pain specialists to tunnel the spinal catheter to the flank, abdomen, or chest wall. In view of the potentially devastating and life-threatening consequences of catheter-induced spinal infection, and the highly favorable risk-to-benefit ratio of the type II tunneled catheter, use of the type I system should, in the author's opinion, be limited solely to the acute setting.
Type II: Subcutaneous Tunneled Catheter Subcutaneously tunneled catheters are usually selected for patients who have a finite need for spinally administered opioids (Fig. 175.2). Patients with pain from major trauma, such as pelvic and long bone fractures and flail chest, are appropriate candidates for a type II system, as are cancer patients with life expectancies of weeks to months who have experienced excellent palliation of symptoms with trial doses of spinal drugs.11,12 The type II system carries significantly less risk for infection than percutaneous catheters do.12 The simplified catheter care and the ease of injection by both medical and nonmedical personnel are also significant advantages of the type II system. The type II system can also be attached to an external continuous infusion pump.
Type III: Totally Implantable Reservoir/Port The totally implantable reservoir is often chosen for cancer patients with life expectancies of months to years who have had excellent relief of symptoms with trial doses of spinal drugs (Fig. 175.3). Significantly less expensive than the type IV or V system, the type III system is a reasonable choice for patients who do not have a third party to cover the cost of a more sophisticated system.13 The type III system is associated with potentially less risk of infection than are the type I and II systems and with a decreased risk of catheter failure. Injection of the type III system is more difficult than with type I and II systems, and this disadvantage can have significant import when training lay people to inject and care for this system. Furthermore, removal or replacement necessitates a surgical incision.
Fig. 175.2 Type II subcutaneous tunneled catheter.
Chapter 175—Implantable Drug Delivery Systems: Practical Considerations 1315
Type IV: Totally Implantable Infusion Pump The totally implantable infusion pump is also used in patients with life expectancies of months to years who obtained relief of symptoms after trial doses of spinal drugs (Fig. 175.4). Type IV delivery systems may also be indicated in a cancer patient with a shorter life expectancy who experiences intermittent confusion from metabolic abnormalities or systemically administered drugs. Clinical experience suggests that such patients may obtain analgesia with fewer side effects with lowdose continuous spinal opioid infusion than with repeated bolus injections into a spinal catheter. Alternatively, a type III implanted port with an external infusion pump may suffice in this situation, although such a system may be more inconvenient and require more support. Because type IV systems require infrequent refills and run continuously, they are ideal for patients with limited medical or nonmedical family support services. The type IV system is usually selected with an auxiliary bolus injection port to take advantage of potential drug options, such as injection of local anesthetics and the ability to inject contrast to troubleshoot the system. Advantages of the type IV system include minimal risk for infection after the perioperative period and the need to inject the pump very infrequently relative to other IDDSs (the pump
reservoir needs to be refilled approximately every 7 to 20 days). The overall high cost of the type IV system is a disadvantage and may occasionally result in the selection of a less effective or more inconvenient analgesic technique.
Type V: Totally Implantable Programmable Infusion Pump The type V totally implantable programmable infusion pump is implanted with the same ease as the type IV system (Fig. 175.5).14 These systems allow a broad spectrum of delivery rates and modes, including occasional bolus injections. Their principal application to date has been intrathecal infusion, especially for the treatment of spasticity in multiple sclerosis and patients with spinal cord injury, but the type V IDDS is also gaining increasing acceptance as the preferred type of IDDS for the long-term administration of spinal opioids.
Conclusion The administration of spinal drugs via an IDDS is a useful addition to the armamentarium of clinicians treating patients with pain or spasticity that does not respond to conventional means. Proper selection of the patient and an appropriate delivery system are crucial if optimal results are to be achieved. The chronic administration of opioids and other drugs into the epidural or subarachnoid space is evolving. Advances in the pharmacology of spinal drugs and the development of new delivery system technology will in time no doubt expand the options available for the relief of uncontrolled pain and spasticity.6
References Full references for this chapter can be found on www.expertconsult.com.
Fig. 175.3 Type III totally implantable reservoir/port.
Fig. 175.4 Type IV totally implantable infusion pump.
Fig. 175.5 Type V totally implantable programmable infusion pump.
V
Chapter
176
Complications of Neuromodulation Timothy R. Deer and Matthew T. Ranson
C h apt e r O u t l in e Introduction 1316 Overview of Complications of Spinal Cord Stimulation and Intrathecal Drug Delivery 1316 Complications of the Neuroaxis Bleeding 1316 Infection 1317 Direct Neurologic Trauma 1318 Complications Outside of the Neuroaxis 1319 Seroma 1319 Bleeding 1319
Introduction The physician must be vigilant to prevent, identify, and resolve complications. Even in the most talented hands, complications occur and may lead to a poor outcome. With use of careful preoperative screening and meticulous operative techniques, the outcomes of neuromodulation are improved, but complications (Table 176.1) persist despite the best efforts of the physician.
Overview of Complications of Spinal Cord Stimulation and Intrathecal Drug Delivery Complications of implantable devices can range from minor problems that may go unnoticed by the physician and patient, to those treated with observation, to major adverse events that lead to paraplegia or serious neurologic injury. In this chapter, the complications are grouped into sections with consideration of the impact of each device on the potential problems that the practitioner may experience.
Complications of the Neuroaxis Bleeding The invasion of the epidural or intrathecal space with needles, leads, and catheters can lead to major bleeding complications. In most patients, this bleeding results in no clinically apparent complication and necessitates no treatment. In some cases, this bleeding may involve an asymptomatic epidural hematoma; but in the absence, of postsurgical imaging, this 1316
Painful Generator 1319 Complications of the Device 1319 Loss of Appropriate Stimulation 1319 Other Lead and Generator Problems 1320 Complications of the Intrathecal Catheters 1321
Complications Involving Intrathecal Agents 1321 Risk Assessment 1321 Risk Reduction Strategies 1322 Conclusion 1323
normally goes unrecognized. Rarely, bleeding progresses to the development of an epidural hematoma and compresses spinal structures. If a developing epidural hematoma progresses, it can lead to numbness, back and leg pain, weakness, and eventual paraplegia. Treatment of clinically significant epidural hematoma necessitates prompt surgical evaluation and evacuation if clinically indicated. This problem must be identified early and treated within 24 hours of the development of symptoms. Patients who undergo surgical evacuation within 12 hours have been shown to have clinically better neurologic outcomes than patients who undergo decompression later than 12 hours.1 After 24 hours from presentation, the chance of a complete recovery diminishes. Patient education is important in the early identification of this complication. The patient should be taught to watch for and report to the treating doctor any new signs of numbness, weakness, and increasing pain in the postoperative period. Weakness in the postoperative period is a red flag that should raise the suspicion of this tragic complication and warrant an immediate computed tomographic (CT) scan of the spine in the patient on a stimulator and immediate magnetic resonance imaging (MRI) with appropriate precautions in the patient on a pump. Risk factors for development of an epidural hematoma include anticoagulation therapy, platelet-inhibiting medications, aspirin, and possibly nonsteroidal drugs. However, the role of low-dose aspirin and nonsteroidal anti-inflammatory drugs in epidural hematoma formation is controversial and has not been established. Most clinicians allow patients to remain on low-dose aspirin and nonsteroidal drugs during the perioperative period. Other factors may include © 2011 Elsevier Inc. All rights reserved.
Chapter 176—Complications of Neuromodulation 1317
Table 176.1 Complications Complication
Diagnosis of Problem
Treatment of Problem
Lead migration
Inability to program
Reprogramming, surgical revision
Current leak
High impedance, pain at leak site
Revision of connectors, generator, or leads
Nerve injury
CT scan or MRI, EMG/NCS/physical examination
Steroid protocol, anticonvulsants, neurosurgery consult
Epidural fibrosis
Increased stimulation amplitude
Lead programming, lead revision
Epidural hematoma
Physical examination, CT scan, or MRI
Surgical evaluation, steroid protocol
Epidural abscess
Physical examination, CT scan or MRI, CBC, blood work
Surgical evaluation, IV antibiotics, ID consult
Postdural puncture headache
Positional headache, blurred vision, nausea
IV fluids, rest, blood patch, neurosurgery consult if evidence of CN palsy
Unacceptable programming
Lack of stimulation in area of pain
Reprogramming of device, revision of leads
Lead migration
Inability to program, x-rays
Reprogramming, surgical revision
Current leak
High impedance, pain at leak site.
Revision of connectors, generator, or leads
Generator failure
Inability to read device
Replacement of generator
Seroma
Serosanguinous fluid in pocket
Aspiration; if no response, surgical drainage
Hematoma
Blood in pocket
Pressure and aspiration, surgical revision
Pain at generator
Pain on palpation
Lidoderm patches, injection, revision
Wound infection
Fever, rubor, drainage
Antibiotics, incision and drainage, removal
Neuroaxis Complication
Device Complication
Non-Neurologic Tissue
CN, cranial nerve; EMG, electromyography; ID, implantable device; IV, intravenous; NCS, nerve conduction study.
difficult percutaneous lead or catheter placement, laminotomy approach to lead placement, and revision of previously placed leads. The need to perform surgical instrumentation and create bony insult dramatically increases the risk of a significant bleed. Spine surgeons often recognize the bleed at the time of surgery and treat it without clinical significance. The diagnosis of epidural hematoma is assisted with clinical suspicion, physical examination, and history, but the confirmatory diagnosis is made with CT scan. MRI can be obtained once the leads are removed and can be obtained in patients with intrathecal infusion systems without delay. However, given the need for prompt surgical evaluation, obtaining a CT scan may be more judicious. Epidural bleeding appears to be a much greater risk with spinal cord stimulation than with intrathecal drug delivery. The catheter is driven within the intrathecal space with pumps, and the insult to the epidural space is minimal. Intrathecal bleeding could result in arachnoid irritation, but the incidence or significance is not known.
Infection The other spinal compressive lesion that causes a complication of the neuroaxis associated with neuromodulation is epidural abscess. This is the most urgent infectious complication associated with implantable devices, although the implanter should be aware of the complications of superficial infections of the incision, pocket infections, diskitis, and meningitis (Figs. 176.1 and 176.2). The most common of these problems is superficial infection, and the risk of epidural abscess
Fig. 176.1 Early cellulitis with partial deshisance of wound.
appears to be much less than one in 1000. Because of the overwhelming potential risks of epidural abscess, the implanter should have a good knowledge of this issue. Epidural abscess may present with severe pain in the area of the lead implant. This may be associated with fever, with most patients experiencing temperatures more than 38°C (101°F). Radiating pain can be severe and may develop if the abscess extends to the foramen or compresses the cord. In some patients, a progression can consist of an initial pain symptom, with an evolution to sensory loss, radicular pain, and then motor weakness and
1318 Section V—Specific Treatment Modalities for Pain and Symptom Management
Fig. 176.2 Infection of device pocket.
eventual paraplegia. Risk factors for abscess include immunocompromised state, including patients with HIV infection and organ transplants, history of chronic oral steroids and immunosuppressive drugs, history of chronic skin infections, history of methicillin-resistant Staphylococcal aureus infection (MRSA) or colonization, chronic diseases such as poorly controlled diabetes mellitus, or local infection at the surgery site. Smoking and obesity may also lead to an increased risk of infection. Infectious complications with intrathecal catheters are uncommon and include meningitis and direct infection of the spinal cord near the catheter tip, resulting in transverse myelitis.2 Most cases of transverse myelitis are not seen with a known infection, and the cause may be undetermined. Clinical indications of infection include the presence of a fever, elevated white blood count, elevated C-reactive protein levels, and elevated erythrocyte sedimentation rate. Epidural abscess is diagnosed with clinical suspicion, history, and physical examination and confirmed with CT scan. MRI may be performed once the spinal cord stimulation (SCS) device is explanted or in patients with an intrathecal delivery device with proper precautions.
Direct Neurologic Trauma Neurologic injury of the spinal cord or nerve roots is another potential risk of percutaneous lead or catheter placement. Because the spinal nerves of the cauda equina float freely within the cerebrospinal fluid (CSF) below the L1-L2 level, this problem less likely if needle entry is below this level. Lateral fluoroscopic views are especially important in percutaneous SCS lead placement because often the surgeon is advancing the needle over the conus medullaris. In addition, lead or catheter placement into the conus medullaris is possible with little production of pain in an awake patient. Injury may occur via needle trauma, lead or catheter placement and removal, or surgical manipulation during paddle lead placement. In many patients, the injury is associated with deep sedation or general anesthesia. Monitored anesthesia care where the patient is freely arousable and communicating with the surgeon is recommended during percutaneous needle placement. In some patients, the inability to tolerate the procedure with sedation leads to the need to perform these devices with general anesthesia. This is acceptable for intrathecal catheter
placement below the level of the conus but should be avoided in spinal cord stimulation unless it is done with an open laminotomy approach. In the immediate postoperative period, a neurologicinjury may present in a confusing manner and may create a diagnostic dilemma. Assessment of the patient in the postanesthesia care unit and documentation of the absence of any new focal neurologic findings are advisable. CT scan may not show an abnormality, and MRI cannot be performed in the case of SCS until the device is surgically removed. With patients on a pump, an MRI is the imaging study of choice with proper precautions. An electromyogram and nerve conduction study may be helpful in determination of injury, but results may not become abnormal for several days after the insult. The treatment of neural injury or irritation depends on the severity. In cases of cord or nerve contusion, the treatment may simply consist of observation because many of these cases often resolve with time. In the immediate postoperative period, intravenous steroids may be helpful in reducing swelling of the neural structures. Less worrisome complications inside the neuroaxis include inadvertent dural puncture with postdural puncture headache. The literature has shown an incidence rate of up to 11% of cases, although that number appears much higher than most implanters may see in their clinical practice. This risk is increased by obesity, calcified ligaments, difficult lead or catheter placement, poor positioning from scoliosis or body habitus abnormalities, patient movement, and previous surgery at the level of needle entry. In spinal cord stimulation, the use of loss of resistance with use of fluoroscopy with an attention to the hanging drop in the syringe may reduce this risk, particularly in the midthoracic and higher levels of entry. In intrathecal catheter placement, the number of attempts is important to reducing the risk of postdural puncture headache. CSF leak and hygroma formation are complications associated with intrathecal drug delivery systems. The use of a pursestring suture to secure the tissue around the CSF entry site may be helpful in reducing these complications. Abdominal binders in the immediate postimplant period may also be helpful, as may conservative measures such as fluid intake, caffeine, and intramuscular sumatriptan. Spinal cord stenosis may develop over time in the vicinity of an implanted lead. This is a rare complication and develops slowly over time. The development of stenosis over the lead is diagnosed with clinical history, CT scan, or CT myelogram. This problem is unlikely with intrathecal catheters because of the compressibility of catheter material. Compression of spinal cord stimulation leads is more likely with paddle leads because of their volume. In cases of stenosis before implant, a paddle implant is the best choice because of the ability to decompress the bony structures via laminotomy before lead placement. Intrathecal drug delivery devices pose additional risks because of the administration of intrathecal medications. Inflammatory masses surrounding the tip of the catheter were first reported in 1999.3 The inflammatory mass appears to be a chronic fibrotic noninfectious mass that develops at the tip of the intrathecal catheter over months to years and is related to high concentrations of opioid at the catheter tip. As the inflammatory mass grows larger, patients often present with neurologic signs and symptoms that reflect direct compression of the spinal cord or other neural elements by the expanding mass.4 Patients may present with initial loss of analgesia followed by progressive neurologic compromise. Because many
Chapter 176—Complications of Neuromodulation 1319 the risk of this complication. In rare cases, fever can develop in the setting of a seroma. This is a complicated situation that can be resolved only with surgical evaluation of the wound.
Bleeding Bleeding can occur in the generator, pump reservoir, or lead and catheter incision sites. This can lead to hematoma and necessitate drainage or wound dehiscence. The best treatment is prevention. This consists of thoughtful tissue dissection, pressure to the area of bleeding, suturing of arterial bleeding, coagulation of ongoing small-vessel hemorrhage, and careful inspection of the wound before closure. The physician should also access the patient for bleeding risks, including medications and diseases that may impact bleeding. Fig. 176.3 Gross seroma of device pocket.
of the reported cases have been directly linked to high concentrations of morphine and hydromorphone, consensus recommendations have suggested that the concentration of morphine be limited to 30 mg/mL and the concentration of hydromorphone to 20 mg/mL. In addition, sufentanyl and fentanyl appear to have a lower risk of granuloma formation. Diagnosis is made with a T1-weighted MRI with and without gadolinium. A CT myelogram can be obtained if MRI is contraindicated. The recommended doses and concentrations of drugs are based on the ideal clinical situation. In some cases, the risks of higher concentrations and doses are believed by the implanter to be worthwhile for a good clinical response and of greater benefit to the patient than the risk of inflammatory mass formation.
Complications Outside of the Neuroaxis Wound infections that involve the generator, pump reservoir, tunneled area, or lead and catheter incision site can occur in 0 to 4.5% of patients based on reported incidence rates.5 This problem is diagnosed with pain, swelling, rubor, and drainage of purulent material. An elevated white blood cell count, sedimentation rate, or C-reactive protein value should create concern regarding the infectious status of the implant. Patients whose conditions respond to antibiotics initially may have development of chronic slow-growing infections that could be subclinical for some time. Recurrent fever should lead the implanter to consider evaluation by an internal medicine specialist, family physician, or infectious disease specialist.
Seroma In some cases, the patient may have a swollen, irritated wound develop that is not related to infectious etiology (Fig. 176.3). This complication, called a seroma, is caused by a buildup of serosanguineous fluid. Seroma is diagnosed with lack of fever and normal blood study evaluation of white blood count. If the diagnosis cannot be determined, incision and drainage with cultures may be necessary to make a conclusive diagnosis. In most cases, seroma can be treated without device removal. Careful dissection and attention to minimizing tissue trauma may reduce
Painful Generator Pain at the generator or reservoir site may occur from neuroma, tissue irritation, or bony contact with a rib or pelvic bones. Neuroma formation is rare and may be reduced with careful dissection and handling of the tissue. To avoid pain on the bony structures, the implanter should carefully access the bony landmarks. In some cases, the patient's body shape or habitus leads to difficulty in finding an ideal position for the generator. With new, smaller generators, the ability to place the pocket near the lead incision site has reduced the problem with pain at the generator in stimulation cases. The size of the pump can lead to pain even in the most carefully placed pocket. The patient with poor nutrition and minimal subcutaneous fat may have pain and pocket complications. Patients with complex regional pain syndrome are thought to be more prone to pain than other chronic pain groups. Treatment can include topical local anesthetic patches, wound injection, or surgical revision.
Complications of the Device Loss of Appropriate Stimulation The most commonly reported complication of SCS devices is loss of paresthesia capture over time and subsequent loss of pain reduction. These reports are often based on older studies with devices that had less ability to capture the spinal fibers and less ability to be programmed in multiple fashions to target many areas of pain generation. Common causes of loss of capture include lead migration, dead zones that do not respond to cathode activation, hypothesized tolerance to stimulation, and increased impedance from either fibrosis under and around the lead or a current leak somewhere in the system. New x-rays can be helpful in confirming any lead shift or migration. Depending on the degree of change, the physician may be able to work with technicians to reprogram the system to create an improved clinical status without the need for surgical correction. If conservative measures fail, a surgical revision may be necessary. The clinician should always be aware that new disease processes can sometimes be confused with a failure of the system and additional workup may be warranted if the history or examination changes from previous evaluations. Lead migration has been reported as a common complication in percutaneous systems (Fig. 176.4 and Table 176.2). In some studies, up to 20% or more of leads have been shown
1320 Section V—Specific Treatment Modalities for Pain and Symptom Management
Table 176.2 Migration Risks Migration Risk
Physician Action
Needle angle
Needle angle of 30 to 45 degrees
Needle entry
Paramedian approach
Fatty tissue at anchoring site
Débridement of fatty tissue around the needle entry site exposing fascia and ligament for proper anchoring
Anchoring to muscle
With use of an exaggerated paramedian approach, the physician should dissect medially until approaching ligament or fascia, avoiding anchoring to muscle, which may lead to migration with contraction.
Lead anchor gap
The anchor should be as close to the lead entry into the ligament or fascia as possible, avoiding room for migration distal to the anchor.
Suturing with silk
Avoid silk sutures when anchoring
Dependence on the anchor
The anchor should be seen as one component of securing the system. Total dependence on the anchor can lead to poor outcomes.
Hematoma below anchor
Hemostasis should be obtained before closing the wound. Bleeding can lead to catheter movement from hematoma compression placing pressure on the anchor.
Minimal migration changes
The catheter should be placed in an area of the spine that is not impacted by minimal migration movements. If the catheter tip is in the spinal cerebral fluid, a good outcome may be preserved even in the presence of movement.
Fig. 176.4 Lead migration.
to migrate.6 This number is based on older data and products, with most clinicians experiencing clinical significance in less than 5% of patients with modern equipment. The problem is diagnosed with anterior-posterior and lateral films with comparison with original implant films. Treatment ranges from simple computer reprogramming to surgical lead revision. A careful attention to anchoring may reduce this complication risk but cannot prevent it from occurring. New anchors have been developed by several manufacturers and have obtained US Food and Drug Administration (FDA) approval for clinical use. The impact of these new titanium-based anchors is not yet known, but regardless of the anchor chosen, the implanter must do an adequate dissection to visualize the fascia and ligament.
Other Lead and Generator Problems Painful stimulation or loss of stimulation can occur from current leakage or loss of system integrity. This problem is often diagnosed with computer analysis showing high impedance compared with baseline. Possible causes include lead migration, poor contacts from fluid in the contacts, or partial or total lead fracture. Lead fracture appears more common with paddle leads. Positional stimulation can occur because of poor lead- to-tissue contact with standing, lying, or bending. This problem sometimes resolves over time but may need revision to a paddle lead that takes up more volume in the epidural space. Positional stimulation is often thought to occur because of lead movement, but physiologically, it is more likely the result of movement of the cord away from the lead and towards the lead with positional change. Some patients experience pain from the generator or pump moving within the pocket. This problem can be reduced by anchoring the generator or pump and by using sizing templates that can be provided by the manufacturers. Proper sizing of the pocket is critical for comfort and to reduce the risk of complications. Situations in which the pocket is too small may lead to poor wound closure, pressure on the tissue, and even erosion over time. If the pocket is too large, it may lead to flipping of the device, pain from device-tissue irritation, or a seroma in the area of the pocket that is not involved in the implant. An anchoring stitch may be helpful to secure the SCS generator.
In cases of implantable pumps, suture loops can be helpful to reduce problems, but anchoring to fascia with a nonabsorbable suture is important. Polytetrafluoroethylene patches can be used to secure the pump but may lead to difficulty with future revisions because of scarring around the pocket. Erosion of device components through the skin can lead to loss of the system. This can occur because of poor tissue health from chronic disease, weight loss, and placement of anchors in the superficial tissues. This does occur more commonly at the generator. When erythema occurs around a generator, the physician should consider surgical revision before the complete loss of tissue integrity of the dermal layers that leads to the need to remove the system. In the placement of peripheral leads, the device should be placed below the dermis. In general, the physician should determine this depth via palpation, needle placement, and observation when making an incision to secure the lead and ensuring anchoring to the thoracolumbar muscle fascia. The use of suture for securing the device without the use of a formal anchor should be considered because many cases of device erosion occur at the silastic anchor site. Erosion may be more problematic when new anchors containing harder substances, such as titanium, are used in peripheral leads.
Chapter 176—Complications of Neuromodulation 1321
Complications of the Intrathecal Catheters The most common device failure in intrathecal pumps is catheter failure. Catheter failure has been reported by Follet and Naumann7 to be 4.5% at 9 months in a prospective observation study. The most common problems associated with the catheter are migration, fracture, and kinking. Migration of the catheter may result in complications that range from lack of analgesia to severe neurologic deficits. Migration into the epidural space or out of the spinal canal produces loss of analgesia and may cause postdural puncture headaches and possibly the development of a hygroma. More worrisome migrations include erosion into the neural foramen, resulting in nerve root irritation and radicular symptoms, or erosion into the spinal cord, producing profound neurologic deficits.8 If migration is suspected with clinical findings, a change in pump refill volumes or examination with an MRI is indicated. Implantation of intrathecal devices with general anesthesia may result in intraparenchymal placement of the catheter. For this reason, many physicians recommend intrathecal catheter placement be performed with monitored anesthesia care with light sedation to avoid this catastrophic complication. In some cases, the patient cannot tolerate lying in the necessary position, and general anesthesia is needed. Other options include spinal anesthesia after the catheter is in position. In addition, the catheter may migrate into the subdural space, resulting in decreased efficacy from inadequate CSF distribution. Again, MRI should be performed in any patient suspected of catheter migration.
Complications Involving Intrathecal Agents Multiple adverse reactions to intrathecal delivery of opioids have been reported and include nausea and vomiting, pruritus, edema, diaphoresis, weakness, weight gain, constipation, difficulty urinating, and decreased libido.9,10 Peripheral edema has a reported incidence rate from 1% to 20% and appears to occur as a result of the effect of intrathecal opioids on the pituitary adrenal axis.11 The development of intrathecal granulomas appears to result from the reaction of the infused drug and was discussed previously and seems to involve morphine more often than other medications. Adjunctive agents commonly used in intrathecal devices include clonidine, bupivicaine, and ziconotide. Clonidine may result in somnolence and hypotension. Bupivicaine can cause muscular weakness and can result in hypotension as well. Ziconotide has many reported side effects, with the most commonly reported including nausea and vomiting, dizziness, confusion, urinary retention, and somnolence.12
Risk Assessment 1. Before any procedures are performed in the neuroaxis a thorough evaluation of the spinal anatomy and coagulation status of the patient is necessary. Imaging studies including MRI, CT scan, and x-rays of the patient's spinal anatomy should be reviewed to assess for critical stenosis, significant loss of disc space height, and complicating factors, such as severe scoliosis, that may make percutaneous access of the neuroaxis both difficult and dangerous.
The physician performing neuroaxial procedures must obtain a careful history, including the presence of coagulopathy and immunocompetency, before the procedure. In addition, the patient's medication list must be reviewed, and any medications that affect bleeding should be discontinued in consultation with the prescribing physician according to the latest guidelines.13 Standard laboratory evaluation should include at a minimum prothrombin time (PT), partial thromboplastin time (PTT), international normalized ratio (INR), and complete blood count (CBC) with platelets. 2. Patients with diseases that result in immunodeficiency should undergo careful assessment, including a review of the underlying disease, preoperative laboratory evaluation, and physical examination, to identify any skin infections that may pose a risk to infection during implantation of a neuromodulation device. Coexisting diseases such as HIV infection and syndrome, neoplastic syndromes, previous MRSA infection, rheumatologic conditions that necessitate long-term steroid treatments, and brittle diabetes and conditions such as morbid obesity all place patients at risk for infection and potential catastrophic outcomes. 3. Wound infections may vary in severity from superficial infection, including frank dehiscence, to catastrophic infections, such as meningitis. Meticulous surgical technique with attention paid to proper wound closure and hemostasis can reduce the incidence of wound infection. 4. The risk of neurologic injury is low in the hands of experienced neuromodulators and is hard to quantify because of the low incidence rate. However, the presence of morbid obesity, critical stenosis, calcified ligaments, epidural fibrosis from prior surgery near the planned implant site, and spinal instrumentation increase the risk of neurologic injury and inadvertent dural puncture in SCS and nerve root injury. CSF in the epidural space can lead to difficulty obtaining adequate stimulation during a SCS trial and can result in postpuncture spinal headache that complicates or confounds the outcome of a SCS trial. The risk of neurologic injury is also increased with uncooperative patients with extensive movement during the operative procedure. 5. Significant spinal stenosis, either pre-existing or acquired after implantation, can result in severe neurologic compromise as a result of spinal compression from the implant. The neuromodulator should pay particular attention to cervical stenosis because the diameter of the spinal canal is significantly smaller that the lumbar and thoracic canals. 6. The development of seromas typically involves the generator or reservoir site and may lead to loss of the device from wound dehiscence. Inadequate hemostasis leading to hematoma formation, history of seroma formation in prior operations, and a history of connective tissues disorders such as lupus, rheumatoid arthritis, and scleroderma may predispose patients to seroma formation. 7. Pain at generator or reservoir site is commonly associated with patients that have a history of complex regional pain syndrome or fibromyalgia. However, it to prediction of which patients will develop pain in this location is impossible, and many will need revision or explantation of the device.
1322 Section V—Specific Treatment Modalities for Pain and Symptom Management 8. Loss of proper stimulation paresthesia or painful stimulation can occur and lead to a reduction in efficacy or increased pain with use of the SCS. Many factors may contribute to decreased efficacy of stimulation, including epidural fibrosis, migration, positional change, or other electrical stimulation factors. Patients with decreased or loss of stimulation should undergo a complete evaluation, including a physical examination, plain film evaluation, and interrogation of the device. In the case of intrathecal drug delivery devices, a dye study and MRI may be useful in determination of loss of analgesia. 9. Lead or catheter migration can lead to decreased efficacy of the device and opioid or baclofen withdrawal in intrathecal drug delivery systems. Movements such as bending at the waist, twisting, reaching overhead, and heavy lifting can all result in lead and catheter migration, particularly in the early postoperative period. Migration of the intrathecal catheter may result in movement into epidural space or completely out of the neuroaxis. Migration of the catheter or lead may occur into the neural foramen, resulting in nerve root irritation and the development of radicular symptoms.8 Intrathecal catheter or SCS lead migration into the spinal cord is possible and may occur without the production of pain. In addition, intraparachymal placement of a catheter or lead is possible during surgical implantation. Good surgical technique during anchoring to the fascia and careful placement of needles with multiplanar fluoroscopy must be used by the surgeon. 10. Fracture of SCS leads appears to be more common in paddle leads, likely because of increased tension from the inability of the paddle to move when force is applied. Placement of a relaxing loop of the lead wires distal to the anchors is advisable and may reduce the tension forces on the paddle lead wires. 11. Improperly anchored pump reservoirs and impulse generators can result in device flipping, which can lead to inability to program or use the SCS system or to access the reservoir for refills. 12. Hardware erosion of leads, anchors, catheters, reservoirs, or generators through the skin can lead to infectious complications that necessitate the removal of the implant or an extensive revision. 13. Finally, patients with a properly functioning SCS with parethesias in the painful areas and normal impedance numbers may experience loss of pain relief.
Risk Reduction Strategies 1. Patients who are on medications that alter hemostasis, including platelet function, must discontinue these medications according to current published guidelines, with consent of the prescribing physician, before undergoing implantation of a neuromodulation device.13 In patients who are unable to discontinue anticoagulation therapy, such as cancer patients with conditions that are hypercoaguable, may be considered for inpatient heparin infusion before surgery. This allows for limited discontinuation of anticoagulation therapy before the implantation operation and reduces, but does not eliminate, the chance of serious sequelae.
2. Perioperative antibiotics should be given at least 30 minutes before incision. Although the use of preoperative antibiotics is considered controversial by some physicians, most experienced implanters consider perioperative antibiotics standard of care. Infectious complications are further reduced with use of extensive preparation with wide draping and careful attention to standard sterile surgical techniques. Physicians with limited surgical training should be mentored by more experienced physicians before performing invasive surgical procedures. All surgical wounds should be irrigated copiously with antibiotic containing irrigation. Proper wound closure techniques are critical to prevention of infection. Patients should be seen within the first postoperative week to allow for early detection of infection, which may present with signs such as rubor, drainage, or painful incisions. Patients with these findings should be considered for incision and drainage to prevent the development serious infections that necessitate the removal of the implanted device. If the infection extends into the pocket or posterior spinal incision, the device must be explanted and an infectious disease consultation should be considered. 3. Neurologic injury can be minimized by educating the patient about movement during the surgical procedure and maintaining anesthetic levels that allow for patient cooperation without disinhibition. Proper patient positioning and fluoroscopic alignment of the spine are critical to correct needle placement. In patients who are unable to tolerate extended periods in the prone or lateral decubitus positions, referral to a spine surgeon should be considered. 4. The risk of dural puncture during SCS implantation can be minimized with use of a paramedian approach with a needle entry angle of less than 45 degrees. In addition, the use of both the hanging drop and loss resistance techniques with lateral fluoroscopic views can reduce the risk of inadvertent dural puncture. 5. Patients who have radiographic evidence of moderate to severe stenosis should be approached with caution before a trial of SCS or permanent implantation procedure. Progression of the stenosis may result in neurologic injury, especially with the addition of leads in a tight stenotic space. Consideration should be given to surgical referral for decompression and paddle lead placement. Caution is also warranted in patients with stenosis who undergo intrathecal catheter placement. 6. Seroma formation occurs as a result of inadequate hemostasis and can lead to disastrous complications, including loss of the implanted device. Although aspiration of a suspected seroma with analysis can help the physician rule out infection, careful attention to avoiding contamination of the wound must be used. Meticulous surgical technique with careful dissection and judicious use of electrocautery can reduce the risk of seroma formation. Some physicians routinely perform the generator or reservoir dissection before placing the leads or catheter and pack the wound with antibiotic-soaked sponges to allow time for tamponade of venous and arterial bleeding. 7. Pain at the generator or reservoir site can lead to patient requests for explantation. Careful planning of
Chapter 176—Complications of Neuromodulation 1323 the implantation site should take into consideration the patient's body habitus, location of the ilium and ribs, and placement of the away from the belt line and avoiding placement too low in the buttock. The device should be placed several centimeters below the dermis, and intramuscular placement should be avoided if at all possible. Newer devices that are significantly smaller have allowed the implantation site to be closer to the spinal incision and will likely decrease the number of revisions necessary as a result of painful device pockets. 8. Loss of paresthesia with SCS can occur over time for reasons that are not well understood. Reprogramming with a change in lead arrays, amplitudes, and pulse widths may restore paresthesias in the painful areas. In addition, the impedances of the leads should be determined through interrogation of the impulse generator. If high impedances are found, the physician may need to perform a revision or consider referral to a spine surgeon for paddle lead placement. Imaging studies should be obtained to assess for lead migration before surgical revision is considered. 9. Lead and catheter migration are often related to improper surgical techniques, either involving the anchor or the angle of needle placement. The anchors must be secured to the underlying fascia and ligaments, and in the case of SCS leads, the anchor must be secured to the leads. Needle insertion should be accomplished with a paramedian approach with an angle less than 45 degrees. Although some physicians advocate bracing, limitation of activity, and restrictions on motion, these recommendations have never been proven to be effective in a prospective fashion. 10. Migration of catheters and leads smf fracture can be avoided with use of a needle insertion angle of less than 45 degrees and placement of strain relief loops both in the spinal incision and under the implantable device. 11. Flipping of the implantable device can be minimized by securing the device to the fascia in the pocket with nonabsorbable suture. In addition, a properly sized pocket helps to prevent this complication by eliminating excess space. 12. Erosion of leads, anchors, or the implantable device may occur over time and is more common in patients with chronic disease and in patients who experience significant weight loss or gain. Erosion can be minimized with placement of the device in the subcutane-
ous tissue below the dermis with adequate tissue to protect the device from pressure. The risk of erosion is higher in patients who undergo peripheral stimulation, particularly in the scalp regions. Silastic anchors appear particularly prone to erosion in areas with little subcutaneous tissue, and some physicians advocate use of suture instead of these anchors. 13. The development of tolerance or severe side effects to intrathecal medications may be unavoidable even with opioid rotation and the addition of adjunct medications. Granuloma formation may necessitate removal of the device if reduction of the medication fails to resolve the inflammatory mass. 14. Loss of stimulation may occur from many factors, such as migration and fibrosis. Even in the presence of adequate stimulation in the painful areas, some patients may eventually lose pain relief and ultimately need explantation. Reprogramming may resolve some cases of loss of pain relief with the SCS. Surgical revision with paddle leads may be an option in some patients, particularly in the case of fibrosis and high impedance. However, some patients are not amenable to revision and reprogramming and ultimately need removal of the device. Neuromodulation is highly effective but may not provide permanent pain relief in all patients, despite heroic physician attempts.
Conclusion Neuromodulation is a highly effective treatment in carefully selected patients with chronic pain. The devices continue to improve, with smaller generators with greater numbers of contacts and newer technologies that allow for greater precision in placement. Miniaturization has allowed an expanded role of SCS and will continue to lead to new treatment options in many patients. Although intrathecal drug delivery is used less commonly because of the increased efficacy of spinal cord sand peripheral stimulation, it is a viable treatment option in refractory cases. The physician must understand and identify the risks associated with these devices and treat them aggressively to prevent permanent neurologic sequelae.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
177
Neuroadenolysis of the Pituitary Steven D. Waldman
CHAPTER OUTLINE History 1326 Indications and Contraindications 1326 Clinically Relevant Anatomy and Technique 1326 Preoperative Preparation 1327 Technique 1327 Postoperative Care 1329
History
Surgery has been used to palliate pain from hormone-dependent tumors since the late 1800s. Early surgical efforts were directed primarily at surgical castration.1 The addition of adrenalectomy followed, as the importance of this gland in the secretion of sex hormones became better understood.2 Advances in the field of endocrinology in the 1950s led to an increasing focus on the pituitary gland. To this end, transcranial hypophysectomy was performed in an effort to induce regression of hormone-dependent tumors and to palliate symptoms. Investigators became aware that pain relief was a more consistent finding than actual tumor regression.3 Unfortunately, transcranial hypophysectomy was a major procedure with significant surgical risk that precluded its use in many of the patients who could most benefit, namely, patients with advanced malignant disease. Consequently, less invasive means of pituitary destruction were undertaken. These attempts included radiation therapy, implantation of radon seeds, and, ultimately, chemical neurolysis of the pituitary.4 Neuroadenolysis of the pituitary (NALP) was first described by Moricca in 1958 as a technique to relieve pain of malignant origin with placement of multiple needles into the pituitary gland and then injection of small amounts of absolute alcohol.5 Moricca's early reports led other investigators to adopt and modify this procedure. To date, more than 14,000 patients with intractable pain have been treated with NALP.6
Indications and Contraindications Indications for NALP are summarized in Table 177.1. NALP is an appropriate treatment for patients with bilateral facial or upper body cancer pain, bilateral diffuse cancer pain, intractable visceral pain, or pain from compression of 1326
Mechanisms of Pain Relief 1330 Results 1330 Incidence of Pain Relief 1330 Complications 1330
Conclusion 1330
neural structures after all antiblastic methods and other analgesic measures have been exhausted. When medical hormonal control of pain no longer works, patients may also benefit from the procedure.4 Most investigators observe better results in patients whose pain is the result of hormone-dependent tumors, although the procedure is also effective for palliation of pain from hormone-unresponsive malignant diseases.7 Contraindications to neuroadenolysis of the pituitary are summarized in Table 177.2 Local infection, sepsis, coagulopathy, significantly increased intracranial pressure, and empty sella syndrome are absolute contraindications to NALP.4,7 Relative contraindications to NALP include poor anesthesia risk, disulfiram therapy, and significant behavioral abnormalities. Obviously, because of the desperate circumstances of most patients considered for NALP, the risk-benefit ratio is shifted toward performing the procedure on both ethical and humanitarian grounds.
Clinically Relevant Anatomy and Technique In an effort to improve on Moricca's original technique, Corssen et al8 and other investigators modified it by decreasing the number of needles used. Levin et al9 further modified the technique with use of a stereotactic head frame. Attempting to reduce the incidence of postoperative cerebrospinal fluid (CSF) leakage, these investigators suggested initial placement of an 18-gauge, 6-inch spinal needle through the floor of the sphenoidal sinus. The needle was then removed, and a smaller, 20-gauge, 6-inch spinal needle was placed through the hole left by the 18-gauge needle. The 20-gauge needle was then advanced into the sella turcica. On occasion, these investigators found it necessary to drill through the floor of the © 2011 Elsevier Inc. All rights reserved.
Chapter 177—Neuroadenolysis of the Pituitary 1327
Table 177.1 Indications for Neuroadenolysis of the Pituitary Failure of all antiblastic treatments Failure of all other appropriate pain-relieving measures Bilateral facial or upper body cancer pain Bilateral diffuse cancer pain Intractable visceral pain Pain from compression of neural structures Loss of hormonal control of pain
Table 177.2 Contraindications to Neuroadenolysis of the Pituitary Local infection
Fig. 177.1 The nose is packed to provide vasoconstriction and mucosal shrinkage.
Sepsis Coagulopathy Increased intracranial pressure Empty sella syndrome
sella turcica with a Kirschner wire because the needle would not pass through dense bone. They also noted the occasional occurrence of CSF leakage until they instituted the injection of ethyl alpha cyanomethacrylate resin through the spinal needles. Waldman and Feldstein10 further modified NALP with use of a needle-through-needle technique, thus eliminating the need for the stereotactic frame or drilling. These modifications made the procedure more suitable for use in the community hospital. Phenol, cryoneurolysis, radiofrequency lesioning, and electrical stimulation in place of alcohol all have been advocated for NALP.11–13 More experience is needed with each of these modalities to determine whether some of the theoretic advantages and disadvantages of each modification translate into clinically relevant benefits.
Preoperative Preparation Screening laboratory tests, consisting of a complete blood cell count, chemistry profile, electrolyte determination, urinalysis, coagulation profile, chest radiography, and electrocardiography, are performed as for any other patient undergoing general anesthesia. Anteroposterior and lateral skull films are also obtained to evaluate the size and relative position of the sella turcica and to rule out sphenoidal sinus infection, which may be clinically silent.4,10 Preoperative treatment of all patients with an intravenous dose of a cephalosporin and aminoglycoside antibiotic 1 hour before induction of anesthesia is indicated to reduce the risk of infection in these immunocompromised patients.10 Most investigators perform NALP with the patient under general endotracheal anesthesia, although because the procedure is relatively painless, it can be performed with local anesthesia.14 Opioids are avoided before and during the operation to avoid pupillary miosis, which might obscure the pupillary dilatation
observed when alcohol spills out of the sella onto the oculomotor nerve (see subsequent discussion).7,10
Technique With the patient intubated in the supine position on a biplanar fluoroscopy table, the nose is packed with pledgets soaked in 7.5% cocaine solution to provide vasoconstriction and shrinkage of the nasal mucosa (Fig. 177.1). After 10 minutes, the packs are removed and the anterior nasal mucosa and face are prepared with povidone-iodine solution. Sterile drapes are placed over the nose and face. The anterior medial mucosa and deep tissues are infiltrated with a solution of 1.0% lidocaine and 1:200,000 epinephrine. During infiltration and subsequent needle placement, care must be taken to avoid Kesselback's plexus, lest vigorous bleeding ensue. The head must be kept precisely in the midline to allow accurate needle placement. A 17-gauge, 3.5-inch spinal needle with the stylet in place is advanced with biplanar fluoroscopic guidance, with care taken to ensure that the needle remains exactly in the midline to avoid trauma to the adjacent structures, including the carotid arteries (Fig. 177.2). The needle is advanced until its tip rests against the anterior wall of the sella turcica (Fig. 177.3). At this point, plain radiographs are taken to confirm the needle position (Fig. 177.4). After satisfactory positioning is verified, the stylet is removed from the 17-gauge needle. A 20-gauge, 13-cm styleted Hinck needle (Cook Incorporated, Bloomington, Ind) is placed through the 17-gauge needle and is carefully advanced through the anterior wall of the sella turcica (Fig. 177.5). This process feels like passing a needle through an eggshell. The Hinck needle is then further advanced with biplanar fluoroscopic guidance through the substance of the pituitary gland, until the tip rests against the posterior wall of the sella turcica (Fig. 177.6). Needle position is again confirmed with plain radiographs (Fig. 177.7). The patient's eyes are then exposed, and alcohol in aliquots of 0.2 mL is injected as the Hinck needle is gradually withdrawn back through the pituitary gland (Fig. 177.8). Depending on the size of the sella, a total of 4 to 6 mL of alcohol is injected. During the injection process, the pupils are constantly monitored for dilation. Pupillary dilation indicates
1328 Section V—Specific Treatment Modalities for Pain and Symptom Management Pituitary gland
Optic n.
Internal carotid a. Oculomotor n. Abducens n.
Trochlear n. Ophthalmic n.
Cavernous sinus Maxillary n. Fig. 177.2 Lateral view of the sphenoidal sinus, sella turcica, and pituitary and of the relationship of the carotid arteries and oculomotor nerve.
Sphenoidal sinus
Pituitary gland Sella turcica Sphenoidal sinus Nasal septum
Fig. 177.3 Drawing of lateral view of the needle trajectory with the tip of a 17-gauge, 3.5-inch spinal needle against the anterior wall of the sella turcica.
A
Fig. 177.5 A 20-gauge, 13-cm Hinck needle is introduced through the 17-gauge needle.
B
Fig. 177.4 Plain radiographs confirming placement of the 17-gauge, 3.5-inch needle in a midline position with the tip resting against the anterior wall of the sella turcica. A, Lateral view. B, Anteroposterior view. (From Waldman SD, editor: Interventional pain management, ed 2, Philadelphia, 2001, Saunders, p 679.)
Chapter 177—Neuroadenolysis of the Pituitary 1329
A
Fig. 177.7 Plain radiograph confirms that the tip of the Hinck needle is resting against the posterior wall of the sella turcica. (From Waldman SD, editor: Interventional pain management, ed 2, Philadelphia, 2001, Saunders, p 680.)
Pituitary gland
Sella turcica
Sphenoidal sinus
B Fig. 177.6 A, The Hinck needle has been placed through the 17-gauge needle, and the Hinck needle's tip is resting against the posterior wall of the sella turcica. B, Drawing of a lateral view of the needle trajectory with the tip of the 17-gauge spinal needle against the anterior wall of the sella turcica and the Hinck needle through it into the substance of the pituitary.
that the alcohol has spilled outside the sella turcica and has come in contact with an oculomotor nerve. If pupillary dilatation is observed, injection of alcohol is discontinued and the needle is withdrawn to a more anterior position. The injection process then resumes. In most instances, if the alcohol injection is discontinued at the first sign of pupillary dilation, any resultant visual disturbance is transitory.15 Monitoring with visual evoked responses during alcohol injection has been suggested as a more sensitive test for visual complications than pupillary dilation.4 After the injection of alcohol is completed, 0.5 mL of cyanomethacrylate resin is injected via the Hinck needle to seal the hole in the sella turcica and to prevent CSF leakage. Both needles are removed. The nasal mucosa is observed for bleeding or CSF leakage. Nasal packing is not generally necessary
Fig. 177.8 The patient's eyes are exposed, and 0.2-mL aliquots of alcohol are injected as the Hinck needle is gradually withdrawn.
with this modified procedure. The patient is then extubated and taken to the recovery room. Approximately 30 minutes is needed to perform NALP.
Postoperative Care All patients are continued on antibiotics for 24 hours. Endocrine replacement, consisting of 15 mg of prednisone and 0.15 mg of levothyroxine sodium (Synthroid) every morning, is necessary for every patient.10 Accurate monitoring of intake and output is mandatory because transient diabetes insipidus occurs in approximately 40% of patients undergoing NALP.16 In most instances, the diabetes insipidus is self limited, but vasopressin administration should be considered for patients who are unable to drink as much as they excrete or whose urinary output exceeds 2.5 L/day.4 Failure to identify and treat diabetes insipidus is the leading cause of morbidity and mortality in patients who undergo NALP.
1330 Section V—Specific Treatment Modalities for Pain and Symptom Management All patients are continued on preoperative levels of oral narcotics for 24 hours, and then doses are tapered. Patients generally resume their normal diet and activities the day of the procedure.
Mechanisms of Pain Relief Levin and Ramirez15 and Bonica7 have reviewed the proposed mechanisms of pain relief after NALP. Early investigators centered their theories on the concept of pain relief from elimination of the pituitary hormones responsible for enhancement of nocioceptive transmission. Later, Yanagida et al11 suggested that pain appears to be independent of the extent of pituitary damage and may be caused by reactionary hyperactivity of the hypophyseal system exerting inhibitory influences on the pain pathways of the brain. In spite of extensive research, the exact mechanism of pain relief after NALP remains unclear, as does whether the procedure produces pain relief by neurodestruction or neuroaugmentation.13
Results Incidence of Pain Relief In 1990, Bonica7 reviewed the world literature on NALP and summarized the data and conclusions. The world literature suggests a success rate (pain relief rated complete to good) of approximately 63%. An additional 23% of patients described their pain relief as fair. Fourteen percent of patients reported poor to no relief of pain after NALP. A closer look at this patient population reveals that patients with hormonedependent tumors experienced better pain relief than did those with non–hormone-dependent tumors.7 Furthermore, investigators who injected larger volumes of alcohol (4 to 6 mL) or who repeated NALP when the first procedure was not successful appeared to obtain better results in terms of pain relief. In spite of the inherent limitations of analyzing data from multiple studies, NALP is obviously an effective treatment for certain patients with cancer pain.7,10,17,18
Complications Complications directly related to NALP are summarized in Table 177.3. Virtually all patients who undergo NALP have a bilateral frontal headache that resolves spontaneously within 24 to 48 hours.10 Diabetes insipidus develops in approximately 40% of patients who undergo the procedure. Approximately 35% of patients experience transient temperature increases up to 1.5°C (35°F) after NALP.10,16 These temperature
Table 177.3 Complications of Neuroadenolysis of the Pituitary Bilateral frontal headache Diabetes insipidus Abnormal temperature regulation Increased pulmonary secretion Ocular disturbances
a berrations are attributed to disturbance of the temperatureregulating mechanism of the hypothalamus.10 About 20% of patients experience an increase in pulmonary secretions and mild orthopnea that clinically resembles congestive heart failure.10 This problem is self limited if careful attention is paid to the patient's fluid status. This phenomenon has been postulated to be centrally mediated. Although the potential exists for serious ocular disturbances, a review of the literature suggests that transient visual disturbances, including diplopia, blurred vision, and loss of visual field, occur in fewer than 10% of patients who undergo neuroadenolysis of the pituitary gland.4,7,16 Permanent visual disturbances occur much less often, with an average incidence rate of approximately 5%.4,7,10,16 CSF leakage, infection, and pituitary hemorrhage develop in fewer than 1% of patients reported but are some of the most devastating complications. If they are not recognized immediately and treated, death can result.4,7,10
Conclusion Neuroadenolysis of the pituitary gland is a safe, effective method for palliating diffuse cancer pain that does not respond to conservative treatment modalities. Its technical simplicity and relative safety make NALP an ideal procedure for cancer patients who have undergone a vast array of treatments. Although spinal administration of opioids has replaced NALP as the procedure of choice for many cancer pain syndromes, many cancer pain specialists believe that NALP is still underutilized today.19 With the needle-through-needle modification described, a more favorable risk-benefit ratio is expected. As Bonica7 has stated, “NALP is one of the most, if not the most, effective ablative procedures for the relief of severe diffuse cancer pain.”
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
178
V
Radiofrequency Lesioning Richard Rosenthal
C h a p t e r O u tl i n e Radiofrequency Lesion Generator 1332 Continuous Impedance Monitoring 1332 Nerve Stimulation 1332 Monitoring of Temperature, Voltage, and Current 1333
Types of Radiofrequency Lesioning 1333 Continuous Lesioning 1333 Pulsed Lesioning 1334
Clinical Applications of Radiofrequency Lesioning 1335 Lumbar Medial Branch Radiofrequency 1335 History 1335 Anatomy 1336 Symptoms and Signs of Facet Joint Pain 1336 Indications 1337 Technique 1337 Postprocedure Advice 1339 Complications 1339 Efficacy 1339 Lumbar Dorsal Root Ganglion Procedure 1340 History 1340 Anatomy 1341 Indications 1341 Technique 1342 Postprocedure Advice 1343 Complications 1344 Efficacy 1344 Cervical Medial Branch Radiofrequency 1345 History 1345
Radiofrequency (RF) current is used in pain medicine to make discrete therapeutic lesions in various targets throughout the nervous system.1–6 The technique is most frequently used to block nociceptive signals from reaching the central nervous system and thereby anesthetize the source of the pain.2 RF is implemented percutaneously by means of an insulated needle with a metal active tip that is placed in the appropriate nerve pathway. Current is then applied such that it alters the function of the nerve and blocks transmission of the painful signal.1 Although RF current does not treat the cause of pain, its palliative effect allows the patient to return to normal daily activities and to function without pain. When appropriately applied to well-selected patients, RF current can produce profound, lasting analgesia sufficient to reverse the deleterious effects of chronic pain on the life of the patient. These effects include sleeplessness, mood disturbance, social isolation, loss of employment, and occa© 2011 Elsevier Inc. All rights reserved.
Anatomy 1345 Patient Selection 1346 Indications 1346 Technique 1347 Sacroiliac Joint Radiofrequency 1352 History 1352 Anatomy 1352 Patient Selection 1353 Indications 1353 Technique 1353 Complications 1355 Efficacy 1355 Thoracic Medial Branch Radiofrequency 1355 History 1355 Anatomy 1355 Patient Selection 1356 Indications 1356 Technique 1356 Efficacy 1356 C2 Radiofrequency Treatment for Cervicogenic Headache 1357 History 1357 Anatomy 1358 Indications 1358 Technique 1359 Efficacy 1360
Conclusion 1360
sionally loss of life. Before the introduction of modern RF equipment, various techniques (e.g., cryosurgery and chemical neurolysis) were used in an attempt to produce localized nervous system lesions; however, none have been as widely used or are as effective as RF.6,7 The use of electricity to treat pain was first described in 1931, when direct current was applied to the gasserian ganglion for the treatment of trigeminal neuralgia.4,8 However, use of direct current was abandoned because it produced lesions of inconsistent size and was associated with complications. High-frequency alternating current was then introduced as a method of producing lesions of a predictable size.9 Soon thereafter, temperature monitoring was found to enhance further the ability to make reliable, consistent lesions. Because the frequencies used (350 to 500 kHz) were also used in radio transmitters, the procedure was termed radiofrequency.5 Today, the frequency used by modern RF machines (just below the AM 1331
1332 Section V—Specific Treatment Modalities for Pain and Symptom Management band) is assigned by the Federal Communications Commission to prevent interference with radio transmissions. The first reported use of RF current in the management of pain focused on percutaneous lateral cordotomy to treat malignant pain.9 The first use for nonmalignant pain began in the 1970s for treatment of trigeminal neuralgia.3,10 At approximately this time, Cosman and Cosman introduced an RF machine that had voltage and time settings and was also capable of monitoring temperature, impedance, and current.11,12 Shealy13 reported the first use of RF current for the treatment of spinal pain. He described a method of treating pain from the zygapophyseal joints (commonly referred to as facet joints or z-joints) by targeting the medial branch. Later, a modified technique was published after anatomic dissections indicated that the electrode placements described in the original paper were not actually on the medial branch.2,14 Uematsu11 used RF to treat radicular pain by targeting the dorsal root ganglion (DRG). His use of a large (14-gauge) electrode to heat the DRG to 75°C (167°F) resulted in nearly complete destruction of the ganglion and severe deafferent pain sequelae.5 Because these early uses of RF for pain treatment had poor outcomes, the technique failed to gain acceptance.3 The widespread use of RF current for the treatment of spinal pain began in 1980, when Sluijter and Metha introduced a 22-gauge cannula through which a thermocouple probe could be inserted.3,5 The smaller electrode meant that the procedure could be performed percutaneously on a conscious patient without causing much discomfort. This development was important because it allowed the patient to be monitored for complications. Shortly after the introduction of the Sluijter-Metha cannula (SMK) needle, a series of studies was published on the use of RF current for the treatment of facet joint pain, diskogenic pain, sacroiliac (SI) joint pain, and sympathetically mediated pain.3,15–23 RF lesioning has since been found to be target specific, safe, and effective for the treatment of pain, and it has supplanted the use of other neurolytics (particularly chemical neurolytics), largely because of the highly focused nature of RF lesions. This chapter is clinically focused to provide the pain practitioner with the means to treat patients. It provides an overview of the RF lesion generator and the two different types of RF lesions, continuous and pulsed. It also updates the reader on the use of RF lesioning for the most common and well-studied procedures and describes the latest, most effective methodology, based on current scientific literature and clinical experience. For example, it presents new methods of performing RF for older procedures, such as the lumbar RF procedure. RF has many other uses in varying stages of development that will expand the use of the modality in the future.
Radiofrequency Lesion Generator An RF lesion generator is a device used to produce lesions in the nervous system or other tissue by the direct application of high-frequency current to selected sites (Fig. 178.1). A typical RF lesion generator has the following systems: continuous impedance monitoring; nerve stimulation; monitoring of voltage, current, and temperature; and pulsed current delivery mode.5,6 The current flows from the electrode tip through the body to a dispersive grounding electrode. RF current alternates at a very high frequency (approximately 500 kHz). The energy is focused around the active tip of the electrode and activates charged molecules (mainly proteins) to oscillate with the rapid changes in alternating current. This produces friction in the tissue that causes heat formation directly around the active
Fig. 178.1 Image of a radiofrequency generator.
tip. Heat is generated as a result of ionic oscillations of the charged molecules in the tissue, rather than direct heating of the electrode element itself. The formation of heat is greatest around the active tip, where the current density is largest. The grounding electrode serves to complete the circuit and to disperse heat buildup, thereby preventing a burn of the skin.2 RF energy can be applied as either continuous or pulsed current. Continuous RF current heats the tissue surrounding the electrode and lyses the targeted nerve. On a pathologic level, continuous RF current heats nerve fibers and results in wallerian degeneration.24–27 On a physiologic level, continuous RF current destroys all fiber types within a nerve and is not selective for any one fiber type.2,28,29 Pulsed RF (PRF) was introduced in 1998. This method delivers RF current in small bursts and thus prevents the accumulation of heat around the electrode. The exact mechanism of action is not currently understood.1,3 One of the prevailing theories postulates that the electrical field generated during a PRF procedure reversibly disrupts the transmission of impulses across small unmyelinated fibers and causes a blockade of pain signals.1,30–32
Continuous Impedance Monitoring When heat lesions are made in the continuous RF mode, impedance monitoring is primarily used to confirm continuity of the electrical circuit. However, in the pulsed mode, impedance monitoring is more crucial because the strength of the electrical field is decreased when impedance is high. Thus, high impedance can reduce the efficacy of the procedure and may be a cause of treatment failure. Typically, impedance varies from 200 to 800 ohms during an RF lesion and is greatly affected by density of the tissues in which the active tip is placed. For example, impedance is high when an electrode is placed in densely packed tissue (e.g., scar tissue), whereas it is low when an electrode is placed inside a blood vessel. Both impedance and current should be noted and monitored d uring the creation of PRF lesions.
Nerve Stimulation Nerve stimulation is important for both the continuous RF and the PRF modes. The two types of stimulation are sensory and motor. Sensory stimulation occurs at 50 Hz and is used to
Chapter 178—Radiofrequency Lesioning 1333
determine the distance between the electrode and the targeted nerve fiber. The minimum sensory threshold (i.e., the minimum voltage required to produce an electrical discharge of the nerve) is directly related to the distance from the nerve fiber.5,33 Thus, sensory stimulation can be used to determine the accuracy of needle placement. This is more important in the pulsed mode than in the continuous mode, as discussed later in the chapter. Motor stimulation occurs at 2 Hz and is used to determine whether a needle is placed too close to motor fibers, typically the ventral rami of the spinal nerve root during the medial branch procedure. This type of stimulation is recommended to avoid unintended damage to neural structures.
Monitoring of Temperature, Voltage, and Current Temperature monitoring facilitates generation of a discrete, controlled lesion of predictable size. Voltage monitoring and current monitoring are of secondary importance when producing a heat lesion, because they are automatically adjusted in accordance with the temperature setting. However, in the pulsed mode, both impedance and current are important, given that the strength of the electrical field is thought to be critical to producing the desired effect. Voltage, impedance, and current output are related as described in the equation V = IR, where V is voltage, I is current, and R is impedance (defined as the electrical resistance in an alternating current circuit). Both voltage and impedance can be regulated during generation of a pulsed lesion; voltage output is adjusted using the generator; and impedance can be decreased by injection of saline solution. The goal is to adjust these variables to produce a current of approximately 200 mA. Temperature is of secondary importance, as long as it remains lower than neurolytic levels (45°C [113°F]).34 Sensory stimulation is helpful for two reasons. First, limited evidence indicates that increasing the proximity between the electrode and the targeted nerve can increase the duration of the effect. Second, sensory stimulation levels of less than 0.05 V are thought to indicate intraneural placement.
Types of Radiofrequency Lesioning Figure 178.2 provides images monopolar, bipolar, and PRF lesions.
Continuous Lesioning The heat generated in the continuous mode causes tissue coagulation in a small, discrete oval surrounding the active tip of the electrode. The largest area of damage is around the long axis of the electrode; very little energy extends distal to the tip. Therefore, to coagulate the largest area of nerve fibers reliably, the electrode must be positioned parallel to the nerve. In addition, because the area of coagulation is quite small (heat diminishes rapidly as the distance from the electrode tip increases), the electrode must be placed directly on the nerve to guarantee neurolysis. If the electrode is as much as one electrode width away from the nerve, it will fail to coagulate the nerve completely.2,3 Continuous RF energy causes nonselective thermal damage to the offending nerve. The size of the lesion depends on several factors:
Fig. 178.2 Images of radiofrequency lesions: bipolar, monopolar, and pulsed.
1 cm
A
B
Fig. 178.3 Image of radiofrequency lesions in meat. A, A 20-gauge needle. B, An 18-gauge needle. (Courtesy of Paul Dreyfuss.)
Tissue temperature: The volume of the lesion expands in direct proportion to the temperature surrounding the electrode, up to a maximum temperature of 90°C. 2 Temperatures higher than 90°C risk charring of tissues, which can cause cavitation and possible sterile abscess formation.35 In a meat model, one can observe the increased lesion size as temperatures are increased (Fig. 178.3).28 n Duration of coagulation: The volume of the lesion grows over time until it reaches its maximal size at approximately 90 seconds, after which time the lesion is stable (Fig. 178.4). At 60 seconds, the lesion reaches 94% of the size attained at 90 seconds. Therefore, the optimal duration of coagulation is between 60 and 90 seconds.2 n Gauge of electrode and length and gauge of active electrode tip: Larger-gauge electrodes and longer active tips produce a larger lesion.5,36 n
The foregoing discussion is clinically relevant. According to the guidelines of the International Spine Intervention Society (ISIS), efficacy is maximized when needle placement
1334 Section V—Specific Treatment Modalities for Pain and Symptom Management 70°C
70°C
70°C
70°C
70°C
0 sec
20 sec
40 sec
60 sec
90 sec
80°C
80°C
80°C
80°C
80°C
20 sec
40 sec
60 sec
90 sec
0 sec
Fig. 178.4 Lesion time versus size and lesion temperature versus size.
is anatomically precise, when larger (e.g., 18- to 20-gauge) needles are used, and when multiple parallel lesions are generated (within one needle width from each other) to account for the variable nerve topography.2 Larger lesions are created using higher temperatures, larger-gauge needles, and longer lesion times (i.e., up to 90 seconds).28 A 60- to 90-second lesion time, at a temperature of 85°C (185°F) to 90°C (194°F) in the cervical spine and 90°C (194°F) in the lumbar spine, is recommended. Heat decreases rapidly as the distance from the electrode tip increases. The average size of a lesion is no more than 1.6 to 2.3 electrode widths.2 For the greatest benefit, two lesions should be made one electrode width from each other. If electrodes are positioned as little as two electrode widths away from each other or from the targeted nerve, incomplete lesioning may occur, resulting in neuritis and possibly therapeutic failure.2 For that reason, larger, 18-gauge electrodes were developed to improve the chance of incorporating the nerve in the lesion and are recommended for use when making heat lesions.2,37 Electrodes placed perpendicular rather than parallel to the nerve may also result in incomplete coagulation and shorter duration of relief. 2,28
60°C
70°C
80°C
60 sec
60 sec
60 sec
Pulsed Lesioning In addition to generating heat, the current from RF energy also produces an intense electrical field. The therapeutic effect of PRF lesioning is thought to be the result of the electrical field, rather than of the thermal effects.1,3 The concept that tissue destruction was the means by which RF current produced its effect was reevaluated in light of certain findings that were inconsistent with this theory.3–5,24,31,32,38–52 First, it was known that heat produced its effect by causing a lesion between the nociceptive focus and the central nervous system; however, Sluijter46 had noticed that electrodes placed distally to the nociceptive focus seemed to produce a therapeutic effect. For example, treatment of radicular pain by heating the DRG seemed to produce a therapeutic effect even though the heat is applied distal to the nociceptive focus (the spinal nerve root). Second, Sluijter noticed that heat lesioning of the DRG produced only transient sensory loss, whereas pain relief lasted much longer. Finally, the role of heat was questioned when Slappendel et al40 published a report that showed no differences in outcome when two different tip temperatures (40°C [104°F] and 67°C
[153°F]) were applied to the cervical DRG for chronic cervical radicular pain. Each of these arguments has since been brought into question. At that time, however, it seemed reasonable to attempt to deliver RF energy in a manner that did not result in the production of heat. These observations provided supporting evidence that led to the development of the PRF procedure. The aim of PRF is to create intense electrical fields while keeping the temperature lower than neurolytic levels. This is done by delivering short bursts of energy (20 milliseconds) twice per second, followed by a quiet phase (lasting 480 milli seconds) during which no current is applied. This approach allows for heat dissipation, thus keeping the tissue temperature lower than the neurodestructive threshold of 45°C.3 Studies in homogeneous nerve tissue suggested that irreversible conduction block occurs at temperatures greater than 45°C (113°F) to 50°C (122°F).53–55 Pulsing the current also allows a substantial increase in the power output of the generator. Voltage in the continuous mode is 15 to 25 V, compared with 45 V in the pulsed mode.5 Because the electric field is strongest at the tip of the electrode, it is recommended that electrodes be placed perpendicular, rather than parallel, to the targeted nerve during creation of a PRF lesion. PRF was originally thought to be a totally nondestructive procedure. However, experimental work indicated that this may not be the case.38,56–58 PRF current appears to have both thermal and nonthermal effects. The thermal effects of PRF were first elucidated by Cosman and Cosman,38 when they noticed heat spikes produced during the 20-millisecond active phase of a PRF current. It is not known whether these brief elevations in temperature have a biologic effect. A mild ablative effect in an in vitro model has also been described, but its significance in a biologic system is unknown.38,56–58 The nonthermal effects may be attributed to an effect on the function of voltage-gated ion channels. Central nervous system effects also appear to be direct results of the RF current.43,45 Convention holds that the word lesion should not be used when referring to a PRF procedure. However, as noted earlier, Cosman and Cosman observed heat bursts with temperatures in the neurodestructive range in a thin layer of tissue immediately surrounding the electrode.38 Experimental evidence also indicates that PRF results in cellular damage that appears to be more pronounced for C fibers.56,57 In a study by Erdine et al,56 electron microscopy showed physical evidence of ultrastructural damage following exposure to PRF. Although the clinical significance of these findings is unknown, this evidence would dispute the currently held belief that PRF does not cause a lesion. Lesion is defined as “a localized pathologic change in a bodily organ or tissue.” Sluijter and van Kleef 59 believed that a PRF procedure clearly meets this criterion. In this chapter, the word lesion is used when referring to a PRF procedure. PRF lesioning is traditionally considered safer than continuous RF because it has no reported neurologic side effects. However, Rosenthal has direct knowledge of a case in which vocal cord paralysis lasting approximately 6 months was induced by a brief delivery of PRF current during a C3 DRG procedure. This suggests that PRF may indeed cause temporary nerve damage and supports the contention that PRF does in fact produce a lesion. However, in most cases, PRF current
Chapter 178—Radiofrequency Lesioning 1335 delivery is a safe method of creating nervous system lesions, because no similar case reports have been published. Although PRF does create a small lesion around the active tip, that cannot completely account for the clinical effects observed. Unfortunately, no single theory fully explains the observed effects. Despite evidence of a mild ablative effect, the current belief is that the electric field is responsible for the clinical effect. Rather than producing local effects surrounding the electrode, as with continuous RF, PRF seems to produce its effect proximal to the point where energy is applied. Indeed, changes within the central nervous system have been observed in response to PRF energy. When PRF energy is applied to the DRG, it induces changes in gene expression within the dorsal horn of the spinal cord. The rapidly alternating current alters pain transmission by activation of a protein called C-Fos. On a cellular level, animal studies showed that exposure of the DRG to PRF current causes both early and late bilateral induction of the protein C-Fos in layers 1 and 2 of the dorsal horn. These effects are not temperature dependent and seem to occur as a result of current fluctuations, rather than tissue heating.3,4,24,38,42,43,45,46,49,50 Other proteins are also produced in response to PRF current, although it remains unclear whether any of these changes are responsible for the observed therapeutic effect.49,50 In addition, investigators believe that strong electrical fields alter the nerve cell membranes and thus affect nerve transmission. This theory is supported by evidence showing that PRF induces changes in synaptic transmission and causes electroporation.46,50 The use of the pulsed mode in clinical practice has been slow to gain widespread acceptance. The reason may be the paucity of evidence showing a clear therapeutic advantage over placebo during the early years of its use. However, since 2005 several studies have demonstrated an advantage over placebo. The role of PRF in clinical practice has been an issue of debate. Some investigators have argued that it is unnecessary because of the availability of continuous RF, which appears to be effective according to well-designed studies. Although this argument is true for treatment of medial branches, it is not relevant when considering the use of RF current for the treatment of radiculopathies and painful peripheral neuropathies. For both these chronic and painful conditions, pain practitioners currently have little to offer these patients. When one considers the benign nature of this treatment and its possibility of real relief, little reason exists not to offer PRF as a therapeutic option. It would appear that the best use for this modality is in the treatment of these two conditions.
Clinical Applications of Radiofrequency Lesioning Lumbar Medial Branch Radiofrequency History The facet joint was characterized as a source of pain as early as 1911.60 In 1933, Ghormely coined the term facet syndrome.61,62 Rees was the first to suggest a treatment.61,63 He used a special scalpel to sever what he thought were the articular branches of the nerves. Later anatomic studies showing the correct location of the articular branches proved that the procedure as proposed was invalid.14,61,64 The nerves were not located where Rees depicted them and were too deep to be cut by a scalpel. Shealy13 was the first to attempt
1336 Section V—Specific Treatment Modalities for Pain and Symptom Management facet denervation using RF electrodes.61,65 Unfortunately, his novel idea exceeded current knowledge of the ideal method to denervate the joints, and the procedure ultimately proved a failure. Finally, an accurate description of the anatomy was elucidated by Bogduk and Long,14 who suggested a technique for denervating the facet joints by placing electrodes against the medial branch of the dorsal ramus (rather than against the articular branches, which are less accessible). The procedure was initially performed by placing electrodes perpendicular to the medial branches to coagulate them. However, this resulted in only short-term relief.28,66 To understand the area of coagulation surrounding the active tip of an RF electrode more clearly, investigators performed RF lesions in experimental media.28 These investigators found that the largest area of coagulation was around the long axis of the electrode with very little heat extending distal to the tip. They also found that larger electrodes created a larger the area of coagulation.28,37 These facts suggested that electrodes should be oriented parallel rather than perpendicular to the nerve to coagulate that longest segment of nerve. In addition, largergauge (16- to 18-gauge) electrodes and more than one lesion were recommended to account for minor variations in the location of the nerves.2,66,67 Finally, an anatomic study by Lau et al67 recommended a technique to align electrodes better to lie parallel to the targeted nerve, to achieve maximum contact along the length of nerve. All these recommendations were incorporated into guidelines produced by the ISIS2 that are summarized as follows: 1. Electrodes should be placed parallel to the targeted nerve to coagulate the longest segment of nerve. 2. Using standard 18- or 20-gauge electrodes, at least two lesions should be made one electrode width apart to ensure that the nerve is incorporated within the area of coagulation. 3. Lesions can be made based on accurate anatomic placement alone without the need to verify electrode placement with sensory stimulation. 4. Lesion times of 90 seconds at 85°C (185°F) produce the largest volume of coagulation without risking boiling of tissues.
Anatomy The medial branches in the lumbar spine are located at the base of the superior articular process (SAP) at their respective vertebral levels (Fig. 178.5). The target is not only at the junction of the SAP and the transverse process (TP), as originally described, but also is slightly up the wall of the SAP at its neck (these points are approximately one to two needle widths apart).67 The nerves curve around the lateral aspect of the neck of the SAP and then give off articular branches to the z-joints at the level of origin and the level above it. The nerves at the L1-4 levels are consistently located as a result of two anatomic features. First, the nerve enters the groove between the SAP and the TP lateral to the SAP through the intertransverse ligament. Second, the nerve exits the compartment beneath the mammilloaccessory ligament (MAL).14,68 These ligaments fix the nerve in place and allow correct anatomic positioning of an RF electrode to locate and ablate the nerve consistently.2 The L1-4 medial branch nerves are accessible for coagulation only for a limited length. Lesions made too proximally
L4-5 ZJ
mb
mb mal
ib
L5 TP lb
Fig. 178.5 The position of the medial branches and the mam milloaccessory ligament. (From Lau P, Mercer S, Govind J, et al: The surgical anatomy of lumbar medial branch neurotomy (facet denervation), Pain Med 5:289– 298, 2004.)
risk coagulation of the dorsal ramus. Lesions made too distally fail to coagulate the nerve as it lies underneath the MAL. The MAL is a thick, fibrous band of tissue that protects the nerves from coagulation.69 The nerve targeted for coagulation at the L5 level is the dorsal ramus. It is longer than the medial branch nerves and follows a rostral course from the sacral ala.68 To anesthetize a given facet joint, both medial branch nerves that innervated the joint must be anesthetized. This procedure requires the practitioner to know the location of the nerves. Numbering the nerves can be confusing because the vertebral segment and numbering of the medial branch do not coincide. Two medial branches innervate each facet joint or z-joint, one from the vertebral level of origin and one from the vertebral level above. For example, the L5-S1 level is innervated by a branch arising from the L4 and L5 vertebral levels. The L4-5 joint is innervated by medial branches from the L3 and L4 levels.
Symptoms and Signs of Facet Joint Pain Patients with facet joint pain commonly present with a deep, aching sensation in the low back that refers in a nondermatomal pattern to the buttocks, the posterior or anterior thigh above the knee, the groin, and the hip (Fig. 178.6). These patients often report morning stiffness. Younger patients may report that the pain followed some type of trauma, but older patients report an insidious onset. The diagnosis is more common in patients older than 65 years and cannot be made solely on the basis of history, physical examination, or laboratory studies, such as radiographs.2,5,70,71 However, certain clinical features have been found to predict a positive response to medial branch block, including pain relieved by recumbency and four of the following six characteristics: age greater than 65 years and back pain not exacerbated by forward flexion, rising from flexion, hyperextension, extension and rotation, or coughing.2,5,70 Mechanical pain must be distinguished from radicular pain. Radicular pain travels in a narrow band in the affected extremity. The pain is typically described as shooting or lancinating, rather than dull or aching. It has both a deep and superficial quality, in that the patient feels both a deep
Chapter 178—Radiofrequency Lesioning 1337
B
A
Fig. 178.6 Lumbar zygapophyseal joint (z-joint) referral maps.
and cutaneous sensation in the affected extremity. This pain is more often felt below rather than above the knee.72 Lower extremity pain associated with a mechanical cause is severe only when the back pain is severe; it never occurs independent of back pain. When attempting to distinguish between these two causes of pain, it is helpful to quantify the percentage of pain in the back versus that in the lower extremity. Of the pain in the lower extremity, one must distinguish between the percentage of pain above the knee and that below it. On physical examination, the patient may report focal tenderness over the facet joints, and extension or lateral side bending may increase the pain.2,6,7,73–75 Patients with only facet joint pain have a normal neurologic examination. Imaging studies may show a normal-looking facet joint, although some patients show degenerative changes of the disks and facet hypertrophy.2,6,74,75 The diagnosis is complicated by the lack of direct correlation between clinical findings and response to medial branch block.70,71,76,77 The outcome of an RF procedure relies on the results of a properly performed series of two medial branch blocks. The medial branch procedure involves placing a small amount (0.3 mL) of local anesthetic on the targeted nerves and quantifying the amount of pain relief reported by the patient.2,66 Diagnoses based on single medial branch block are not considered valid because of the high false-positive response rate, which can be as high as 40%.2 An RF p rocedure is indicated if the patient reports greater than 80% relief after each of two medial branch procedures, provided the pain is emanating from the facet joint alone. However, because a given patient may have more than one cause of back pain, some investigators have suggested that greater than 50% pain
relief is an adequate criterion. Other investigators have suggested that complete pain relief in a distinct topographic area is adequate to constitute a positive response.2 The target specificity of the medial branch procedure was established by Dreyfuss et al,78 who showed that, with properly placed needles, injected contrast dye incorporated the medial branch nerves without spread to the adjacent spinal nerve. The blocks were also shown to have both face validity and construct validity and are therefore predictive of a positive outcome for a properly performed RF procedure.
Indications The indication for this procedure is pain that has persisted for more than 3 months and has not responded to conservative therapy. In addition, the patient must not be abusing analgesics. The patient must have responded positively on two separate occasions to medial branch blocks with greater than 80% pain relief.2
Technique The patient is placed prone on the fluoroscopy table, and the back is prepared and draped in sterile fashion. A small amount of intravenous or oral sedation is administered. The patient must remain awake enough to communicate during the procedure because it is crucial that he or she report any discomfort felt. This is especially important given that the electrodes can be misplaced onto the spinal nerve and can cause coagulation of the major motor and sensory nerve to the lower extremity. An awake patient can immediately report any burning sensations in the lower extremity.
1338 Section V—Specific Treatment Modalities for Pain and Symptom Management The target for the L1-4 medial branches is located proximal to the MAL but distal to the dorsal ramus. The classically described location of the nerve is at the junction of the SAP and the TP. However, the nerve can also be located at the lateral surface of the neck of the SAP.67 At the L5 level, a lesion is made to the dorsal ramus, instead of the medial branch. It is located at the junction of the S1 SAP and the sacral ala, and not slightly up the wall of the SAP, as at the L1-4 levels. Lau et al67 made several recommendations that altered how the procedure is performed. First, these investigators recommended using larger-gauge needles (i.e., 16 or 18 gauge). Second, they recommended that multiple parallel lesions be made one needle width apart (the first at the base of the SAP and the second slightly up the wall), to account for the variable topography of the nerve. Third, they recommended that, for the electrode to lie parallel to the nerve, it must be inserted from an oblique, cephalocaudad trajectory. This has been referred to as a pillar view. The trajectory places the electrode parallel to the nerve and maximizes the length of active tip in contact with the nerve, a placement that has been shown to increase the duration of effect.28,37,66 Fourth, Lau et al67 recommended that needle placements be assessed in multiple views. The target zone in a pillar view is located against the lateral neck of the SAP. In an anteroposterior (AP) view, the needle should be well applied to the SAP. However, for the L1-4 levels, the needle must be passed at an angle from the sagittal plane to avoid the tip of the electrode being deflected laterally by the MAL. In a lateral view, the middle two fourths (2⁄4 to 3⁄4) of the SAP are targeted. For the L5 dorsal ramus, the target zone is the middle and posterior one third of the neck of the SAP at S1. To obtain a pillar view, first the disk space at the targeted level is visualized in an AP view. Then, the image intensifier is rotated obliquely approximately 30 degrees to the ipsilateral side or until the SAP is projected a generous one third of the way across the image of the vertebral body. A pointer is then placed approximately one vertebral level below the targeted nerve. The image intensifier is declined caudally, approximately 30 degrees, until the pointer is projected directly over the SAP at the targeted nerve level. Finally, small adjustments are made both obliquely and cephalocaudally until the lateral cortical margin of the SAP is clearly defined. 67 In this view, the nerve lies against the lateral aspect of the SAP. For example, to target the L3 medial branch, the superior end plate of L4 is squared to open the disk space between the L3 and L4 vertebral bodies. The C-arm is then rotated obliquely as described earlier. A pointer is placed over the SAP of L4 (which is the level below the targeted level), and the C-arm is moved caudally until the image of the groove between the SAP and the TP at the L3 level comes into view and overlies the pointer. Then, final adjustments are made until the lateral margin of the L3 SAP is “crisp.” The needle is passed “down the beam” until the base of the SAP is contacted at its lateral margin. The needle is then viewed in an additional three views (AP, steep oblique, and lateral), and small adjustments are made in each view. In the AP view, the needle should be seen resting tightly against the SAP and above the TP. In a steep oblique view (at least 45 degrees), the needle should be seen across the “ear” of the “Scotty dog,” with the tip resting at the leading edge of the SAP. In the lateral view, the needle should cover the middle two fourths of the SAP at the L1-4 levels, whereas at the L5 level, it should cover the middle and posterior one third of the SAP. It should also
be resting on the TP, which is located posterior to the inferior aspect of the foramen. If the needle is seen above the TP (above the inferior aspect of the foramen), it is too high (cephalad) and should be adjusted inferiorly. The needle should never be located anterior to the posterior aspect of the vertebral foramen when viewed in a lateral view. The needle is too posterior if it lies posterior to the image of the SAP. In this position, the nerve lies under the MAL and is not accessible for coagulation. If the needle is seen to be anterior to the posterior aspect of the foramen, it is too ventral, and the neural foramen can be inadvertently entered. Once the needle position is established, it is wise to check the electrical impedance to ensure the overall integrity of the RF system.6 Traditionally, location of the targeted nerves is based on radiographic landmarks, as well as on sensory and motor stimulation. However, no comparative studies have documented the benefit of sensory stimulation over radiographic landmarks alone to determine optimal needle placement. Motor stimulation at 1.0 V is used to confirm needle placement posterior to the DRG. Multifidus muscle contraction may be noted during this procedure and is considered normal.6 Sensory stimulation is no longer considered necessary according to the ISIS guidelines, for the following reasons2: 1. Dreyfuss et al79 showed that sensory stimulation thresholds did not correlate with improved outcome. These investigators found that correct anatomic placement of the electrode produced reliable nerve coagulation. 2. Evoked sensations may be falsely positive. 3. Electrical stimulation may cause an evoked sensation, but not necessarily close enough to coagulate the nerve. 4. Rigorous sensory testing requires testing at three different locations: at the location where the lowest sensory threshold is obtained, at a location both cephalad and caudad to the first location showing higher sensory thresholds, and at each location compared with the original location. The ISIS guidelines argue that just as many electrode placements are required in making subsequent lesions after making the initial lesion. Thus, radiographic landmarks are the primary tool to localize final needle position before lesioning. After confirmation of correct placement with fluoroscopy and motor stimulation, 1 mL of 2% lidocaine is injected through each of the cannulas, and 30 to 60 seconds are allowed to pass while waiting for production of anesthesia. Then, the generator is turned on in the automatic mode, and lesions are created at a temperature of 85°C (185°F) applied for 60 to 90 seconds. After completion of the first lesion, a second lesion is performed one needle width cephalad to the first lesion, slightly up the wall of the SAP. The position of the second lesion is established in the same pillar view used for the initial placement of the needle. The needle positions described earlier apply only to the lumbar medial branches from L1 to L4 (Fig. 178.7). At the L5 level, the anatomy is slightly different, in that the L5 dorsal ramus is much longer and more easily accessible than at typical lumbar levels. Therefore, at the L5 level, the dorsal ramus, and not the medial branch, is lesioned. The dorsal ramus runs along a groove formed between the ala of the sacrum and the base of the S1 SAP. The area exposed for lesioning is much
Chapter 178—Radiofrequency Lesioning 1339
A
C
B
D
Fig. 178.7 Fluoroscopic images of medial branch (MB) radiofrequency lesioning at L1-4. A, Pillar view showing correct placement at the L3 MB. B, Anteroposterior view of correct needle position; note the needle tip above the transverse process. C, Steep oblique view showing lesion points 1 and 2. D, Lateral view showing correct needle position for L4 MB; note the needle positioned behind the foramen. (Courtesy of Paul Dreyfuss.)
longer than of a typical medial branch; therefore, once the first lesion is completed, the needle is repositioned caudally for a second lesion (rather than up the wall of the SAP). This procedure allows a longer length of nerve to be coagulated and thus increases the period of time before nerve regrowth. In the lumbar spine, patients who fail to obtain relief after medial branch RF lesioning can be assessed by segmental multifidus electromyography to evaluate the technical success of the procedure (Fig. 178.8).79 For patients who obtain good relief but in whom the pain recurs, the effects of the procedure can be successfully reinstated 85% of the time.80
Postprocedure Advice The patient should be advised that it could take up to 3 or 4 weeks before the full effect of the procedure is experienced. During the first week following the procedure, the patient may notice increased pain, which should be treated with analgesics. During subsequent weeks, the physician may refer the patient to physical therapy for a deep muscle relaxation technique, such as deep tissue massage or augmented soft tissue manipulation, which should relieve any muscle tightness or trigger points that may have been caused by chronic inflammation associated with the facet joint syndrome. Physical therapy also facilitates healing of any small, procedure-related hematoma.
Complications Expected procedure-related side effects are minor and selflimited. These include back pain that usually resolves within 1 to 2 weeks and neuritic pain lasting less than 2 weeks. In a review of 92 patients who received 616 lesions, neither complication had an incidence higher than 0.5%. No cases of infection or new motor or sensory deficits were reported.81 In a patient rendered unconscious from intravenous sedation or general anesthesia, needle placement that is inadvertently too close to the spinal nerves could result in severe injury and even permanent motor and sensory deficits. The ISIS guidelines reported just such a case, in which a patient under general anesthesia had the ventral ramus of the spinal nerve coagulated during the procedure.2 To avoid this complication, the operator is urged to keep the patient conscious at all times during the procedure. The ISIS guidelines also described a case in which a patient suffered full-thickness burns when a spinal needle (instead of the usual dispersive grounding electrode) was used to ground the patient. This type of complication should never occur if a physician is properly trained.2
Efficacy Bogduk et al66 wrote an excellent review on the lumbar medial branch neurotomy procedure. In that review, these investigators pointed out that to evaluate the outcome of any
1340 Section V—Specific Treatment Modalities for Pain and Symptom Management
A
C
B
D
Fig. 178.8 Lumbar L5 dorsal ramus. A, Pillar view: L5 radiofrequency. B, Anteroposterior (AP) view: L5 lesion point 1. C, AP view: L5 lesion point 2. D, Steep oblique view: L5. (Courtesy of Paul Dreyfuss.)
rocedure, one must first assess whether the procedure was p performed properly, that is, in a manner expected to produce the desired result. They further stated that, of the six randomized controlled trials performed to date, three should not be considered as evidence, based on improper patient selection (patients not selected based on positive response to two correctly performed medial branch blocks) or improper surgical technique (electrodes not correctly aligned parallel to nerve). Although the remaining three trials were suboptimal in terms of patient selection or proper anatomic technique, all showed positive results when compared with placebo. In addition, three descriptive studies were published that used proper patient selection and anatomic technique, and all three showed positive outcomes. These investigators believed that when these results were “pooled,” they presented strong evidence supporting efficacy of the procedure. In Table 178.1, the results of the best studies performed to date are summarized. Five additional randomized controlled trials (Gallagher et al, 1994; van Kleef et al, 1999; Leclaire et al, 2001; van Wijk et al, 2005; and Tekin et al, 2007) had significant methodologic problems and were excluded from the table. More specifically, the studies were flawed as a result of improperly selected
patients based on the results of two medial branch blocks or appropriate positioning of the electrodes to create complete lesions of the medial branch nerves.
Lumbar Dorsal Root Ganglion Procedure History Uematsu11 was the first to attempt DRG lesioning for the treatment of radicular pain by heating the DRG with the use of a large 14-gauge cannula. As expected, it caused damage to the pain fibers as well as to the motor and sensory fibers and resulted in near destruction of the spinal nerve. The procedure was quickly abandoned. DRG lesioning was reintroduced in 1980 after Sluijter developed small-diameter electrodes that fit inside a 22-gauge needle.3 This approach permitted both smaller lesion size and less pain during the procedure. At that time, the recommended tip temperature for treatment of the DRG was 67°C (153°F). The lower temperatures and smaller lesions prevented the complications associated with the Uematsu procedure.11 However, many patients still developed complications as a result of heating of the DRG. These complications included neuroma formation, allodynia, and
Chapter 178—Radiofrequency Lesioning 1341
Table 178.1 Radiofrequency of the Lumbar Medial Branch Randomized Controlled Trial Authors
Study Design
N
Efficacy
Tekin et al, 2007
Randomized controlled trial
60
Effect of RF maintained at 6 mo and 1 yr; only 40% of patients using analgesics at 1-yr follow-up
Nath et al, 2008*
Randomized controlled trial
40
Patients in treatment group reported significant improvements in pain and quality of life
van Kleef et al, 1999†
Randomized controlled trial
31
At 6 and 12 months after treatment, significantly more successful outcomes in RF group compared with placebo group
N
Efficacy
30
Prospective Uncontrolled Trials Authors
Study Design
Dreyfuss et al, 200079
Prospective audit
15
Gofeld et al, 2007‡
Prospective audit
174
Burnham et al, 2009
§
Prospective cohort
44
12 months after procedure, 60% of patients experienced 90% relief of pain; 87% had ≥60% relief 68.4% had good to excellent pain relief lasting 6–24 mo Patients reported significant improvements in pain, disability, analgesic requirement; and satisfaction; effects peaked at 6 mo after procedure
*Nath S, Nath CA, Pettersson K: Percutaneous lumbar zygapophysial (facet) joint neurotomy using radiofrequency current, in the management of chronic low back pain: a randomized double-blind trial, Spine 33:1291, 2008. † van Kleef M, Barendse GAM, Kessels A, et al: Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain, Spine 24:1937–1942, 1999. ‡ Gofeld M, Jitendra J, Faclier G: Radiofrequency denervation of the lumbar zygapophysial joints: 10-year prospective clinical audit, Pain Physician 10:291, 2007. § Burnham RS, Holitski S, Dinu I: A prospective outcome study on the effects of facet joint radiofrequency denervation on pain, analgesic intake, disability, satisfaction, cost, and employment, Arch Phys Med Rehabil 90:201, 2009. RF, radiofrequency.
dysesthesias.39 Geurts et al82 studied the heat procedure in a double-blind, randomized, controlled trial. These investigators concluded that “lumbosacral radiofrequency lesioning of the dorsal root ganglion failed to show advantage over treatment with local anesthetics.” Thus, the use of this procedure in the treatment of radicular pain was not recommended. PRF was introduced in 1998. This method allows delivery of high-frequency electric current without the development of heat. Given the potential for nerve damage with heating of the DRG, PRF was introduced as a method of treatment for radicular pain that had the potential for therapeutic efficacy without the attendant risks. Pulsed treatment of the DRG has shown increasing evidence of efficacy in studies conducted to date. For these reasons, only PRF treatment of the DRG is presented here.
Ventral horn of spinal cord Dorsal root Dorsal root ganglion (DRG) Spinal n. root
Ventral ramus of spinal n. Ventral root
Anatomy Five paired nerves exit their respective intervertebral foramina from L1-2 to the L5-S1 levels (Fig. 178.9). Just as the orientation of the lumbar z-joint differs from L1-2 to L5-S1, the lumbar nerves exit their respective foramina at different angles from L1 through L5. At L1, the nerves exit downward and forward at an acute angle, whereas at L5, the nerves exit more horizontally and at a more obtuse angle.3,44,72 These anatomic features have important corollaries for positioning of the fluoroscope. For example, imaging the L5-S1 foramen requires much more obliquity than when imaging the L1-2 foramen. In addition, the C-arm must be tiled in a caudal direction to square the end plate at L1, whereas it should be cephalad for L5. The lumbar ventral roots find their cell bodies of origin within the spinal cord at the T9-11 vertebral level.83 Rootlets come off the dorsal and ventral surface of the spinal cord to form the dorsal and ventral roots. The dorsal and ventral roots then join to form the spinal nerve root. The DRG contains cell bodies that provide sensation, proprioception, and pain.44
Dorsal horn of spinal cord
Fig. 178.9 Cross-sectional anatomy of the spinal cord. (From Mathis JM, Golovac S: Image-guided spine interventions. New York, 2010, Springer.)
The spinal nerve root immediately divides to form the dorsal and ventral rami. The ventral ramus is the larger branch and travels to the lower extremity. The dorsal ramus divides into three branches: medial, lateral, and intermediate. The lateral and intermediate branches supply sensation and motor function to the skin and muscles of the back, whereas the medial branch provides sensation to the z-joint and motor function to the multifidus muscles.14
Indications In general, the indication for PRF is neuropathic pain that is confined to the distribution of a known nerve.3,39,42,46 The specific indication for PRF treatment of the DRG is radicular pain
1342 Section V—Specific Treatment Modalities for Pain and Symptom Management or radiculopathy that is completely but temporarily relieved by transforaminal injection of local anesthetic performed on two separate occasions. The local anesthetic injections are performed diagnostically to identify the location of the origin of the pain and to confirm the nerve levels involved. The procedure has been used for both acute and chronic radicular pain and radiculopathy.3–5,42,46,48,50–52,84–88
block.2 With this approach, the target lies at the intersection of two lines. In a lateral view, the first line runs longitudinally between the posterior half and the anterior half of the foramen and divides the foramen into two equal halves. The second line runs in a transverse direction between the superior one third and the inferior two thirds of the foramen. The intersection serves as a starting point for locating the DRG, however, it can lie anywhere between the midaspect and the most anterior aspect of the foramen in the AP plane.
Technique PRF lesioning of the DRG requires extremely careful, precise placement of the electrode (Fig. 178.10). Therefore, the operator should have very soft hands (a gentle touch) and excellent needle handling skills before attempting this procedure. Although PRF lesioning of the DRG is possible at all spinal levels, this discussion is limited to the use of PRF in the lumbar spine. The discussion also focuses only on the PRF procedure, because continuous RF current applied to the DRG was found to be no more effective than control treatment with local anesthetics.82 The retroneural approach is the best method of needle placement to reach the DRG. It is well described in the ISIS guidelines presented in the chapter on lumbar spinal nerve
A
Fig. 178.10 Fluoroscopic images of dorsal root ganglion radiofrequency lesioning. A, Oblique view. B, Anteroposterior view. C, Lateral view.
Identify the target For PRF to be effective, the electrode must be meticulously positioned, pointed directly perpendicular and very close to the targeted nerve. To identify the target, the operator should obtain an oblique view, similar to that used for a t ransforaminal procedure. More specifically, after squaring the superior end plate at the involved level, the operator should rotate the image intensifier into an oblique view until the SAP is projected one third of the distance across the image of the vertebral body (approximately 25 degrees). In this view, the starting point for the needle is slightly inferior
B
C
Chapter 178—Radiofrequency Lesioning 1343
and lateral to that used for a transforaminal injection. The target lies at a point just beneath the pedicle, one third of the way down the foramen. As the needle is advanced, the image is rotated into an AP projection to assess the depth of insertion. If further insertion is required, the image is rotated back to an oblique view and the needle continues to advance. When the needle tip approaches the lateral aspect of the vertebral body, it is best to advance further in an AP view. When the needle is advanced it must be done very slowly (only 1 mm at a time) to avoid damage to the nerve. This aim can be achieved by pinching the needle shaft at the point of skin entry. If the operator is having difficulty locating the nerve, the needle tip is usually too medial and should be corrected in an oblique view so that the tip is located directly beneath the pedicle on a line that bisects it. Because evidence indicates that a small lesion does occur around the electrode tip, it may be unwise to allow the electrode to penetrate neural tissue. The operator should warn patients that they will feel paresthesia and should not make any sudden movements. Because the greatest current density is projected from the tip of the needle, it is best to point the needle tip directly toward nerve tissue and not against the vertebral body (i.e., the needle tip rather than the shaft should be perpendicular to the targeted nerve). Once the patient reports paresthesia, the operator places the electrode into the needle and begins testing. One must be very careful when handling the needle at this time because any movement risks spearing and damaging the nerve. A modification of the foregoing technique is required to perform the procedure at the S1 nerve level. In the case of the S1 nerve, the procedure is performed at the level of the ventral ramus, rather than directly at the DRG, because the ventral ramus is located more proximally within the spine. The procedure is performed differently than a typical S1 transforaminal injection. First, the operator adjusts the cephalocaudal tilt in a cephalad direction to optimize the view of the foramen. The C-arm should remain in an AP view (rather than in the ipsilateral oblique position recommended for a transforaminal injection). The needle entry site is at the inferior and lateral quadrant of the foramen with the trajectory superior and medial. This follows the course of the nerve. The needle should first touch the posterior shelf of the sacrum before it enters the foramen. This technique gives a sense of depth and provides a warning before the needle enters the foramen. Once inside the foramen, the needle is advanced very slowly (1 mm at a time) toward the nerve. When contact is established, the operator performs sensory testing and proceeds as usual. If the operator is unable to locate the nerve after three or four attempts, he or she should withdraw the needle and find a new starting place. This is necessary because of the limitation in needle adjustments imposed by the foramen (i.e., the foramen confines the needle such that only a limited territory of space that can be searched).
etermine the minimum sensory threshold (the lowest voltage d at which the patient can still perceive a sensation) and a second time to determine reproducibility. During stimulation the second time, the operator slowly increases the voltage by 0.05 V until the patient reports perceiving a stimulus. This should be within 0.05 V of the first stimulation test. If the patient does not feel the current at the required level of less than 0.2 V, the needle is advanced slightly (no more than 1 mm) or is repositioned altogether and retested. Values lower than 0.05 V may reflect intraneural placement, and the needle should be retracted slightly.5 Motor stimulation is unnecessary during PRF because the modality does not damage motor fibers.
Determine proximity between needle tip and nerve Electrical stimulation tests are used to determine proximity between the needle tip and the nerve. Adequate placement requires that the patient feel reproducible stimulation (tingling in the distribution of the stimulated dermatome) at less than 0.2 V. Two stimulation tests are conducted, once to
Postprocedure Advice
Lower impedance The next step is to lower the impedance sufficiently to produce a current of 150 to 200 mA during the procedure. The maximum impedance should be less than 400 ohms and ideally less than 250 ohms. To achieve this goal, the operator injects a small amount (1 mL) of local anesthetic (0.5 mL of 0.5% lidocaine [Xylocaine]) or saline solution through the needle. When fluid is injected through the needle, the position of the needle must be secured by one hand at the skin to prohibit movement, which could cause severe pain and possible needle trauma to the nerve. If any resistance is felt during injection, the operator should stop, retract the needle slightly, inject again, and then replace the needle in its original position. Liquid should flow easily through a 20-gauge needle. The minimal stimulation threshold and impedance should be recorded before treatment. Begin pulsed radiofrequency treatment At this point, the operator turns on the power in the PRF mode, slowly increases the voltage to 45 V, and verifies that the patient feels pulsing. The needle must be close enough to the target nerve to produce a perceptible electrical discharge in the treated extremity with each pulse. The absence of a pulsing sensation may indicate that the needle is not close enough to the targeted nerve tissue to produce an effect. If this is the case, the operator repositions the needle and begins treatment again. Although no study has demonstrated that this step is necessary, it can be another useful test to verify proximity to the targeted neural tissue. If desired, this step can be performed before lesioning the nerve, because it is unlikely that the patient will feel pulsing once the nerve has been anesthetized. The standard protocol is to proceed with PRF treatment for 3 to 4 minutes at 45 V (as long as the temperature does not exceed 42°C [108°F]), two pulses per second, with current applied for 20 milliseconds during each pulse. However, an alternative protocol is to increase the voltage as high as necessary to produce a current of at least 150 mA, which may cause additional heating around the needle. The temperature can be allowed to rise as high as 45°C (113°F), if necessary, to produce the higher current (of at least 150 mA). Because treatment protocols may vary among operators, the operator should consult the literature for other examples of lesion parameters.
The patient usually feels immediate relief on completion of the procedure, as a result of the injection of local anesthetic into the affected nerve. When the effect wears off, the patient may begin to feel sore. The patient should be advised that he or she may continue to feel sore for the first week and better the second week, and that the full effect can take 3 to 4
1344 Section V—Specific Treatment Modalities for Pain and Symptom Management weeks to develop. During this time, the patient is not required to restrict activities except as needed to relieve pain. Deep tissue massage once a week for the first 3 weeks following the procedure may relieve soreness related to the procedure, as well as chronic trigger points that may have developed over the course of the disease.
Complications The most common complication noted during any spinal procedure is vasovagal syncope.89 This symptom is more common during a cervical than lumbar procedure (8% versus 1%).90 Other complications include transient nonpositional headache, increased back pain, facial flushing (if steroids are used) and increased leg pain, ischemia of the anterior spinal artery if particulate steroid is injected, infection (epidural abscess, meningitis, diskitis), and other complications related to injected medications.4,91,92 A potential risk of neural trauma is associated with this procedure, but this has not been specifically studied. Certainly, with proper needle handling techniques, the complication should be rare. In Rosenthal's experience, after performance of more than 1000 procedures, no incidence of neural trauma occurred. During injection of local anesthetic to anesthetize the nerve, fluid can be inadvertently injected into the axon bundle, thus leaving the patient with persistent motor or sensory deficits. This complication should never
occur in a properly performed procedure and can be detected by resistance to flow of fluid on injection. If any resistance is encountered during injection, especially if it is accompanied by pain, the operator should stop injecting and retract the needle slightly before continuing. Hematoma may occur just under the skin or in the deeper muscle layers as a result of the procedure. Most patients report mild discomfort in the treated extremity that spontaneously resolves within approximately 3 weeks.93 All complications have a low incidence.
Efficacy Some investigators studied the efficacy of PRF lesioning of DRG by targeting the lumbar, thoracic, or cervical spine. Most of these studies were prospective uncontrolled trials or retrospective studies, and one was a randomized controlled trial. Each of the four prospective uncontrolled trials concluded that PRF lesioning of the DRG was a safe and effective pain treatment, and each of the five retrospective studies reported similarly positive results. These data are summarized in Table 178.2. Although the foregoing studies appear promising, none included a control group, and most reported only relatively short-term efficacy. To date, only one double-blind, randomized, placebo-controlled trial of PRF lesioning has been conducted, and that trial studied 23 patients with chronic cervicobrachial pain for 6 months.48 Patients underwent either
Table 178.2 Radiofrequency of the Dorsal Root Ganglia Randomized Controlled Trial Authors
N
Type of Pain
Efficacy
23
Cervical radicular
82% achieved ≥50% improvement in global perceived effect and ≥2-point reduction of VAS at 3 mo
N
Type of Pain
Efficacy
Sluijter et al, 1998
15
Lumbar radicular
53% achieved ≥2-point reduction of VAS at 6 mo, and 40% did so at 1 yr
Pevzner et al, 2005163
28
Lumbar radicular Cervicobrachial
2 patients had “excellent” pain relief, 12 had “good” pain relief, and 9 had “fair” pain relief at 3 mo
28
Spinal neuropathic
82% achieved ≥30% reduction of VAS at 3 mo, and 68% of did so at 1 yr
76
Lumbar radicular
Patients reported an average 4.3-point decrease in pain scores, with a 3.18-mo average duration of success
N
Type of Pain
Efficacy
Van Zundert et al, 2003
18
Cervicobrachial
72% achieved ≥50% pain relief at 2 mo, 56% did so at 3 to 11 mo, and 33% did so for >1 yr
Teixeira et al, 200584
13
Lumbar radicular
92% achieved ≥5-point improvement in NRS at 1 yr
Cohen et al, 2006164
13
62% achieved ≥50% pain relief at 6 wk and that 54% did so at 3 mo
Abejón et al, 2007
54
Thoracic segmental Herniated disk Spinal stenosis FBSS Lumbar radicular Cervical radicular
45% of patients with lumbar pain (n = 116) and 55% of patients with cervical pain (n = 49) achieved ≥50% relief at 3 mo
Van Zundert et al, 2007
48
Prospective Uncontrolled Trials Authors 31
Shabat et al, 200693 Simopoulous et al, 2008
51
Retrospective Studies Authors 47
Chao et al, 2008162
85
154
40% of patients with herniated disks (n = 29) and 40% of patients with spinal stenosis (n = 12) achieved “successful treatment” at 180 days after treatment; treatment not as successful in patients with FBSS (n = 13)
FBSS, failed back surgery syndrome; NRS, numerical rating scale; VAS, Visual Analog Scale.
Chapter 178—Radiofrequency Lesioning 1345
PRF lesioning (n = 11) or sham lesioning (n = 12) at the C5-7 nerve levels.At 3 months, significantly more patients in the treatment group (83%) than in the control group (33%) reported at least 50% improvement in global perceived effect, an effect that was also maintained at 6 months. Similarly, at 3 months, significantly more treatment-group patients (82%) than control-group patients (25%) reported at least a 20-point decrease in Visual Analog Scale (VAS) score, although the effect was not maintained. This study has been criticized because (1) recruitment challenges limited its statistical power, (2) the two study groups were not comparable in terms of average age and baseline VAS scores, and (3) the effect was not maintained at 6 months. Despite these shortcomings, this study is important because it is the first prospective controlled trial to show a treatment effect. Martin et al94 proposed that the efficacy of PRF lesioning of the DRG is directly related to the proximity of the RF electrode to the targeted neural structure and the amount of delivered current (Table 178.3). These investigators recommended using a stimulation voltage between 0.1 and 0.3 volts to position the electrode properly. They also suggested that higher current delivery (150 to 200 mA) improves outcomes. Considering the preponderance of the evidence presented earlier, it appears that PRF does indeed have a clinical effect for the treatment of radicular pain. Further research is required to bolster the data presented here and to prove the long-term utility of the procedure. However, enough evidence currently exists to support the use of PRF lesioning in clinical practice for the treatment of radicular pain.
Cervical Medial Branch Radiofrequency (Table 178.4) History Lord et al95 published the first randomized, double-blind, placebo-controlled trial illustrating that, when performed accurately (i.e., based on results of anatomic studies), cervical medial branch RF lesioning was clearly efficacious. This land-
Table 178.3 Stimulation Voltage versus Duration of Effect Based on Studies Sensory Stimulation (V)
Duration (mo)
Simopoulos et al, 200851
0.6
3.18
Teixeira et al, 2005
0.22
15.8
Chao et al, 2008162
80% relief) to SI joint injections on two occasions to be considered a candidate for an SI joint RF procedure. Contraindications include local or systemic bacterial infection, bleeding diathesis, and possible pregnancy.
Technique Two techniques that have emerged as having promise in the treatment of SI joint pain are strip lesion RF ablation and cooled-probe RF ablation. Because the cooled-probe RF technique requires the use of special equipment and a specific lesion generator, it is not discussed here. Instead, only the strip lesion technique is addressed because it can be performed with standard RF equipment, and no special lesion generator is required. A strip lesion can be produced by several methods. One can create either a monopolar or a bipolar lesion, or the practitioner can use the Simplicity III device made by NeuroTherm, which contains three electrodes on a single probe. All three methods are very similar, so only the monopolar technique is discussed in detail here. To begin the procedure, the L5-S1 disk space is opened by moving the C-arm into a cephalad tilt, to look into the L5-S1 disk space. The C-arm is then very slightly obliquely toward the ipsilateral side to visualize the groove between the sacral ala and the SAP of S1 fully. The L5 dorsal ramus is then approached in a pillar view, as previously described in the section on lumbar medial branch RF. A 10- or 15-cm needle with a 10 mm active tip is advanced directly down the beam until it contacts periosteum. Because this technique requires some manipulation of the needle as it rests against the bone, it is best to anesthetize the bone by injecting 1 to 2 mL of 2% lidocaine (Xylocaine) through the needle to prevent pain while the cannula is slid into proper position. The needle is then carefully advanced by making small back and forth twisting motions until the active tip lies in the previously described groove. Once the needle is properly located in the pillar view, the needle should be observed in three additional views: AP, lateral, and steep oblique. In the AP view, the needle should be resting against the SAP of S1; in the lateral view, it should be at the base of the SAP of S1; and in the steep oblique view,
1354 Section V—Specific Treatment Modalities for Pain and Symptom Management it should lie across the base of the S1 SAP. A second needle is then placed by starting on the skin at or just below the S2 foramen. The needle is carefully advanced down to periosteum, such that it touches bone slightly lateral and inferior to the S1 foramen. The needle is then carefully advanced cephalad until the needle is two active tips (10 mm) cephalad to the S1 foramen. A third needle is started on the skin inferior to the S4 foramen and advanced in similar fashion until it is located similarly against the S2 foramen. As the nerves exit their respective foramina, they may take any path as they travel to the joint, including directly lateral, lateral and cephalad, or lateral and caudal. Therefore, one should take care to locate the needles near, but never directly in, the sacral foramen, to catch the nerves before they begin to separate significantly from one another as they travel to the joint. Once the sacral needles are in place, a lateral view is obtained. In the lateral view, the needles should
A
be closely applied to the posterior aspect of the sacrum, rather than located in the soft tissue above the sacrum. In addition, it is important to ensure that the needles have not entered the sacral foramina and are placed in the epidural space. Motor testing at 2 Hz and 1 V is performed to ensure that no contraction of the muscles innervated by the ventral rami has occurred. Then, 1 mL of 2% lidocaine is infiltrated through each needle, and 60 seconds are allowed to pass while the anesthetic takes effect. Finally, each nerve is ablated for 60 to 90 seconds at 80°C to 85°C. The needles are then pulled down the length of the active tip, and second, third, and forth lesions are produced. By creating multiple lesions, the active tip of the cephalad needle is retracted caudally, 10 mm at a time, until it reaches the starting position of the needle below. This leaves a continuous strip lesion from L5 to S2 and ensures that all possible locations of the lateral branches have been burned (Fig. 178.21).
B
C Fig. 178.21 A, Image of L5 and S1 needles in place for the first radiofrequency (RF) lesion. B, Second position for the S1 RF lesion. C, Lateral view showing S1 and S2 needles in place for the RF lesion.
A bipolar variation on this procedure uses two needles. The needles are placed as described earlier, with the caveat that the tips lie 2 to 4 mm from each other. Then, rather than pulling each needle down for successive lesions, the cephalad needle is removed and replaced as the caudad needle. A third variation on this technique involves use of the Simplicity III probe. The probe is placed from a single location just slightly below and lateral to the S4 foramen. It is then advanced to its final position at the sacral ala. Because the probe is not hollow, anesthetic must be placed using a spinal needle. For further instruction on placement of this probe, contact NeuroTherm.
Complications Possible complications related to RF lesioning of the SI joint include those described in the section on lumbar medial branch RF. An additional risk is the possibility that the needles could enter the sacral foramina and cause heating and damage to the sacral nerve roots. Because the patient is awake and conversant during the procedure, this complication should not occur, given that the patient will feel a sensation of heating in the legs that can be communicated immediately.
Efficacy Approaches to RF lesioning of the SI joint include intraarticular, cooled-probe RF ablation, bipolar or monopolar strip lesions, and a combination of ligamentous and neural RF ablation. This discussion focuses on cooled-probe RF ablation and bipolar or monopolar strip lesions. Cooledprobe RF ablation is a relatively new method of treating SI joint pain that can increase lesion size by a factor of 8.134 To date, its use has been published in two papers. The first described a randomized, placebo-controlled study of 28 patients with SI joint pain confirmed by a single intraarticular diagnostic block.141 The study compared sham and cooled-probe denervation of the S1-3 lateral branches, with conventional lesions performed at L4 and L5 medial branches. Patients in the treatment group reported significant improvement in pain (a reduction by 60%, 60%, and 57%, at 1, 3, and 6 months, respectively) compared with the patients in the placebo group, none of whom reported significant improvement. Patients in the treatment group also reported improvement in functional capacity and medication usage. The other article described a retrospective case series including 27 patients with SI joint pain confirmed using dual diagnostic blocks.142 Thirteen of the patients (50%) reported at least a 50% decrease in pain 3 to 4 months following treatment. Strip lesions are another relatively new method of treating SI joint pain. The technique was used in a prospective observational study that included nine patients with SI joint pain confirmed by local anesthetic joint and lateral branch nerve blocks.127 The strip lesions were created adjacent to the lateral dorsal foraminal aperture, with conventional monopolar lesions at the L5 dorsal ramus. Eight of the nine patients were satisfied with the treatment, and 78%, 67%, 67%, 89%, and 67% reported being very satisfied at 1, 3, 6, 9, and 12 months. Median improvement in pain intensity was 4.1 on a 10-point rating scale, and reduction in disability was 17.8 on the Oswestry Disability Index. Finally, a meta-analysis of 10 studies in which RA ablation was used to treat SI joint pain demonstrated that the
Chapter 178—Radiofrequency Lesioning 1355 procedure is an effective treatment a3 and 6 months.143 Diminished outcomes after 6 months are likely the result of nerve regeneration and regrowth.
Thoracic Medial Branch Radiofrequency History When RF neurotomy was first introduced as a therapeutic modality, attention was largely focused on treatment of cervical and lumbar pain. Few studies were directed toward treatment of thoracic facet joint pain, possibly because of the lower incidence of complaints in that region. In addition, no anatomic dissections of the thoracic medial branches had been published, and poorly performed anatomic studies, described in a textbook by Hovelacque in 1927,144 suggested that thoracic medial branch anatomy was analogous to that of the lumbar medial branches. Therefore, early attempts at thoracic facet joint RF were directed at the junction of the SAP and the TP, and outcomes were poor.16,145,146 Despite using the same anatomic targets as earlier studies, Stolker et al16 reported that 16 out of 36 patients (44%) were pain free 31 months after the procedure. Subsequent anatomic studies revealed that the thoracic medial branch nerve is located on distal tip of the superior aspect of the TP,147 which redirected the target for RF procedures. Whether this change will improve efficacy remains to be seen.
Anatomy The thoracic facet joints are innervated by the medial branches of the dorsal rami.98,147–150 The location of the thoracic medial branches is basically the same at all levels of the thoracic spine, but their course differs slightly at the midthoracic levels. A careful anatomic study of multiple adult human cadavers found that the archetypical medial branches are located on the superior lateral aspects of the TPs and assume a consistent course.147 On exiting the IVF, the dorsal rami immediately divide, giving off the medial, lateral, and intermediate branches. The medial branch nerves pass mostly laterally within the intertransverse space until they cross the TP at the superolateral corner. They then pass medially and inferiorly across the posterior surface of the TP before ramifying into the multifidus muscles. The exception to this pattern appears at the T4-8 levels, where the inflection point is superior to the TP. These nerves are often referred to as floating because they may be retracted into the muscles above the TP rather than actually touching the periosteum. The medial branch nerves located at the T12 and L1 vertebral levels (i.e., the T11 and T12 medial branches) are found in an analogous location to the lumbar medial branch nerves (i.e., at the junction of the SAP and the TP). The precise location of the medial branch along the TP varies from cadaver to cadaver, with some medial branches are located slightly more toward the midline than others. Thus, the target for RF lesioning is an area along the distal TP, rather than a discrete point. The nomenclature used to identify specific nerves can be confusing. Because the spine has seven cervical vertebrae and eight cervical nerves, the C8 medial branch nerve is located at the T1 vertebra. Consequently, the nomenclature for each subsequent nerve is associated with the vertebra below it. For example, the T7 medial branch rests on the T8 TP. In addition, two nerves innervate each joint, one from the segmental level of origin and one from the level below it. For example,
1356 Section V—Specific Treatment Modalities for Pain and Symptom Management the T8 and T9 medial branches innervate the T8-9 joint. To ensure clear communication about any spinal procedure performed, it is necessary to specify the nerves involved, their location on the vertebral body, and the joints they innervate. For example, a report of a medial branch block could read as follows: the T7 and T8 medial branches were blocked at the T8 and T9 vertebral levels to anesthetize the T8-9 joint.151
Patient Selection Midback pain is an important albeit uncommon pain complaint. Investigators have estimated that 5% to 15% of all patients referred to a typical outpatient pain clinic complain of thoracic spinal pain.152,153 The prevalence of facet joint pain in this group of patients is 42%. Before evaluating the origin of musculoskeletal pain in the thoracic spine, one should first exclude medical causes. This is particularly critical in the thoracic area, given the important structures that reside there. For example, thoracic pain can arise from diseases of the cardiovascular, pulmonary, or gastrointestinal systems. Serious causes of pain must also be considered such as malignant disease, infection, or impending cardiac disasters (myocardial infarction, rupturing thoracic aneurysm). Once medical causes have been excluded, the physician must differentiate between mechanical and radicular causes of pain. Thoracic radicular pain is most often of a burning, shooting, or electrical nature and radiates around to the front of the chest or abdomen. The pain is constant and not usually influenced by activity. In contrast, thoracic facet joint pain is mechanical, often manifesting as a constant ache that worsens with activity and eases with rest, and it may radiate in a nondermatomal pattern. Once a mechanical cause is identified, it may be difficult to determine whether the pain source is a facet joint, a costovertebral joint, or a costotransverse joint, given that no clinical features allow differentiation among the three joints. Because these joints are in close proximity, sequentially anesthetizing each is the best way to determine which joint is causing the pain. A patient whose pain is relieved by a correctly performed medial branch block can be assumed to have facet disease. An additional confounding factor in the evaluation of upper thoracic pain is that pain originating from the lower cervical facet joint refers to the upper thoracic spine. Thus, patients presenting with upper thoracic pain (e.g., pain between the shoulder blades) should first undergo a cervical medial branch block.
Indications The indications for facet joint denervation include chronic midback pain with or without radiation in a nondermatomal pattern, focal tenderness over one or several facet joints, and positive response to a medial branch block with greater than 80% relief on two occasions. The only absolute contraindications are infection in the overlying soft tissues, systemic infection, bleeding diathesis, and possible pregnancy.
Technique The RF techniques for thoracic medial branch neurotomy published to date have emphasized a single-needle approach. However, in the absence of definitive studies regarding an
optimal approach, a two-needle bipolar technique with chemical neurolysis is presented here. The advantage of the bipolar technique is that it creates a larger burn and thus increases the likelihood of trapping the nerve between the two electrodes, a maneuver that, in turn, increases the probability of adequate neurolysis. In addition, the use of 6% phenol diluted in contrast dye may aid in achieving neurolysis, particularly of the floating nerves located at the T4-8 levels that do not rest directly on the TP. The patient is positioned prone on the fluoroscopy table, and the back is prepared and draped in sterile fashion. If sedation is given, it should be light enough that the patient is awake and conversant throughout the procedure. The target for the medial branches is the lateral aspect of the TPs. To begin, a straight AP view with the vertebral end plates squared is obtained. The TP at the targeted level should be clearly visible. If it is not, it sometimes helpful to move the C-arm such that the TP of interest is visualized at the periphery of the screen to improve contrast and decrease the “whiteout” caused by the lungs. Once the TP is clearly visualized at the targeted levels, a skin wheal is placed slightly below the inferior aspect of the TP. A 20-g 10-cm RFK needle with a 10-mm active tip is advanced from inferior and lateral to superior and medial toward the superior border of the lateral aspect of the TP. A second needle is then similarly advanced, slightly medial to the first, such that the needles form a V shape with the heads more lateral than the tips. This technique interference between the needle heads that can cause shifting in the location of the active tips. Once in final position, the needle tips should be separated by 2 to 4 mm or one to two needle widths. The needles are advanced from an inferior position in an attempt to place them parallel to the nerve, to provide a larger area of burn. Sensory testing can be implemented at 0.3 to 0.5 V, although this may not have an impact on outcome.79 One can also perform motor stimulation to ensure adequate distance from the ventral ramus by using parameters of 2 Hz and 1 V, which should not result in muscle contraction in the anterior chest wall. Once the needles are in final position, a lateral view is obtained to confirm that the needles have not advanced off the TP. The nerves are then anesthetized by placing 0.5 mL of 2% lidocaine through each needle, and RF current is applied for 60 to 90 seconds at 80°C to 90°C. On completion of the lesion, 0.1 to 0.2 mL of 6% phenol diluted in contrast dye is injected through each needle, so the patient receives both chemical and thermal lesions. Phenol should be used only on the T1-10 medial branches (i.e., at the T2-11 vertebral levels), where the nerves are located on the tips of the TPs (Figs. 178.22 and 178.23).
Efficacy RF lesioning of the thoracic facet joints is not well studied. Only a few articles have been published, and the lesioning techniques reported are inconsistent. Some techniques incorrectly target the junction of the SAP and the TP, whereas others use the anatomically correct target.16,147 In an unpublished case report, the use of bipolar RF lesioning with the addition of phenol decreased a patient's pain from a 9/10 to 2/10 on a VAS. The neurotomy was performed at the distal aspect of the TPs.109 A cadaveric study of a bipolar
Chapter 178—Radiofrequency Lesioning 1357
A
B
C Fig. 178.22 A, Anteroposterior view with needles in place for thoracic bipolar radiofrequency (RF). B, View after injection of 6% phenol. C, Lateral view of needles in place for thoracic bipolar RF.
technique using interspinous ligament tissue demonstrated that heating two electrodes simultaneously appears to coagulate a wider area than a monopolar lesion and potentially produces better results in less time.154 Tzaan and Tasker22 reviewed 118 cases of RF denervation performed on 90 patients. The procedures were not limited to the thoracic spine and also included cervical and lumbar procedures. The patients were followed for an average of 5.6 months, and success was defined as greater than 50% reduction in pain. Of the 17 patients who underwent thoracic RF lesioning (the exact method of lesioning was not described), 15 met the criteria for success at follow-up. The most frequent complications were sensory loss and transient neuritis in the cutaneous branches of the posterior rami.22
C2 Radiofrequency Treatment for Cervicogenic Headache (Table 178.5) History The most common cause of cervicogenic headache of spinal origin is injury to the C2-3 joint. Rarely, the C1-2 and C0-1 joints are involved. The suspicion that the upper cervical joints could be responsible for headache was first proposed in the early 1900s.2,155 However, upper cervical joint injury as a primary cause of headaches in whiplash victims remained largely unrecognized for many years.5 In a study by Lord et al156 in whiplash victims who reported headache as the primary symptom, the prevalence of C2-3 joint pain was 53%.156 In an attempt to prove the C2-3 joint as a source of
1358 Section V—Specific Treatment Modalities for Pain and Symptom Management headache, Dwyer et al105 injected contrast dye into the C2-3 joint of normal volunteers and was able to induce a characteristic headache in the occipital area.2 Bogduk and Marsland157,158 showed that anesthetizing the TON could relieve pain emanating from the joint. Dreyfuss et al159 performed a similar study of the atlantoaxial joint and was able to induce pain at the base of the skull. Bogduk2,160 described a technique of
A
anesthetizing the C2 spinal nerve as a means of diagnosis. Later, the idea of directly anesthetizing the joint as a means of diagnosis was proposed.
Anatomy The anatomy of the upper cervical spine is complex because several communicating branches are present among the C1, C2, and C3 dorsal rami.5 The confusion is compounded by the trigeminal cervical system. The trigeminal nucleus descends into the upper cervical segments of the spinal cord possibly as far down as C3.110 Stimulation of the occipital nerves has a facilitatory influence on input from the dura. Furthermore, stimulation of muscle afferents produces more input than skin afferents, a finding suggesting that increases in cervical muscle tone may increase input into the cervical trigeminal system. This may explain why anesthetizing the occipital nerves relieves tensiontype headache. For this group of patients, it may make sense to perform a PRF lesion of the C2 DRG because this is the sensory nucleus of the occipital nerve. For those patients with headache of spinal origin, it most commonly emanates from the C1-2 or C2-3 joint (Fig. 178.24). The TON innervates the C2-3 joint, whereas C1-2 innervation derives from the C2 dorsal ramus. Finally, for patients with pain from occipital neuralgia caused by chronic tension headache, the greater occipital nerve derives its roots from the C2 nerve. Therefore, PRF procedures performed at the C2 and C3 levels would be expected to treat all three causes of pain.
Indications The diagnosis of cervicogenic headache should be suspected in patients with headache pain of unknown origin. Distinguishing pain emanating from the C1-2 and C2-3 joints
0 0 0 0 0 0 T1 0
B Fig. 178.23 A, Anteroposterior view of the course of the medial branch nerve tracking back to the dorsal ramus and spinal nerve root. B, Lateral view showing dye from the medial branch nerve sheath tracking into the epidural spaces.
Fig. 178.24 C1-2 joint referral maps and C1-2 cervical facet joint referral map.
Table 178.5 Radiofrequency for Cervicogenic Headache Authors
Study Design
N
Efficacy
Haspeslagh et al, 2006
Randomized controlled trial
30
No difference between group treated with occipital nerve block using steroids and group treated with cervical facet joint radiofrequency and upper cervical dorsal root ganglion radiofrequency
Chao et al, 2008162
Retrospective analysis
49
55.10% had ≥50% pain relief at 3-mo follow-up
161
is difficult.5 Patients often complain of pain at the base of the skull that sometimes radiates up the back of the head. They may report focal tenderness in the suboccipital area. The pain is often unilateral. The pain may be increased with turning of the head, axial loading, or bending toward the affected side. The pain is continuous but is often increased by activity and lessened by rest. Patients describe it as a dull aching or throbbing sensation. Neurologic symptoms are not usually associated with the pain. This pain can be extremely debilitating, and some patients give up their work or school activities to cope with it. The cause is thought to be tearing of the joint capsule surrounding one or more of the upper cervical joints. Another cause of chronic posterior headache pain is tension-type headache. Many of these patients complain of a dull aching or a squeezing sensation bilaterally at the posterior aspect of the head that radiates into the temporal, frontal areas. The pain is usually not associated with nausea, vomiting, photophobia, or phonophobia. Patients with this type of pain can usually function in spite of it, in contradistinction to patients with migraine headache, who usually must lie down in a dark room to cope with the pain. Anecdotally, patients with tension headaches originating in the occipital area have been found to respond to treatment with an interventional procedure (described in the next subsection) at the C2 DRG level. Although no data show a clear advantage of this procedure, the theoretical basis for treatment is sound. PRF lesioning of the C2 DRG should be undertaken only when more conservative treatment options have failed. The patient should have responded on two occasions with greater that 80% relief to diagnostic blocks (TON for C 2-3 joint pain, C2 DRG for atlantoaxial joint pain, and occipital nerve blocks for headache pain).
Chapter 178—Radiofrequency Lesioning 1359 target. Once the needle is properly aligned, the needle is passed in a tunnel vision view down to the lamina of C2. Contact with lamina before passing the needle to the final target is done to give a sense of depth before advancing to the target. With the needle on the lamina, the operator retracts the needle slightly and redirects it toward the target. At this point, an AP view is obtained, and the needle should be seen resting on the lateral aspect of the articular pillar. If visualizing the needle tip is difficult, an open-mouth view is helpful. The needle tip is carefully and slowly advanced toward the target. In the AP view, the target is usually directly over or slightly inferior to the midaspect of the atlantoaxial joint. When the needle approaches this area, the operator should warn the patient and advance only 0.5 mm at a time while monitoring for paresthesia. Once the patient feels mild paresthesia, needle advancement is stopped, and sensory testing is performed. With correct needle placement, the patient should
Technique The patient is positioned in the lateral position on the operating room table with the head built up sufficiently that it is parallel to the operating room table and directly perpendicular to the shoulders. This position facilitates proper imaging (Fig. 178.25). The neck is prepared and draped in sterile fashion, and monitors are applied if intravenous sedation is planned. If intravenous sedation is given, it should be very light, to facilitate continuous communication between the patient and the operator. This serves as a monitor for any type of complication that may occur. The target point is in the anterior aspect of the dome created by the C1-2 lamina. Specifically, the point lies in the midaspect of the dome from cephalad to caudad and in the anterior aspect from dorsal to ventral. A needle placed down to this point is not expected to contact periosteum and can be placed directly through the spinal cord. Checking multiple AP views during needle insertion to assess the needle during needle placement is essential to prevent this complication. A skin wheal overlying this target point is raised, and a 22-gauge SMK needle with a 4-mm active tip is advanced through the skin wheal directly down the beam toward the target. Caution should be taken to make certain that the needle tip is not advanced into the muscle layers until it is pointed directly toward the intended target. In addition, if the skin wheal is placed more than 3 mm off target, a new starting point should be made, and the needle should be reinserted directly over the
A
B Fig. 178.25 Fluoroscopic images of a C2 dorsal root ganglion radiofrequency procedure. A, Anteroposterior view: C2 procedure. B, Lateral view: C2 procedure.
1360 Section V—Specific Treatment Modalities for Pain and Symptom Management report a tingling sensation in the back of the head at less than 0.2 V. No need exists for motor stimulation during a PRF procedure. Before lesioning, one should check the final needle position in two views. In the lateral view, the needle is seen in the anterior aspect of the dome created by the C1-2 lamina and in a midposition from cephalad to caudad. In an AP view, the needle is seen at or slightly below the atlantoaxial joint in the middle aspect of the articular pillar from lateral to medial. Lesioning in the pulsed mode is done by slowly turning up the voltage while monitoring the patient. It is not uncommon to note muscle contractions during the procedure. These contractions are normal and should not cause alarm.
Efficacy PRF lesioning of the nerves at this level of the cervical spine has not been well studied. Only one article specifically studied this issue. The study was a randomized controlled trial comparing the results of occipital nerve block with RF treatment of the upper cervical area in patients with occipital headache. Each group had 30 patients: 15 received RF treatments and 15 underwent occipital nerve blocks. The RF group first underwent RF of the C3-6 z-joints from a posterolateral approach by using 22-gauge SMK needles with a 4-mm active tip. If this procedure failed to relieve symptoms, diagnostic nerve blocks were performed at either the C2 or C3 levels followed by RF lesioning at the relevant level. The second group received an occipital nerve block. If the patient failed to obtain sufficient relief after 8 weeks, a second block was performed. Finally, if the patient remained symptomatic at 16 weeks, he or she was treated with transcutaneous electrical nerve stimulation. The results revealed no statistical difference of either treatment between the groups. The study can be criticized on multiple points. First, the RF procedure as performed would be unlikely to coagulate the TON and therefore relieve the most common cause of spinal headache. In addition, RF lesions performed at other levels (C3-6) are superfluous in the treatment of cervicogenic headache. Next, the investigators did not specify how the DRG procedure was performed. As reported in an earlier section of this chapter, PRF lesioning of the cervical DRG had an effect in relieving pain, whereas DRG performed with heat (in the lumbar spine) clearly did not.119 Two other small studies looked at outcomes from pulsed DRG treatment at the cervical levels. While not specifically studied, both reports included patients treated for headache with DRG lesioning at the C2 or C3 levels. The first study, reported earlier, included six patients treated at either the C2 or C3 DRG for headache. Out of six patients, three reported no effect, and three reported pain relief averaging 20 months (two patients had 18 months of relief, and one patient reported 24 months of relief). All three patients rated their pain relief at 7 on the Likert scale, a finding corresponding to greater than
75% improvement. A second study reported results of PRF lesioning at the C3-7 levels. At 1 year, 57% of patients reported satisfactory pain relief.47,120
Conclusion RF treatment has been used for various painful conditions including trigeminal neuralgia, facet-mediated pain, and radicular pain syndromes. As is often the case with novel treatments for challenging medical conditions, the early use of RF current for chronic pain was fraught with problems. At first, investigators recognized the value of the modality, but did not know how to best apply it. The advent of better equipment in 1980 (in particular the SMK needle and the Cosman RF generator) prompted anatomic and clinical studies that fostered rapid advances in knowledge. Flaws in previous studies were corrected with improvements in patient selection and technique. Thanks to pioneering studies by Bogduk, Lord, Govind, Dreyfuss, and others, proper anatomic targets for the cervical and lumbar medial branch procedures were identified and were used to devise the optimal means of destroying the nerves. This research helped to confirm the efficacy of both procedures. Through experimentation with the use of continuous RF, the PRF mode was developed, thus allowing the treatment of targets for which heat is contraindicated. Researchers in multiple disciplines have appreciated the importance of this modality. Increasing numbers of clinical studies, when considered collectively, suggest that PRF is effective. In addition, ongoing in vitro and animal studies will bolster the evidence in this area of study. As is often the case during the development of a treatment, no single theory has been able to explain the mechanism of action for PRF fully. However, clinical data support the notion that, when PRF is properly used to treat well-selected patients, it is an effective tool for some types of chronic pain syndromes (most notably radicular pain and peripheral neuropathies). These patients in particular are often refractory to medication and, in the absence of PRF, may require more expensive and invasive treatments (e.g., spinal cord stimulation). To date, most studies show only short-term efficacy (approximately 3 months). Further research is needed to determine the best methods of applying PRF for longerterm pain relief. This chapter summarizes best practices in the use of RF, describes new methods of RF application, and presents data on PRF to support its use in clinical practice.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
179
V
Cryoneurolysis Lloyd R. Saberski
C hapt e r O u t l i n e Historical Considerations 1355 Physics and Cellular Basics for Cryoanalgesia 1355 Indications and Contraindications 1357 Clinically Relevant Anatomy 1357 Clinical Pearls and Tricks of the Trade 1357
Chronic Pain Management 1359 Applied Cryoanalgesia for Chronic Pain 1360 Lower Extremity Pain 1365 Craniofacial Pain 1365
Future Directions 1368
Postoperative Pain Management 1357 Popular Cryodenervation Techniques for Postoperative Pain Management 1357
Cryoanalgesic therapy has widespread and diverse applications in the fields of pain management and neurosurgery. This chapter introduces the practitioner to the proper use and limitations of this relatively new technology so that appropriate clinical decisions can be made. Examples of applications are presented, but the intent is not to address all potential uses of cryoanalgesia.
Amoils9 developed a simpler hand-held unit that used carbon dioxide or nitrous oxide. These devices were the prototypes for the current generation of cryoprobes used in cryoanalgesia (Figs. 179.1 and 179.2). The coldest temperature used today is approximately −70°C.
Historical Considerations
Physics and Cellular Basics for Cryoanalgesia
Cryoanalgesia is a technique in which cold is applied to produce pain relief. The analgesic effect of cold has been known to humans for more than 2 millennia.1 Hippocrates (460–377 bc) provided the first written record of the use of ice and snow packs applied before surgery as a local pain-relieving technique.2 Early physicians, such as Avicenna of Persia (980– 1070 ad) and Severino of Naples (1580–1656) recorded using cold for preoperative analgesia.3,4 In 1812, Napoleon's surgeon general, Baron Dominique Jean Larrey,5 recognized that the limbs of soldiers frozen in the Prussian snow could be amputated relatively painlessly. In 1751, Arnott6 described using an ice-salt mixture to produce tumor regression and to obtain an anesthetic and hemostatic effect. Richardson introduced ether spray in 1766 to produce local analgesia by refrigeration; this was superseded in 1790 by ethyl chloride spray. Contemporary interest in cryoanalgesia was sparked in 1961, after Cooper described a cryotherapy unit in which liquid nitrogen was circulated through a hollow metal probe that was vacuum insulated except at the tip. With this equipment, it was possible to control the temperature of the tip by interrupting the flow of liquid nitrogen at temperatures within the range of room temperature to −196°C. Because the system was totally enclosed, cold could be applied to any part of the body accessible to the probe. The first clinical application of this technique was in neurosurgery for treatment of parkinsonism.7,8 In 1967, © 2011 Elsevier Inc. All rights reserved.
The working principle of a cryoprobe is that compressed gas (nitrous oxide or carbon dioxide) expands. The cryoprobe consists of an outer tube and a smaller inner tube that terminates in a fine nozzle (Fig. 179.3). High-pressure gas (650 to 800 psi) is passed between the two tubes and is released through a small orifice into a chamber at the tip of the probe. In the chamber, the gas expands, and the substantial reduction in pressure (80 to 100 psi) results in a rapid decrease in temperature and cooling of the probe tip. (Absorption of heat from surrounding tissues accompanies expansion of any gas, according to the principles of the general gas law; this is the adiabatic principle of gas cooling and heat extraction, also known as the JouleThomson effect.) The low-pressure gas flows back through the center of the inner tube and back to the console, where it is vented. The sealed construction of the cryoprobe ensures that no gas escapes from the probe tip, handle, or hose. The rapid cooling of the cryoprobe produces a tip surface temperature of approximately −70°C (–94°F). Tissue in contact with the tip cools rapidly and forms an ice ball. The ice ball varies in size, depending on probe size, freeze time, tissue permeability to water, and the presence of vascular structures (heat sink). The ice ball typically measures 3.5 to 5.5 mm in diameter. Further increase in size is prevented when thermal equilibrium is attained. 1355
1356 Section V—Specific Treatment Modalities for Pain and Symptom Management
Fig. 179.1 An early hand-held cryoprobe with ice ball. (From Holden HB: Practical cryosurgery, London, 1975, Pitman.)
Fig. 179.2 Contemporary hand-held Lloyd cryoprobes. (Courtesy of Westco Medical Corporation, San Diego.)
Precise levels of gas flow through the cryoprobe are essential for maximum efficiency. Inadequate gas flow does not freeze tissue. Excessive gas flow results in freezing down the stem of the probe and the associated risk of cold skin burns. The cryoprobe console is fitted with a regulator and an indicator that are adjusted for optimal performance. The application of cold to peripheral nerves, whether by direct cooling of localized segments or complete immersion of tissue in a cold medium, induces reversible conduction block. The extent and duration of the effect depend on the temper ature attained in the tissues and the duration of exposure.1 When nerve fibers are progressively cooled, a conduction block similar to that produced by local anesthetic develops. At 10°C, larger myelinated fibers cease conduction before unmyelinated fibers, but at 0°C (32°F), all nerve fibers entrapped in the ice ball stop conduction. Some fibers resume conduction on rewarming. To obtain a prolonged effect from a cryolesion, the intracellular contents of the nerve must be turned into ice crystals. The clinical difference is minimal as long as the temperature is less than −20°C (−4°F) for 1 minute.10 When the nerve is frozen amid other tissues, the duration of exposure becomes more important. Within the limitations of a specific cryoprobe and its steady state of thermal equilibrium, prolonging application of the cryoprobe increases the size of the ice ball and the likelihood that the nerve will become entrapped by a cryolesion. In practice, a freeze of 2 to 3 minutes' duration produces a good result.
Fig. 179.3 A and B, Cross sections of two commonly used cryoprobe designs. High-pressure gas goes in through the outer tube at 650 to 800 psi. Low-pressure gas is vented out at 80 to 100 psi. Gas flow is at 7 to 9 L/minute. Test conditions: The tip is inserted into water at 36°C (97°F) ± 1°C (34°F). An ice ball is formed within 60 seconds.
Prolonged exposure and repeated freeze-thaw cycles likely are beneficial with percutaneous techniques, especially when abundant surrounding soft tissue and nerve localization are poor.1 Histologically, the axons and myelin sheaths degenerate after cryolesioning (wallerian degeneration), but the epineurium and perineurium remain intact, thus allowing subsequent nerve regeneration. The duration of the block is a function of the rate of axonal regeneration after cryolesioning, which is reported to be 1 to 3 mm/day.10 Because axonal regrowth is constant, the return of sensory and motor activity is a function of the distance between the cryolesion and the end organ.1 The absence of external damage to the nerve and the minimal inflammatory reaction to freezing ensure that regeneration is exact. The regenerating axons are unlikely to form painful neuromas. (Surgical and thermal lesions interrupt perineurium and epineurium.) Other neurolytic techniques (alcohol, phenol) potentially can produce painful neuromas because the epineurium and perineurium are disrupted. A cryolesion provides a temporary anesthetic block. Clinically, a cryoblock lasts weeks to months. The result depends on numerous variables, including operator technique and clinical circumstances. The analgesia often lasts longer than the time required
for axons to regenerate.16 The reasons are still a matter of speculation, but it is obvious that cryoanalgesia is more than just a temporary disruption of axons. Possibly, sustained blockade of afferent input to the central nervous system (CNS) has an effect on CNS windup. One report suggested that cryolesions release sequestered tissue protein or facilitate changes in protein antigenic properties.11 The result is an autoimmune response targeted at cryolesioned tissue. The first report of such a response was from Gander et al,12 who showed tissuespecific autoantibodies after cryocoagulation of male rabbit accessory glands. This report was followed by a parallel clinical report of regression of metastatic deposits from prostatic adenocarcinoma after cryocoagulation of the primary tumor.13 The significance for pain management is unclear; however, it does indicate that tumor growth and regression are affected by immune function. Perhaps immune mechanisms play a role in the analgesic response after cryoablation.
Indications and Contraindications Cryoanalgesia is best suited for clinical situations when analgesia is required for weeks or months. Permanent blockade does not usually occur because the cryoinjured axons regenerate. The median duration of pain relief is 2 weeks to 5 months.14,15 Cryoanalgesia is suited for painful conditions that originate from small, well-localized lesions of peripheral nerves (e.g., neuromas, entrapment neuropathies, and postoperative pain).16 Longer than expected periods of analgesia have been reported and may result from the patient's ability to participate more fully in physical therapy or from an effect of prolonged analgesia on central processing of pain (preemptive analgesic effect). Sustained blockade of afferent impulses17–20 with cryoanalgesia may reduce plasticity (windup) in the CNS and may decrease pain permanently.21 Cryoablative procedures can be open or closed (percutaneous), depending on the clinical setting. Most often, open procedures are performed as part of postoperative analgesia. Under direct visualization, the operator identifies the neural structure of concern, and the cryoprobe is applied for 1 to 4 minutes, depending on tissue heat, which is a function of blood supply and distance of the probe from the nerve. Care is taken not to freeze adjacent vascular structures. The cryoprobe is withdrawn only after the tissue thaws because removing it earlier can tear tissue. Percutaneous (closed) cryoablation is the technique of choice for outpatient chronic pain management. It has the advantages of easy application and few complications. Percutaneous (closed) cryoablative procedures have been used successfully for many benign and malignant pain syndromes. Few scientific studies have been published, however, in part because interest was minimal until more recently in pain management techniques and because of a lack of industry funding for advanced research. Patients must give informed consent for the procedure. The consent form should describe the risk-to-benefit ratios of cryoanalgesia and of regional anesthesia. Patients should be fully aware that a cryoanalgesia procedure usually is not a permanent solution. It can ameliorate symptoms, however, and can allow the patient to participate in physical therapy more fully. In some cases, when CNS windup has occurred, cryoanalgesia may serve as a form of preemptive anesthetic and may facilitate prolonged relief. Cryoanalgesia for chronic pain syndromes always should be preceded by diagnostic or prognostic local
Chapter 179—Cryoneurolysis 1357 anesthetic injections. After a test block with local anesthetic, the examiner should inquire about the patient's tolerance to the numbness and the extent of pain reduction. If the patient's response to the test injections is inadequate, the patient will not have a good response to cryodenervation. Patients also should be aware that numbness can replace pain, and small areas of skin depigmentation can occur if the ice ball frosts skin because the probe is not deep enough or is inadequately insulated from tissues. All procedures are performed with appropriate sterile preparation. As a general rule, infected areas are avoided.
Clinically Relevant Anatomy For any given procedure, it is essential that the provider of cryoanalgesia be aware of the regional anatomy of interest. Because cryoanalgesia has widespread applications, thorough knowledge of neuroanatomy and of regional anesthesia is required. In the next section, detailed descriptions and illustrations are provided for numerous procedures. The reader is referred to standard anatomy textbooks for more detailed discussions.
Clinical Pearls and Tricks of the Trade Postoperative Pain Management The postoperative use of cryoanalgesia should be widespread, but in the United States, cryoanalgesia is used routinely for postoperative patients in only a few centers. The reasons are several, among them a lack of controlled studies and physicians' reluctance to add time and costs to procedures, especially when they believe that patients already are receiving adequate care. At many institutions, cryoanalgesia is reserved for patients with special analgesia needs and patients at high risk who cannot receive standard postoperative treatment. Of the handful of studies that have been done,22–26 most indicated significant reductions in pain and medication requirements. The use of postoperative cryoanalgesia will likely increase if investigators can show cost savings and improved long-term outcomes. Cryoanalgesia procedures are provided intra-operatively by surgeons who have access to involved peripheral nerve and pain management specialists participating in the operative procedure. At times, pain specialists are called on to provide cryoanalgesia postoperatively, in which case they must decide whether some other alternative is more suitable than open or closed cryodenervation.
Popular Cryodenervation Techniques for Postoperative Pain Management Post-thoracotomy pain Intra-operative intercostal cryoneurolysis was first described by Nelson et al27 in 1974. Since that time, a large body of literature has supported the use of cryodenervation as a component of a postoperative analgesia plan.22–24,28 Post-thoracotomy cryoanalgesia is most effective for treating incisional pain, but it is ineffective for pain from visceral pleura supplied by autonomic fibers or for ligament pain of the chest secondary to rib retraction. Post-thoracotomy cryoanalgesia often has little effect on chest tube pain, for the same reasons. Patients treated with cryotherapy during thoracotomy have relatively
1358 Section V—Specific Treatment Modalities for Pain and Symptom Management less postoperative discomfort and fewer opioid requirements in the immediate postoperative period and over subsequent weeks. Only one report of neuritis has been documented as a complication of cryoneurolysis.29 Sensory anesthesia lasts longer than 6 months along the sensory field of treated intercostal nerves. For effective intra-operative cryoneurolysis, intercostal nerves on each side of the thoracotomy incision are lesioned. If a rib is removed, that intercostal nerve also undergoes cryolesioning. The intercostal nerves are best cryoablated just lateral to the transverse process, before the collateral intercostal nerve branches (Fig. 179.4). Only a small area of skin innervated by the dorsal primary ramus is missed. Care is taken to separate the intercostal nerves from the intercostal vessels, thus removing a large heat sink that would be counterproductive to cryotherapy. The vessels also are protected from cold-induced thrombosis. A cryolesion sufficient to produce visible evidence of freezing is required. In general, such a lesion takes 1 to 2 minutes. A second lesion can be placed after tissue thaws, but whether that is necessary when freezing of the first lesion is complete remains to be determined. A retrospective study examined the medical records of patients who received percutaneous cryoanalgesia following successful intercostal nerve blockade for chronic chest pain. Sixty percent of the patients (N = 43) reported significant pain relief immediately following their procedure. Three months after cryoanalgesia, 50% continued to report significant pain relief. No cases of neuritis or neuroma formation were reported, and only three patients had a pneumothorax. This work provided evidence that cryoanalgesia is a safe and
Fig. 179.4 Cross-sectional view of intercostal nerve anatomy. (From Chung J: Thoracic pain. In Sinatra RS, Hord AH, Ginsberg G, et al, editors: Acute pain, St. Louis, 1991, Mosby.)
efficacious method of providing analgesia for chronic thoracic pain resulting from intercostal neuralgia.30 A comparison of epidural analgesia and intercostal nerve cryoanalgesia for post-thoracotomy pain as part of a randomized control study31 cast some doubt on the long-term utility of cryoanalgesia for post-thoracotomy pain. The study looked at 107 adult patients, allocated randomly to thoracic epidural bupivacaine and morphine or to intercostal nerve cryoanalgesia. Acute pain scores and opioid-related side effects were evaluated for 3 postoperative days. Chronic pain information, including incidence, severity, and allodynia-like pain, was acquired on the first, third, sixth, and twelfth months postoperatively. No significant difference was noted on a numerical rating scale (NRS) at rest or on motion between the two groups during the 3 postoperative days. The patient satisfaction results were also similar between the groups. The side effects, especially mild pruritus, were reported more often in the epidural group. Both groups showed a high incidence of chronic pain (42.1% to 72.1%), with no significance between the groups. The incidence of allodynia-like pain reported in the cryoanalgesia group was higher than that in epidural group in any postoperative month, with significance on the sixth and the twelfth months postoperatively (P < .05). More patients rated their chronic pain intensity as moderate and severe in the cryoanalgesia group and reported that the pain interfered with daily life (P < .05). Both thoracic epidural analgesia and intercostal nerve cryoanalgesia produced satisfactory analgesia for post-thoracotomy acute pain. The incidence of post-thoracotomy chronic pain is high. Cryoanalgesia may be a factor that increases the incidence of neuropathic pain.
Postherniorrhaphy pain Cryoneurolysis after herniorrhaphy was first described by Wood et al in 1979.32 A cryolesion of the ilioinguinal nerve reduced analgesic requirements during the postoperative period. The follow-up study in 1981 compared recovery from herniorrhaphy among three study groups: patients treated with oral analgesics, patients undergoing cryoanalgesia, and patients receiving paravertebral blockade (the last two treatments supplemented with oral analgesics as needed). The study indicated that the cryoanalgesia group not only had less pain in the postoperative period, but also used less opioid, resumed a regular diet earlier, were mobilized faster, and returned to work sooner.25 Despite these successes, the technique is not widely used. Given its effectiveness and freedom from side effects, it is ideal for ambulatory surgery. After repair of the internal ring, posterior wall of the inguinal canal, and internal oblique muscle, the ilioinguinal nerve on the surface of the muscle is identified and mobilized. The surgeon elevates the nerve above the muscle, and an assistant performs the cryoablation.
Chronic Pain Management For management of chronic pain, open cryoablation is avoided whenever the procedure can be performed effectively percutaneously. Before committing to cryoablation, the provider must perform a series of test blocks to determine presence of a consistent analgesic response. A favorable response before cryoablation occurs when the local anesthetic injection decreases pain, and the numbness that replaces the pain is tolerated by the patient. Care always must be taken to ensure correct positioning of the needles. When necessary, fluoroscopic guidance should be used. The smallest amount of local anesthetic required to achieve blockade must be used. A tuberculin syringe that injects 0.1 mm at a time ensures that the anesthetic does not contaminate other structures, which otherwise would make interpretation of the block difficult. This contributes to accurate localization of the primary pain generator. If the block is successful, an appropriate dermatomal representation of the analgesia is present. Subsequently, the patient is assessed for subjective changes in pain; however, this alone is insufficient to determine suitability for cryoablation. Many patients with chronic pain have suffered for a long time and are hopeful that the next procedure is going to be the longawaited successful treatment. These patients are responsive to suggestion and placebo effect. To identify such effects, the first test injection is done with lidocaine and the second with bupivacaine. In appropriate responders, a significantly longer duration of analgesia can be found with bupivacaine, assuming that all other variables remain the same. The effects of peripheral blockade on windup and chronic pain are not clearly understood. To responsive patients, a cryoablative procedure can be offered. For patients who do not have the desired response to bupivacaine or lidocaine, further testing is necessary, including differential blockade with local anesthetics and normal saline solution and consideration of consultation with a clinical psychologist. To perform percutaneous cryoablation successfully, the cryoprobe must be placed properly. This is a disadvantage compared with open cryoablative techniques used for postoperative pain management. The operator must ensure proper
Chapter 179—Cryoneurolysis 1359 cryoprobe placement by using a combination of techniques (see later) that improve the chances that the ice ball will be made precisely on the pain generator. In addition, special care must be taken when using the cryoprobe for percutaneous procedures. Bending the probe during percutaneous introduction can distort the lumen of the low-pressure outer tube, increase the resistance pressure to the expanding nitrous oxide gas, and convert a low-pressure exhaust system to one of higher pressure. That eventuality would impede gas expansion, inhibit ice ball formation, and limit cooling of the probe. To maintain the integrity of the cryoprobe, the probe should be placed through an introducer. The preferred introducers are large-bore intravenous catheters: 12-gauge, 14-gauge, or 16-gauge catheters, depending on the size of the cryoprobe. The operator always should check to see that the cryoprobe fits through the lumen of the catheter. The depth at which the probe emerges from the distal tip of the catheter should be marked on the proximal shaft of the cryoprobe to ensure that the cryoprobe tip extends far enough beyond the catheter to create a full-sized ice ball. Several techniques are used to enhance precise placement of the cryoprobe, as follows: 1. Careful palpation with a small blunt instrument, such as a felt-tipped pen, can help to localize a soft tissue neuroma or another palpable pain generator. 2. An image intensifier (fluoroscopy) can identify bony landmarks. 3. Contrast medium improves definition of tissue planes, capsules, and spaces. (Nonionic contrast medium should be used in areas close to neural tissue.) 4. The nerve stimulator at the tip of the cryoprobe is used to produce a muscle twitch in a mixed nerve. The stimulator is set at 5 Hz for recruitment of motor fibers. The probe is closest to the nerve when the lowest output produces a twitch response. In general, twitches should occur at 0.5 to 1.5 V. Small sensory branches contain no motor component and do not twitch with electrical stimulation. These fibers are localized by using higher-frequency (100-Hz) stimulation, which produces overlapping dysesthesia in the distribution of the small sensory nerve. This procedure may reproduce the patient's pain. Use of low-output (3 mo Spinal cord compression History of disabled back not from VCF Dementia Inability to walk before VCF
Primary end point
Roland Morris Disability Questionnaire disability and pain at 1 mo
Pain at 3 mo
SF-36 at 1 mo
BKP, balloon kyphoplasty; ER, emergency decompressive surgery; f/u, follow-up; fx, fracture; NSM, nonsurgical management; OVCF, osteoporotic vertebral compression fracture; QOL, quality of life; VB, vertebral; VCF, vertebral compression fracture; VP, vertebroplasty.
Vertebroplasty Buchbinder et al64 studied 78 patients, with 91% of participants followed up at 6 months. Study enrollment commenced in 2004 and concluded in 2008, with goal follow-up of 2 years. These investigators selected patients who had 12 months or less of back pain and who had the presence of 1 or 2 VCFs of grade 1 or higher with edema or a fracture line noted on MRI. For this study, 468 patients were screened; 248 did not meet inclusion criteria, and 141 (plus 1 death) were not willing to participate. Of the 78 patients who met inclusion criteria, 38 underwent vertebroplasty, whereas 40 underwent a sham procedure. The sham procedure involved the placement of a 13-gauge needle to the lamina, replacement of the sharp stylet with a blunt stylet, and gentle tapping to simulate vertebroplasty. These investigators also mixed the PMMA so that the smell permeated the room. All participants underwent basic testing as well as “up and go testing,” which involved measuring the time required to rise from a standard arm chair, walk 3 m, turn around, return to the chair, and sit down again. Also separated were the acuity of the fractures (6 weeks). The primary outcome was the overall pain score measured on a scale of 0 to 10, whereas secondary outcomes included quality-of-life measures, pain at rest and pain in bed at night, and Roland Morris Disability Questionnaire measures. Measurements were taken at 1 week, 1 month, 3 months, and 6 months. Mean pain reduction in the vertebroplasty and placebo groups was 2.6 ± 2.9 and 1.9 ± 3.3, respectively. The investigators concluded that at 6 months, vertebroplasty had no beneficial effect over a sham procedure at any time point. The investigators admitted to a selection bias based on the finding that only 78 patients were enrolled, whereas 141 declined to participate. Critics65 of the study cited multiple other flaws with the study, such as the following: Patients did not require edema, only a fracture line on MRI, even though the investigators stated that bone marrow edema indicated an acute fracture. n The definition of “acute” in this study included fractures up to 1 year old, whereas most clinicians would define an acute fracture as one that occurred within the previous 4 to 6 weeks. n The sham procedure was performed with local anesthetic at the facet joint. n The primary outcome of pain as overall pain may not have been reflective of back pain because it was a report of overall body pain. n The investigators did not report whether back pain was from fracture, by percussing the spinous process systematically to find a level of maximal tenderness. n The investigators did not report pain severity and functional compromise of the patients who met criteria but who refused to enroll in the study. n
Kallmes et al66 studied 131 patients with 1 to 3 VCFs that were either fractures less than 1 year old and defined by the onset of pain and a pain score of at least 3 (0 to 10) or were fractures of uncertain age that were examined by MRI or bone scan to assess for edema. Only the patients with fractures of uncertain age underwent imaging, and those with fractures with edema were eligible for inclusion. Of the 1813 patients who were screened, 300 patients who fit criteria declined to participate. Of the 131 patients enrolled, 68 underwent
Chapter 180—Vertebroplasty and Kyphoplasty 1379 v ertebroplasty, and 63 underwent a sham procedure. The sham procedure involved placement of local anesthetic at the skin and subcutaneous tissues and infiltration of the periosteum of the pedicles with 0.25% bupivacaine. Then, instead of placement of 11- or 13-gauge trocars, verbal and physical cues of pressure were given on the patient's back, and the methylmethacrylate monomer was opened. Primary outcomes measured included modified Roland Morris Disability Questionnaire and pain scores at various times over 1 year, with the goal to evaluate the outcome at 1 month as the primary outcome. Secondary outcomes included scores on health status questionnaires, the physical and mental component summary of Short Form-36 (SF-36) version 2, and opioid use. At 1 month, the mean pain scores of the vertebroplasty and control group were 3.9 ± 2.9 and 4.6 ± 3.0, respectively. The mean Roland Morris Disability Questionnaire score was essentially the same for both groups. Forty-three percent of patients who underwent the control procedure crossed over to the vertebroplasty group, whereas only 12% did the reverse (vertebroplasty to control). No significant difference was noted in any of the secondary outcome measures, but the trend was toward more meaningful improvement in pain in the vertebroplasty group than in the control group (64% versus 48%). The investigators concluded that no significant difference existed at 1 month between the two groups, and they cited the following limitations of their study: Cross-over at 1 month complicated the interpretation of data. n The study did not compare the study groups with respect to medical treatments received that could have affected outcomes. n Persistence of pain after vertebroplasty or fracture healing may have indicated causes of pain other than the fracture. n Vertebroplasty may be beneficial only for fractures of a certain age or healing stage, and this possibility was not taken into account. n Kyphoplasty was not evaluated. n
Critics65 of the study cited the following weaknesses: Selection bias occurred. Patient selection criteria were poor because they did not require edema on MRI or bone scan for all patients. n Pain severity and functional compromise of the patients who met criteria but who refused to enroll were not reported. n The sham procedure was a facet block instead of a dry needle approach. n The investigators did not report whether back pain was from fracture, by percussing the spinous process systematically to find a level of maximal tenderness. n n
The results of these studies were quite shocking to the “spine” community. Practitioners who have performed vertebral augmentation over the years have clinically seen profound relief of pain in those patients who had acute VCFs, and numerous large case series, prospective and retrospective, have demonstrated dramatic pain relief. What the studies most clearly demonstrate are the need for improvement in patient selection criteria for vertebral augmentation and the difficulties in performing randomized, double-blinded, placebocontrolled studies in patients in severe pain. Important physical
1380 Section V—Specific Treatment Modalities for Pain and Symptom Management examination and imaging findings need to be included, along with a comparison of the outcomes of those patients who fit criteria for inclusion but who choose not to enroll in the study. This issue may be assessed further by the investigators of the foregoing studies by retrospective review of the patients who chose not to enroll in those studies but who met inclusion criteria. Future studies should take this factor into account rather than jump to the conclusion that vertebral augmentation is no better than placebo.
Kyphoplasty Wardlaw et al67 studied 300 patients with VCFs by randomly assigning these patients to receive kyphoplasty or nonsurgical care (this study is also known as the FREE [Fracture REduction Evaluation] trial). These investigators used the following inclusion criteria: One to three VCFs from T5 to L5 At least one fracture with edema shown by MRI n At least one fracture associated with greater than 15% height loss n The requirement that single fractures had to meet both criteria n n
The primary outcome was the change in SF-36 score from baseline to 1 month. This score showed a decrease in 7.2 points in the kyphoplasty group as opposed to 5.2 points in the nonsurgical group. These investigators also noted no difference in frequency of adverse reactions between the groups and concluded that kyphoplasty is a safe and effective procedure for patients with acute VCFs. This is the only prospective, randomized, double-blind study of kyphoplasty. The only drawback is that it has no placebo control.
Other Studies for Osteoporotic Fractures Taylor et al54 performed a systematic review and metaregression to compare the efficacy and safety of kyphoplasty and vertebroplasty for the treatment of VCFs and to examine the prognostic factors that predict outcome. These investigators reviewed studies that compared kyphoplasty with conventional medical therapy, vertebroplasty with conventional medical therapy, and vertebroplasty with kyphoplasty. Based on a total of 74 studies, none of which were randomized, these investigators concluded that level III evidence supports vertebral augmentation for osteoporotic fractures refractory to conventional medical therapy. The ratio of benefit over harm was favorable for both procedures, and kyphoplasty had a better adverse event profile. These investigators later followed up with a study demonstrating that patients undergoing kyphoplasty experienced superior improvements in pain, functionality, vertebral height, and kyphotic angle at least up to 3 years after the procedure. These investigators also concluded that prospective studies of low bias, with follow-up of 12 months or more, demonstrate that kyphoplasty is more effective than conventional medical management of osteoporotic VCFs and is at least as effective as vertebroplasty. Eck et al55 performed a meta-analysis to assess both pain relief and risk of complications associated with vertebroplasty versus kyphoplasty. These investigators included 168 studies that met inclusion criteria. They concluded that vertebroplasty caused a significantly greater improvement in Visual Analog Scale (VAS) scores compared with kyphoplasty
(mean VAS decrease, 5.68 versus 4.60, respectively), but it also had a statistically greater risk of cement leakage and new fracture. Masala et al68 evaluated the efficacy and cost effectiveness of vertebroplasty by comparing 58 patients who accepted and underwent vertebroplasty versus 95 who refused the procedure and underwent conservative medical therapy. These investigators found that significant reduction in VAS and improvement in ambulation and activities of daily living were observed in both groups at 1 week, 3 months, and 12 months. The results were significantly superior in the vertebroplasty group at 1 week and 3 months, and vertebroplasty was more cost effective than conventional medical management with regard to VAS and activities of daily living at 1 week. By 3 months, vertebroplasty was more cost effective with regard to ambulation. However, no significant cost difference was noted at 12 months between the 2 groups. Kyphoplasty has been touted to restore vertebral body height and sagittal alignment. Only a few retrospective reviews discuss this benefit. Hiwatashi et al69 noted no significant difference between vertebroplasty and kyphoplasty in restoring vertebral body height and wedge angles. Kim et al70 concluded that balloon kyphoplasty after postural reduction and intraoperative kyphotic angle correction is well tolerated and effective for treating severe osteoporotic VCFs.
Vertebral Augmentation in Multiple Myeloma and Metastases Studies in patients with multiple myeloma and spinal metastases have also been completed. Fourney et al71 retrospectively reviewed 56 patients who underwent vertebroplasty or kyphoplasty (total of 97 procedures) for either myeloma or metastases. These investigators reported complete pain relief in 84% and no change in 9% of patients who underwent the procedures. No patient was worse, and asymptomatic cement extravasations occurred in 9.2%. Significant improvement in pain scores was noted at 1 year, and analgesic consumption was reduced after 1 month. The CAFÉ (Cancer Patient Fracture Evaluation) study72 randomly assigned 134 patients with various types of cancers and up to 3 painful VCFs to receive immediate kyphoplasty (n = 70) or nonsurgical supportive care (n = 64). These investigators excluded patients with primary bone tumors, osteoblastic tumors, or solitary plasmacytoma at the fracture site. The primary outcome measure was the Roland Morris Disability Questionnaire at 1 month, results of which were found to be significantly improved in the kyphoplasty group (−8.3) versus the nonsurgical care group (−0.1). Secondary measures included VAS scores, which were also improved (−4.1 versus −0.5). No significant difference was noted in serious adverse reactions between the groups. The investigators concluded that the improvements in disability and pain with kyphoplasty were both statistically and clinically significant without an increase in adverse reactions. Pflugmacher et al73 found that the mean VAS and Oswestry Disability Index significantly improved in patients with lumbar or thoracic VCFs secondary to metastases who underwent balloon kyphoplasty. Sixty-five patients were prospectively followed over 24 months, and sustained improvement in both scores was reported. These investigators also noted a 12% rate of cement leakage and an 8% incidence of vertebral fracture. No symptomatic cement leaks occurred.
Other retrospective reviews74,75 have demonstrated positive results with vertebroplasty in patients with spinal metastases and multiple myeloma, with marked pain reduction and decreased analgesic consumption, along with minimal complications.
Conclusion Osteoporosis and VCFs are significant public health concerns with high morbidity. Management of VCFs should start with prevention. In the presence of a painful VCF, all measures should be taken to keep the patient weight bearing and functional. This should start with medical management including opioids, NSAIDs, back bracing, and physical therapy. If at any time the patient cannot perform weight-bearing exercises despite appropriate medical management, interventions should be considered. A comprehensive history and physical examination, particularly neurologic and musculoskeletal examinations along with proper review of imaging studies, will help to target interventions. If the pain is determined
Chapter 180—Vertebroplasty and Kyphoplasty 1381 to be related to the VCF, an experienced practitioner should determine which procedure should be done to augment the fracture. Both vertebroplasty and kyphoplasty have excellent safety profiles when these procedures are performed appropriately. Kyphoplasty is approved only when performed in the operating room and is more expensive than vertebroplasty, which can be completed in an office based facility (with fluoroscopy). Randomized trials demonstrated that kyphoplasty is efficacious for the treatment of painful VCFs related to osteoporosis, whereas the results of vertebroplasty, although controversial, are no better than placebo. Either procedure can be performed for VCFs related to cancer. Patient selection and proper technique are the most important factors in determining whether interventional procedures will relieve pain and thus improve quality of life.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
181
Intradiskal Electrothermal Annuloplasty Michael L. Whitworth
CHAPTER OUTLINE Historical Considerations 1388 Indications 1389 Anatomy and Pathology 1389 Technique 1389
Historical Considerations Since the mid-1990s, intradiskal radiofrequency heating has been considered for the treatment for diskogenic pain. Cadaver studies demonstrated that placement of a bipolar probe did not result in end-plate or vertebral body damage and was associated with a temperature change at the edges of the disk of 3°C (37°F) to 4°C (39°F).1 Later experiments evaluated the thermal diffusion capacity of the intervertebral disks. Investigators discovered an age-related differential in thermal dissipation: the disk of a 32-year-old person has 250% the thermal diffusion capability of the disk of a 61-year-old person.2 Ostensibly, this phenomenon is the result of the relatively greater aqueous content of the younger disk. Interest in diskogenic disease—and its causes—heightened after the seminal 1997 article demonstrating the presence of neural ingrowth into the inner anulus and nucleus 0% of the time in diskogram-negative disks but 57% of the time in diskogram-positive disks.3 Additional sources of potential nociception transmission were also found in the vertebral end plate in patients with severe disk degeneration. The end plate in such cases was associated with increased sensory nerve innervation and neoangiogenesis adjacent to the end plates.4 Tony Yeung, a pioneer in endoscopic spine surgery, attempted to use a prototype intradiskal radiofrequency probe during endoscopic spine surgery but found that the temperatures produced in tissues were erratic. He later developed endoscopic laser annuloplasty. Interest in the radiofrequency intradiskal approach continued with subsequent clinical studies, but with disappointing results. A prospective randomized human trial using a 90-second intradiskal radiofrequency lesion at 70°C (158°F) did not produce any differences from controls.5 A later study comparing two heating protocols of 120 and 360 seconds at 80°C (176°F) failed to produce long-term positive results. At 6 months after the procedure, Visual Analog Scale (VAS) scores had returned to baseline, although the short-term response to the procedure was statistically significant.6 1388
Complications 1390 Outcome Studies 1391 Conclusion 1392
The Saals selected a thermoresistive heating element as a means of producing sufficient heat to cause interruption in intradiskal neural transmission—if not overt intradiskal neural destruction. Although their energy source remained a radio frequency generator, the energy was not directly imparted to the nucleus pulposus or the anulus fibrosus because the “spine wand” was insulated. Instead, unlike intradiskal radiofrequency application of energy, the radiofrequency current was used to heat a resistive coil inside the insulated intradiskal portion of the device that secondarily heated the surrounding tissues with thermal energy. An initial report on the procedure, termed intradiskal electrothermal (IDET) annuloplasty, was published in 1999.7 In early 2000, a preliminary report on a 20-patient study was published with the results that 72% of patients received 50% relief.8 A 1-year outcome study using the IDET device was published in October of 2000. The study had 62 participants with chronic low back pain and diskogram-positive findings; some improvement was found at 1 year in 71% of the patients.9 Unfortunately, this trial was not controlled, and although the investigators cautioned that the results should be verified by placebo-controlled randomized trials, these follow-up studies were not forthcoming for several years. A company was formed very early to market the device aggressively to physicians through training courses for them. As a result, the device had tens of thousands of uses before the first validated clinical trials were released. During a training conference in 1999, the company manufacturing the device at that time reported that reimbursement for the procedure was in the range of $3500 to $7000 and that the company had a reimbursement department for physician use. Eventually, insurers became increasingly reluctant to pay for an expensive procedure with so little clinical data and with marginal results. Insurers subsequently began to block payment for the procedure in their medical policies. At the time of this writing, in the United States, very few major insurers will cover the IDET procedure because it is considered “investigational.” © 2011 Elsevier Inc. All rights reserved.
Chapter 181—Intradiskal Electrothermal Annuloplasty 1389
Other alternatives to IDET, such as endoscopic annuloplasty, the discTRODE intra-annular radiofrequency procedure, and bipolar annuloplasty, began to appear around the turn of the millennium. However, few studies have been conducted on these procedures, and these studies have only marginal results.
Indications The indications for and contraindications to annuloplasty are summarized in Table 181.1. The International Spine Intervention Society publishes Practice Guidelines: Spinal Diagnostic and Treatment Procedures, which represents the only validated operating guidelines for this and many other spinal procedures. These guidelines detail IDET theory, practice, and controversy. Table 181.2 compares IDET with other forms of intradiskal therapy in common use.
Table 181.1 Indications for and Contraindications to Annuloplasty No evidence of emergency spinal intervention indicators No medical contraindications Absence of radiculopathy and myelopathy Negative Lasègue sign MRI with no other disorders correlating to the pain production No evidence for spinal instability or spondylolisthesis at the level of interest No significant untreated or uncontrolled psychiatric issues Motivated patient with realistic outcome expectations No greater than 25% loss of disk height Criteria for intradiskal disease satisfied: Disk stimulation is positive at low pressures (6/10) Disk stimulation reproduces concordant pain CT diskography reveals a grade 3 or greater annular tear Control disk stimulation is negative in at least one adjacent disk CT, computed tomography; MRI, magnetic resonance imaging.
Anatomy and Pathology Painful annular radial fissures, as seen during diskography, are evidence of internal disk disruption, which is the sole indication for IDET.10 It is known that these fissures are associated with vascular and neural ingrowth from the outer anulus, that leakage of diskal enzymes that are toxic to extradiskal materials may occur, and that mechanical changes in the disk occur with disk degeneration. The mechanism by which IDET actually works is not known but is thought to be by sealing off the fissures with thermal energy, destroying nociceptor nerve ingrowth, and stabilizing the collagen and biomechanics of the disk. Some studies of these mechanisms have been conducted in cadavers,11–13 but clearly this model has little to do with the dynamic human intervertebral disk and the processes of tissue healing. The annular fissures are both radial and circumferential, and they split the laminar layers of the anulus. Provocative manometric diskography with a negative control disk and postdiskography computed tomography (CT) or magnetic resonance imaging (MRI) are the absolute minimum requirements for proper selection of patients for IDET. Fluoroscopic diskography may demonstrate annular fissures, but the threedimensional location of the radial tears cannot be determined accurately with fluoroscopy. Both circumferential and radial annular tears may be visualized on postdiskography CT scans. The fissures are thought to begin peripherally and gradually expand as the degree of internal disk disruption expands to involve increasing amounts of the nucleus pulposus by cavitation.
Technique In the United States, the acquisition cost of the SpineCath (Smith & Nephew, Inc., Andover, MA) is more than $1200, so it is prudent to select patients carefully. At times, it is impossible to advance the SpineCath into the area containing the annular tear as demonstrated on CT diskography. At other times, the SpineCath folds over on itself and becomes it utterly useless from that point on in the procedure. In such cases, a new SpineCath is required, thereby making the IDET an extremely expensive procedure to the entity purchasing
Table 181.2 Advantages and Disadvantages of Intradiskal Thermal Delivery Systems Delivery System
Advantages
Disadvantages
Good access to disease Excellent decompression effect for radiculopathy
High expense Poor temperature control
Easy intradiskal placement Cost effectiveness Safety Minimal invasiveness
Poor heating of low-water-content diskal tissues Poor decompressive effect Small treatment area Inability to reach posterior disk easily
Easy intradiskal placement Broad target zone Cost effectiveness Safety Minimal invasiveness
Poor decompressive effect Inability to reach collapsed disks Poor results for radicular pain
Laser Fiberoptic
Energy source: laser Delivery method: straight or side-firing fiberoptic catheter Radiofrequency Electrode
Energy source: radiofrequency Delivery method: straight electrode
Intradiskal Electrothermal Catheter
Energy source: electroresistive coil Delivery method: navigable catheter
1390 Section V—Specific Treatment Modalities for Pain and Symptom Management
Fig. 181.3 Technique for threading the SpineCath catheter.
Fig. 181.1 Radiograph showing positioning of the intradiskal electrothermal needle.
Fig. 181.2 The target for the needle tip is halfway between the end plates and just medial to the medial pedicular line, at the inner aspect of the anulus fibrosus.
the device. A posterolateral approach is used that targets the superior articular process with a 17-gauge IDET needle with a relatively smooth beveled edge, to avoid shearing the catheter (Fig. 181.1). The trajectory of the needle is usually between 25 and 40 degrees to the sagittal plane, with an entry point on the contralateral side from the CT-demonstrated radial tears. The target for the needle tip is halfway between the end plates and just medial to the medial pedicular line, at the inner aspect of the anulus fibrosus (Fig. 181.2). Once the needle is placed into the inner annular fibers and outer nucleus pulposus, the SpineCath is slowly inserted and, as much as possible, is “guided” into place by the flexible bent tip (Fig. 181.3). However, the catheter frequently lodges in irregularities in the inner anulus or travels in a circumferential annular tear or even creates its own separation of the
lamina of the anulus fibrosus (Fig. 181.4). In any case, the final resting place of the SpineCath tip is across the posterior anulus, to cover the CT-demonstrated location of the radial tear (Fig. 181.5). Frequent manipulations of the catheter may be necessary, and in some cases where excessive force would bend the catheter, a contralateral or bilateral approach is necessary with dual heatings (Fig. 181.6). The SpineCath has two markings—one at the tip and one more proximally—that denote the location of the thermoresistive coil, which is the active heating element. The patient must be awake enough to render feedback regarding potential nerve root heating, although this is uncommon. A manufacturer heating protocol is usually incorporated in which the temperature is gradually ramped up to 90°C (194°F) for 16.5 minutes. The safest method of catheter removal is en bloc, with the needle and catheter removed as a unit. If antibiotic is to be administered into the disk, this should be done before the catheter is introduced into the needle or, if the catheter can easily be removed through the needle, after the heating. Controversy continues regarding the location of the catheter with respect to any circumferential fissures. Some investigators believe that the SpineCath should be placed deep into the anulus fibrosus within the circumferential tear, whereas others use the more traditional approach of the anulus-nucleus junction. Manipulation of the catheter may, at times, be very time consuming, requiring up to an hour. However, experienced physicians are usually able to place the catheter and needle carefully within several minutes.
Complications Shortly after the first published reports of IDET, several serious complications were described in the literature. The first noted complication was cauda equina syndrome.14 Postprocedure pain flare-ups are relatively common, and they seem to be temperature dependent.15 Intradural migration from a broken SpineCath that ultimately required surgery for the resultant radiculopathy has been reported.16 Osteonecrosis of the vertebral body after IDET has also been reported in the literature.17,18 During subsequent endoscopic disk surgery, Whitworth observed charring of diskal tissues from IDET. The complications of the procedure are divided into access issues and heating issues. Clinicians not versed in diskography may not understand the anatomic barriers to the disk, such as the furcal nerves, the iliac crest's overriding the disk space in
Chapter 181—Intradiskal Electrothermal Annuloplasty 1391 A
B
C
D
E
F
Fissure
Fig. 181.4 Problems with catheter advancement. A, Desired catheter position. B, Needle is advanced too far, causing acute deflection. C, Deflection angle is too acute, and the catheter does not follow the anulus. D, Needle is intra-annular, and the catheter cannot be advanced. E, Catheter tip enters the annular tear, and the catheter cannot be advanced. F, Intracanal catheter placement.
Fig. 181.6 Advancing the coil against significant resistance causes the catheter to bend within the intervertebral disk. (From Kapural L, Goyle A: Fig. 181.5 Anteroposterior view of the intradiskal electrothermal resistive coil final position. The coil is within the L4-5 intervertebral disk and clearly away from the end plates. (From Kapural L, Goyle A: Imaging for interventional management of chronic pain: imaging for provocative discography and minimally invasive percutaneous procedures for treatment of discogenic lower back pain, Tech Reg Anesth Pain Manag 11:73, 2007.)
the oblique fluoroscopic rotation, the safe access zone shape and size, the potential for end-plate damage, and the risk of diskitis (septic and aseptic). The IDET catheter may travel outside the posterior anulus fibrosus into the epidural space or even into the dura or nerve roots (Fig. 181.7). Heating may cause radicular-type pain that cannot be readily explained in the absence of proximity to nerve roots.
Imaging for interventional management of chronic pain: imaging for provocative discography and minimally invasive percutaneous procedures for treatment of discogenic lower back pain, Tech Reg Anesth Pain Manag 11:73, 2007.)
Outcome Studies Many of the IDET studies grouped their results effectively into nonresponders and responders. Patients who did respond were then given an average VAS reduction citation. The adoption of this methodology appears to connect failure to respond with poor patient selection, inadequate technical placement of the SpineCath, or disease that was so severe that IDET with its 2-mm thermal excursion could not help. Such methodology also calls into question the validity of the technique as an effective treatment. Bogduk19 published an excellent review
1392 Section V—Specific Treatment Modalities for Pain and Symptom Management placed IDET in a more positive light and suggested that IDET may be a reasonable “first option” in patients who have failed to respond to conservative therapy.21
Conclusion
Fig. 181.7 This fluoroscopic image shows the intradiskal electrothermal catheter tip passing posteriorly through the annular fissure. Such inappropriate placement of the catheter may result in heat dissipation to the epidural space and neural elements. It is necessary to reposition the catheter and recheck it in the lateral and anteroposterior views. (From Kapural L, Goyle A: Imaging for interventional management of chronic pain: imaging for provocative discography and minimally invasive percutaneous procedures for treatment of discogenic lower back pain, Tech Reg Anesth Pain Manag 11:73, 2007.)
of the IDET literature and methodology. The first placebocontrolled trial demonstrated a powerful placebo effect on pain relief that suggested caution in the adaptation of IDET.20 However, the entire effect of pain relief could not be entirely explained by placebo; therefore, IDET was believed to have a positive but modest effect. Other studies generally revealed a modest reduction in pain in the 50% responders (usually 3 points on a 10-point VAS scale), with no relief in the other 50%. A more recent evidence-based review of the literature
Because of the lack of financial reimbursement, electrothermal annuloplasty is only occasionally practiced in the United States today. The elevation of physician and corporate avarice to a level that superseded scientific demonstration of the effectiveness of the technique has cast a pall on future use of this technique. One hopes that interventional pain practitioners will learn from this tragic episode and will become more acutely aware of their role as stewards of monetary resources available for the treatment of pain and as gatekeepers against wholesale acceptance of experimental techniques. The technique actually did work in the treatment of some patients, and practitioners should build on that knowledge to advance the potential modifications necessary to enhance effectiveness. Perhaps improvements on the IDET model could be made in the future, such as bipolar radiofrequency electrode energy applied across the posterior anulus, a more expansive heating device, or consideration of neuromodulation of the posterior anulus. Outcome studies for both discTRODE (a flexible radiofrequency catheter that splits the lamellae of the anulus circumferentially)22,23 and intradiskal endoscopic laser annuloplasty have shown modest improvements in pain.24 The future of the development of techniques to treat annular fissures will be partially predicated on fiscal responsibility to the medical system by demonstrating effectiveness before massive release and promotion of a product. As the understanding of the pathologic process of internal disk disruption increases, practitioners may be able to develop enhanced therapies that may include intradiskal injections along with structural support methods.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
182
V
Percutaneous Diskectomy: Automated Technique Steven D. Waldman
CHAPTER OUTLINE Indications 1393 Clinically Relevant Anatomy 1393 Technique 1393
Indications Percutaneous diskectomy using the automated technique is indicated for a specialized subset of patients who are suffering from low back and radicular pain thought to be caused by contained disk protrusion1 (Fig. 182.1). In this group of patients, conservative therapy consisting of a trial of simple analgesics, nonsteroidal anti-inflammatory agents or cyclooxygenase-2 inhibitors, bed rest, and epidural steroids should have failed. Some pain management specialists also recommend that a trial of transforaminal epidural steroid nerve blocks should also be attempted before percutaneous diskectomy.2 To optimize patient selection, the ideal candidate for nucleoplasty should have magnetic resonance imaging (MRI) findings, evidence on diskography, and electromyographic changes that correlate with the patient's radicular pain pattern.
Clinically Relevant Anatomy From a functional anatomic viewpoint, lumbar disks must be thought of as distinct from cervical disks insofar as a source of pain is concerned. Radicular symptoms originating solely from disk herniation are much more common in the lumbar region when compared with the cervical and thoracic regions.3,4 The reason for this finding is twofold: (1) for the lumbar disk to impinge on the lumbar nerve roots, it must herniate posteriorly and laterally; the lumbar nerve roots are not protected from impingement from lumbar disk herniation by the bony wall of the facet joints, as are the cervical nerve roots; and (2) the posterior longitudinal ligament in the lumbar region is only a single layer, which is thinner and less well developed in its lateral aspects; lumbar disk herniation with impingement on exiting nerve roots is most likely to occur in this lateral region. The nuclear material in the lumbar disk is placed more posteriorly than in its cervical counterpart. The gelatinous © 2011 Elsevier Inc. All rights reserved.
Side Effects and Complications 1395 Conclusion 1396
nucleus pulposus of the lumbar disk is surrounded by a dense, laminated fibroelastic network of fibers known as the anulus fibrosus.4 The annular fibers are arranged in concentric layers that run obliquely from adjacent vertebrae. This annular layer receives sensory innervation from various sources. Posteriorly, the anulus receives fibers from the sinovertebral nerves, which also provide sensory innervation to the posterior elements, including portions of the facet joints.4 Laterally, fibers from the exiting spinal nerve roots provide sensory innervation, with the anterior portion of the disk receiving fibers from the sympathetic chain. Whether some of or all these fibers play a role in diskogenic pain is a subject of controversy among pain specialists. The lumbar nerve roots leave the spinal cord and travel laterally through the intervertebral foramina. If the posterior lumbar disk herniates laterally, it can impinge on the lumbar root as it travels through the intervertebral foramen and can thus produce classic radicular symptoms. If the lumbar disk herniates posteromedially, it may impinge on the spinal cord itself and produce myelopathy that may include lower extremity as well as bowel and bladder symptoms. Severe compression of the lumbar spinal cord may result in cauda equina syndrome, paraparesis, or, rarely, paraplegia.
Technique The patient is placed in the lateral or prone position with a pillow under the abdomen to flex the lumbar spine slightly as if for a lumbar sympathetic block. Computed tomography (CT) scans or fluoroscopic views are taken through the disks to be imaged, and the relative positions of the lung, ribs, aorta, vena cava, kidneys, nerve roots, and spinal cord are noted1 (Fig. 182.2). The spinous process of the vertebra just above the disk to be evaluated is palpated. At a point just below and 11⁄2 inches lateral to the spinous process, the skin is prepared with antiseptic solution, and the skin and subcutaneous tissues are 1393
1394 Section V—Specific Treatment Modalities for Pain and Symptom Management infiltrated with local anesthetic.1 A small stab wound as made at the point of needle entry to facilitate the placement of the introducer cannula. The stylet is placed into the introducer cannula, and the cannula is then advanced through the skin under fluoroscopic or CT guidance, with the target being the middle of the disk to be decompressed (Figs. 182.3 to 182.5). If fluoroscopic guidance is used, oblique images may be helpful.1 Given the proximity of the somatic nerve roots, paresthesia in the distribution of the corresponding lumbar paravertebral nerve may be elicited. If this occurs, the needle should be withdrawn and redirected slightly more cephalad. The needle is again readvanced in incremental steps under CT or fluoroscopic guidance. Sequential imaging is always indicated to avoid advancing the needle completely through the disk and into the lower limits of the spinal cord or cauda equina.1 The pain management
specialist must also take care not to allow the needle to track too laterally into the lower pleural or retroperitoneal space. When the cannula is in a satisfactory position in the center of the disk, the stylet is removed, and a small amount of contrast material is injected into the disk to confirm mid-disk needle placement and to identify any significant disruption of the anulus1 (Fig. 182.6). The automated disk decompressor probe is then advanced through the cannula into the center of the disk nucleus until the probe extends beyond the end of the cannula (Fig. 182.7). The activation switch of the device is then turned to the “on” position for 15-second increments, with the total combined time that the device is activated not to exceed 5 minutes. Under CT or fluoroscopic guidance, the device may be gently advanced toward the anterior anulus of the disk being treated, with care taken to avoid impinging on the anulus itself. Disk material will begin to appear in the clear collection chamber after approximately 1 mL of disk has been removed. After an adequate amount of disk material has been removed, the automated disk decompressor probe is removed from the cannula. A slight rotation of the probe may aid in the
L5-S1
Fig. 182.1 Lumbar spine computed tomography axial image at the L5-S1 level. Note: (1) the median disk protrusion (black arrow) abutting the left, and particularly the right, nerve roots (small white arrows) and indenting the dural tube anteriorly. R, right side of the patient. (From Giles LGF: CT versus MRI for lumbar spine intervertebral disc protrusion, 100 challenging spinal pain syndrome cases, ed 2, New York, 2009, Churchill Livingstone.)
Fig. 182.3 Lateral view of the cannula within the disk. (From Waldman SD: Atlas of interventional pain management, ed 3, Philadelphia, 2009, Saunders Elsevier.) Left hepatic v. Esophagus
Rectus abdominis m. Heart Costal cartilage
Middle hepatic v.
Aorta
Inf. vena cava Stomach
Rib
Spleen
Right hepatic v.
Serratus ant. m.
Right lung
Latissimus dorsi m.
Illiocostalis m.
Longissimus Multifidus m. dorsi m.
Intercostal vessels
Left lung
Fig. 182.2 Computed tomography or fluoroscopic views are taken through the disks to be imaged, and the relative positions of the lung, ribs, aorta, vena cava, kidneys, nerve roots, and spinal cord are noted. (From El-Khoury GY, Bergman RA, Montgomery WJ, et al: Sectional anatomy by MRI and CT, ed 3, New York, 2007, Churchill Livingstone, p 492.)
Chapter 182—Percutaneous Diskectomy: Automated Technique 1395
easy withdrawal of the probe. The cannula is then removed, and a sterile dressing is placed over the operative site. After the procedure is completed, the patient is observed for 30 minutes before discharge. The patient should be warned to expect minor postprocedure discomfort, including some soreness of the paraspinous musculature. Ice packs placed on the
injection site for 20-minute time periods will help decrease these untoward effects. The patient should be instructed to call immediately if any fever or other systemic symptoms occur that could suggest infection.
Side Effects and Complications Complications directly related to percutaneous diskectomy using the automated technique are generally self-limited, although occasionally, even with the best technique, severe complications can occur.6 The most common severe complication of percutaneous diskectomy using the automated technique is infection of the disk, which is commonly referred to as diskitis (Fig. 182.8). Because of the limited blood supply of the disk, such infections can be extremely difficult to eradicate. Diskitis usually manifests as an increase in spine pain several days to a week after percutaneous diskectomy. Acutely, no change will be evident in the patient's neurologic examination as a result of disk infection.
Fig. 182.4 Lateral view of the cannula within the disk. (From Waldman SD: Atlas of interventional pain management, ed 3, Philadelphia, 2009, Saunders.)
Fig. 182.6 Contrast medium is placed through the cannula into the disk.
Activation switch
Moveable depth marker
1.5-mm cannula
Removable collection chamber Probe tip Fig. 182.5 Posteroanterior view of the cannula within the disk. (From Waldman SD: Atlas of interventional pain management, ed 3, Philadelphia, 2009, Saunders.)
Fig. 182.7 The automated disk decompressor probe is then advanced through the cannula into the center of the disk nucleus until the probe extends beyond the end of the cannula. (From Waldman SD: Atlas of interventional pain management, ed 3, Philadelphia, 2009, Saunders.)
1396 Section V—Specific Treatment Modalities for Pain and Symptom Management
L2
L3
L4
L5
urine cultures should be taken, antibiotics started, and an emergency MRI scan of the spine obtained to allow identification and drainage of any abscess formation, to prevent irreversible neurologic deficit. In addition to infectious complications, pneumothorax may occur after percutaneous diskectomy. This complication should rarely occur if CT guidance is used during needle placement. A small pneumothorax after percutaneous diskectomy using the automated technique can often be treated conservatively, and tube thoracostomy can be avoided. Trauma to retroperitoneal structures, including the kidney, may also occur if CT guidance is not used to avoid and localize these structures. Direct trauma to the nerve roots and the spinal cord can occur if the needle is allowed to traverse the entire disk or is placed too laterally. These complications should rarely occur if incremental fluoroscopic or CT scans are taken while the needle is advanced. Such needle-induced trauma to the lower lumbar spinal cord and cauda equina can result in deficits, including cauda equina syndrome and paraplegia.
Conclusion
Fig. 182.8 Sagittal lumbar spine gadolinium-enhanced magnetic resonance imaging showing postoperative diskitis and complete collapse of the L5-S1 disk space. (From Harris AE, Hennicke C, Byers K, et al: Postoperative discitis due to Propionibacterium acnes: a case report and review of the literature, Surg Neurol 63:538, 2005.)
Epidural abscess, which can rarely occur after percutaneous diskectomy, generally manifests within 24 to 48 hours. Clinically, the signs and symptoms of epidural abscess are high fever, spine pain, and progressive neurologic deficit.5n If either diskitis or epidural abscess is suspected, blood and
Percutaneous diskectomy using the automated technique is a straightforward procedure that is a reasonable treatment option in carefully selected patients. Proper patient selection is based on correlation with the patient's symptoms and physical examination, MRI, diskogram, and electromyogram results. The use of CT guidance adds an additional measure of safety when compared with fluoroscopy, because CT allows the pain specialist to identify anatomic structures and needle position clearly. These advantages more than outweigh the possible added cost when compared with fluoroscopically guided procedures.
References Full references for this chapter can be found on www.expertconsult.com.
Chapter
183
V
Percutaneous Laser Diskectomy Michael L. Whitworth
CHAPTER OUTLINE Historical Considerations 1397 Indications 1398 Technical Aspects of Lasers 1399 Laser Safety 1399 Interactions of Lasers with Intervertebral Disks 1400 Cadaver and Animal Disk Laser Research 1400 Live Animal Laser Research 1400
Anatomy and Pathology of Herniated Disks 1400 Techniques of Laser Disk Decompression 1402 Stepwise Laser Disk Decompression 1402
Historical Considerations Since 1934, when open diskectomy was first introduced at Massachusetts General Hospital, millions of diskectomies have been performed in the United States, with the rate now approaching 500,000 operations per year. The search for a less invasive approach to laminectomy/diskectomy began in the 1960s with chymopapain—Lyman Smith in 1964;1 microdiskectomy by Yasargil in 1968; percutaneous diskectomy introduced by Hijikata in 1975; endoscopic monitoring of disk removal by Leu in 1982; endoscopic diskectomy first used by Schreiber and Suezawa in 1986 and improved by Mayer, Brock, and Mathews; arthroscopic diskectomy by Kambin in 1983; nucleotome introduction by Onik in 1984; percutaneous nonendoscopic laser diskectomy by Ascher in 1986;1 and Choy et al2 in 1987 and endoscopic laser diskectomy by Mayer et al3 in 1992 and Savitz4 in 1994, and the subsequent refinement of endoscopic laser methods by Yeung. In 2000 to 2001, newer minimally invasive methods of diskectomy were introduced, such as coblation nucleoplasty followed by disk decompression. Lasers were first reported to be clinically used in the intervertebral disk in 1977 as part of an open thoracic diskectomy using a CO2 laser (Fig. 183.1).5 Animal models for use of the same laser during canine anterior cervical open diskectomy did not occur until 1984.6 In the 1980s, several lasers were available for treatment of ocular disorders including the argon, carbon dioxide, and excimer (XeCl) laser. The road to published science behind percutaneous diskectomy with a laser began in 1989 when an excimer laser was used on cadaveric disk tissue,7 even though the first percutaneous diskectomy had occurred several years earlier in 1986. The © 2011 Elsevier Inc. All rights reserved.
Laser Diskectomy Techniques 1402 LASE System 1402 Nonendoscopic Laser Fiber Diskectomy (Modified Choy Technique) 1403 Rigid-Scope Endoscopic Laser Diskectomy 1404 Nonlumbar Systems 1405
Outcome Studies 1405 Ho:YAG 1405 Nd:YAG 1405
Complications 1406 Conclusion 1407
neodymium:yttrium/aluminum/garnet (Nd:YAG) laser was applied in laboratory applications and clinically from 1986 to 1990 and was first introduced to the scientific literature by Yonezawa et al8 in 1990. The KTP laser (green) was used at least as far back as 1990 for diskectomy.9 The early 1990s saw a proliferation of other laser development with the introduction of Ho:YAG, Er:YAG, and excimer lasers for widespread use in medicine and dentistry. Because of practical considerations, the Ho:YAG (Fig. 183.2) became the tool of choice for most physicians performing laser diskectomy.10 This is largely due to the fact that a fiberoptic waveguide can be employed instead of a mirror system, the penetration depth into tissue is very low giving fine control of tissue modulation and ablation, and the laser output power available is very high—up to 100 watts. Much of the history of development of lasers for diskectomy was not published until many years later, partially because of financial considerations tied to patent and technique development. The most expansive description of one author's quest to develop laser for intradiskal therapy is found in Choy's book Percutaneous Laser Disc Decompression.11 Choy pioneered the development of laser coronary angioplasty with an argon laser, having performed the first such surgery in September 1983.12 From 1984 to 1986 Choy and his colleagues worked on the basic science and animal models before introducing the laser for human diskectomy. The initial experiments, published much later, included proving the hypothesis that a minimal volumetric decompression of a pressurized disk using a laser would result in a disproportionately greater reduction in intradiskal pressure.13 An Nd:YAG laser at 1064 nm was used to deliver 1000 J of energy to create 20 mm by 6 mm elliptical tracks in the nucleus of fresh cadaver disks loaded to 260 to 410 kPa (37 to 59 psi). Control disks were used in which the laser 1397
1398 Section V—Specific Treatment Modalities for Pain and Symptom Management
kPa 50 45 40 35 30 25 20 15 10 5 0
Decrease in Intradiscal Pressure after NdYAG Laser 1000J (Choy)
Laser Control
Preload
Loaded
End-Lase
Post-Lase
Post-lase is 9 minutes after end of laser application Fig. 183.3 Decrease in intradiskal pressure after Nd:YAG laser at 1000 J. (From Choy DS, Altman P: Fall of intradiskal pressure with laser ablation, J Clin Laser Med Surg 13[3]:149, 1995.)
Fig. 183.1 Carbon dioxide laser.
for percutaneous laser disk decompression (PLDD) owing to the availability of fiberoptic waveguides and the high powers available with the Nd:YAG. Other experiments were conducted using bovine disks demonstrating temperature rises of less than 2°C (36°F) in the neural foramina, the anterior surface of the spinal canal, and 1 cm away from the laser tip directly in the line of fire of the laser. Next, experiments with mongrel dogs where employed under institutional research board (IRB) approval. PLDD was performed through an 18-gauge needle with 1000 J of energy delivered. The dogs were subsequently sacrificed and on autopsy, there were no extradiskal injuries. Clinical use in humans began in February 1986 in Austria, when Choy performed the first PLDD successfully. Because of bureaucratic obstacles in obtaining IRB approval, it was not until September 1988 when the first U.S. use occurred. Food and Drug Administration approval of PLDD was received in 1991, and since that time it is estimated that there have been over 100,000 users worldwide of intradiskal laser for intervertebral disk decompression.
Indications
Fig. 183.2 Ho:YAG laser.
was not turned on. The results are presented in Figure 183.3. Next, different lasers were examined as to their capability of disk ablation. At 900 J of energy, the mass of disk ablated ranged from 120 to nearly 200 mg of disk tissue. Er:YAG, Nd:YAG (1318 and 1064 nm, respectively), CO2, argon, excimer, and Ho:YAG lasers were evaluated. The most effective in disk ablation was the pulsed CO2 laser and erbium laser, but all other lasers were nearly as effective. However, the Ho:YAG lasers of that time were very weak compared to later lasers. For practical purposes, the Nd:YAG 1064 nm was chosen by Choy
Relative indications for this technique depend partially on the technologies employed and partially on the specific targeted pathology. In general, the major indication is the presence of a contained intervertebral disk herniation (confirmed by magnetic resonance imaging [MRI], computed tomography [CT] scan, or CT myelogram) in addition to a clinical presentation of radicular pain with or without neurologic deficits, and a minimum of 6 weeks of conservative treatment without significant improvement. Exclusion criteria are patients with foraminal or central canal stenosis, symptoms of facet syndrome, previous spinal surgery in the same region, bony deformities (such as congenital abnormalities, spondylolisthesis, and hemivertebrae), cauda equina syndrome, other symptoms of myelopathy, and pregnancy. It should be noted that a contained disk herniation is not simply a diffuse bulge, but should be less than 25% of the circumference of the anulus fibrosus and usually contacts the nerve roots or cord (for cervical or thoracic presentations). Technically, a contained disk herniation is one in which there is displaced disk tissue that is
Chapter 183—Percutaneous Laser Diskectomy 1399 Feedback Electromagnetic Radiation Out
Active medium Rear mirror (100% reflection)
Excitation mechanism
Output coupler
Fig. 183.4 Schematic representation of the mechanism of laser function.
wholly within an outer perimeter of uninterrupted outer anulus or capsule. Extruded disk fragments are not treatable by this technique because there is no continuity with the central nucleus pulposus. Using the selection criteria (leg pain, positive physical findings such as motor/sensory/reflex deficits and/or straight leg raise, contained disk herniation confirmed by diskography) and exclusion criteria (normal physical examination, presence of stenosis, spondylolisthesis, extruded disk fragment, leakage of diskographic dye from the outer anulus, multiple prior lumbar surgeries), the performance of laser disk decompression resulted in a success rate of 71%, whereas those who did not meet all the section criteria were successful only 29% of the time.14 Some authors advocate the use of disk decompression for the treatment of spinal stenosis that is primarily caused by a significant disk bulge. Intradiskal and extradiskal endoscopic diskectomy with laser assistance can be performed in the hands of experts using a posterior or posterolateral approach (foraminal).
Technical Aspects of Lasers Laser stands for light amplification through stimulation of emitted radiation and is used universally as an acronym for obvious reasons. The original equations describing its operation were developed by Albert Einstein in 1917.15 The first optical laser was developed by Gordon Gould in 1958. Theodore Maiman developed the first solid-state laser, the ruby laser, in 1960 and was followed shortly thereafter by Ali Javan with the first gas laser (He Ne) in 1960, and the CO2 laser by Kumar Patel in 1964. Now there are more than 100 known lasing media. Lasers produce an extremely focused monochromatic light that is virtually uniform in wavelength. The mechanism of laser function is presented in Figure 183.4. There is usually a primary wavelength and several secondary wavelengths of lesser amplitude produced from each laser. A resonating chamber is used (cylindrical tube) containing a lasing medium (gas, liquid, crystal) and a full mirror on one end of the tube with the other end partially mirrored. External energy is applied to the tube through the application of electricity, a flash lamp, or another laser and this causes the electrons in the lasing medium to become excited to a higher orbit. When they fall back to their baseline orbit, the electrons give off monochromatic photons, which are reflected back and forth internally until the energy of the photons is sufficient to break through the partially mirrored end. These photons are collected in a fiberoptic or mirrored waveguide and are transmitted to the target. Different lasing media produce different
wavelengths of light. The CO2 laser generates an infrared light of 10,600 nm, whereas the Er:YAG generates 2940 nm; Ho:YAG produces 2150 nm; Nd:YAG produces wavelengths of 1318 nm and 1064 nm; KTP generates 532 nm; and the excimer laser produces 193 nm. More recently, diode lasers, especially in parallel arrays, have been shown to give wavelengths up to 2100 nm. The lasing medium is often a crystal that is doped with a rare earth impurity (holmium, neodymium, erbium) during the growth of the crystal. In reality, most lasers generate more than one wavelength of light, and in fact some, such as the CO2 laser, generate dozens. But in most lasers, the light generated at each wavelength is coherent (i.e., the waves generated are all in phase with each other). Lasers are very inefficient, with usually less than 1% of the input energy being converted to the laser beam. The remainder is emitted as heat.16 With a laser that operates at an efficiency of 2% and has an output of 80 watts, the excess heat produced is about 4000 watts. When the heat generation is excessive and cannot be diffused, the laser crystal medium may fracture. Therefore, in larger lasers, forced air or circulating water is used to dissipate heat. The efficiency of the typical YAG laser is 0.1% to 1%; the excimer laser is 2%; and CO2 lasers have an efficiency up to 20%. Laser output power is measured in watts, whereas the tissue effect is measured in joules (watts times seconds). Pulsed lasers deliver small pulses of energy with time for thermal dissipation to occur in tissues when the pulses are far enough apart and the pulse width is narrow enough. Double-pulsed lasers can result in summation effects of thermal energy rather than permitting dissipation, thereby approximating the effect of a continuous-wave laser. Because not all lasers are visible (e.g., Ho:YAG, Nd:YAG, Er:YAG), a second laser is used as an aiming laser through the same fiberoptic waveguide. Usually a low-power helium laser is employed (bright red) and the intensity of the aiming laser may be varied. If the aiming laser is interfering with visualization of tissue vaporization from the primary laser, the aiming laser can often be turned off.
Laser Safety It is imperative to consider the hazards of a laser beam before engaging in laser use. Most manufacturers have laser courses designed to educate both the staff and physician about radiation hazards from the powerful laser beams. Hospitals and surgery centers usually have a “laser safety officer” who should be well versed in laser safety. Nd:YAG lasers can cause permanent retinal damage and absolutely require safety glasses. All lasers with wavelengths in the ultraviolet (UV) (excimer) or visible spectrum (KTP) and below 1.55 microns in wavelength (Nd:YAG) can seriously damage the retina by causing punctate lesions, thereby permanently reducing vision. The effect of a milliwatt laser in this wavelength range striking the eye is similar to that of staring into the sun. Laser beam energy can enter the orbit from direct beam (e.g., end of the laser fiber, disconnect in the coupling, and so on) or indirectly (reflective surfaces from needles, cannulas, instrumentation), both with devastating effects on the retina. Lasers with wavelengths longer than 1.55 m (Ho:YAG, Er:YAG) cannot reach the retina but can do damage to the cornea and skin. CO2 lasers can be so powerful that they can cut through any tissue because they are available in output powers up to 15,000 watts. Laser glasses are designed to be specific for different laser wavelengths,
1400 Section V—Specific Treatment Modalities for Pain and Symptom Management and certainly for wavelengths below 1.55 microns (1550 nm). They are mandatory for everyone in the room, including the patient. The laser beam must never ever be pointed at a person, and when removing the laser from the patient, the laser operator must switch to standby mode. The laser may never be fired toward a paper drape or gown.
Interactions of Lasers with Intervertebral Disks Almost immediately after the introduction of lasers, the concern regarding tissue interactions was of research interest.17,18
Cadaver and Animal Disk Laser Research The search for the optimal laser for use in the intervertebral disk began in the 1980s with surveys of absorption of laser energy by intervertebral disk material.19 It was found that the higher wavelengths such as Nd:YAG 1320 nm and mid-infrared lasers had a higher absorption than the lower-wavelength Nd:YAG 1064 nm or argon lasers. A higher amount of absorbed energy would theoretically be advantageous. However, control of the degree of heating of the disk is also necessary because with Nd:YAG 1320 nm powers above 20 W, instead of tissue shrinkage, a thermal bubble develops that ruptures tissues.20 When intradiskal tissues reach 65°C (149°F), permanent changes are introduced to the disk, resulting in both morphology changes in the disk and also a permanently increased tension in the disk with a volume loss of 20% to 70% of the nucleus pulposus. Using an Ho:YAG laser, radial bulging is increased with low-energy level laser application whereas after 1500 J, the radial bulge and transverse disk diameter decrease.21 One group claims that Ho:YAG lasers without cooling (as is the case with nonarthroscopic applications) cause immediate tissue damage to surrounding tissues, whereas in the case of arthroscopy there is irrigation cooling—thereby avoiding damage to surrounding tissues. The same group found that Nd:YAG lasers were much more dependent on the color of the tissue for ablation, with the highly colored tissue causing an increased absorption of energy, thereby concluding that the Nd:YAG is the superior laser for intradiskal ablation.22 Of course, the disk material that is herniated is usually not highly colored, therefore it is perplexing why these conclusions were reached. A study of power and energy from an Ho:YAG laser with respect to ablated disk material mass and time demonstrated that temperature does not rise any more after the application of 500 J to the disk, and that the mass of ablated material was related to energy, but not to power.23 Similarly, in another cadaver study, it was discovered that energy, not time, power, or pulse frequency, best determined the rate of disk ablation, and the rate of ablation was enhanced through suction application.24 The same group determined that end plate damage and adjacent tissue damage is avoided if the laser remains in the middle of the disk, and that there is little tissue damage 1 cm from the tip of the laser. The amount of disk material removed with an Ho:YAG laser was determined via experiment on human cadaver spines to be 104 mg/kJ.25 MRI correlation with histology in cadaver disks subjected to different energy pulses of Ho:YAG radiation demonstrated cavitation with end plate involvement at high pulse energies of 1 to 2 J/pulse, whereas low pulse energy of less than 1 J/pulse produced tissue modulation with end plate sparing. The overall loss of mass was determined by total
energy applied rather than pulse energy.26 Tissue absorption and ablation of an Ho:YAG laser is limited to approximately 500 microns, which makes aggressive ablation of the disk difficult, but also reduces the likelihood of the laser contacting dura or nerve roots. In summary, we may conclude the following from this research: There are different mechanisms of laser-tissue interaction at low power and high power. Low-power laser application (20 W), inadequate outflow of the irrigation, or excessive lasing in one location without laser tip movement (Fig. 183.8), carbonization will occur and the disk tissues will become blackened; visualization will degrade with blackened fragments floating in the field of view.
It is preferred to lase for 5 seconds on, then 5 seconds off because during lasing, the cavitation obscures the optical resolution of the tissues being lased. If the tip approaches the end plate, a bright flashback can occur with reflection of the laser beam off the bone and back through the waveguide toward the laser source. This can damage the end plate (very undesirable) and potentially the laser itself if there is inadequate flashback protection built into the laser. Typically one to two disks may be treated with a single laser wand. The optics of the fiberoptic system can degrade with extended use and the tip of the laser fiber itself may degrade. If the laser fiber is not polished, it is possible to cut the laser fiber back with a special laser fiber knife and resume the LASE procedure. After termination of the procedure, the laser wand and needles are withdrawn with local anesthetic injected in the needle track outside the neuroforamen. It is not desirable to inject local anesthesia near the DRG or exiting nerve root because if there exists a rare neurologic deficit after the termination of the procedure, the effect of the local anesthetic could muddle the diagnosis and result in significant diagnostic delay.
Nonendoscopic Laser Fiber Diskectomy (Modified Choy Technique) The original Choy procedure used lateral decubitus patient positioning and did not employ targeting the safe operating zone of the neuroforamen. Choy used a fixed 10-cm lateral entry from the midline and an initial 45-degree angulation. Of course, in obese patients a fixed distance from the midline skin needle entry will result in a trajectory that is less than 45 degrees to the sagittal plane and potential entry into the disk at the site of exiting nerve root owing to deflection of the needle by the SAP. Very thin patients have the opposite issue with a fixed needle skin entry site and it may result in excessively posterior needle placement if the SAP is targeted and potential
1404 Section V—Specific Treatment Modalities for Pain and Symptom Management pithing of the exiting nerve root if a 45-degree entry angle is selected. Therefore the technique has been modified to use the standard precision “down the barrel” pain medicine method. With the patient in the prone position, for central disk targeting the fluoroscopy beam is used to provide a horizontal trajectory across the end plates; then the beam is rotated obliquely approximately 45 degrees at L3-4 and L4-5 and 35 to 40 degrees at L1-2 and L2-3. The angle at L5-S1 is as far oblique as possible until the iliac crest overrides the superior articular process. At each level the lateral-inferior border of the SAP is targeted at the junction between the superior end plate and the disk. An aliquot of local anesthetic is infiltrated in the skin at the selected entry site, and then a 6-inch spinal needle is passed in the selected trajectory to, but not beyond, the SAP, during which time local anesthetic is infiltrated. A 20 cm, 18-gauge needle is subsequently advanced in the anesthetized track and the SAP is contacted. On advancement across the neuroforamen (slowly), the patient may experience some intense back pain but should not experience any radicular pain. Repositioning is necessary if there is radicular pain, which can be due to a hypersensitized DRG, furcal nerve contact, or overt contact with a displaced exiting nerve root. When annular cannulation has occurred, the end point of needle advancement is on anterior-posterior projection, halfway between the lateral border of the spinous process and the medial border of the pedicle. On lateral fluoroscopic projection, the needle tip should reside at the junction of the posterior quarter of the disk with the anterior three quarters. An Nd:YAG fiber is inserted through the needle to the tip and 1cm beyond. The needle is subsequently not moved. Lesioning at 20 W with 5 seconds between 1-second pulses is used. If a flashback is observed, the laser tip is retracted and inspected for damage. If the tip is damaged, the tip is cut and the laser reinserted. The total energy applied is 1000 J or up to 1500 J if the patient is greater than 165 cm in height. (Note: The energy used with this technique incorporating an Nd:YAG laser is only one tenth of that required with the Ho:YAG laser.) If the disks have a narrowed height, the amount of energy applied is reduced by 25%. During lasing, the patient should alert the physician of any new radicular pain. (Note: This method is completely blind and is incapable of guiding the laser tip. It also does not employ any aqueous irrigation, which can lead to charring and end plate damage. However, numerous publications attest to the safety of this procedure.) An alternative laser source is an Ho:YAG fiber or multidiode laser, but the same limitations apply. With an Nd:YAG laser, the lesion produced is 2 cm long and 6 mm wide (Figs. 183.9 and 183.10). An Ho:YAG laser produces a much smaller lesion in the disk tissue unless the laser fiber is moved; this system is not desirable because of potential laser fiber fracture within the disk.
Rigid-Scope Endoscopic Laser Diskectomy This technique of endoscopic laser diskectomy uses a rigid scope in contrast to the LASE (flexible, steerable fiberoptic scope). The optics and visualization are much better than the fiberoptic scope and the working channels in the scope permit introduction of dissection and probing instruments. The two systems used in pain medicine are the PercScope by Clarus and the YESS scope by Wolf. The PercScope uses a 30,000-pixel fiberoptic bundle housed in a 5.2 mm rigid scope housing and
Fig. 183.9 Laser tracts formed in nucleus pulposus by 1000 J of laser energy at 1.32 μm on the left and a 1.06 μm Nd:YAG laser on the right. (From Choy DSJ: Percutaneous laser disc decompression: history and scientific rationale, Techniques Reg Anesth Pain Manage 9[1]:50–55, 2005.)
Fig. 183.10 Histologic appearance of a laser tract in the nucleus pulposus. There is a central hole surrounded by a zone of protein denaturation and then vacuoles, which are probably steam pockets. (From Choy DSJ: Percutaneous laser disc decompression: history and scientific rationale, Techniques Reg Anesth Pain Manage 9[1]:50–55, 2005.)
contains a large 3.1 mm working channel. This size of working channel will permit the introduction of a variety of instruments, as depicted subsequently, that permit laser-assisted dissection. The lasers may be either a nonsteerable bare fiber, fiberoptic steerable laser, or rigid laser housing for side-firing or end-firing laser output. The Wolf system uses a 7-mm outer diameter (OD) cannula for a 6 mm OD scope. The working channel is 2.7 mm, but there are several irrigation ports. The optical system uses a rigid rod system with crystal-clear nonpixelated viewing. There is a European scope with a much larger working channel (Fig. 183.11), up to 4 mm, that will permit introduction of large dissection instruments and automated rotating dissectors and burrs. Fundamentally, both systems incorporate the same basic technique of disk access and dissection. The cannula systems are so large that primary introduction is not possible without a guidewire (Fig. 183.12). An initial posterolateral placement of an intradiskal needle is the first step. When the disk has been entered, an injection of indigo carmine blue/iodinated
Chapter 183—Percutaneous Laser Diskectomy 1405
Fig. 183.11 PercScope working channel.
Fig. 183.13 Laser through YESS endoscope.
deflecting the laser at right angles to the wand. This has several advantages, including that a more posterior laser diskectomy may be performed. Care must be taken not to excessively weaken the posterior anulus fibrosus by firing the laser in one location onto the anulus. With the PercScope system, the procedure is terminated at this point, whereas with the Wolf system, the laser dissection is usually followed by an aggressive articulating forceps used to grasp the neck of the herniation, pulling the hernia back inside the disk and out through the cannula. At the termination of the procedure, the cannula is removed and the patient may receive steroids along the nerve root to help control postoperative periradicular edema.
Fig. 183.12 PercScope access cannulas and surgical instruments.
contrast is rendered into the nucleus pulposus. Indigo carmine has been shown to selectively stain the degenerative/herniated parts of intervertebral disks blue.49 A guidewire is then inserted through the needle, and the needle is removed. Next, a dilator is placed over the guidewire under fluoroscopic guidance to avert bending the guidewire. A cannula is placed over the dilator which is advanced to the external anulus fibrosus. With the cannula held in place, the external anulus is probed with the dilator for underlying nerve roots. If none are discovered, the dilator is removed and the cannula is held firmly in place; a trephine or annulotome is advanced to the anulus. If the trephine is used, the cannula is simply advanced into the intervertebral disk. However, if the annulotome is used, the dilator is replaced through the cruciate incision of the anulus, and subsequently is advanced into the nucleus pulposus. The cannula is then slid off the dilator into the nucleus pulposus. Following removal of the dilator, the endoscope is inserted with continuous saline or bacitracin containing saline irrigation flowing into the nucleus pulposus. Pituitary forceps are inserted through the endoscope to clear disk tissue from the end of the cannula. The blue-stained material is targeted with the forceps and then the laser, as this represents the herniated and severely degenerative portion of the disk (Fig. 183.13). An end-firing or side-firing laser wand may be placed through the working channel, and the Ho:YAG laser at 20 to 40 W is used to clear the area under the disk herniation. The usual laser energy applied is between 5000 and 25,000 J. A side-firing laser has a mirror placed at a 45-degree angle near the tip of the scope,
Nonlumbar Systems The cervical and thoracic areas can be approached with a laser technique for diskectomy. The lower three thoracic disks can often be accessed inferior to the transverse process, whereas the mid and upper thoracic levels may require obtuse angulations. The LASE system is ideal for these applications. Cervical diskectomy may be performed with a special cervical LASE system or a 2.5-mm cannulated system such as a Blackstone or other access system. Usually the cervical disk is approached very much like cervical diskography, except extreme care must be used in the anterior cervical spine owing to the carotid and jugular systems being in the line of the needle trajectory. It is suggested that cervical diskectomy not be performed unless the physician has immense experience with both lumbar and thoracic diskectomy and with cervical diskography.
Outcome Studies Ho:YAG Using 1500 J energy at 15 watts through an 18-gauge needle, one group had a 91% successful outcome rate at 18 months' follow-up.50 Using a laser-assisted disk decompression with a side-firing laser placed through an endoscope, success was achieved on 1 year's follow-up at a 90% level51 and at 87% at 2 years' follow-up.52
Nd:YAG The results for nonendoscopic lumbar disk decompression with an Nd:YAG laser are variable, but generally range from 70% to 90% good to excellent results. A 4-year follow-up study of 200 patients with Nd:YAG 1064 nm nonendoscopic laser
1406 Section V—Specific Treatment Modalities for Pain and Symptom Management diskectomy produced a 74% success rate.53 Another study used nonendoscopic Nd:YAG diskectomy in 42 patients with thoracic disk extrusions and protrusions, with improvement in all clinical parameters in 41 of the 42 patients.54 Choy's experience with 389 patients using a nonendoscopic laser diskectomy with the Nd:YAG laser demonstrated a 75% success rate according to good and excellent results by the modified MacNab criteria,55 although in his book Percutaneous Laser Disc Decompression he states the success rate in later cases rose to 89%.
Complications Generally the complication rate for laser diskectomy is relatively low, around 1%. The specific complication profile for cervical, thoracic, and lumbar diskectomy are different, because of anatomic considerations, and are listed in Table 183.1. Most complications are relatively mild and involve transient increases in pain caused by prone patient positioning when the patient may not have assumed that position in years, muscle spasm from the needle/cannula, and subcutaneous or intramuscular hematomas. However, on rare occasions serious complications will occur. This author has had one case of a Brown Séquard syndrome when an access cannula displaced a protruding disk herniation fragment into the cervical spinal cord, with only partial long-term neurologic recovery. Poor patient selection can lead to severe complications such as cauda equina syndrome in very rare cases.56 When larger cannulas are used to access the disk, a finite percentage (about 5% to 7%) will develop a transient complex regional pain syndrome type II (CRPS II) syndrome,57 but this does not seem to occur as frequently with a needle access system. Both osteomyelitis and diskitis have been reported after laser diskectomy,58,59 although these are rare, and most are aseptic. It is highly probable that most instances of aseptic diskitis are caused by over-reading postoperative MRI scans or mistaking end plate laser damage for diskitis. The potential for long-term disk degeneration acceleration is a very real concern when using the larger cannulas for disk access because the sheep model for long-term degeneration is coring the anulus fibrosus The use of slit lesions with a 2.5-mm device caused
much less disk degeneration and instability than did the use of a box window excision of the disk,60 which implies that if the larger cannulae are to be used, they should be preceded by an annulotome incision. Excessive removal of disk is also potentially deleterious owing to the removal of the central nucleus pulposus support with a biomechanical weight transfer to the anulus fibrosus. The anulus is not designed to hold significant weight and undergoes progressive collapse with annular bulging. Another significant concern is the damage to the end plates that are the nutrient conduits to the avascular nucleus pulposus. The cartilaginous end plates gradually become sclerotic with subchondral bone formation because there is increased force affecting the trabecular bone when the disk is no longer serving as a hydraulic shock absorber. Additionally, Ito has demonstrated a direct correlation between calcification of the nutrient canaliculi and MRI grade of disk degeneration.61 Adams et al62 demonstrated that even minor damage to the vertebral end plates may lead to progressive structural changes in the adjacent disk. One study demonstrated that after endoscopic laser diskectomy, subchondral marrow abnormalities were identified in 41 of 109 patients. However, in a subset of patients examined 5 to 7 years after laser diskectomy, both back pain and marrow abnormalities improved on MRI.63 The nature of such subchondral osteonecrosis was examined on MRI imaging and was found to include a wedge-shaped area of low signal intensity on T1 images, of high and low signal intensity on T2-weighted images, and of gadolinium-enhanced high signal intensity on T2-weighted images, respectively. The speculative causes of such changes were thought to include thermal energy and photoacoustic shock.64 An experimental animal model of Nd:YAG laser injury to the end plates revealed an early decrease in vascularization at 1 month after laser application; however, by 2 months after laser application, the vascularization of the end plate had effectively doubled.65 Using an experimental guinea pig model with a carbon dioxide laser fired at the end plates, as little as 300 J of energy was required to damage the end plates.66 However, it was demonstrated by Hoogland67 that curettage of the end plates of severely degenerative disks may later reverse some of the MRI changes of disk degeneration, including that of disk
Table 183.1 Potential Complications of Laser Diskectomy Cervical Complications
Thoracic Complications
Lumbar Complications
Disk access complications
Perforation of carotid, jugular, thyroid, esophagus, trachea
Pneumothorax, cord or nerve root penetration, chylothorax, hemothorax, CSF leak
CSF leak, nerve root injury, bowel penetration, epidural hematoma, epidural abscess, cord injury (above L2)
Laser/needle complications
Needle perforation of the end plates, cord with Brown Séquard syndrome, nerve root penetration, diskitis, CSF leak, PLL destruction, lasing the cord or nerve roots, late disk space collapse or degeneration, pseudodiskitis, epidural hematoma from lasing of epidural vessels
Lasing the cord, nerve root thermal injury, aortic/caval injury, diskitis, epidural hematoma, epidural abscess, end plate damage/pseudodiskitis
Iliac penetration, sympathetic chain injury, end plate damage/pseudodiskitis, diskitis, bowel injury, genitofemoral nerve injury, late disk degeneration, disk space collapse with increased disk bulge
CSF, cerebrospinal fluid; PLL, posterior longitudinal ligament.
desiccation. The latter finding, however, was based on limited clinical evidence; therefore the modus operandi at this juncture would invoke end plate preservation.
Conclusion Laser diskectomy is an alternative to open or microdiskectomy for selected patients at a small fraction of the cost. Least expensive is the Choy technique, but it has the theoretical disadvantage of increased risk of end plate damage because the laser fiber angle cannot be controlled when the laser waveguide is inserted through the needle. Although the other techniques are more expensive, they provide steerability of the laser, which is useful in avoiding the end plates. The Nd:YAG laser is much more aggressive than the Ho:YAG; therefore tissue ablation will occur at a much more rapid rate. The advantage of the Ho:YAG is the safety imparted through a 500-micron controlled tissue penetration, especially when operating in a continuously irrigated field.
Chapter 183—Percutaneous Laser Diskectomy 1407 The major barriers to more widespread use of laser disk decompression include high cost of a laser ($50,000 to $180,000); reluctance of hospital medical staff to open laser use to pain medicine because of infrequent use by the specialty; equipment costs (endoscopes, light sources, cannula systems, video system, and flexible laser wands); lack of double-blind controlled studies; alternative, more simple solutions (coblation nucleoplasty, disk decompression); and global skill level deficits of most pain physicians in endoscopy of the spine. However, most hospitals and some surgery centers have acquired lasers (e.g., Ho:YAG lasers are often used to perform laser lithotripsy of kidney stones) and already own the video towers and cameras necessary to perform video procedures. PLDD is effective 75% to 90% of the time in selected patients at a fraction of the cost of microdiskectomy or open diskectomy.
References Full references for this chapter can be found on www.expertconsult.com.
V
Chapter
184
Percutaneous Fusion Techniques David Petersen
CHAPTER OUTLINE Background 1402 Indications 1402 Anatomy 1403
Background The TruFUSE (facet joint spinal stabilization or fusion) procedure represents a new, more biologic way of performing an established technique that has been part of the gold standard for posterior spinal fusion for many decades. In the past, the facet joints were either drilled or burred and packed with unstable chips of bone, allowing them to continue to grind until fusion occurs, causing the patient pain during recovery and allowing for the joint to settle with possibly more foraminal stenosis. Now a precision, “press-fit,” stable grafting of the joint can be accomplished, relieving the patient's mechanical back pain very rapidly by separating the arthritic joint surfaces and stabilizing them immediately with a Morse tapered dowel without instrumentation and the risks/recovery and longterm issues associated with hardware (Fig. 184.1). The joint can also be theoretically reduced and held there for a more anatomic fusion (Fig. 184.2). The concept of facet angle or tropism (Fig. 184.3) becomes important in preoperative planning to assist in determining the opening angle for fluoroscopy and to see if there may be obstructions to graft placement (Fig. 184.4).
Technique 1404 Complications 1407 Clinical Pearls 1407
very useful for revision surgery to fuse an adjacent segment to avoid redoing large, old fusion constructs with additional hardware or in some cases of pseudoarthrosis (Fig. 184.5). Patients suffering from facet joint arthropathy whose pain is temporarily relieved with intra-articular facet joint injections and/or radiofrequency ablation procedures but in whom pain relief is not long lasting are also good candidates for TruFUSE. Rigid constructs in spine surgery are essential for deformity correction (scoliosis), tumors (segmental loss), gross instability, and fractures and in some cases of spondylolisthesis. It makes a great deal of biologic sense to use the TruFUSE technique within rod/screw constructs to act as bleeding surface with reamed
Indications The indications for facet fusion (TruFUSE) are generally the same as those for any posterior fusion method. It is another way to perform a posterior fusion, when instrumentation is not needed. As a standalone procedure it is used for facet arthropathy or intractable mechanical low back pain unresponsive to nonoperative measures. It is often used as an adjunct after laminectomy/decompression, or with microinstability (less than 2 mm motion on lateral flexion/ extension films), or after anterior spinal fusion to supplement a 360-degree fusion (posterior lumbar interbody fusion, anterior lumbar interbody fusion, extreme lateral interbody fusion, or on the contralateral side of a transforaminal lumbar interbody fusion). It has been used with several of the spinous process distraction devices (X-Stop, Aspen, and Spire plates) to fuse the decompressed level in a distracted position. It is 1402
A
B Fig. 184.1 A, Proper graft placement within the facet joint. B, Schematic drawing of proper graft placement within the facet joint. © 2011 Elsevier Inc. All rights reserved.
Chapter 184—Percutaneous Fusion Techniques 1403
compacted autograft and a stable allograft dowel spanning the facet joint for primary bony healing to occur across rigidly fixed segments. This is preferable to placing stress-shielded graft in the posterior lateral gutter on non–weight-bearing structures and hoping that structurally sound bone will form. Nerve
This technique does not burn bridges and allows for conversion to rod/screw stabilization surgeries without additional risk or surgical times should the patient's symptoms recur or progress following the TruFUSE posterior facet joint spinal fusion. The bone graft is a precision-cut Morse tapered allograft dowel placed into an undersized Morse tapered, press-fit, compaction reamed tunnel into the middle one third of the facet joint (Figs. 184.6 and 184.7).
Anatomy Foramen
Facet joints are synovial joints. They possess a joint capsule, are lined with synovium, and contain joint fluid. They are formed by the articulations of the superior and inferior
A
Foramen Vertebra
Disc
B
Front of vertebra
Fig. 184.2 A, Displaced degenerative facet joint. B, Reduced facet joint demonstrating positional or indirect decompression.
Fig. 184.3 Facet joint angle or tropism.
Fig. 184.4 Preoperative planning—facet approach difficulties.
Fig. 184.5 “workaround.”
Pseudoarthrosis—hardware
1404 Section V—Specific Treatment Modalities for Pain and Symptom Management articular processes of adjacent vertebrae. The joint capsule is richly innervated and frequently acts as a pain generator. Cervical and lumbar facet joints are more susceptible than thoracic facet joints to arthritic changes and trauma secondary to a wide variety of mechanisms. Regardless of the mechanism, damage to facet joints can result in pain secondary to synovial joint inflammation and ultimately degeneration as a final pathway (Fig. 184.8). Each facet joint receives innervation from up to three spinal levels. Each joint receives fibers from the dorsal ramus at the same level as the vertebra, as well as fibers from the dorsal ramus of the vertebrae above it. This is why facet-mediated pain can be difficult to localize and explains why the nerve from the level above the offending level must also be blocked, when an extra-articular block is performed, in order to provide complete pain relief, which is not the case if an intra-articular injection is performed for at least diagnostic purposes. Occasionally, a patient may experience long-lasting relief from an intra-articular injection because the inflammatory effect from the synovium decreases, at least for a time.
Fig. 184.6 Anatomic graft placement within the facet joint.
L2
L2
L3 L3 Fig. 184.7 Schematic of graft placement within the facet joint.
Fig. 184.8 A, Oblique x-ray. B, Computed tomography scan view of a degenerative facet joint, severe facet arthropathy.
A
Technique After the patient receives an appropriate level of anesthesia/ sedation (and/or local anesthetic), the patient is placed in the prone position on a fluoroscopy table. Most patients are given prophylactic antibiotics preoperatively per routine. Longitudinal rolls or a Wilson frame (which can be adjusted for lumbar flexion with the patient prone on the frame) is placed on the fluoroscopy table before the patient. Any commonly available spine surgery adjustable fluoroscopic table will work equally well. The lumbar spine is flexed to reestablish facet joint height lost during the degenerative process. This also helps to reopen the foramina and pull the superior articular process back out of the foramina, termed indirect decompression (see Fig. 184.2). Alternatively, a small incision can be made over the spinous processes and a lamina spreader can be used to open the foramina during the procedure and then the lamina spreader can be removed before wound closure. The facet joint(s) to be fused are next identified on an anteroposterior (AP), lateral, and oblique fluoroscopic view, before setting up a sterile field, to be sure that adequate visualization is possible. After the patient is prepped and draped in a standard sterile fashion, a true AP x-ray view is obtained at the level to be fused. Next, the superior end plate is “flattened” by angling the fluoroscope either caudally or cranially, and then gradually increasing the oblique angle of the fluoroscope until the opening angle has been maximized. The opening angle should be measured preoperatively with either a magnetic resonance imaging (MRI) scan (coronal section) or more ideally a computed tomography (CT) scan with thin slices through the facet joint, not only to predetermine the facet angle but also to look for obstructive osteophytes and to help decide if the patient is a candidate for the procedure (see Figs. 184.3 and 184.4). Finally, the point at which the superior end plate intersects with the middle one third of the open facet joint will serve as the target (+) for the spinal needle or Steinmann pin (see Figs. 184.6 and 184.7). This approach will increase your accuracy in graft placement into the middle one third or “sweet spot” of the facet joint and will reduce the risk of nerve root injury since the nerve root will be at the top of the foramina and if the pin goes in too deep the pin will pass through the bottom of the foramina well out of the way of the exiting nerve root. After the target has been identified, a spinal needle or the Steinmann pin is then passed down through the soft tissues and into the opening of the facet joint. If a spinal needle is used, it will then need to be changed out for the Steinmann pin (Figs. 184.9 and 184.10).
B
A
Chapter 184—Percutaneous Fusion Techniques 1405
The pin should appear as a dot on the x-ray image before it is hammered into the facet joint and fully seated (Fig. 184.11). The pin is then tapped with the hammer lightly into the middle one third of the facet joint approximately 1 cm until it stops when it contacts the superior articular process. The pin will slightly distract the facet joint and will confirm you are in the joint. A lateral x-ray view is checked to be sure you are not too deep, the pin should bottom out posterior to the foramina, and the pin should be directed toward the superior end plate. Following this, the contralateral pin is placed in a similar fashion. Next, a small (Wiltse approach) incision is made through the skin and subcutaneous tissues in a longitudinal fashion to free the pin up from the skin and subcutaneous tissues to allow the rest of the instruments clear passage into the
joint. The cannulated spatula is then placed over the pin and twisted over the pin repeatedly clockwise and counterclockwise (approximately 180 degrees) to gently pass the instrument thru the soft tissue and fascia down to the joint (Fig. 184.12). Once it is confirmed on the lateral x-ray view to be at the level of the joint, the vertical lines on the spatula are oriented in line with the facet joint plane and the blade of the spatula is advanced by impacting it slowly into the joint approximately 1 cm. Be careful not to loosen or move the pin while advancing the spatula; the pin is your guidewire at this point. After satisfactory placement of the spatulas bilaterally (confirmed radiographically) the drill guide is placed over the spatula on one side (Fig. 184.13). While holding the spatula firmly with one hand to stabilize it as you would a
Video: Percutaneous technique Video: Percutaneous technique
Fig. 184.9 Spinal needle is replaced by the Steinmann pin.
Video: Percutaneous technique
Fig. 184.10 Steinmann pin placement within the facet joint.
Fig. 184.12 Spatula slowly twisted over the pin through the fascia.
Video: Percutaneous technique
Fig. 184.13 Drill guide is inserted unilaterally.
Fig. 184.11 Proper pin placement. The pin will appear as a dot in the center one third of the facet joint.
1406 Section V—Specific Treatment Modalities for Pain and Symptom Management guidewire, the drill guide is rotated down through the skin, subcutaneous tissues, and fascia in a similar 360-degree clockwise and then a 360-degree counterclockwise fashion repeatedly until it gets down to the first horizontal line on the spatula (Fig. 184.14A). (This is similar to a warning track at a baseball field to warn the fielder that the wall is coming soon.) Advancing the drill guide replaces the spatula with the teeth to maintain the joint separation. Now that the first line is visible, only rotate the drill guide 30 to 40 degrees back and forth (with the drill guide's handle nearly perpendicular to the patient's body) until the second line appears on the spatula (Fig. 184.14B), and then stop rotating the drill guide. The lines on the top of the drill guide must be aligned with the vertical lines on the shaft of the spatula to ensure proper intra-articular placement of the drill guide teeth (Fig. 184.15). Stabilize the drill guide at the patient's skin with your nondominant hand and hold a firm downward pressure on the drill guide for the rest of the procedure, maintaining the angle of the guide during the drilling and graft placement. Now
Fig. 184.14 A, First line. B, Second line. C, Third line.
A(1)
A(2)
hammer the drill guide, next to the spatula (Fig. 184.16), down into the joint to fully seat the drill guide's teeth; stop when the third horizontal line becomes visible (Fig. 184.14C). Do not release the downward pressure on the drill guide from your hand until you are completely done hammering the allograft bone into place in the joint. The Steinmann pin and spatula are then removed while maintaining the downward pressure on the drill guide with your hand. The reaming/drilling is carried out with short 2-second bursts so that the chips of the subchondral bone that are created and impacted into the facet joint are not burned. This may cause osteonecrosis, which will compromise your fusion results. The reaming/drilling is continued until the drill has been advanced to the stop, which is in contact on the top of the drill guide (Fig. 184.17), a distance of 1 cm. This allows the posterior portion of the facet allograft to be countersunk approximately 2 mm below the posterior surface of the facet joint. Once the drill bit has bottomed out to the drill guide stop, ream another 2 to 3 seconds to help create a good bleeding surface on each side of the facet joint before dowel placement (the drill bit
A(1)
B(1)
C(1)
A(2)
B(2)
C(2)
B(1)
B(2)
Fig. 184.15 Lining up the vertical lines of the drill guide and the spatula.
Fig. 184.16 Impacting the drill guide, close to the spatula, down into the facet joint.
Chapter 184—Percutaneous Fusion Techniques 1407
has side-cutting teeth). After reaming/drilling has been completed, the TruFUSE facet fusion allograft dowel is placed into the graft holder block to ensure the graft is properly oriented so the smaller end will go into the compacted tunnel first and ensure a solid press-fit. It is then loaded into the insertion device. The TruFUSE facet fusion allograft dowel in the holder is placed down into the drill guide and then impacted into the facet joint with the impactor (Fig. 184.18). When the graft is fully seated into the tunnel and countersunk 2 mm, the drill guide is carefully removed from the joint by pulling it straight out of the joint so the allograft is not dislodged by the drill guide's teeth. The same procedure is then followed for the contralateral side. The wounds are closed in layers and sterile dressings are applied. The patient is then placed in a back brace to limit flexion, extension, and lateral bending for 6 to 8 weeks. Figure 184.19 shows an x-ray of the graft in place, and Figure 184.20 shows a patient's recent postoperative CT scan.
Clinical Pearls The approach to L5-S1 can be very challenging and is best done similar to a diskogram angle (Fig. 184.21). The pin should enter the top of the joint and not the middle one third as with the other levels to ensure better bony purchase for the graft (Fig. 184.22).
Complications Posterior spinal fusion is a salvage procedure and should always be viewed that way, regardless of the ease of this new variation of an old technique. The dura and exiting nerve roots are just beyond the bottom of the incisions, and this makes it imperative that this procedure only be performed by those well versed in the regional anatomy and experienced in performing either open or at least mini-open interventional pain management techniques. This procedure should not be performed on patients who are not cleared for surgery and who do not need rods/screws.
Fig. 184.19 Oblique x-ray—graft within the facet joint.
Video: Percutaneous technique
Fig. 184.17 Facet joint reaming.
Video: Percutaneous technique
Fig. 184.18 Graft impacted and countersunk within the facet joint.
Fig. 184.20 CT scans—graft within the facet joint.
1408 Section V—Specific Treatment Modalities for Pain and Symptom Management
Fig. 184.21 L5-S1 approach similar to diskogram angle.
The best surgical candidates are those who have experienced good, albeit transient, pain relief following intraarticular facet injections with local anesthetic and/or steroid (for localization of the pain-generating degenerative facet joint) and for those who have failed to achieve long-lasting relief with radiofrequency ablation. This technique is straightforward when performed by those skilled in placement of needles into the facet joints. Postprocedure bracing will improve long-term outcomes and should be used in all patients undergoing posterior facet joint spinal fusion with the TruFUSE allograft dowel. Bone stimulators are medically necessary in patients with diabetes, smokers who will not stop smoking, pseudoarthrosis patients, anyone who has been on steroids recently, Down syndrome patients, and patients with multilevel fusions. Posterior facet joint spinal fusion is a reasonable procedure for patients who suffer from intractable mechanical
Fig. 184.22 Angle for TruFUSE at L5-S1.
low back pain not relieved by nonoperative measures. It may be caused by facet joint arthropathy, adjacent segment degeneration next to long-standing hardware, or microinstability following decompressive spine surgery. The procedure is frequently used as a standalone technique or as an adjunct to other spinal fusion and/or decompression procedures.
Index Note: Page numbers followed by b indicate boxes, f indicate figures, and t indicate tables.
A
Abdominal aneurysm aortic, femoral neuropathy due to, 826 CT scan of, 674, 677f low back pain in, 699 Abdominal crunches, for sacroiliac joint disorders, 762 Abdominal muscles, contraction of, 674, 676f Abdominal pain in acute pancreatitis, 682 in chronic pancreatitis, 685, 685f in ilioinguinal neuralgia, 687 management of limitations in, 945, 945t prolotherapy in, 1040–1041, 1040f transcutaneous electrical nerve stimulation in, 996 Abdominal wall pain, 674–681 in anterior cutaneous nerve entrapment, 674–677, 675f, 676f, 677f in liver disease, 679–681, 679f, 680f, 681f in slipping rib syndrome, 677–679, 678f Abducens nerve (VI) evaluation of, 44t palsies associated with, 376, 377t Abduction release test, resisted, for trochanteric bursitis, 361, 362f A-beta fibers classification of, 10, 11t properties of, 11 Abortive therapy, for cluster headache, 446–451 Abrasions, corneal, 484, 484f Abscess brain, headache in, 252, 252f, 255 epidural. See Epidural abscess iliac, femoral neuropathy due to, 826 lung, 654, 654f retropharyngeal space, 500, 502f Abused substances. See Drug abuse. under named drug Acetabular fracture, CT scan of, 98 Acetaldehyde accumulation, after celiac plexus block, 1203 Acetaminophen, 882–883 contraindications to, 883 dosing guidelines for, 882–883 for cancer pain, 304, 305t for osteoporosis, 704 hepatic injury caused by, 73 indications for, 883 mechanism of action of, 882 pharmacokinetics of, 883 Acetazolamide for chronic arachnoiditis, 749 for postoperative dural sac deformities, 785 Acetylsalicylic acid. See Aspirin Achilles bursitis, 367–368, 368f Achilles tendinitis, 863–864, 863f, 864f Achilles tendon, 860, 862f rupture of, 864–865 Achondroplasia (dwarfism), 78 Acoustic nerve (VIII), evaluation of, 44t Acromioclavicular joint. See also Shoulder anatomy of, 580f painful, 79, 579–581, 581f treatment of, 579–581, 581f Action potentials, in nerve conduction, 178 Active straight leg raising test, 777, 778f Acupuncture, 1019–1026. See also Alternative medicine adverse effects of, 1025–1026 anatomic aspects of, 1021–1023 auricular, 1023 channels and collaterals in, 1022–1023 complications and pitfalls of, 1025–1026 De Qi sensation in, 1022
Acupuncture (Continued) electroacupuncture, 1023 example of, 1019, 1020f for cancer pain, 1025 for chronic arachnoiditis, 749 for low back pain, in pregnancy, 779 for neuropathic pain, 211 for phantom pain, 300 for piriformis syndrome, 792 historical considerations in, 1019–1020 morphogenetic singularity theory and, 1021 neurohumoral mechanisms of, 1020–1021 outcomes of, 1025 principles of, 1020–1021 provider credentialing for, 1026 safety of, 1025–1026 scalp, 1023–1024 techniques of, 1023–1024 therapies concomitant with, 1024 yin-yang theory and, 1020, 1020f Acupuncture needles, manufacture and use of, 1025 Acupuncture points, 1021, 1022f types of, 1022 Acupuncture research, issues in, 1025 Acute chest syndrome, in sickle cell disease, 245 Acute pain in burn patients, 229 management of, 216–227 hypnosis in, 964 technique of, 965 narcotic analgesics in, 218–219, 218f neural blockade in, 219–227, 220f, 221f, 222f, 223f, 224f, 225f, 226f, 226t. See also Nerve block(s), for acute/ postoperative pain nonprescription analgesics in, 878–879 nonsteroidal anti-inflammatory drugs in, 217–218, 217f, 217t prophylactic measures in, 216 transcutaneous electrical nerve stimulation in, 996 obturator nerve block for, 1245 thoracic epidural nerve block for, 1181 Addiction, to opioids, 898, 898f vs. dependence, 308–309 Adductor tendinitis, 363–364, 363f, 364f A-delta fibers, 703 classification of, 10, 11t properties of, 11 Adenoma, pleomorphic, of parapharyngeal space, 500, 501f Adhesions, epidural, lysis of, 1138–1141, 1258–1272. See also Epidural adhesiolysis Adhesive capsulitis (frozen shoulder), 566, 567f Adjunctive therapy for herpes zoster, 270–271 for neuropathic pain, 210–211 Adson's test, for cervical radiculopathy, 525, 526t Adult hemoglobin (Hb A), 243 Afferent(s) activation of, 19–20, 20f dorsal horn projections of, 11t, 12, 13f in nerve injury sensitivity changes of, 26 sprouting of, 26 in tissue injury, 20, 20f primary, 10–12 classification of, 10, 11t properties of, 10–12, 11f transmitters in, 17–18, 18f supraspinal projections of, 15–16, 15f, 16f with high thresholds, 12 Afferent line labeling, in pain processing system, 17
Afferent transmitter systems in nociception, pharmacology of, 17–18, 18f primary, 32f Alanine aminotransferase (ALT), 71 Albumin, 67, 72 Alcohol intoxication with, 74 neurolytic blockade with, 325–327, 325t subarachnoid, 1216–1218, 1217f Alcohol use/abuse acute pancreatitis and, 682, 683f chronic pancreatitis and, 684 triggering cluster headache, 440, 441 Alcoholism, screening for, 74 Alendronate, for complex regional pain syndrome, 285 Alfentanil, 907 Alkaline phosphatase (ALP), 71 Alkaloids, phenanthrene, 893t, 901–903. See also specific agent, e.g., Morphine Allergies, contrast-induced in diskography, 123 in epidurography, 143 Allochiria (mirror-image pain), 8 Allodynia in postmastectomy pain, 662t tactile, 12 Alpha2-adrenergic agonists, mechanism of action of, 30, 30f Alpha-amino-3-hydroxy-5-methyl-4isoxazolepropionic acid (AMPA) receptor, 31, 32f Alternative medicine, 934–940 acupuncture in, 936t, 939, 1019–1026. See also Acupuncture biostimulation techniques in, 939 chiropractic therapy in, 938–939 classification of, 935, 936t comfort measures in, 939 definition of, 935 hypnosis in, 936t, 938, 963–966. See also Hypnosis intercessionary prayer and, 937–938 low-power laser therapy in, 939 magnetic field therapy in, 939 music therapy in, 937 office of, 936 relaxation therapy in, 938. See also Relaxation technique(s) scope of, 937 spinal manipulation in, 1009–1018. See also Spinal manipulative therapy spiritual healing and, 937–938 transcutaneous electrical nerve stimulation in, 939. See also Transcutaneous electrical nerve stimulation (TENS) vs. holistic medicine, 935 Aluminum sulfate, for herpes zoster, 271 Alveolar nerve, inferior, 1070 Alvimopan, 912 Amine release, in tissue injury, 21t Amitriptyline, 914f, 915 for acute arachnoiditis, 748 for cancer pain, 309 for migraine prophylaxis, 426 for mononeuritis multiplex, 671 for peripheral neuropathies, 267 for phantom pain, 297 for postmastectomy pain, 663t for post-thoracotomy pain syndrome, 639 for proctalgia fugax, 805 for tension-type headache, 434t for vulvodynia, 799 Ammonium compounds, in neurolytic blockade, 325t, 327 Amoxapine, for tension-type headache, 434t
1415
1416 Index Amphetamine abuse, screening for, 74 Amplitude, in electromyography, 179 Analgesia ilioinguinal-iliohypogastric nerve block with, 1238 technique of, 1240 patient-controlled, 219 for post-thoracotomy pain, 667 postoperative, thoracic epidural nerve block in, 1181 Analgesic agents. See also specific agent adjuvant for cancer pain, 309 for peripheral neuropathies, 267, 267t for burn pain based on valid pain assessment, 240 excessive use of, complications from, 240–241 nonopioid, 234 for mononeuritis multiplex, 671 for occupational back pain, 724 for osteoarthritis, 393 opioid, 890–912. See also Opioid(s) role of, in patient with analgesic overuse headache, 455. See also Medication overuse headache simple (nonprescription), 878–883. See also Acetaminophen; Nonsteroidal antiinflammatory drugs (NSAIDs) classification and relationships of, 878–879, 879f overview of, 878–879 topical, for neuropathic pain, 210 Analgesic rebound headache, mechanisms of, 456, 457f Anemia definition of, 58 in giant cell arteritis, 479 Anesthesia general, for burn pain, 234–235 local. See Local anesthetics nerve blocks with. See Nerve block(s); specific nerve block Anesthetic agents for caudal epidural nerve block injection of, 1254, 1254f selection of, 1254–1255 for celiac plexus block, 1099–1100 for cervical epidural nerve block injection of, 1132, 1133f selection of, 1132–1133 for cervical facet block, 1124 for cervical plexus block, 1099–1100 for lumbar facet block, 1227 for lumbar sympathetic nerve block, 1235 for thoracic epidural nerve block, 1183 Aneurysm(s) abdominal aortic, femoral neuropathy due to, 826 CT scan of, 674, 677f low back pain in, 699 carotid artery, in cavernous sinus, 490–491, 490f cavernous sinus, 377, 377f, 490–491, 490f Aneurysmal bone cyst, magnetic resonance imaging of, 647f Anger, in cancer patients, 345 Angina spinal cord stimulation for, 1309 stellate ganglion block for, 1104 thoracic epidural nerve block for, 1181 Angiofibroblastic hyperplasia, in rotator cuff disorders, 570–571 Anhedonia, 948–949 Animals, laser research in, 1400 Ankle, radiography of, 84 Ankle pain disorders causing, 861t in arthritis, 860–862, 862f in bursitis, 367–368, 368f, 865 nerve blocks for, 1296–1297 Ankle sprains, osteopathic manipulative therapy for, 1007 Ankylosing spondylitis, demographics of, 39t Annuloplasty, intradiskal electrothermal, 1388–1392. See also Intradiskal electrothermal annuloplasty Anorexia AIDS-related, 342 cancer-induced, 342
Anterior apprehension test, for rotator cuff disorders, 574, 574f Anterior cruciate ligament anatomy of, 834–835, 836f integrity of, anterior drawer test for, 840–841, 841f Anterior cutaneous nerve entrapment, 674–677, 675f, 676f, 677f Anterior drawer test, for anterior cruciate ligament integrity, 840–841, 841f Anterior horn cell disorders, electrodiagnosis of, 185 Anterior interosseous syndrome, 611–613, 612f, 613f electrodiagnosis of, 184 Anterior scalene syndrome, 534–535 Anterocollis, 559–560 muscles involved in, 562t Antiarrhythmics, for mononeuritis multiplex, 671–672 Antibiotics, for epidural abscess and infective spondylitis, 742 Anticoagulants aspirin and, 880 knee pain and, 839 preoperative management of, for epidural adhesiolysis, 1260 Anticonvulsants, 919–923. See also specific agent, e.g., Gabapentin category 1, 919–922, 920f category 2, 922 classification of, based on mechanism of action of, 919, 920t for cancer pain, 309 for herpes zoster, 270 for migraine prophylaxis, 426–427 for mononeuritis multiplex, 671 for neuropathic pain, 209–210 for phantom pain, 297–298 Antidepressants classification of, 913–918, 914t for herpes zoster, 270 for mononeuritis multiplex, 671 for vulvodynia, 799 in pain management, 913–918 clinical use of, 918 neuropathic, 210 monoamine oxidase (MAO) inhibitors, 917–918. See also Monoamine oxidase (MAO) inhibitors noradrenergic reuptake inhibitors, 917, 917f selective serotonin reuptake inhibitors, 915–916. See also Selective serotonin reuptake inhibitors (SSRIs) serotonin and noradrenergic reuptake inhibitors, 917, 917f tricyclic, 913–915. See also specific agent, e.g., Amitriptyline absorption and metabolism of, 914 abuse potential of, 915 common, 914f, 915, 915f for anterior interosseous syndrome, 612 for cancer pain, 309 for complex regional pain syndrome, 284 for facial complex regional pain syndrome, 512 for intercostal neuralgia, 640–641 for migraine prophylaxis, 426 for phantom pain, 297 for postmastectomy pain, 662, 663t for post-thoracotomy pain syndrome, 639 for proctalgia fugax, 805 for radial tunnel syndrome, 614 for tension-type headache, 434, 434t mechanism of action of, 914 overdosage of, 915 side effects of, 914–915, 914t withdrawal of, 915 Antiepileptics for postmastectomy pain, 662 for vulvodynia, 799 Anti-inflammatory agents, for rheumatoid arthritis, 401 Antimony poisoning, screening for, 74 Antinuclear antibody (ANA) test, 61–63 for scleroderma, 407 for systemic lupus erythematosus, 404 Antiviral agents, for herpes zoster, 270 Anulus fibrosus, anatomy of, 118
Anxiety cancer-related, palliative care for, 343 in burn patients, overlooking, 241 in chronic pain, 949 pain associated with, 192, 206 relaxation-induced, 975 in biofeedback, 961–962 Anxiolytics, for burn pain, 234 Aortic aneurysm, abdominal, femoral neuropathy due to, 826 Appetite disturbances, cancer-related, palliative care for, 342 Aquatic therapy, 987. See also Hydrotherapy Arachnoid webs, 783, 784f Arachnoiditis, 56, 743–750 acute, treatment of, 748 causes of, 743 chronic, treatment of, 748–749 nonconventional, 750 clinical features of, 746–747 diagnosis of, 745–748 correlative, 747–748 electrodiagnostic studies in, 745 epiduroscopy and myeloscopy in, 745 focal, 783, 784f in failed back surgery syndrome, 771–772, 771f, 772f laboratory findings in, 745 pain mechanisms in, 744, 744f prevention of, 748 radiologic studies in, 745–746, 745f, 746f, 747f treatment of, 748–750 interventionism in, 749–750 nonconventional, 750 Arsenic poisoning, screening for, 74 Arteritis, temporal. See Giant cell arteritis Arthritis biofeedback for, 955 degenerative. See Osteoarthritis of ankle, 860–862, 862f of foot, 860–862, 862f of wrist and hand, 616–619, 617f, 617t, 618f osteo-. See Osteoarthritis painful, therapeutic scintigraphy for, 93, 93f rheumatoid. See Rheumatoid arthritis Arthritis Self-Management Program (ASMP), 969 Arthroplasty, hip, femoral neuropathy after, 826 Arthroscopic debridement, for osteoarthritis, 394 Arthroscopic subacromial decompression, 577, 577f Arthroscopic surgery fluoroscopically-guided of hip, 85, 86f of shoulder, 85, 86f for rotator cuff disorders, 577, 577f, 578f Asanas/postures, in yoga, 974t Asbestos-related pleural disease, 657, 657f Ascending projection system transmitters, 18 Ascending spinal tracts anatomy of, 14–15 plasticity of, 17 Aspartate aminotransferase (AST), 71 Aspirin, 879–881 action of, 879 anticoagulants and, 880 benefits of, 879 characteristics of, 885–886 chemical structure of, 217f, 885f contraindications to, 881 dosing guidelines for, 879–880 drug interactions with, 881 for cancer pain, 305t for tension-type headache, 433t half-life of, 880–881 indications for, 881 mechanism of action of, 879 pharmacokinetics of, 880–881 pharmacology of, 887t Reye's syndrome and, 880, 881 Assistive devices, for rheumatoid arthritis, 402 Asthma, 651 Asthma inhalers, impeding biofeedback, 962 Athletes iliopsoas bursitis in, 817 injury to. See Sports injury(ies) spondylolysis in, 752, 752t
Atlantoaxial nerve block, 1051–1053 indications for, 1051, 1052t side effects and complications of, 1053 technique of, 1052–1053, 1052f, 1053f Atlantoaxial pain, differential diagnosis of, 1051, 1052t Atlantoaxial subluxation, in rheumatoid arthritis, 546, 546f Atlanto-occipital nerve block, 1047–1049 indications for, 1047 side effects and complications of, 1048–1049 technique of, 1048, 1049f, 1050f Atropine, chemical structure of, 896f Auditory canal, external, pain in, 495–497, 497f, 498f Aura, in migraine headache, 422t, 423, 423t persistent, 424 symptoms of, 423 Auricular acupuncture, 1023. See also Acupuncture Auricular pain, 494–495, 496f, 497f Auriculotemporal nerve, irritative neuropathy of, 1372–1373 Autogenic training, 968–969. See also Relaxation technique(s) technique of, 971 Autonomic nervous system (ANS) anatomy of, 1192, 1192f changes in, cluster headache and, 442 Autonomic reflex testing, in peripheral neuropathy, 266 Avascular necrosis in sickle cell disease, 247 vs. iliopsoas bursitis, 819, 819t Avoidance strategies, for burn pain, 235–237 Axillary brachial plexus block, 1148–1150. See also Brachial plexus block anatomic aspects of, 1148, 1149f indications for, 1148 side effects and complications of, 1150 technique of, 1148–1149, 1148f, 1149f, 1150f Axolemma, 178 Axon(s). See also Nerve fibers diffuse injury of, magnetic resonance imaging of, 107 Axonotmesis, 182, 532–533, 532f Azotemia, 69–70
B
B cells, 59, 64 Babinski's sign, in epidural abscess, 739–741 Back exercises, for lumbar radiculopathy, 713 Back pain acute, 722, 723f cervical. See Neck pain chronic, 728–730 euphemistic, 725–726 lumbar, 694–700. See also Low back pain lumbar facet joints and, 1116 occupational, 722–736. See also Occupational back pain Back schools, 713 Back surgery syndrome, failed, spinal cord stimulation for, 1308–1309 Background pain, in burn patients, 229–230, 230f management of, 232–233 Backpack (rucksack) paralysis, 535 Baclofen for cluster headache, 450 for complex regional pain syndrome, 285 for glossopharyngeal neuralgia, 474, 474t for muscle spasms, 927 for neuropathic pain, 210–211 for tension-type headache, 433t Bacterial meningitis, headache in, 252, 254–255 Baker's cyst, 839, 853–855, 853f, 854f, 855f in rheumatoid arthritis, 398, 398f rupture of, 853, 853f Balloon compression, percutaneous, for trigeminal neuralgia, 468–469 Balloon sign, 618 Ballottement test, for joint effusions, 839, 840f Basal cell carcinoma, of auricle, 495, 497f Basic calcium phosphates (BCPs), in osteoarthritis, 390 Basilar artery migraine, 424–425, 424t. See also Migraine headache Bed rest, for lumbar radiculopathy, 712–713
Index 1417 Behavior(s), associated with peripheral neuropathy, 263, 263t Behavioral pain, transcutaneous electrical nerve stimulation for, 996 Behavioral therapy, for lumbar radiculopathy, 713 Bell's palsy, 375, 376t, 379 Benzodiazepines, for phantom pain, 298 Beta blockers for migraine prophylaxis, 426 for phantom pain, 298 Betamethasone, intrathecal use of, for cancer pain, 323 Biceps tendinitis, 354–356, 354f, 355f, 356f, 585–587 diagnostic tests for, 585–586 differential diagnosis of, 586–587, 587t historical considerations in, 585 signs and symptoms of, 585, 586f treatment of, 587, 587f complications and pitfalls in, 587 Biceps tendon, wear and tear of, 585, 586f Biliary obstruction, intrahepatic, 72 Bilirubin, 71 Bioelectromagnetic applications, 936t Biofeedback, 954–962 adaptation phase of, 959 applied, 954, 955 autogenic, 959 baseline phase of, 959 biomedical engineering and cybernetics in, 955 blood volume pulse, 956 drug effects in, 962 efficacy of, 955, 956t electromyography-assisted, 957, 958f for arthritis, 955 for chronic pain, 956 for facial complex regional pain syndrome, 512 for migraine headache, 956 for pain disorders, 955, 956t for Raynaud's disease/phenomenon, 956–957 for temporomandibular joint disorders, 957 for tension-type headache, 956 historical considerations in, 955 indications for, 955–957, 956t muscle discrimination in, 960 muscle scanning in, 960 practitioner/patient considerations in, 960–961 psychophysiology and, 955 reactivity phase of, 959–960 recovery phase of, 960 relaxation-induced anxiety in, 961–962 resources for, 962 side effects and complications of, 961–962 skill learning and maintenance in, 961 skin conductance-assisted, 957 skin temperature-assisted, 958–959 techniques of, 957–961 general approach in, 957–959, 958f practitioner and patient considerations in, 960–961 specific approach in, 959–960 thermal-assisted, 956–957, 959 vs. vestibulectomy, 956 Biomechanical spine pain, cryoanalgesia for, 1366–1369, 1367f, 1368f, 1369f Biomedical engineering, in biofeedback, 955 Biopsy, of temporal artery, for giant cell arteritis, 478, 478t Biopsychosocial treatment model, for chronic pain, 461, 462f Biostimulation techniques, 939 Bismuth poisoning, screening for, 74 Bisphosphonates for bone metastases, radiation therapy with, 316 for osteoporosis, 705 for trochanteric bursitis, 816 Bites, tick, knee pain due to, 839 Bladder dysfunction, in arachnoiditis, 747 Bleeding. See Hemorrhage Blind technique of ganglion of Walther (impar) block, 1281–1282, 1281f of hypogastric plexus block single-needle, 1274, 1274f two-needle, 1276–1277, 1277f of lumbar epidural nerve block, 1210–1212 of suprascapular nerve block, 1175, 1175f
Blisters, suction, in cold-type complex regional pain syndrome, 277 Blood glucose, control of, for mononeuritis multiplex, 672 Blood pressure cuff test, for Achilles tendon rupture, 864–865 Blood supply, to intervertebral disk, 119 Blood urea nitrogen (BUN), 69 elevated, 69–70 Blood volume pulse (BVP) biofeedback, 956 Blue dot sign, in testicular torsion, 795 Bone cyst, aneurysmal, magnetic resonance imaging of, 647f Bone diseases, associated with pain, 701, 702t Bone harvest, iliac crest, cryoanalgesia for, 1366, 1367f Bone marrow edematous lesions in, 110–111 complex regional pain syndrome causing, 111, 113f degenerative conditions associated with, 111 vascular causes of, 111, 112f magnetic resonance imaging of, 110–111 Bone metastases bisphosphonates for, radiation therapy with, 316 lumbosacral, 696–697, 697f painful, therapeutic scintigraphy for, 92–93, 93f Bone pain evaluation of, baseline blood testing in, 702t nonpharmalogic interventions for, 703–704, 704f osteoporosis-related fracture causing, 701. See also Osteoporosis pharmacologic interventions for, 704–705 relief of, additional points for, 705–706 Bony spur, posterior, 542–543 Borrelia burgdorferi, in Lyme disease, 64 Botulinum neurotoxin for cervical dystonia, 561–562 trials of, 562, 563t for migraine prophylaxis, 427 for phantom pain, 299 for piriformis syndrome, 792 for tension-type headache, 435, 435t in neurolytic blockade, 327 Bouchard nodes, 81, 386, 386f, 399–400, 400f, 618 Boutonnière deformity in rheumatoid arthritis, 399, 399f of finger, 618, 618f Brachial neuritis, 380–381, 381f Brachial plexopathy, 529–540 anatomic aspects of, 529–532, 530f, 531f, 532f classification of, 533–536, 533t clinical presentation of, 533–536 complications of, 540 computed tomography in, 539 diagnosis of, 536–539, 538t, 539t electromyography in, 536–538, 538t historical perspectives of, 529, 529f iatrogenic, 535–536 in backpack (rucksack) paralysis, 535 in costoclavicular syndrome, 534–535 in Parsonage-Turner syndrome, 536, 537f, 538f in pectoralis minor syndrome, 534–535 in thoracic outlet syndrome, 534–535, 535f information sources for, 540b lower, 533–534 magnetic resonance imaging in, 537f, 539 myelography in, 539 neoplastic, 536, 536t, 537f nerve conduction studies in, 536–538, 538t nerve vs. muscle involvement in, 539t pathophysiology of, 532–533, 532f radiation therapy for, 317, 317f radiation-induced, 536, 536t radiography in, 539 sensory evoked potentials in, 538, 539t traumatic, 534–535, 534f, 535f treatment of pharmacologic, 540 rehabilitation in, 539–540 surgical, 540 upper, 533
1418 Index Brachial plexus anatomy of, 529–532, 530f, 531f, 532f, 1142, 1143f postfixed, 531 prefixed, 531 tumors of, 533t, 536, 537f Brachial plexus block, 1142–1150 anatomic aspects of, 1142, 1143f axillary, 1148–1150 differential, 155 historical considerations in, 1142 interscalene, 1142–1145 supraclavicular, 1145–1148 Brain abscess, headache in, 252, 252f, 255 Brain metastases, radiation therapy for, 317–318 Brain stimulation. See also Spinal cord stimulation peripheral, cortical, and deep, 1310 Brain tumor, headache in, 253, 254f, 256 Brainstem, morphine injection into, 28 Brainstem auditory evoked potentials (BAEPs), 188 Breakthrough pain, 943–944 in burn patients, 229–230, 230f management of, 233 spontaneous, 944 Breast cancer, metastatic, yoga therapy for, 970 Breathing deep, for burn pain, 237–238 relaxed. See also Relaxation technique(s) relaxed, 971 Bridge (transition) therapies, for medication overuse headache, 460–461, 461t Brief Pain Inventory, 196–197, 198f Bronchitis, 651, 652f Brown-Séquard syndrome, 528, 646, 647f Brucella infection, of spine, 739, 741f Buccinator nerve, 1070 Bulbospinal systems in tissue injury, 23, 24f opioids in, 28 Bunionette (tailor's bunion), 870f, 871 Buoyancy, in hydrotherapy, 988 Bupivacaine, 931t, 932t Bupivacaine/methylprednisolone injections for Achilles bursitis, 367–368, 368f for acromioclavicular joint pain, 579–580, 581f for anterior cutaneous nerve entrapment, 676, 677f for Baker's cyst, 854–855, 855f for biceps tendinitis, 587, 587f for bicipital tendinitis, 355 for costosternal syndrome, 633–634 for gluteal bursitis, 809–810, 810f for ilioinguinal neuralgia, 688, 689f for iliopsoas bursitis, 818f, 819 for infrapatellar bursitis, 848, 848f, 851 for ischiogluteal bursitis, 811, 00105:t0035 for osteitis pubis, 788–789, 790f for osteoarthritis, 567 for pes anserine bursitis, 849, 850f for post-thoracotomy pain, 666 for prepatellar bursitis, 846, 847f for quadriceps expansion syndrome, 856–858, 859f for sacroiliac joint disorders, 761 for slipping rib syndrome, 678, 678f for sternalis syndrome, 636 for sternoclavicular joint syndrome, 644 for subdeltoid bursitis, 583, 583f for suprapatellar bursitis, 844–845, 845f for supraspinatus tendinitis, 352 for trochanteric bursitis, 362, 362f, 815–816 for vulvodynia, 799–800 Buprenophine, 911 chemical structure of, 911f Burn depth, definitions of, 229, 229f Burn pain, 228–242 acute, 229 assessment of, 229, 230 background, 229–230, 230f management of, 232–233 breakthrough, 229–230, 230f management of, 233 chronic, 00025:s0320 classification of, 229–230, 230f clinical settings in, 229–230, 230f definition of, 229 differential diagnosis of, 231 duration of, 230 from first-degree burns, 229, 230f
Burn pain (Continued) from second-degree burns, 229, 230f from third-degree burns, 229, 230f historical considerations in, 228–229 management of, 231–242 anesthetics in, 234–235 anxiolytics in, 234 avoidance in, 235–237 cognitive restructuring in, 239–240 complications in, 240–242 coping styles in, 232t, 235, 241 deep breathing in, 237–238 distraction techniques in, 235–236 future directions in, 242 general philosophy in, 00025:f0025, 231–232 hypnosis in, 236–237, 965 technique of, 966 imagery in, 236 institutional guidelines in, 00025:f0025, 231 nonopioid analgesics in, 234 nonpharmacologic, 235–240 operant techniques in, 238–239 opioids in, 233–234 overlooking anxiety in, 241 patient participation in, 240 patient teaching in, 239 pharmacologic, 233–235 positive reinforcement in, 238–239 progressive muscle relaxation in, 238 quota system in, 238 reappraisal in, 239–240 regular medication scheduling in, 238 relaxation techniques in, 237–238 setting schedules in, 240 side effects of, 240–242 thought stopping in, 239 virtual reality in, 237, 237f wound care in, 240, 241–242 physical findings in, 229–230, 229f, 230f postoperative, 229–230, 230f management of, 233 procedural, 229–230, 230f management of, 232–233 psychological aspects of, 241 staff changeover and, 241 unplanned procedures and, 241 Burn Specific Anxiety Scale, 241 Burners, 534, 535f. See also Brachial plexopathy Burning pain, in arachnoiditis, 747 Burning thigh sign, in meralgia paresthetica, 821, 823f Bursae associated with greater trochanter, 813, 814f gluteal, anatomy of, 808, 809f iliopsoas, 817, 818f ischial, anatomy of, 810 of knee, 835, 836f subdeltoid, abnormalities of, 582, 583f suprapatellar, 843, 844f Bursitis cubital, 598, 600f, 603–605, 604f, 605f gluteal, 808–810, 809f, 810f iliopsoas, 817–820, 818f, 819f, 819t in scleroderma, 406 ischiogluteal, 810–811, 811f of ankle and foot Achilles, 367–368, 368f retroachilleal, 865 retrocalcaneal, 865 sub-Achilles, 865 subcutaneous calcaneal, 865 subtendinous, 865 of knee, 843–852 infrapatellar deep, 835, 836f, 850–851, 850f treatment of, 851 superficial, 847–848, 847f treatment of, 848, 848f pes anserine, 848–850, 849f treatment of, 849–850, 850f prepatellar (housemaid's knee), 365–366, 365f, 845–847, 845f, 846f treatment of, 846, 847f suprapatellar, 843–845, 844f, 845f treatment of, 844–845, 845f treatment of, complications and pitfalls in, 851–852 olecranon, 601–603, 602f, 603f, 604f subdeltoid, 582–584, 583f treatment of, 582–584, 583f trochanteric, 361–363, 361f, 362f, 813–816
Butorphanol, 910 chemical structure of, 910f Butterfly rash, in systemic lupus erythematosus, 403, 403f Bystander disease, 1030–1031, 1031f correction of, 1031, 1031f neuropraxia and, 1031–1032
C
Cachexia, cancer, pain management and, 944 Cadavers, laser research in, 1400 Calcaneal jump sign, in plantar fasciitis, 370, 370f Calcific tendinosis, of shoulder, 79, 80f Calcification(s) in ligamentum flavum, 545, 545f in scleroderma, 406f, 407, 407f Calcinosis, subcutaneous, 405–406, 406f Calcitonin for complex regional pain syndrome, 285 for osteoporosis, 705 for phantom pain, 297 Calcitonin gene-related peptide (CGRP), 440 Calcium channel(s), 00003:s0135 Calcium channel blockers, for migraine prophylaxis, 426 Calcium imbalance, 70–71 Calcium pyrophosphate dehydrate (CPPD) crystal(s), in osteoarthritis, 390 Calcium pyrophosphate dehydrate (CPPD) crystal deposition disease, 81 Calcium-regulating drugs, for complex regional pain syndrome, 285 Cancer. See also at anatomic site. specific neoplasm gastroparesis in, 340–341 palliative care for, 336–348. See also Palliative care, of cancer patient Cancer pain acupuncture for, 1025 anesthetic approach to, 309–311, 310t. See also Cancer pain, nerve blocks for assessment of, 302 Edmonton Classification System in, 338, 339f multidimensional, 338–343 barriers to management of, 346, 347f cervical epidural nerve block for, 1127, 1127t diagnosis of, 303 epidemiology of, 337 epidural steroid injections for, 321–322 etiology of, 329 hypnosis for, 964 technique of, 965 invasive procedures for, 942 nerve blocks for, 309–310, 310t. See also under specific nerve block diagnostic, 320, 320t differential, 320 intrathecal glucocorticoids in, 321–323 analgesic effects of, 323 indications for, 321–322 safety of, 323 local anesthetic injections in, 319–321 neurolytic, 311, 324–328. See also Neurolytic blockade prognostic, 320–321 regional anesthetic techniques in, 321 continuous, 321 neuropathic. See Neuropathic pain neurostimulation for, 311 neurosurgery for, 311, 333–335 nonpharmacologic approach to, 309, 310t, 346t palliative care for, 336–348. See also Palliative care, of cancer patient clinical assessment of, 337–345 community issues and adjunct treatments with, 345 interventional procedures in, 346, 348t principles of, 346, 346t, 347f WHO definition of, 336–337 pharmacologic approach to, 304–309, 305t, 306t, 308t, 346, 346t. See also specific drug therapy advantages of, 942 limitations of, 942–943 opioids in, spinal, 330–331, 331t, 332t physiatric approach to, 311 psychological approach to, 311
Cancer pain (Continued) radiation therapy for, 312–318. See also Radiation therapy, palliative indications for, 312 technique of, 313–316, 313f, 314t relaxation procedures for, 970 therapeutic approach to, 303–304 thoracic epidural nerve block for, 1181–1182 transcutaneous electrical nerve stimulation for, 996 treatment plan for, 329–331 trigger point injections for, 321 types of, 303t, 338 WHO analgesic ladder in, 346, 347f, 655f, 656 Cancer therapy. See also specific therapy, e.g., Radiation therapy femoral neuropathy due to, 826 pain associated with, 303t pharmacologic, 330, 330f primary, 329 Candida albicans, in vulvodynia, 798–799 Cannabinoids, for appetite stimulation, 342 Capitellum, osteochondritis dissecans of, 79, 80f Capsaicin for cluster headache, 450 for facial complex regional pain syndrome, 512 for herpes zoster, 271 for osteoarthritis, 393 for osteoporosis, 705 for postmastectomy pain, 663 in neurolytic blockade, 325t, 327 Carbamazepine, 920–921, 921f dosing guidelines for, 921 for glossopharyngeal neuralgia, 473, 473t for trigeminal neuralgia, 467 monitoring protocol for, 921, 921t Carbon dioxide laser, 1397, 1398f. See also Laser diskectomy. Laser therapy in animal research, 1400 Cardiovascular disorders in cluster headache, 440 opioid-induced, 896 Carisoprodol, 925, 925t for tension-type headache, 433t Carotid artery aneurysms, in cavernous sinus, 490–491, 490f Carotid chemoreceptor, in cluster headache, 443 Carotid-cavernous fistula, 491, 492f Carotidynia, 501–502 Carpal tunnel syndrome, 357–359, 357f, 379–380, 620–621 anatomic aspects of, 357–358, 357f clinical features of, 620–621, 621f demographics of, 39t diagnosis of, 621 differential diagnosis of, 00042:f0100, 00042:s0125 etiology of, 620 signs and symptoms of, 00042:f0085, 00042:f0090, 00042:f0095, 00042:s0115 tests for, 00042:s0120 treatment of, 00042:f0105, 00042:s0130, 621, 621f median nerve block in, 1165, 1166f yoga therapy in, 970 Cartilage, magnetic resonance imaging of, 114 Catching tendon sign, in trigger finger, 626, 627f Catheter intradiskal electrothermal advantages and disadvantages of, 1389t placement problems with, 1390, 1391f intrathecal, complications involving, 1321 percutaneous, 1313t, 1314, 1314f Racz, for epidural adhesiolysis, 1140, 1140f subcutaneous tunneled, 1313t, 1314, 1314f Catheterization in caudal epidural nerve block, 1256 in cervical epidural nerve block, 1136 inadvertent catheter placement in, 1136–1137 interpleural, anesthetic instillation via, 310 periaortic, in celiac plexus block, 1200 transforaminal, in epidural adhesiolysis, 1264–1266, 1265f, 1266f, 1267f, 1268f Cauda equina syndrome, 695 Caudal epidural nerve block, 1248–1257. See also Epidural nerve block, caudal Cauliflower ear, 494–495, 496f Causalgia, 290–291. See also Complex regional pain syndrome, type II
Index 1419 Cavernous sinus aneurysms of, 377, 377f, 490–491, 490f thrombosis of, 492 tumors of, 491, 491f Cavernous sinus syndromes, 489–492 CD4 cells, in HIV infection, 64 CD8 cells, in HIV infection, 64 Celecoxib, 889, 889f. See also Cyclooxygenase-2 (COX-2) inhibitors for acute arachnoiditis, 748 for tension-type headache, 433t pharmacology of, 887t Celiac ganglia, anatomy of, 1193 Celiac plexopathy, radiation therapy for, 317 Celiac plexus anatomy of, 221, 221f, 1193 structures surrounding, 1193, 1193f Celiac plexus block anatomic aspects of, 1192–1193 complications of, 222, 1202–1204 contraindications to, 1192 CT-guided for acute pancreatitis, 683–684, 684f for chronic pancreatitis, 686 diagnostic, 149 differential, 156t drugs for, 1200–1201 for acute/postoperative pain, 221–222, 221f for cancer pain, 310 for liver pain, 680–681, 680f future directions for, 1203f, 1204 historical considerations in, 1191 indications for, 1192 needle selection for, 1201 periaortic catheterization in, 1200 radiographic guidance in, 1201, 1201f technique of, 1193–1200 anterior approaches to, 1198–1199, 1198f, 1199f choice of, 1201–1202 classic retrocrural, 1193–1195, 1194f, 1195f transaortic, 1195–1198 CT-guided, 1196–1198, 1197f fluoroscopically-guided, 1196 transcrural, 1195 with splanchnic nerve block, 1200, 1200f Cellulitis after spinal cord stimulation, 1317–1318, 1317f periorbital, 483 Central autonomic dysregulation, in complex regional pain syndrome, type I, 276–277 Central canal (lamina X) neurons, 12t, 13 Central facilitation, in tissue injury, 22–24 Central nervous system (CNS) disorders electrodiagnosis of, 185 opioid-induced, 895–896 Central nervous system (CNS) trauma, pain from, 208 Central sensitization, migraine headache and, 421 Cerebral blood flow, in cluster headache, 442 Cerebrospinal fluid, circulation of, 781 Cerebrospinal fluid leaks after spinal cord stimulation, 1318 in arachnoiditis, 743 Cerebrospinal fluid pressure, increased, epidural injections causing, 168 Certification, for occupational back pain, 726–727 Cervical diskectomy, laser, 1405. See also Laser diskectomy Cervical diskography, technique of, 131–135, 133f, 134f, 135f Cervical dorsal root ganglia, herpetic/ postherpetic neuralgia of, vs. trigeminal neuralgia, 466 Cervical dystonia, 558–563 clinical presentation of, 559–560, 559f, 560t complications of, 563 diagnostic tests for, 560–561 differential diagnosis of, 560, 561t genetic factors in, 558 historical considerations in, 558, 559f imaging studies in, 561 muscle involvement in, 562t pathogenesis of, 558–559 post-traumatic, 560 psychogenic origin of, 560, 560t treatment of, 561–563 botulinum neurotoxin in, 561–562 trials of, 562, 563t
Cervical epidural nerve block, 1126–1137. See also Epidural nerve block, cervical Cervical facet block, 1116–1125 anatomic aspects of, 1118–1119, 1118f anesthetic agents for, 1124 cervical medial branch, 1121–1124, 1122t lateral approach in, 1123–1124, 1124f posterior approach in, 1121–1123, 1123f complications of, 1124 contraindications to, 1117, 1117t diagnostic, 148, 1117–1118 technique of, 517–518, 518f historical considerations in, 1116 indications for, 1116–1118, 1117t intra-articular, 1119–1121 lateral approach in, 1120–1121, 1121f, 1122f posterior approach in, 1119, 1120f protocol for, 86–87 technique of, 1119–1124 therapeutic, 1118 Cervical facet syndrome, 55, 00006:t0030, 516–521 clinical features of, 516–517, 517f, 518f diagnosis of, 517–518, 518f differential diagnosis of, 518 historical considerations in, 516 imaging in, 517 pain distribution in, 517, 517f, 518f prevalence of, 517 treatment of, 518–520, 519f cervical fusion in, 520 complications and pitfalls in, 520, 521t cryoanalgesia in, 1369 intra-articular facet joint injections in, 519, 519f medial branch blocks in, 519 medial branch neurotomy in, 520 radiofrequency lesioning in, 1345–1357. See also Cervical medial branch radiofrequency rehabilitation in, 518–519 whiplash injury and, 517 Cervical fusion, for cervical facet syndrome, 520 Cervical ganglia, 1095f Cervical medial branch radiofrequency, 1345–1357, 1345t anatomy in, 1345–1346, 1346f complications of, 1352 efficacy of, 1352 history in, 1345 indications for, 1346–1347 patient selection for, 1346, 1347f technique of, 1347–1357 posterolateral approach in, 1348–1352, 1351f prone approach in, 1347, 1348f, 1349f, 1350f, 1351f Cervical myelopathy, 541–557 calcification of ligamentum flavum in, 545, 545f causes of, 541, 542t classification of, 549, 549f, 549t clinical symptoms in, 548–549 destructive spondyloarthropathy in, 548 diagnosis of, 548–555 disk herniation in, 545, 545f epidural abscess in, 547, 548f evaluation of, 550, 551t, 552t radiologic, 550–555, 554f ossification of posterior longitudinal ligament in, 544, 544f, 545f pathology of, 541–548, 542f, 543f, 544f, 545f, 546f, 547f, 547t, 548f physical examination in, 549–550 rheumatoid arthritis in, 546, 546f, 547f, 547t spinal anomaly in, 547–548, 548f spinal tumors in, 546–547 spondylitic, 542–544, 542f, 543f, 544f surgery for approaches to, 555–557, 556t indications for, 555 therapeutic strategies for, 555–557 Cervical nerve root block, CT-guided, 88 Cervical plexus anatomy of, 1092–1095, 1092f, 1093f, 1094f, 1095f deep, 1093, 1095f superficial, 1093, 1094f
1420 Index Cervical plexus block, 1091–1102 anatomic aspects of, 1092–1095, 1092f, 1093f, 1094f, 1095f anesthetic agents for, 1099–1100 complications of, 1100–1101, 1100f, 1101f contraindications to, 1092 deep, 1091 Heidenhein's (Labat's) method of, 1096 interscalene, 1096–1097, 1098f nerve stimulator method of, 1097, 1098f posterior approach to, 1098–1099, 1099f technique of, 1096, 1097f single-injection, 1096–1097, 1098f Wertheim and Rovenstine's method of, 1097–1098, 1099f future directions for, 1101–1102 history of, 1091 indications for, 1091–1092 pitfalls in, 1100 superficial, 1091 technique of, 1095–1096, 1095f, 1096f Cervical radicular pain, 55, 55t Cervical radiculopathy, 522–528 clinical features of, 522–524 definition of, 522–523 diagnostic tests for, 525–527 differential diagnosis of, 526–527 at symptomatic level, 527 diskography in, 526 etiology of, 524 examination maneuvers for, 526t historical considerations in, 522, 523f imaging studies in, 525–526 neurologic features of, 524, 525t neurophysiologic tests for, 526 physical examination of, 524–525 prevalence of, 524 provocative tests for, 525, 526t signs and symptoms of, 524–525, 525t treatment of, 527–528 complications of, 528 conservative, 527 interventional pain management in, 527–528 surgical, 528 vs. nonsurgical management, 528 vs. ulnar tunnel syndrome, 1171 Cervical spine anomalies of, 547–548, 548f destructive change in, 548 radiography of, 75–76, 76f rheumatoid arthritis involving, 546, 546f, 547f, 547t spondylitic changes in, 542–544, 542f dynamic mechanical factors in, 543–544, 543f, 544f ischemic factors in, 544 static mechanical factors in, 543, 543f Cervical sympathetic chain, 531, 532f Cervical sympathetic nerves, anatomy of, 1103, 1104f, 1105f Cervicogenic headache atlanto-occipital nerve block for, 1047–1049, 1049f, 1050f radiofrequency lesioning for, 1357–1360, 1358t anatomy in, 1358, 1358f efficacy of, 1360 history in, 1357–1358 indications for, 1358–1359 technique of, 1359–1360, 1359f C-fibers, 703 classification of, 10, 11t in respiratory system, 650, 650f, 658, 659f properties of, 10–12, 11f Chaddock's sign, in epidural abscess, 739–741 Chamberlain's lines, 546, 546f Chemical dependency. See Drug abuse. under specific agent Chemical heating pads, 980 Chemical ice packs, 985f, 986 Chemical neurolysis, of stellate ganglion, 1112, 1112f efficacy of, 1115 Chemonucleolysis, for lumbar radiculopathy, 714 Chemoreceptor(s), carotid, in cluster headache, 443 Chest, flail, 658
Chest pain after thoracotomy, 655, 655f. See also Post-thoracotomy pain syndrome causes of specific, 651, 651t visceral, 651–653 clinical features of, 650–651 from cough, 658, 659f from lung abscess, 654, 654f from mediastinal tumors, 657–658 from mesothelioma, 657, 657f from Pancoast tumors, 656–657 from pneumothorax, 655, 655f, 655t from pulmonary embolism, 653–654, 654f from pulmonary infection, 654, 654f from systemic inflammatory conditions, 655 in asthma, 651 in bronchitis, 651, 652f in histoplasmosis, 654 in lung cancer, 656–658, 656f in lymphangioleiomyomatosis, 651–652 in Pancoast-Tobias syndrome, 656–657, 657f in pneumonia, 654, 654f in pulmonary hypertension, 653 in pulmonary Langerhans cell histiocytosis, 652 in sarcoidosis, 652–653, 653f in sickle cell disease, 656 traumatic, 658, 658f cough-induced, 653 visceral, 649–650, 650f causes of, 651–653 Chest wall pain, 632–645, 633t complications and pitfalls in, 645 differential diagnosis of, 644–645, 645f in costosternal syndrome, 632–634, 633f, 634f in intercostal neuralgia, 640–641, 640f in rib fractures, 636–638, 637f, 638f in sternalis syndrome, 635–636, 636f, 637f in sternoclavicular joint syndrome, 643–644, 643f, 644f in Tietze's syndrome, 634–635, 634f, 635f in xiphisternal syndrome, 641–643, 641f, 642f, 643f pleuritic, 649, 650, 653–656 post-thoracotomy, 638–640, 638t, 639f, 655, 656f Children abuse of, neuropathic pain and, 206 acetaminophen dosages for, 883 aspirin dosages for, 880 cluster headache in, 438 complex regional pain syndrome in, 287 infective spondylitis and epidural abscess in, 737–738 Chin adduction test, for acromioclavicular joint dysfunction, 579, 581f Chinese bodywork (tui na), 1024 Chinese medicine acupuncture in, 1019–1026. See also Acupuncture cupping and scraping (gua sha) in, 1024 food therapy (diet) in, 1024 herbal remedies in, 1024 historical considerations in, 1019–1020 moxibustion in, 1024 qi gong in, 1024 Qi in, 1020 tai chi in, 1024 tui na in, 1024 Chiropractic therapy, 938–939 Chloroprocaine, for celiac block, 1193 Chlorpromazine, for cluster headache, 450 Chlorzoxazone, 925–926, 925t for tension-type headache, 433t Cholangiocarcinoma, intrahepatic, CT scan of, 680f Cholesteatoma, 495–497, 497f Cholesterol granuloma, maxillary, 500, 500f Choline magnesium trisalicylate for cancer pain, 305t pharmacology of, 887t Chondroblastoma, of tibia, 851, 852f Chondrocalcinosis, 81 Choy technique, modified, of laser diskectomy, 1403–1404, 1404f Chronic pain anxiety in, 949 cognitive-behavioral therapy for, 950 efficacy of, 952 comprehensive multimodal therapy for, 950–952
Chronic pain (Continued) cryoanalgesia for, 1365–1373 applied, 1366–1371 depression in, 948–949 drug abuse and, 952 hypnosis for, 965 technique of, 966 in burn patients, 00025:s0320 in elderly, 944 insomnia in, 949 intractable, in sickle cell disease, 247 legal issues and, 953 malingering and, 953 management of biofeedback in, 956 invasive procedures in, 942 obstacles to, 952–953 operant conditioning in, 949–950 therapy effectiveness in, 952 obturator nerve block for, 1245–1246 osteopathic manipulative therapy for, 998–1008. See also Osteopathic manipulative therapy personality disorders and, 949 pharmacotherapy in, limitations of, 943, 943t psychiatric disorders and, 952–953 psychological aspects of, 948–949 psychotherapeutic approaches to, 949–952 Chylothorax, in lymphangioleiomyomatosis, 651–652 Circulating water heating pads (K-pads), 980 Civamide, for cluster headache, 450–451 Clavicle, distal, osteolysis of, 79 Clinical practice, pitfalls in, 57 Clodronate, for complex regional pain syndrome, 285 Clomiphene, for cluster headache, 450 Clonidine for cluster headache, 449–450 for complex regional pain syndrome, 512 for neuropathic pain, 210–211 for postmastectomy pain, 663 Clonus, in epidural abscess, 739–741 Clostridial collagenase injections, for Dupuytren's contracture, 624 Clostridial neurotoxin. See also Botulinum neurotoxin in neurolytic blockade, 327 Clunk sign, 586–587 Cluster headache, 436–452. See also Headache age of onset of, 438 associated symptoms in, 439, 440, 440t autonomic changes in, 442 biochemical changes in, 443 carotid chemoreceptor in, 443 chronic, 441–442 chronobiologic changes in, 443 clinical features of, 437–440, 438t definition of, 436 demographic factors in, 39t, 437–438 diagnosis of, 445 differential diagnosis of, 445–446, 445t epidemiology of, 437 familial occurrence of, 437–442 genetic factors in, 437–442 hemodynamic changes in, 442 history of, 436–437 hormonal changes in, 443 Horner syndrome in, 440, 488, 489f in women, 441 International Headache Society classification of, 438t pain in, 38 characteristics of, 438–440 ocular/periocular, 488–489, 489f source of, 442 pathophysiology of, 442–444 synthesis of, 443–444 periodicity of, 438 personality factors in, 440–441 photophobia in, 440 prevalence of, 437 psychologic factors in, 440–441 secondary, 446 signs associated with, 437t terminology of, 436–437 treatment of, 446–452, 446t, 447t abortive, 446–451 baclofen in, 450 capsaicin in, 450
Cluster headache (Continued) chlorpromazine in, 450 civamide in, 450–451 clomiphene in, 450 clonidine in, 449–450 cocaine in, 447 corticosteroids in, 448 cyproheptadine in, 450 dihydroergotamine in, 447 doxepin in, 450 eletriptan in, 447 ergotamine derivatives in, 449 gabapentin in, 449 histamine desensitization in, 451 hypothalamic stimulation in, 452 indomethacin in, 449 lidocaine in, 447 lithium carbonate in, 448–449 melatonin in, 451 methysergide in, 449 naratriptan in, 450 occipital nerve blockade in, 450 oxygen therapy in, 446–447 pramipexole in, 450 prophylactic, 447t, 448 sumatriptan in, 447 surgical, 451–452, 451t tizanidine in, 450 topiramate in, 449 valproic acid in, 449 verapamil in, 448 zolmitriptan in, 447 trigeminal neuralgia with, 465 trigger factors in, 440 variants of, 444–445 vascular changes in, 442 vs. trigeminal neuralgia, 445 Cluster-tic syndrome, 465 Coagulation, 60 parameters in, 60 Cocaine abuse of, screening for, 74 for cluster headache, 447 Coccygodynia, 801–803, 802f, 00103:f0025, 803f cryoanalgesia for, 1370 Coccyx, anatomy of, 1250, 1250f Codeine, 895t, 903 chemical structure of, 218f for cancer pain, 306t Cognitive evoked potentials, 190 Cognitive impairment, assessment of in cancer patients, 343–345, 343f, 344f, 344t pain in, 200t, 201, 201t Cognitive restructuring, for burn pain, 239–240 Cognitive-behavioral therapy for chronic pain, 950 efficacy of, 952 for neuropathic pain, 209 Cold therapy. See also Cryoanalgesia for bone pain, 703–704 for proctalgia fugax, 805–806 for rheumatoid arthritis, 402 in pain management, 984–986 choice of, 984–986, 985f physiologic effects of, 984 indications for, 984t precautions and contraindications to, 984t Cold-type complex regional pain syndrome, 277 Colicky pain, 699 Colitis, ulcerative, relaxation techniques for, 970 Collateral ligament(s). See Lateral collateral ligament; Medial collateral ligament Collaterals, acupuncture, 1022–1023 Collimators, in radiography, 75 Comfort measures, in pain management, 939 Communication, in palliative care, 345 Community issues, in palliative care, 345 Compensation, for occupational back pain, 731–732 Complementary medicine. See Alternative medicine Complementary strategies, for neuropathic pain, 211 Complete blood count (CBC), 58–60 in headache, 250 Complex regional pain syndrome, 207–208 magnetic resonance imaging of, 111, 113f spinal cord stimulation for, 1309 stellate ganglion block for, 1104 transient, after laser diskectomy, 1406
Index 1421 Complex regional pain syndrome (Continued) type I, 272–289 autonomic abnormalities in, 276–277 central autonomic dysregulation in, 276–277 clinical presentation of, 274–275, 274t cold type, 277 definition of, 273 denervation supersensitivity in, 276 diagnosis of, 280–283, 281t tests in, 280f, 281–282, 282f diagnostic criteria for, 281t validation of, 282 differential diagnosis of, 282–283 epidemiology of, 273 facial, 506–513 clinical presentation of, 1f, 506–508, 507f, 507t, 508f, 509t, 510f diagnostic tests for, 511–512 IASP classification of, 506, 507t pathophysiology of, 510–511 treatment of, 512–513 vs. somatic, 506, 507t genetic factors in, 275 history of, 273, 273f HLA antigens in, 275 IASP classification of, 273 in children, 287 incidence and prevalence of, 273 motor abnormalities in, 277–279 neurogenic inflammation in, 277, 278f pathophysiology of, 275–280, 276f, 278f prevention of, 287 prognosis of, 287–288 psychological aspects of, 275 somatosensory abnormalities in, 275–276, 276f spatial distribution of, 274 stages of, 275 sympathetically maintained pain in, 273, 279–280, 279f time course of, 274 treatment of, 283–287 guidelines in, 287, 288f interventional, at sympathetic nervous system level, 285–286 occupational therapy in, 286 pharmacologic, 283–285, 284t physical therapy in, 286 psychotherapy in, 287 spinal drug application in, 286 stimulation techniques in, 286 surgical, 286 vs. post-traumatic neuralgia, 282–283 type II after spinal cord injury, 290–291 after stroke, 290 clinical presentation of, 290 definition of, 290 diagnosis of, 291 differential diagnosis of, 291 epidemiology of, 290 IASP classification of, 290 pathophysiology of, 290–291 prognosis of, 291 vs. post-traumatic neuralgia, 291 Comprehensive multimodal therapy, for chronic pain, 950–952 Compression fractures, vertebral. See Vertebral fractures, compression Compression neuropathy(ies). See Entrapment neuropathy(ies) Compression tests, for sacroiliac joint disorders, 760 Computed radiography, 75 Computed tomography (CT), 95–101 diagnostic strengths of, 99–101, 100f first-generation scanners in, 95 fourth-generation scanners in, 96 in arachnoiditis, 745–746, 746f in brachial plexopathy, 539 in headache, 250–251 in palliative radiation therapy, 313, 313f in peripheral neuropathy, 266 in pregnancy, 778 multi-detector row, 96 of orthopedic trauma, 97–98, 98f of pancreatic pseudocyst, 682, 683f, 685–686, 685f of spine, 98–99, 99f, 100f, 101f
Computed tomography (CT) (Continued) of sternal chondroma, 641, 641f of thoracic contents, 637, 637f of vertebral compression fractures, 1378, 1379f principles of, 95–97 second-generation scanners in, 96 spiral/helical, 96 third-generation scanners in, 96 three-dimensional, 97, 97f Computed tomography myelography, 139–140, 140f of spinal cord atrophy, 554, 554f Computed tomography-guided technique of celiac plexus block, 1196–1198, 1197f of ganglion of Walther (impar) block, 1282, 1283–1284, 1283f of hypogastric plexus block, 1279–1280, 1280f single-needle, 1274–1275, 1276f, 1277f, 1278f two-needle, 1277–1278 Conduction, heat therapy via, 979–981 chemical heating pads, 980 circulating water heating pads, 980, 980f hydrocollator packs, 979–980, 980f microwavable heating pads, 980–981, 981f paraffin baths, 981, 981f Conjunctival injection and tearing, short-lasting unilateral neuralgiform headache attacks with, 444–445 Conjunctivitis, 484–485, 484f Connective tissue disease(s), 396–412, 397t. See also specific disease, e.g., Systemic lupus erythematosus common features of, 397t laboratory tests for, 61–63, 62t, 63t Conn's syndrome, 61 Conscious pain mapping, 1370–1371 Consensus paper, on spinal canal endoscopy, 166 Constipation, opioid-induced, 307–308 Contracture, Dupuytren's, 624–625, 625f Contrast agents allergies to, 123, 143 in cervical epidural space, 1139–1140, 1139f Contrast baths in hydrotherapy, 994 in pain management, 985f, 986 Convection, heat therapy via, 982 fluidotherapy, 982, 982f hydrotherapy, 982, 982f Conversion, heat therapy via, 982–984 microwave diathermy, 984 short-wave diathermy, 983, 984f ultrasound, 983 Convulsions, opioid-induced, 896 Cooling sprays, evaporative, 985–986 Coordination, lack of, in peripheral neuropathy, 261t Coping styles, in burn pain management, 232t, 235 mismatch of techniques and, 241 Cordotomy, anterolateral, for cancer pain, 334, 334f Core strengthening exercises, for low back pain, in pregnancy, 779 Cornea abrasions of, 484, 484f innervation of, 483 Corner lesion, in Pott's disease, 738–739, 741f Coronoid notch palpation of, 1076, 1076f trigeminal nerve block via, 1076–1078, 1077f, 1078f Corticosteroids epidural. See also Epidural nerve block for cervical radiculopathy, 527 for lumbar radiculopathy, 713 for thoracic radiculopathy, 646–647 side effects of, 1212 for cancer pain, 309 for cluster headache, 448 for complex regional pain syndrome, 285 for dermatomyositis, 409 for giant cell arteritis, 480–481, 481t for herpes zoster, 270 for neuropathic pain, 211 pulse therapy with, 211 intra-articular for acromioclavicular joint pain, 579–580, 581f for cervical facet syndrome, 519, 519f
1422 Index Corticosteroids (Continued) for coccydynia, 801–803, 802f for costosternal syndrome, 633–634, 634f for golfer's elbow, 599, 600f for lumbar facet syndrome, 720 for osteoarthritis, 394, 567, 569f for sternalis syndrome, 636, 637f for sternoclavicular joint syndrome, 644, 644f for Tietze's syndrome, 635, 635f for trigger finger, 626 for xiphisternal syndrome, 642–643, 643f intralesional for anterior interosseous syndrome, 612 for Baker's cyst, 854–855, 855f for biceps tendinitis, 587, 587f for carpal tunnel syndrome, 621, 621f for cubital bursitis, 598, 600f, 605, 605f for cubital tunnel syndrome, 608, 608f for Dupuytren's contracture, 624 for foot and ankle arthritis, 861 for gluteal bursitis, 809–810, 810f for iliopsoas bursitis, 818f, 819 for infrapatellar bursitis, 848, 848f, 851 for intercostal neuralgia, 641 for ischiogluteal bursitis, 811, 00105:t0035 for meralgia paresthetica, 821–823, 823f for olecranon bursitis, 603, 604f for pes anserine bursitis, 849, 850f for piriformis syndrome, 792 for plantar fasciitis, 874 for post-thoracotomy pain syndrome, 639–640 for prepatellar bursitis, 846, 847f for pronator syndrome, 610, 611f for quadriceps expansion syndrome, 856–858, 859f for Quervain's tenosynovitis, 622–623, 623f for subdeltoid bursitis, 583, 583f for suprapatellar bursitis, 844–845, 845f for trochanteric bursitis, 815–816 knee pain due to, 839 Cost-containment issues, in electromyography, 186 Costoclavicular syndrome, 534–535 Costosternal joints anatomy of, 632, 633f irritation of, 632–633, 633f swelling of, in Tietze's syndrome, 634, 634f Costosternal syndrome, 632–634, 633f, 634f Cough, 658, 659f chest wall trauma caused by, 653 C-polymodal nociceptors, 11, 12 Crandall and Batzdorf classification, of cervical myelopathy, 549, 549t Cranial nerves. See also specific cranial nerve, e.g., Trigeminal nerve (V) anatomy of, 375, 376f examination of, 43–46, 44t, 45f, 46f inadvertent blockade of, in cervical plexus block, 1101 Craniofacial pain, cryoanalgesia for, 1371–1373, 1372f, 1373f C-reactive protein, measurement of, 58 Creak sign, for Achilles tendinitis, 863–864, 864f Creatine kinase, measurement of, 72 Creatine phosphokinase, elevated levels of, after celiac plexus block, 1204 Credentialing, for acupuncture, 1026 Crescent sign, in avascular necrosis of hip, 81, 83f CREST syndrome, 407, 407f Cross-arm test, 587 Cross-body adduction test, 591 Cross-tolerance, to opioids, 897 Cruciate ligaments. See Anterior cruciate ligament; Posterior cruciate ligament Cryoanalgesia, 1361–1374. See also Cold therapy anatomic aspects of, 1363 case report of, 1373b, 1373t cellular basics for, 1361–1363 closed vs. open procedures in, 1363 contraindications to, 1363 cryoprobes for, 1361, 1362f duration of, 1370 for biomechanical spine pain, 1366–1369, 1367f, 1368f, 1369f for cervical facet syndrome, 1369 for chronic pain, 1365–1373 for coccygodynia, 1370
Cryoanalgesia (Continued) for craniofacial pain, 1371–1373, 1372f, 1373f for genitofemoral neuropathy, 1370–1371, 1370f for iliac crest bone harvest, 1366, 1367f for iliohypogastric neuropathy, 1370–1371 for ilioinguinal neuropathy, 1370–1371 for intercostal neuralgia, 1366, 1366f for interspinous ligament pain, 1370 for lower extremity pain, 1371 for mechanical spine pain, 1370 for neuromas, 1366 for perineal pain, 1370 for peroneal nerve injury, 1371 for postherniorrhaphy pain, 1365 for postoperative pain, 1363–1365 for post-thoracotomy pain, 1363–1364, 1364f for superior gluteal neuralgia, 1371 future directions for, 1374 historical considerations in, 1361, 1362f indications for, 1363 informed consent for, 1363 of intercostal nerve, 1189f physics of, 1361–1363 Cryoglobulins, 69 Cryoneurolysis, CT-guided, for post-thoracotomy pain, 667 Cryoprobe(s), 1361, 1362f placement of, techniques in, 1365 rapid cooling of, 1361 working principle of, 1361, 1362f Cubital bursitis, 598, 600f, 603–605, 604f, 605f Cubital tunnel syndrome, 606–609, 607f, 608f vs. golfer's elbow, 607–608, 1161, 1164f Cue-controlled relaxation, 973 Cullen's sign, in acute pancreatitis, 682, 684f Cupping, in Chinese medicine, 1024 Cutaneous nerve, neuralgia secondary to irritation of, 1371 Cybernetics, in biofeedback, 955 Cyclic vulvitis, 798 Cyclobenzaprine, 925t, 926 for tension-type headache, 433t Cyclooxygenase (COX) inhibition by acetaminophen, 882 by nonsteroidal anti-inflammatory drugs, 884 in tissue injury, 22, 23f Cyclooxygenase-2 (COX-2) inhibitors, 889. See also Nonsteroidal anti-inflammatory drugs (NSAIDs) for cancer pain, 304 for migraine headache, 426 for osteoarthritis, 393–394 for rheumatoid arthritis, 401 Cyproheptadine, for cluster headache, 450 Cyst aneurysmal bone, magnetic resonance imaging of, 647f Baker's. See Baker's cyst nerve root, in failed back surgery syndrome, 767, 767f suprapatellar pouch, noncommunicating, 844f Cytokine release, in tissue injury, 21t
D
Dactylitis (hand-foot syndrome), in sickle cell disease, 246 Dantrolene, for muscle spasms, 927–928 Day unit, sickle cell pain management in, 247–248 De Qi sensation, in acupuncture, 1022 De Quervain's tenosynovitis, 81, 359–361, 360f, 361f, 622–623, 623f Debridement, arthroscopic, for osteoarthritis, 394 Decompression insufficient, in failed back surgery syndrome, 767–768 laser disk. See also Laser diskectomy stepwise, 1402, 1402f techniques of, 1402 microvascular for trigeminal neuralgia, 469–470 of glossopharyngeal nerve root, 475, 1084–1085, 1085f percutaneous disk, for lumbar radiculopathy, 713 surgical, for Quervain's tenosynovitis, 622–623
Decremental differential nerve blocks, 158–159, 158f Deep breathing for burn pain, 237–238 slow, 971 Deep tendon reflexes, examination of, 48–49, 48t, 49f Degenerative arthritis. See Osteoarthritis Delirium definition of, 343 in cancer patients, 343–345 detection of, 343, 343f etiology of, 343, 344t therapeutic approach to, 343, 344f Delta (δ) opioid receptor, 892, 892t Deltoid ligament strain, 366–367, 366f Denervation, supersensitive, in complex regional pain syndrome, 276 Denervation hypersensitivity, 7–8 Deoxyribonucleic acid (DNA), changes in, growth factors and, 1027, 1028f Depression cancer-related, palliative care for, 342–343 in chronic pain, 948–949 in vulvodynia, 798 pain associated with, 192, 206 Dermatomyositis, 408–409, 408f, 409f Desipramine, 915 for postmastectomy pain, 663t for tension-type headache, 434t Destructive spondyloarthropathy, 548 Dexamethasone for cancer pain, 309 for cluster headache, 448 for medication overuse headache, 461 for nausea, 341f Dextrose, effects of, on growth factors, 00194:f0040 Diabetes insipidus, 61 Diabetes mellitus, 60, 60f diagnosis of, 60, 60t Diabetic amyotrophy, 824 Diabetic nephropathy, peripheral, 207 Diabetic neuropathy, 824 femoral nerve, 826 Diacetylmorphine, chemical structure of, 894f Diaphragmatic breathing, slow, 971 Diaphragmatic pain, referred to supraclavicular region, 679, 679f Diathermy microwave, 984 short-wave, 983, 984f Diazepam, for muscle spasms, 927 Diclofenac for cancer pain, 305t pharmacology of, 887t Diet, 936t in alternative medicine, 936t in Chinese medicine, 1024 restrictions in, MAO inhibitors and, 917t Dietary supplements, for osteoarthritis, 391t Diffuse axonal injury (DAI), magnetic resonance imaging of, 107 Diffuse idiopathic skeletal hyperostosis (DISH) of spine, 77, 77f vs. osteoarthritis, 390–391 Diflunisal characteristics of, 886 for cancer pain, 305t for tension-type headache, 433t pharmacology of, 887t Digital nerve block for foot pain, 1297–1298 for hand pain, 1171–1173, 1172f Digital scleroderma, 405–406, 405f Dihydroergotamine for cluster headache, 447 for medication overuse headache, 460–461, 461t for migraine headache, 425–426 Dimethylsulfoxide, for complex regional pain syndrome, 285 Diphenhydramine, for medication overuse headache, 461t Disability, from phantom pain/sensation, 293–294 Discoid cutaneous lesions, in systemic lupus erythematosus, 403, 403f Discoid lupus erythematosus, 403, 403f Disease-modifying drugs, for rheumatoid arthritis, 401
Disk, intervertebral. See Intervertebral disk Diskectomy complications of, 766–772. See also Failed back surgery syndrome for lumbar radiculopathy, 714 percutaneous automated, 1393–1396. See also Percutaneous diskectomy, automated laser, 1397–1407. See also Laser diskectomy Diskitis after automated percutaneous diskectomy, 1395, 1396f after diskography, 135–136 Diskography cervical, technique of, 131–135, 133f, 134f, 135f complications of, 135–136 contraindications to, 122–123 documentation in, 135 historical considerations in, 119–121 in cervical radiculopathy, 526 indications for, 122 informed consent for, 123, 137 interpretation of findings in, 127–128, 128f, 129f lumbar interpretation of, 137–138 procedure in, 137 sample procedure note in, 137 technique of, 124–126, 124f, 125f, 126f, 127f patient selection for, 122–123 physician training in, 122 postprocedure considerations in, 135 preprocedure and periprocedure considerations in, 123–124 provocation, 123 technique of, 123–135 thoracic, technique of, 129–131, 130f, 131f, 132f validation of, 121–122 Disrepair factors, in soft tissue restoration. See also Prolotherapy Disrepair factors, in soft tissue restoration, 1027, 1028f Distal interphalangeal joint, arthritis of, 618–619, 618f Distraction techniques, for burn pain, 235–236 Distraction test, for sacroiliac joint disorders, 760 Divalproex, 923 Diverticula, dural cuff, 783–784, 784f DNA (deoxyribonucleic acid), changes in, growth factors and, 1027, 1028f Documentation, in diskography, 135 Donepezil for cancer-related fatigue, 340 for opioid-induced sedation, 342 Dopamine, in opioid addiction, 898, 898f Dorsal funicular projection systems, 14 Dorsal horn neurons of, 12–14 anatomic localization of, 12–13, 13f functional properties of, 14 in nerve injury, reorganization of, 26–27 in tissue injury, 21–22, 21f, 22f nociceptive-specific, 14 spinal. See Spinal dorsal horn Dorsal root entry zone (DREZ) lesioning, for cancer pain, 333–334, 334f Dorsal root ganglion, cross-talk with neuroma, 26 Dorsal root ganglionotomy, lumbar, 1340–1345. See also Lumbar dorsal root ganglionotomy Dorsum, of hand, 616 Double-crush syndrome carpal tunnel syndrome and, 380, 380f cubital tunnel syndrome and, 607–608 meralgia paresthetica and, 821 sciatic nerve entrapment and, 808 Double-line sign, in magnetic resonance imaging, 111, 112f Doxepin for cluster headache, 450 for postmastectomy pain, 663t for tension-type headache, 434t Drainage, of epidural abscess, 742 DRD5 gene, in cervical dystonia, 558 Drowsiness, cancer-related, palliative care for, 342
Index 1423 Drug abuse chronic pain and, obstacles to treatment in, 952 laboratory tests for, 72–74 noncontrolled, in pain history, 41t Drug therapy. See also named drug or drug group associated with peripheral neuropathy, 261–262, 262t FDA classification of, in pregnancy, 779 for cancer pain, 304–309, 305t, 306t, 308t, 346, 346t, 941. See also specific drug advantages of, 942 limitations of, 942–943 for chronic pain, 942. See also specific drug limitations of, 943, 943t limitations of, in pain managment, 941–945 monitoring of, 72–74 risk-to-benefit ratio in, 941 teratogenicity in, 779 Dry needling, for piriformis syndrome, 792 Dupuytren's contracture, 624–625, 625f Dura mater, anatomy of, 168–169 Dural cuff diverticula, 783–784, 784f Dural puncture after celiac plexus block, 1202 after spinal cord stimulation, 1318 inadvertent, in cervical epidural nerve block, 1136 Dural sac postoperative deformities of, 781–785. See also specific deformity diagnosis of, 784–785 treatment of, 785 protective function of, 781 Dural sac dilatation, 783, 783f treatment of, 785 Dural sac ectasia, 782–783, 783f treatment of, 785 Durotomy, incidental, in failed back surgery syndrome, 766 Dwarfism (achondroplasia), 78 Dynorphin, in nerve injury, 27 Dysesthesia, in postmastectomy pain, 662t Dysesthetic vulvodynia, 798. See also Vulvodynia Dyspnea, cancer-related, palliative care for, 341–342 Dystonia cervical, 558–563. See also Cervical dystonia definition of, 558 DYT genes, in cervical dystonia, 558
E
Eagle syndrome, 501–502, 502f Ear. See also specific part cauliflower, 494–495, 496f innervation of, 494, 496f Ear pain, 494–498, 495t anatomic aspects of, 494, 496f auricular, 494–495, 496f, 497f in external auditory canal, 495–497, 497f, 498f in mastoiditis, 498, 499f in myringitis, 497 in otitis media, 497–498, 498f in Ramsay-Hunt syndrome, 494, 496f Ecchymosis after caudal epidural nerve block, 1256 after cervical epidural nerve block, 1137 in acute pancreatitis, 682, 684f Edema, disc, in optic neuritis, 487–488, 487f Edmonton Classification System, for cancer pain, 338, 339f Edmonton Symptom Assessment System (ESAS), 337–338 Education in management of medication overuse headache, 460 in management of osteoarthritis, 391t, 392 in management of rheumatoid arthritis, 402 in management of sacroiliac joint dysfunction, 761 patient, vulvodynia and, 799 Effusion joint, ballottement test for, 839, 840f pleural. See Pleural effusion Elbow anatomy of, 601, 602f, 604 corticosteroid injection at for cubital tunnel syndrome, 608, 608f for golfer's elbow, 599, 600f
Elbow (Continued) entrapment neuropathy(ies) of, 606–614 anterior interosseous syndrome, 611–613, 612f, 613f pronator syndrome, 609–611, 609f, 610f, 611f radial tunnel syndrome, 613–614, 613f, 614f tardy ulnar palsy (cubital tunnel syndrome), 606–609, 607f, 608f golfer's (medial epicondylitis), 598–600, 599f, 600f vs. cubital tunnel syndrome, 607–608, 1161, 1164f median nerve block at, 1157–1159, 1157f, 1158f, 1160f painful. See also Elbow, golfer's (medial epicondylitis); Elbow, tennis (lateral epicondylitis) prolotherapy for, 1042–1043, 1042f radial nerve block at, 1154–1157, 1155f, 1156f, 1157f radiography of, 79–80, 80f tennis (lateral epicondylitis), 356–357, 356f, 357f, 594–597, 595f differential diagnosis of, 594 signs and symptoms of, 594, 596f testing for, 594, 596f treatment of, 594–596, 597f vs. radial tunnel syndrome, 613–614, 614f, 1153, 1153f ulnar nerve block at, 1159–1162, 1161f, 1162f, 1163f, 1164f Elderly chronic pain in, 944 iliopsoas bursitis in, 817 pain assessment in, 200t, 201, 201t Electric heating pads, thermal injury associated with, 980, 980f Electrical stimulation, for sacroiliac joint disorders, 761 Electroacupuncture, 1023. See also Acupuncture Electroconvulsive therapy, for phantom pain, 300 Electrodes in electromyography, 176–177, 177f in spinal cord stimulation, selection of, 1305 Electrolyte imbalance, 61 Electromyography, 175–186 basic examination in, 177–178 clinical correlations in, 182–185 cost-containment issues in, 186 diagnostic in anterior horn cell disorders, 185 in arachnoiditis, 745 in CNS disorders, 185 in compression neuropathy, 183–185 in entrapment neuropathy, 183–185 in mononeuropathy, 183–184 in nontraumatic neuropathy, 183 in painful myopathies, 185, 185t in peripheral neuropathy, 265–266 in plexopathy, 185 in polyneuropathy, 176f, 183 in radiculopathy, 185 in traumatic neuropathy, 182–183 in uncommon neuropathy, 184–185 methods of, 176–177 equipment for, 176, 176f, 177f findings in, normal and abnormal, 185–186, 186f history of, 175–176 in brachial plexopathy, 536–538, 538t in cervical dystonia, 561 nerve conduction studies and, 180–182, 181f F wave in, 180–182 H-reflex in, 182 of muscle amplitude in, 179 insertional activity in, 179, 179f interference pattern in, 179–180, 180f, 181f spontaneous activity in, 179, 179f voluntary activity in, 179–180, 180f waveforms in, 179 of ulnar nerve entrapment, 606–607 physiologic mechanisms of, 177–178, 178f precautions with, 176–177 quantitative sensory testing in, 182 timing of, 186 Electromyography machine, 176, 176f Electromyography-assisted biofeedback, 957, 958f
1424 Index Electrothermal annuloplasty, intradiskal, 1388–1392. See also Intradiskal electrothermal annuloplasty Eletriptan, for cluster headache, 447 Embolus (embolism) pulmonary, 653–654, 654f saddle, imaging of, 653, 654f Emergency department, sickle cell pain management in, 248 Emesis. See Nausea and vomiting Emotional distress, of family members, concerning terminal illness, 345 Endocrine system, opioid effects on, 897 Endoscopic laser diskectomy, rigid-scope, 1404–1405, 1405f Endoscopy, spinal canal, 162–174. See also Spinal canal endoscopy Enterococcus infection, of spine, 737 Enthesofascial/intra-articular prolotherapy, 1027–1028, 1032. See also Prolotherapy Entrapment neuropathy(ies), 606–614 anterior cutaneous nerve, 674–677, 675f, 676f, 677f anterior interosseous syndrome, 611–613, 612f, 613f carpal tunnel syndrome. See Carpal tunnel syndrome cubital tunnel syndrome (tardy ulnar palsy), 606–609, 607f, 608f de Quervain's tenosynovitis, 81, 359–361, 360f, 361f, 622–623, 623f electrodiagnosis of, 183–185 femoral nerve, 826 gluteal nerve, 809, 810f lateral femoral cutaneous nerve, 821, 822f pronator syndrome, 609–611, 609f, 610f, 611f radial tunnel syndrome, 613–614, 613f, 614f sciatic nerve, 808 suprascapular nerve, 591 tarsal tunnel syndrome, 382–383 Enzyme(s), phosphorylating, in tissue injury, 23 Enzyme immunoassay testing, for HIV infection, 64 Eosinophilia, 59 Epicondyle lateral, anatomy of, 594, 595f medial, anatomy of, 598, 599f Epicondylitis lateral (tennis elbow), 356–357, 356f, 357f, 594–597, 595f differential diagnosis of, 594 signs and symptoms of, 594, 596f testing for, 594, 596f treatment of, 594–596, 597f vs. radial tunnel syndrome, 613–614, 614f medial (golfer's elbow), 598–600, 599f, 600f vs. cubital tunnel syndrome, 607–608, 1161, 1164f Epididymectomy, for orchialgia, 797 Epidural abscess, 737–742, 737f after automated percutaneous diskectomy, 1396 after spinal cord stimulation, 1308 definition of, 737 in children, 737–738 signs and symptoms of, 739–742 spinal, 547, 548f testing for, 742 treatment of, 742 Epidural adhesiolysis, 167–168, 1258–1272 anticoagulant management for, 1260 cervical, 1138–1141, 1266–1267, 1269f, 1270f, 00169:f0140, 00169:f0145, 00169:f0150, 00169:f0155, 00169:f0160, 00169:f0165, 00169:f0170 anatomic aspects of, 1138 complications of, 1140–1141 contrast medium injection in, 1139–1140, 1139f drugs for, 1140 indications for, 1138 patient preparation for, 1138 Racz catheter in, 1140, 1140f technique of, 1138–1140, 1139f, 1140f complications of, 00169:f0180, 00169:f0185, 00169:f0190, 1269 contraindications to, 1259 Current Procedural Terminology for, 1259 indications for, 1259 laboratory studies for, 1260
Epidural adhesiolysis (Continued) mapping in, 1268 neural flossing in, 00169:f0175, 1268 outcomes of, 1269–1271 patient preparation for, 1259–1260 technique of, 1260–1267 caudal approach, 1260–1264, 1260f, 1261f, 1262f, 1263f, 1264f 3-D, 1266–1267, 1269f, 1270f, 00169:f0140, 00169:f0145, 00169:f0150, 00169:f0155, 00169:f0160, 00169:f0165, 00169:f0170 transforaminal catheters in, 1264–1266, 1265f, 1266f, 1267f, 1268f thoracic, 1267–1268 Epidural arteries, 1128–1129 Epidural fibrosis in failed back surgery syndrome, 767, 767f pathophysiology of, 1258–1259 radiologic diagnosis of, 1259 Epidural injections increased cerebrospinal fluid pressure and, 168 of corticosteroids. See Corticosteroids, epidural Epidural mapping, 1268 Epidural nerve, anatomy of, 223–224, 223f Epidural nerve block caudal, 1248–1257 anatomic aspects of, 1250, 1250f, 1251f catheterization in, 1256 complications of, 1256–1257 contraindications to, 1249 drug injection in, 1254, 1254f drug selection in, 1254–1255 for proctalgia fugax, 805–806 historical considerations in, 1248–1249 indications for, 1249, 1249t needle placement pitfalls in, 1255–1256, 1255f, 1256f needle selection for, 1252 patient positioning for, 1251, 1251f sacral hiatus localization in, 1252–1253, 1252f, 1253f, 1254f technique of, 1250–1256 cervical, 1126–1137 anatomic aspects of, 1127–1129, 1128f, 1129f, 1130f catheter placement in, 1136 complications of, 1136–1137 contraindications to, 1127, 1127t drug injection in, 1132, 1133f drug selection in, 1132–1133 epidural space boundaries and, 1127–1128, 1128f, 1129f epidural space identification in, 1131–1132 for cancer pain, 1127, 1127t historical considerations in, 1126 indications for, 1126–1127, 1127t needle insertion in pitfalls in, 1129 structures encountered during, 1129, 1130f needle selection for, 1131 patient positioning for, 1129 preblock preparation for, 1130–1131, 1131f technique of, 1129–1136 loss-of-resistance, 1131–1132, 1132f, 1133f transforaminal approach in, 1133–1135, 1134f, 1135f, 1136f complications of, 225 differential, 154–155 for acute/postoperative pain, 223–225, 223f, 224f for cancer pain, 310, 321–322 for phantom pain prevention, 296–297 lumbar, 1205–1213 anatomic aspects of, 1207 complications of, 1212–1213 disadvantages of, 1206t historical considerations in, 1205 indications for, 1205–1206 nonsurgical, 1207t rationale for, 1206–1207, 1206t, 1207t side effects of corticosteroid-related, 1212 local anesthetic-related, 1212 procedure-related, 1212–1213 technique of, 1207–1212 blind, 1210–1212 fluoroscopic, 1207–1210, 1208f, 1209f, 1210f, 1211f, 1211t
Epidural nerve block (Continued) thoracic, 1179–1184 anatomic aspects of, 1179–1180, 1180f cardiovascular effects of, 1180 complications of, 1184 contraindications to, 1182 drugs for, 1183 for acute pain, 1181 for acute pancreatitis, 1182 for angina, 1181 for cancer pain, 1181–1182 for herpes zoster, 1181 for postherpetic neuralgia, 1181 for post-thoracotomy pain, 666 for rib fractures, 1181 for surgical procedures, 1181 for vertebral fractures, 1181 historical considerations in, 1179 Horner's syndrome and, 1181 in postoperative analgesia, 1181 in spinal cord stimulation, 1182 indications for, 1181–1182 laminar approach in, 1183 midline approach in, 1182–1183, 1183f paramedian lateral approach in, 1183 pitfalls in, 1183–1184 pulmonary effects of, 1180 Epidural space anatomy of, 168 cervical boundaries of, 1127–1128, 1128f, 1129f contents of, 1128–1129 identification of, 1131–1132 contents of, 171 thoracic anatomy of, 1179–1180, 1180f pressure in, 1180 Epidural veins, 1128 Epidurography anatomic aspects of, 141–142 historical considerations in, 141 indications for, 141 materials for, 142 side effects and complications of, 143 technique of, 142–143, 142f, 143f Epiduroscopy. See Spinal canal endoscopy Epinephrine, for cervical plexus block, 1099 Epistaxis (nosebleed), sphenopalatine ganglion block causing, 220 Equinanalgesia, 895 Erb-Duchenne palsy, 534, 534f. See also Brachial plexopathy Ergotamine for cluster headache, 449 for migraine headache, 425–426 Erythema migrans, 839, 839f in Lyme disease, 65, 67f Erythematous malar rash, in systemic lupus erythematosus, 403, 403f Erythrocyte sedimentation rate (ESR), 58 in headache, 250 Erythrovirus B19, in complex regional pain syndrome, 277 Essential vulvodynia, 798. See also Vulvodynia Etanercept for osteoporosis, 705 for rheumatoid arthritis, 401–402 Ethanol, toxic levels of, after celiac plexus block, 1203 Etidocaine, 931t, 932t Etodolac for tension-type headache, 433t pharmacology of, 887t Euphemistic back pain, 725–726 Euphoria, opioid-induced, 895 Evaporative cooling sprays, 985–986 Eversion test, for deltoid ligament insufficiency, 366, 366f Evoked potentials, 187–190 brainstem auditory, 188 cognitive, 190 instrumentation for, 187 somatosensory, 189–190, 189f specific tests for, 187–190 visual, 187–188, 188f Excretion, of opioids, 901 Exercise(s). See also See also specific type of exercise for lumbar radiculopathy, 713 for osteoarthritis, 391t, 392
Exercise(s) (Continued) for rotator cuff disorders, 576 for sacroiliac joint disorders, 762 neural flossing, 00169:f0175, 1268 water-based, 989–993, 991f, 992f, 993f. See also Hydrotherapy Extensor tendon sheaths, of wrist and hand, 617f External auditory canal, pain in, 495–497, 497f, 498f Extracorporeal shock wave therapy, for plantar fasciitis, 874 Eye. See also Ocular. Visual entries. specific part examination of, in peripheral neuropathy, 265 painful, 482–493. See also Ocular/periocular pain sensory innervation of, 482–483, 483f Eyelid, drooping, 376
F
F wave, 180–182 definition of, 180–181 variability in, 182 Fabere maneuver, 760 Faces Pain Scale, 200f, 201 Facet joint(s) anatomy of, 1409–1410 cervical, pain in, 00006:t0030. See also Cervical facet syndrome distribution of, 517, 517f, 518f fusion techniques for, 1408–1414. See also Facet joint fusion lumbar anatomy of, 716, 717f, 1223 blockade of, 1221–1229. See also Lumbar facet block pain in, 56, 716–721. See also Lumbar facet syndrome nerve block of CT-guided, 87 fluoroscopically-guided, 85–87, 87f Facet joint fusion, 1408–1414 anatomic aspects of, 1409–1410, 1410f background in, 1408, 1408f, 1409f candidates for, 1414 challenges of, 1413, 1414f complications of, 1413 identification of joints in, 1410 indications for, 1408–1409, 1409f, 1410f patient preparation for, 1410 technique of, 1409–1410 drill guide insertion in, 1411–1412, 1411f, 1412f drill guide stabilization in, 1412, 1412f graft in, 1413, 1413f joint reaming in, 1412–1413, 1413f Steinmann, pin placement in, 1410, 1411, 1411f Facet syndrome(s) cervical, 516–521. See also Cervical facet syndrome lumbar, 716–721. See also Lumbar facet syndrome Facial complex regional pain syndrome, biofeedback for, 512 Facial nerve (VII) anatomy of, 375, 376f evaluation of, 44t Facial nerve palsy Bell's, 375, 376t, 379 differential diagnosis of, 376t Facial pain atypical (of unknown origin), 379, 467b criteria for, 467b vs. trigeminal neuralgia, 467 in trigeminal neuralgia. See Trigeminal neuralgia Facial scleroderma, 405–406, 406f Fade test, for sacroiliac joint disorders, 760 Failed back surgery syndrome, 763–774 arachnoiditis in, 771–772, 771f, 772f definition of, 765 diagnosis of, 772–773, 773f, 773t epidemiology of, 765–766 epidural fibrosis in, 767, 767f excessive surgical interventions and, 765 historical perspectives on, 764–765 incidental durotomy in, 766
Index 1425 Failed back surgery syndrome (Continued) infections in, 769, 770f insufficient decompression in, 767–768 intrathecal hematoma in, 766, 766f laminectomies and fusions in, rationalization for, 765 loose disk fragments in, 766 mechanical instability in, 768 minimally invasive access and, 768 nerve root cysts in, 767, 767f peridural hematoma in, 766 prognosis of, 774 pseudoarthrosis in, 769, 769f pseudomeningocele in, 770, 770f residual/recurrent/adjacent herniated nucleus pulposus in, 768, 768f spinal cord stimulation for, 1308–1309 spinal stenosis in, 769, 770f spondylolisthesis in, 769, 769f, 770f surgery at wrong level and, 770–771 symptoms in, 773 treatment of, 774 Family history, in peripheral neuropathy, 262–263 Family involvement, in palliative care, 345 Fasciitis, plantar, 369–370, 369f, 370f, 872–874, 873f Fat, epidural, 1128, 1180 Fatigue, cancer-related, palliative care for, 339–340 Felty syndrome, 398–399 Female genitalia, external, 798, 799f Femoral cutaneous nerve, lateral. See Lateral femoral cutaneous nerve entries Femoral herniorrhaphy, femoral neuropathy due to, 827 Femoral nerve, anatomy of, 824–827, 825f Femoral nerve block, 1292–1293, 1292f Femoral nerve palsy, after ilioinguinaliliohypogastic nerve block, 1240–1241 Femoral neuropathy, 824–827, 825f, 825t Femoral stress fractures, vs. iliopsoas bursitis, 819, 819t Femoral-patellar joint, anatomy of, 834, 836f Femoral-tibial joint, anatomy of, 834, 835f Fenoprofen for cancer pain, 305t for tension-type headache, 433t pharmacology of, 887t Fentanyl, 906–907 for cancer pain, dosage of, 331t for post-thoracotomy pain, 666 transdermal administration of, 900, 900f Fetal exposure, to ionizing radiation, 778 Fetal hemoglobin (Hb F), 59 Fever knee pain with, 838 low back pain and, 695–696 Fibromyalgia, 371–373 hypnosis for, 965 osteopathic manipulative therapy for, 1007–1008 relaxation techniques for, 969–970 water-based exercises for, 990 Fibrosis epidural in failed back surgery syndrome, 767, 767f pathophysiology of, 1258–1259 radiologic diagnosis of, 1259 in scleroderma, 406 Ficat classification, of osteonecrosis of hip, 81 Fight-or-flight response, 967 Film badges, for x-ray staff, 104 Finger(s) deformities of, 618, 618f trigger, 626–627, 627f Finkelstein test, for de Quervain's tenosynovitis, 360, 361f, 622, 623f First (worst) syndrome, 37–38 First-degree burns, 229, 230f Fistula(s), carotid-cavernous, 491, 492f Flail chest, 658 Flank ecchymosis, in acute pancreatitis, 682, 684f Flexor tendon sheaths, of wrist and hand, 617f Fluidotherapy, heat application with, 982, 982f Fluoroscopy, 85–90 in arthroscopic procedures hip, 85, 86f shoulder, 85, 86f
Fluoroscopy (Continued) in celiac plexus block, 1196 in ganglion of Walther (impar) block, 1281–1283, 1282f, 1283f in hypogastric plexus block, 1278–1279, 1279f, 1280f single-needle, 1274, 1275f two-needle, 1275f, 1276–1277, 1276f in lumbar epidural nerve block, 1207–1210, 1208f, 1209f, 1210f, 1211f mean levels of contrast flow in, 1211t patient positioning for, 1207, 1208f in spinal procedure(s), 75–76 facet joint block, 85–87, 87f sacroiliac joint injection, 87–88, 88f selective nerve root block, 88–89, 89f vertebroplasty, 89–90, 90f in stellate ganglion block, 1107, 1107f, 1108f Fluoxetine, 916, 916f Flurbiprofen, for tension-type headache, 433t Folliculitis, nasal, 498 Folstein Mini-Mental State Examination, 43, 44t Food therapy. See also Diet in Chinese medicine, 1024 Foot examination of, in peripheral neuropathy, 263–264, 264f radiography of, 84 Foot pain digital nerve block for, 1297–1298 disorders causing, 861t in arthritis, 860–862, 862f in bursitis, 865 Morton's neuroma and, 866–868, 867f, 868f prolotherapy for, 1035, 1036f anterior, 1035–1036, 1036f medial, 1036–1037, 1036f, 1037f Forearm, median nerve entrapment at. See Pronator teres syndrome Forebrain, opiates in, 28 Foreign body(ies) in cornea, 484, 484f in external auditory canal, 497, 498f Fortin's finger test, 760 Fournier's gangrene, 795 Fracture(s) compression, vertebral. See Vertebral fractures, compression hip, from osteoporosis, 701 pars, 752, 753f, 754. See also Spondylolysis pelvic, CT scan of, 98, 98f rib, 636–638, 637f intercostal nerve block for, 638, 638f thoracic epidural nerve block for, 1181 treatment of, 658 stress, femoral, vs. iliopsoas bursitis, 819, 819t Free radical scavengers, for complex regional pain syndrome, 285 Freiberg test, for piriformis syndrome, 792 Frequency encoding, in pain processing system, 17 Frequency-dependent differential nerve blocks, 158–159, 158f Frontal nerve, 1069 Frovatriptan, for medication overuse headache, 461 Frozen shoulder (adhesive capsulitis), 566, 567f Functional Assessment of Cancer TherapyAnemia Scale, 340 Functional brain imaging, in neuropathic pain, 204–205 Functional Pain Scale (FPS), 201, 201t, 702–703, 703f Funicular projection systems dorsal, 14 ventral, 14 Fusion techniques, for facet joints, 1408–1414. See also Facet joint fusion
G
Gabapentin, 922, 922f for acute arachnoiditis, 748 for cluster headache, 449 for complex regional pain syndrome, 285 for facial complex regional pain syndrome, 512 for glossopharyngeal neuralgia, 473, 473t for intercostal neuralgia, 641 for mononeuritis multiplex, 671
1426 Index Gabapentin (Continued) for peripheral neuropathies, 267, 267t for phantom pain, 297–298 for post-thoracotomy pain syndrome, 639 for proctalgia fugax, 805 for vulvodynia, 799 Gabapentinoid agents, mechanism of action of, 21, 30f Gaenslen's test, 760, 777 Gait examination of, 49, 1003 iliopsoas bursitis and, 817 Gallstones acute pancreatitis and, 682 chronic pancreatitis and, 684 Gamma globulins, 68 Gamma knife radiosurgery for cluster headache, 452 for trigeminal neuralgia, 469 Gamma-aminobutyric acid (GABA) in spinal modulatory systems, 33 loss of, in nerve injury, 26 mechanism of action of, 30, 30f Gamma-aminobutyric acid (GABA) agonists, for complex regional pain syndrome, 285 Gamma-aminobutyric acid (GABA) receptor, in spinal modulatory systems, 33 Gamma-glutamyltransferase (GGT), 71 Gangliolysis intraoperative, 1199 percutaneous, 1198–1199, 1198f, 1199f Ganglion. See specific ganglion Ganglion of Walther (impar) block, 1281–1284 anatomic aspects of, 1281–1284 complications of, 1284 for coccydynia, 803, 803f technique of blind and fluoroscopic, 1281–1282, 1281f, 1282f CT-guided, 1282, 1283–1284, 1283f fluoroscopic, 1282–1283, 1283f transcoccygeal, 1282 Ganglionotomy, lumbar dorsal root, 1340–1345. See also Lumbar dorsal root ganglionotomy Gangrene Fournier's, 795 in systemic lupus erythematosus, 404f Gasserian ganglion anatomy of, 1069, 1069f, 1075, 1075f destruction of, indications for, 1068 Gasserian ganglion block, 1068–1073 anatomic aspects of, 1069–1070, 1069f, 1070f contraindications to, 1068–1069 historical considerations in, 1068 indications for, 1068–1069, 1069t practical considerations in, 1071–1072 technique of, 1070–1072, 1070f, 1071f, 1072f, 1073f Gastrointestinal disorders hypnosis for, 965 opioid-induced, 896–897 Gastrointestinal hypermotility, after celiac plexus block, 1202 Gastroparesis, in cancer, 340–341 Gate control theory, of pain, 3 General anesthesia, for burn pain, 234 Genetic factors in cervical dystonia, 558 in cluster headache, 437–442 in complex regional pain syndrome, 275 in spondylolysis, 752 Genetic predisposition, to neuropathic pain, 205–206 Geniculate neuralgia, vs. trigeminal neuralgia, 466 Genitalia, female, external, 798, 799f Genitofemoral nerve block for genitofemoral neuralgia, 691, 691f for vulvodynia, 800, 800f Genitofemoral neuralgia, 691–692, 691f after lumbar sympathetic nerve block, 1235 vs. orchialgia, 794–795, 795t Genitofemoral neuropathy, cryoanalgesia for, 1370–1371, 1370f Genitourinary disorders, opioid-induced, 897 Giant cell arteritis, 410–411, 410f, 411f, 476–481 arterial biopsy in, 478, 478t clinical features of, 476–478, 477f demographics of, 39t
Giant cell arteritis (Continued) diagnostic tests for, 478–479, 478t differential diagnosis of, 411 epidemiology of, 478, 478t etiology of, 479–480 headache in, 253, 255–256, 476 histologic features of, 479, 479f, 479t historical considerations in, 476 imaging in, 480 pathogenesis of, 479–480, 480f polymyalgia rheumatica and, 413, 415, 478 prognosis of, 481 signs and symptoms of, 410, 412f treatment of, 411, 480–481, 481t vs. cluster headache, 445 Gilbert's syndrome, 71–72 Gingival hyperplasia, phenytoin-induced, 919, 921f Glaucoma, 485–486 angle-closure, 485–486, 485t, 486f open-angle, 485, 485f, 485t optic disc cupping in, 485, 486f optic disc enlargement in, 45, 46f Globulin, 67 Glomus tumor, of hand, 628–629, 628f, 629f Glossopharyngeal nerve (IX) evaluation of, 44t irritative neuropathy of, 1373, 1373f Glossopharyngeal nerve block, 474, 474f, 1081–1085 anatomic aspects of, 474, 474f, 1082, 1082f complications of, 1083–1084, 1083t contraindications to, 1081, 1082t extraoral approach to, 1082–1083, 1082f, 1083f historical considerations in, 1081 indications for, 1081, 1082t intraoral approach to, 1083, 1083f neurodestructive procedures of, 1084, 1084f, 1085f technique of, 474–475, 474f, 475f, 1082–1083, 1082f, 1083f Glossopharyngeal nerve root, microvascular decompression of, 475, 1084–1085, 1085f Glossopharyngeal neuralgia, 471–475 characteristics of, 472 demographic considerations in, 471, 472f, 472t evaluation of, 472, 472f historical considerations in, 471 laboratory tests for, 472 pain localization in, 471, 472f treatment of, 472–475 drug therapy in, 473–474, 473t, 474t nerve block in, 474–475, 474f, 475f neurodestructive procedures in, 475 vs. trigeminal neuralgia, 465–466 Glucocorticoids for cancer pain, 321–323 analgesic effects of, 323 indications for, 321–322 safety of, 323 for giant cell arteritis, 481 Glucose testing, 60–61, 60f, 60t Glutamate receptors, in tissue injury, 22, 23f Glutamate release, in nerve injury, 26 Gluteal bursae, anatomy of, 808, 809f Gluteal bursitis, 808–810, 809f, 810f Gluteal nerve entrapment of, 809, 810f neuralgia secondary to irritation of, 1371 Gluteal tendinitis, trochanteric bursitis and, 815 Glycerol, in neurolytic blockade, 325t, 327 Glycerol rhizotomy, for trigeminal neuralgia, 468 Glycine, loss of, in nerve injury, 26 Gold therapy, for rheumatoid arthritis, 401 Golfer's elbow (medial epicondylitis), 598–600, 599f, 600f vs. cubital tunnel syndrome, 607–608, 1161, 1164f Golfer's elbow test, 598, 600f Gonyalgia paresthetica, 828 Gout, 71 Granuloma, maxillary cholesterol, 500, 500f Greater occipital nerve block, 1059–1060. See also Occipital nerve block Greater trochanter, bursae associated with, 813, 814f
Greater trochanter pain syndrome. See Trochanteric bursitis “Green back pain,”, 726 Ground electrodes, in electromyography, 176–177, 177f Group therapy, for neuropathic pain, 209 Growth factors dextrose effects on, 00194:f0040 in soft tissue restoration, 1027, 1028f. See also Prolotherapy released, life of, 00194:f0030 soft tissue, 00194:f0035 therapeutic injects of. See Prolotherapy Gua sha, in Chinese medicine, 1024 Guided imagery, 969. See also Relaxation technique(s) technique of, 971
H
Hair, examination of, in peripheral neuropathy, 265, 265t Hallux rigidus, 869–870, 870f Hallux valgus, 869, 870f Haloperidol, for nausea, 341, 341f Hampton's hump, 653 Hamstring muscles, anatomy of, 835 Hand anatomy of, 616, 617f glomus tumor of, 628–629, 628f, 629f osteoarthritis of, 81, 386, 386f radiography of, 80–81 Hand pain differential diagnosis of, 616, 617t digital nerve block for, 1171–1173, 1172f Hand warming therapy, in migraineurs, 958 Hand-foot syndrome (dactylitis), in sickle cell disease, 246 Hattori and Kawai classification, of cervical myelopathy, 549, 549f Hawkins impingement test, 573, 573f, 586–587 Headache, 249–257 age and, 249 cervicogenic atlanto-occipital nerve block for, 1047–1049, 1049f, 1050f radiofrequency lesioning for, 1357–1360, 1358t. See also Cervicogenic headache, radiofrequency lesioning for chronic classification of, 454–455, 454t mechanisms of, 456, 457f cluster, 436–452. See also Cluster headache complete blood count in, 250 CT scan in, 250–251 diagnostic tests for, 250–251 differential diagnosis of, 251–253, 251f, 252f erythrocyte sedimentation rate in, 250 hypertensive, 253, 256 in bacterial meningitis, 252, 254–255 in brain abscess, 252, 252f, 255 in brain neoplasms, 253, 254f, 256 in giant cell arteritis, 253, 255–256, 476 in infectious disorders, 252, 252f, 254–255 in inflammatory disorders, 253 in pseudotumor cerebri, 253, 256 in stroke, 251–252, 251f, 253–254 in subarachnoid hemorrhage, 251–252, 251f, 254, 254f magnetic resonance angiography in, 251 magnetic resonance imaging in, 107, 251 management of, 253–256 hypnosis in, 965 medication overuse, 453–463. See also Medication overuse headache migraine, 420–427. See also Migraine headache neurologic examination in, 250 occipital, 503–505, 1063–1065 after cervical plexus block, 1101 organic causes of, 249, 250t physical examination in, 250 signs and symptoms of, 249–251, 250t site of pain in, 249 tension-type, 428–435. See also Tension-type headache Healing, spiritual, 937–938 Heart, effects of thoracic epidural nerve block on, 1180 Heat, specific, in hydrotherapy, 988
Heat therapy contraindications to, 979t for bone pain, 703–704 for herpes zoster, 270 for proctalgia fugax, 805–806 for rheumatoid arthritis, 402 for sacroiliac joint disorders, 761 in pain management choice of, 978–979, 979t deep, 982–984 via conversion, 982–984, 984f physiologic effects of, 978–979, 979t superficial, 979–982 via conduction, 979–981, 980f, 981f via convection, 982, 982f indications for, 979t Heating pads chemical, 980 circulating water, 980 electric, thermal injury associated with, 980, 980f microwavable, 980–981, 981f Heberden nodes, 81, 386, 399–400, 400f, 618 Heel wedges, in management of osteoarthritis, 392 Heidenhein's method, of cervical plexus block, 1096 Hematoma after caudal epidural nerve block, 1256 after cervical epidural nerve block, 1137 intrathecal/peridural, in failed back surgery syndrome, 766, 766f Hemicrania, paroxysmal, 444 Hemiplegic migraine, 423. See also Migraine headache clinical example of, 423–424, 424t familial, 423 sporadic, 423 Hemorrhage after spinal cord stimulation, 1319 neuroaxial, 1316–1317 iliac, femoral neuropathy due to, 825–826 subarachnoid, headache in, 251–252, 251f, 254, 254f Hemorrhoids, vs. proctalgia fugax, 804 Hemothorax, traumatic, 658f, 00080:p0540 Henderson-Hasselbalch equation, 930 Hepatic crisis, in sickle cell disease, 246 Hepatotoxicity, acetaminophen-induced, 883 Herbal medicine, 936t Herbal remedies, in Chinese medicine, 1024 Hereditary diseases, peripheral neuropathy and, 262t Hering-Breuer reflex, 650 Herniation definition of, 107–108. See also Intervertebral disk, herniation of of nucleus pulposus, in failed back surgery syndrome, 768, 768f Herniorrhaphy(ies) cryoneurolysis after, 1365 femoral neuropathy due to, 827 orchialgia after, 795 Heroin, 904, 904f for cancer pain, 306t Herpes zoster, 268–271 complications of, 271. See also Postherpetic neuralgia in Ramsay Hunt syndrome, 268 signs and symptoms of, 268–269, 269f stellate ganglion block for, 269, 1104–1105 thoracic epidural nerve block for, 1181 treatment of, 269–271 adjunctive, 270–271 drug therapy in, 269–270 nerve blocks in, 269, 270f options in, 269–270 Herpes zoster ophthalmicus, 492–493, 492f Herpetic pain, 268 Herpetic/postherpetic neuralgia, vs. trigeminal neuralgia of cervical dorsal root ganglia, 466 of trigeminal nerve, 466 Heterocyclic antidepressants. See Antidepressants, tricyclic Hiccups complications of, 1089t persistent or intractable, 1088 causes of, 1089t pharmacologic management of, 1089t phrenic nerve block for, 1088, 1089t
Index 1427 Hilldreth's test, for glomus tumor, 628 Hill-Sachs lesions, 575 Hip osteoarthritis of, 81, 82f osteonecrosis of, 81, 83f radiography of, 81–82, 82f, 83f Hip abduction, for sacroiliac joint disorders, 762 Hip adduction, for sacroiliac joint disorders, 762 Hip adduction test, resisted, for iliopsoas bursitis, 817, 818f Hip arthroplasty, femoral neuropathy after, 826 Hip extension, for sacroiliac joint disorders, 762 isometic, 762 Hip fractures, from osteoporosis, 701 Hip pain, prolotherapy for, 1040–1041, 1040f Histamine, triggering cluster headache, 440 Histamine desensitization, for cluster headache, 451 Histoplasmosis, 654 HLA antigens, in complex regional pain syndrome, 275 Hoffmann (H) reflex, 182 Hoffmann's sign, in cervical radiculopathy, 525, 526t Holistic medicine, vs. alternative medicine, 935 Hooking maneuver test, for slipping rib syndrome, 678, 678f Hordeolum (stye), 483, 483f Hormone changes, in cluster headache, 443 Hormone release, inhibition of, opioid-induced, 897 Hornblower's sign, 572, 572f Horner's syndrome after thoracic epidural nerve block, 1181 causes of, 512 findings in, 533–534 partial, in cluster headache, 440 Hospice, 944 Hospital(s) Joint Commission Pain Assessment and Management Standards for, 193, 193t sickle cell pain management in, 248 Housemaid's knee (prepatellar bursitis), 845–847. See also Prepatellar bursitis (housemaid's knee) Ho:YAG laser, 1397, 1398f. See also Laser diskectomy. Laser therapy in cadaver research, 1400 results with, 1405 H-reflex, 182 5-HTTLPR gene, 205 Hubbard tank, in hydrotherapy, 993–994. See also Hydrotherapy Human immunodeficiency virus (HIV) infection, laboratory tests for, 64 Human leukocyte antigen (HLA), in cluster headache, 437 Humerus, radial nerve block at, 1151–1153, 1152f, 1153f Hyaluronan injections for osteoarthritis, 394 for osteoporosis, 705 Hyaluronidase, with local anesthetics, 932 Hydrocele, 795 Hydrocodone, 904–905 chemical structure of, 894f Hydrocollator packs, 979–980, 980f Hydrogen ion release, in tissue injury, 21t Hydromorphone, 895t, 905 chemical structure of, 894f, 904f for cancer pain, 305–306, 306t, 307 Hydropneumothorax, radiography of, 645f Hydrostatic pressure, 988 Hydrotherapy, 987–994 contrast baths in, 994 definition of, 987 historical considerations in, 987–988 Hubbard tank in, 993–994 physical effects of, 988–989, 988t principles of, 988, 988t techniques of, 989–994 therapeutic effects of, 989, 989t water-based exercises in, 989–993, 991f, 992f, 993f whirlpools in, 993–994 with heat, 982, 982f Hydroxychloroquine, for rheumatoid arthritis, 401 5-Hydroxytryptamine (5-HT), in supraspinal modulatory systems, 33–34
Hyoid syndrome, 501–502 Hyperactivity, neuronal, 7–8 Hyperalgesia, 12 in complex regional pain syndrome, 274, 275–276 in postmastectomy pain, 662t nerve injury-induced, 24–27. See also Pain processing system, in nerve injury opioid-induced, 897–898 tissue injury-induced, 20–24. See also Pain processing system, in tissue injury Hyperbilirubinemia, unconjugated, 71–72 Hypercalcemia, 70 Hyperemia, of conjunctiva, 484–485, 484f Hyperhidrosis, in complex regional pain syndrome, 276 Hyperkalemia, 61 Hypernatremia, 61 Hyperparathyroidism, 70 Hyperpathia evoked, in nerve injury, 26–27 in postmastectomy pain, 662t Hyperphosphatemia, 70 Hyperreflexia, in arachnoiditis, 747 Hypersensitivity, denervation, 7–8 Hypertension, pulmonary, 653 Hypertensive headache, 253 treatment of, 256 Hypertonic solutions, in neurolytic blockade, 327 Hyperuricemia, definition of, 71 Hypnosis, 936t, 938, 963–966. See also Alternative medicine anatomic aspects of, 965 for burn pain, 236–237, 965 technique of, 966 for phantom pain, 300 historical considerations in, 963–964, 964f indications for, 964–965 side effects and complications of, 966 technique of, 965–966 Hypoalgesia, in complex regional pain syndrome, 275–276 Hypocalcemia, 70 Hypoesthesia, in complex regional pain syndrome, 275–276 Hypogastric plexus, anatomy of, 793, 794f, 1273, 1274f Hypogastric plexus block, 1273–1278 anatomic aspects of, 1273, 1274f complications of, 1280–1281 superior, differential, 156t technique of CT-guided, 1279–1280, 1280f fluoroscopic, 1278–1279, 1279f, 1280f single-needle, 1273–1278 blind and fluoroscopic, 1274, 1274f, 1275f, 1277f CT-guided, 1274–1275, 1276f, 1277f, 1278f transdiscal, 1278 two-needle, 1275–1276 blind and fluoroscopic, 1275f, 1276–1277, 1276f, 1277f CT-guided, 1277–1278 Hypoglossal nerve (XII), evaluation of, 44t Hypokalemia, 61 Hyponatremia, 61 Hypophosphatemia, 70 Hypophysectomy, for cancer pain, 335 Hyporeflexia, in cervical radiculopathy, 524 Hypotension, after celiac plexus block, 1202 Hypothalamic stimulation, for cluster headache, 452 Hypovolemia, in pancreatitis, 682, 684, 686 Hysterectomy, femoral neuropathy after, 826
I
Ibuprofen, 881–882 chemical structure of, 217f for cancer pain, 304, 305t for tension-type headache, 433t pharmacology of, 887t Ice packs, 984, 985f chemical, 985f, 986 for herpes zoster, 270 Ice rubs, 985 Ice slushes, 984 Iced whirlpool baths, 985
1428 Index Iliac abscess, femoral neuropathy due to, 826 Iliac crest bone harvest, cryoanalgesia for, 1366, 1367f Iliac hemorrhage, femoral neuropathy due to, 825–826 Iliacus compartment, 825 hemorrhage in, 825–826 Iliohypogastric nerve block. See Ilioinguinaliliohypogastic nerve block Iliohypogastric neuralgia, 689–690, 690f Iliohypogastric neuropathy, cryoanalgesia for, 1370–1371 Ilioinguinal nerve, sensory distribution of, 687, 688f Ilioinguinal neuralgia, 687–689, 688f, 689f vs. orchialgia, 794–795, 795t Ilioinguinal neuropathy, cryoanalgesia for, 1370–1371 Ilioinguinal-iliohypogastric nerve, 1237 Ilioinguinal-iliohypogastric nerve block, 1237–1241 analgesic, 1237 technique of, 1240 anatomic aspects of, 1238, 1239f, 1240f anesthetic, 1238 technique of, 1238–1240, 1241f ultrasound-guided, 1239–1240, 1241f complications of, 1240–1241 diagnostic, 1237 technique of, 1240 for iliohypogastric neuralgia, 690, 690f for ilioinguinal neuralgia, 688, 689f for vulvodynia, 799–800, 800f historical considerations in, 1237 indications for, 1237–1238 side effects of, 689, 690 Iliopsoas bursitis, 817–820, 818f, 819f, 819t Iliotibial band syndrome, 817 Imagery, for burn pain, 236 Imaging. See also specific modality, e.g., Computed tomography (CT) Imipramine for postmastectomy pain, 663t for tension-type headache, 434t Immunoglobulins, 68 Immunologic disorders, opioid-induced, 897 Immunosuppressives for mononeuritis multiplex, 672 for rheumatoid arthritis, 401–402 Impar block. See Ganglion of Walther (impar) block Impedance monitoring, in continuous and pulsed radiofrequency mode, 1332 Impingement syndrome arthroscopic surgery for, 577, 577f rotator cuff disorders and, 570 Implantable drug delivery systems, 1311–1315 classification of, 1313–1315, 1313t complications of, 1313 costs of, 1313 history of, 1311 patient selection for, 1311–1313 patient's support system for, 1313 preimplantation trial for, 1312, 1312t patient's ability to assess results of, 1312–1313, 1312t side effects of, 1312 symptom relief with, 1311 type I: percutaneous catheter, 1313t, 1314, 1314f type II: subcutaneous tunneled catheter, 1313t, 1314, 1314f type III: totally implantable reservoir/port, 1313t, 1314, 1315f type IV: totally implantable in fusion pump, 1313t, 1315, 1315f type V: totally implantable programmable infusion pump, 1313t, 1315, 1315f Implantable infusion pump, 1313t, 1315, 1315f for arachnoiditis, 749–750 opiate delivery via, 750 programmable, 1313t, 1315, 1315f Implantable reservoir/port, 1313t, 1314, 1315f Implanted pulsed generator pain at site of, 1320 types of, 1305, 1305f Incident pain, 944 Incidental durotomy, in failed back surgery syndrome, 766
Incontinence, urinary after caudal epidural nerve block, 1256–1257 after cervical epidural nerve block, 1137 in arachnoiditis, 747 Indomethacin for acute arachnoiditis, 748 for cancer pain, 305t for cluster headache, 449 for paroxysmal hemicrania, 444 pharmacology of, 887t Infection(s). See also specific infection after caudal epidural nerve block, 1256 after cervical epidural nerve block, 1137 after spinal cord stimulation, 1308, 1317–1318, 1317f, 1318f after thoracic epidural nerve block, 1184 headache in, 252, 252f, 254–255 in failed back surgery syndrome, 769, 770f spinal, 737–742 Inferior hypogastric plexus, anatomy of, 793, 794f Inflammation bronchial, 651, 652f headache and, 253 nerve injury and, 27. See also Neurogenic inflammation systemic, pleurisy associated with, 655 Infliximab, for rheumatoid arthritis, 401–402 Informed consent for cryoanalgesia, 1363 for diskography, 123, 137 for subarachnoid neurolytic block, 1214 Infraorbital nerve, irritative neuropathy of, 1372, 1372f Infrapatellar bursitis, 835, 836f deep, 835, 836f, 850–851, 850f treatment of, 851 superficial, 847–848, 847f treatment of, 848, 848f Infusion continuous. See also Implantable infusion pump; Nonimplantable infusion pump of analgesia, 219 opiate, for arachnoiditis, 750 Inguinal herniorrhaphy, femoral neuropathy due to, 827 Inhaled nitrous oxide, for burn pain, 234 Inhalers, asthma, impeding biofeedback, 962 Injection test, for rotator cuff disorders, 573–574 Insertional muscle activity, in electromyography, 179, 179f Insight-oriented therapy, for neuropathic pain, 209 Insomnia, chronic pain and, 949 Instability, mechanical, in failed back surgery syndrome, 768 Institutional guidelines, for burn pain management, 00025:f0025, 231 Intercessionary prayer, 937–938 Intercostal nerve anatomy of, 225–226, 1185, 1186f, 1364f anterior cutaneous branch of, 674, 675f Intercostal nerve block, 1185–1190 complications of, 226 diagnostic, 148 for acute/postoperative pain, 225–226, 226f for cancer pain, 309 for fractured ribs, 638, 638f for liver pain, 680–681, 681f with local anesthetic, 1185–1187 anatomic aspects of, 1185, 1186f complications of, 1187, 1189f indications for, 1185, 1186f technique of, 1185–1186, 1186f, 1187f, 1188f with radiofrequency lesioning, 1188–1190 anatomic aspects of, 1188, 1190f complications of, 1189–1190 indications for, 1188 technique of, 1188, 1190f Intercostal neuralgia, 640–641, 640f cryoanalgesia for, 1366, 1366f Intercostobrachial nerve block, 1153–1154, 1154f, 1155f Interdigital neuroma, Morton's, 866–868, 867f, 868f Interference pattern, in electromyography, 179–180, 180f, 181f
International Association for Study of Pain (IASP) classification, of complex regional pain syndrome, 273, 290, 506, 507t International Association for Study of Pain (IASP) definition, of neuropathic pain, 202–203 International Headache Society classification, of cluster headache, 438t International normalized ratio (INR), 60 Interphalangeal joint(s), arthritis of, 618–619, 618f Interpleural catheter analgesia, for cancer pain, 310 Interpleural nerve block, for post-thoracotomy pain, 666–667 Interscalene brachial plexus block, 1142–1145. See also Brachial plexus block indications for, 1142–1144, 1143f side effects and complications of, 1144–1145 technique of, 1144, 1144f, 1145f, 1146f Interscalene cervical plexus block, 1096–1097, 1098f Intersection syndrome, 622 Intersegmental projection systems, 14–15 Interspinous ligament pain, cryoanalgesia for, 1370 Intertarsal joints, 860–861 Interval headache, 428. See also Tension-type headache Interventional strategies at sympathetic nervous system, for complex regional pain syndrome, 285–286 for neuropathic pain, 211 Intervertebral disk anatomy of, 118–119, 118f, 119f cervical, herniation of, 541, 542f, 545, 545f CT scan of, 98–99, 99f, 100f, 101f degeneration of, 78, 78f, 79f CT scan of, 99, 100f diskography of, 117–138. See also Diskography disorders of, 78 herniation of anatomic aspects of, 1401–1402 atypical presentation of, 712, 713t CT scan of, 99, 99f diagnosis of, 711, 711f epidural steroids for, 1181 pain in. See Lumbar radiculopathy; radicular pain pathology of, 1400–1402 infection of. See Diskitis loose fragments of, in failed back surgery syndrome, 766 magnetic resonance imaging of, 107–108, 109f Interview, in pain history, 37–38 Intradiskal electrothermal annuloplasty, 1388–1392 advantages and disadvantages of, 1389t anatomic aspects of, 1389 complications of, 1390–1391, 1392f contraindications to, 1389, 1389t efficacy of, 1391–1392 future directions for, 1392 historical considerations in, 1388–1389 indications for, 1389, 1389t technique of, 1389–1390, 1390f, 1391f Intradiskal electrothermal catheter advantages and disadvantages of, 1389t placement problems with, 1390, 1391f Intraspinal therapies, for postmastectomy pain, 663 Intrathecal agents, complications involving, 1321 Intrathecal catheter, complications involving, 1321 Intrathecal hematoma, in failed back surgery syndrome, 766, 766f Intravenous access, for diskography, 123 Intravenous bolus, analgesia delivery via, 219 Intravenous regional sympatholysis, for complex regional pain syndrome, 285–286 Ion channels, increased expression of, 25 Iontophoresis, of opioids, 901 Irritable bowel syndrome, relaxation techniques for, 970 Ischemia of spinal cord, 544 spinal cord stimulation for, 1309
Ischiogluteal bursitis, 810–811, 811f Isocarboxazid, for migraine prophylaxis, 426 Isometic hip extension exercises, for sacroiliac joint disorders, 762
J
Japanese Orthopaedic Association Cervical Myelopathy Evaluation Questionnaire, 550, 552t Japanese Orthopaedic Association Scoring System, for cervical myelopathy, 550, 551t Jaundice, 72 Jobe's relocation test, 573–574 Joint(s). See named joint Joint Commission on Accreditation of Healthcare Organizations (JCAHO), pain assessment standards of, 193–201, 193t Joint effusions, ballottement test for, 839, 840f Joint pain, water-based exercises for, 990 Jump sign calcaneal, in plantar fasciitis, 370, 370f in fibromyalgia, 371, 372f Juvenile rheumatoid arthritis, 396–397 aspirin dosing guidelines for, 880
K
Kager's fat pad, 860 Kappa (k) opioid receptor, 892, 892t Kegel exercises, 779 Kernig's sign, 252 Ketoprofen, 882 for cancer pain, 305t for tension-type headache, 433t pharmacology of, 887t Ketorolac chemical structure of, 217f for tension-type headache, 433t pharmacology of, 887t Killer headache, 436, 439. See also Cluster headache Kinin release, in tissue injury, 21t Klumpke's palsy, 534. See also Brachial plexopathy Knee anatomy of, 834–835, 835f, 836f Baker's cyst of, 839, 853–855, 853f, 854f, 855f bursitis syndromes of, 843–852. See also under Bursitis housemaid's (prepatellar bursitis), 845–847. See also Prepatellar bursitis (housemaid's knee) osteoarthritis of, 82–83, 83f, 385, 385f, 386f radiography of, 82–83, 83f Knee braces, in management of osteoarthritis, 392 Knee extension test, for quadriceps expansion syndrome, 856, 858f Knee pain, 834–842 acute, 837 age and, 837, 838t anticoagulants and, 839 approach to, 837–842 chronic, 837 classification of, 837t common conditions causing, 836–837, 837t corticosteroid-related, 839 evaluation of, testing modalities in, 841–842 in Lyme disease, 839, 839f nerve blocks for, 1294–1296, 1296f physical examination for, 839–841, 839f anterior drawer test in, 840–841, 841f McMurray's test in, 841, 842f palpation in, 839, 840f posterior drawer test in, 841, 841f valgus stress test in, 840, 840f varus stress test in, 840, 841f prolotherapy for, 1037, 1037f, 1038f targeted history for, 837–839, 838t traumatic, 837 with fever, 838 with muscle weakness, 838 with polyarthralgias, 838 with rash, 838 with weight changes, 838–839 K-pads (circulating water heating pads), 980 KTP laser, 1397. See also Laser diskectomy. Laser therapy Kummell's disease, 78, 80f
Index 1429 Kyphoplasty, 89, 1381–1382, 1381f, 1382f outcomes of, 00180:s0066 PMMA preparation and delivery in, 1382–1383, 1383f vs. vertebroplasty, 1384t Kyphosis, thoracic, 77
L
Labat's method of cervical plexus block, 1096 of sciatic nerve block, 1290 Labor and delivery, effect of low back pain on, 780 Laboratory test(s), 57–74 basic, 57–58, 58t complete blood count, 58–60 C-reactive protein, 58 creatine kinase, 72 electrolytes, 61 erythrocyte sedimentation rate, 58 for acute phase proteins, 58 for calcium, phosphorus, and magnesium disorders, 70–71 for connective tissue diseases, 61–63, 62t, 63t for drug monitoring and abuse, 72–74 for HIV infection, 64 for neuropathy, 65–67, 68t for spirochetal diseases, 64–65, 65f, 66f, 67f for uric acid disorders, 71 for vasculitis, 61–63, 62f, 62t, 63t glucose, 60–61, 60f, 60t hematologic, 58–60 liver function, 71–72 osmolality, 70 prostate-specific antigen, 63–64 renal function, 69–70 serum protein, 67–69, 69f thyroid function, 63 toxicology, 74 Lacrimal nerve, 1069 Lacrimation, in cluster headache, 439 Lactate dehydrogenase (LDH), 71 Laminectomy, rationalization for, in failed back surgery syndrome, 765 Lamotrigine, 921–922, 921f dosing guidelines for, 922 Langerhans cell histiocytosis, pulmonary, 652 Laparoscopy, femoral neuropathy after, 826 LASE system, of laser diskectomy, 1402–1403, 1403f Lasègue test, for lumbar radiculopathy, 707, 708f Laser(s). See also specific laser low-power, 939 safety of, 1399–1400 technical aspects of, 1399, 1399f Laser diskectomy, 1397–1407 cadaver disk research in, 1400 complications of, 1406–1407, 1406t disadvantages of, 1407 historical considerations in, 1397–1398, 1398f indications for, 1398–1399 live animal disk research in, 1400 results of, 1405–1406 safety of, 1399–1400 technical aspects of, 1399, 1399f technique(s) of, 1402–1405 LASE system, 1402–1403, 1403f nonendoscopic laser fiber diskectomy (modified Choy), 1403–1404, 1404f nonlumbar, 1405 rigid-scope endoscopic laser diskectomy, 1404–1405, 1405f stepwise laser disk decompression, 1402, 1402f types of lasers in, 1397–1398, 1398f Lateral collateral ligament, integrity of, varus stress test for, 840, 841f Lateral epicondylitis (tennis elbow), 356–357, 356f, 357f vs. radial tunnel syndrome, 613–614, 614f, 1153, 1153f Lateral femoral cutaneous nerve anatomy of, 381, 382f, 821, 822f, 1242, 1243f entrapment of, 821, 822f ultrasonography of, 821–823, 823f Lateral femoral cutaneous nerve block, 1242–1244, 1243f, 1243t, 1244f, 1293 Laterocollis, 559–560 muscles involved in, 562t
Lead(s), neurostimulator. See Neurostimulator lead(s) Lead apron, for radiation procedures, 104 Lead poisoning, screening for, 74 Learned tolerance, to opioids, 897 Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) Pain Scale, 199, 199f Leflunamide, for osteoporosis, 705 Left upper quadrant syndrome, in sickle cell disease, 246 Leg length discrepancy, in trochanteric bursitis, 814, 815, 816 Leg pain lower anterior, prolotherapy for, 1035–1036, 1036f lower medial, prolotherapy for, 1036–1037, 1036f, 1037f Leg ulcers, in sickle cell disease, 246–247 Lesser occipital nerve block, 1059–1060. See also Occipital nerve block Leukocytosis, 59 Levator scapulae, anatomy of, 589–590, 590f Levo-alpha acetyl methadol (LAAM), 908 Levophanol, 906 Lhermitte's sign in cervical myelopathy, 549 in cervical radiculopathy, 525, 526t Lidocaine chemical structure of, 146f for celiac block, 1193 for cluster headache, 447 topical, for mononeuritis multiplex, 672 Lidocaine patch, for herpes zoster, 271 Lidocaine/bupivacaine, for cervical plexus block, 1099–1100 Lifestyle changes, 936t Liftoff test, 572 Ligament(s). See also named ligament magnetic resonance imaging of, 113–114, 114f Ligament of Struthers, median nerve entrapment by, 610, 1159 Ligamentum flavum, calcification of, 545, 545f Lingual nerve, 1070 Lipid mediators, in tissue injury, 22, 23f Lipidic acid release, in tissue injury, 21t Lipoma arborescens, 854, 855f Lithium carbonate, for cluster headache, 448–449, 489 Lithotomy positions, femoral neuropathy after, 827 Litigation, ongoing, chronic pain and, 953 Liver disease, pain in, 679–681, 679f, 680f, 681f referred, 679 Liver function tests, 71–72 Liver metastases, palliative radiation therapy for, 317 Load and shift maneuver, for rotator cuff disorders, 574, 574f Local anesthetic toxicity, 931t, 932–933, 932f, 933f after caudal epidural nerve block, 1256 Local anesthetics, 929–933. See also specific agent alkalinization of, 930 chemistry of, 929–931, 929f, 930f, 931f duration of, 930–931, 931t epidural, complications of, 1212 for burn pain, 235 for cancer pain, 319–321 for postmastectomy pain, 662–663 generic and trade names of, 933t hyaluronidase with, 932 in clinical use, 933, 933t intercostal nerve block with, 1185–1187 anatomic aspects of, 1185, 1186f complications of, 1187, 1189f indications for, 1185, 1186f technique of, 1185–1186, 1186f, 1187f, 1188f intravenous, mechanism of action of, 30, 30f oral, for cancer pain, 309 pharmacodynamics of, 931 pharmacokinetics of, 931–932, 932t sensitivity to, nerve fiber size and, 150–151, 151t topical, 933t Log roll swim exercises, 991–992, 993f Long dorsal sacroiliac ligament palpation, 777 Long Q-T syndrome, stellate ganglion block for, 1105
1430 Index Long-term care, for medication overuse headache, 462 Loss-of-resistance technique, of cervical epidural nerve block, 1131–1132, 1132f, 1133f Low back pain, 694–700 cauda equina syndrome and, 695 causes of mechanical, 699–700, 700f nonmechanical, 695–699, 696f, 697f, 698f, 699f chronic, 206–207 definition of, 694 diagnosis of, degenerative changes in, 731, 731t differential diagnosis of, 776, 776t disorders associated with, 694, 695t epidemiology of, 775 fever and, 695–696 from abdominal aneurysms, 699 from lumbar spondylosis, 700, 700f from lumbosacral strain, 699–700 from vertebral osteomyelitis, 695–696, 696f in pregnancy, 775–780. See also Pregnancy, low back pain in initial evaluation of, 694–695 local vertebral column, 697–698, 698f morning stiffness and, 698–699, 699f natural history of, 694 osteopathic manipulative therapy for, 1006–1007 physical examination in, 695 postpartum, 780 radicular. See Lumbar radiculopathy radiography of, 77–78, 77f, 78f, 79f, 80f visceral, 699 water-based exercises for, 990 weight loss and, 695–696 with recumbency, 696–697, 697f yoga therapy for, 970 Lower extremity. See also specific part pain in, cryoanalgesia for, 1371 peripheral nerve blocks for, 1289–1298 at ankle, 1296–1297 at knee, 1294–1296, 1296f digital, 1297–1298 femoral nerve, 1292–1293, 1292f historical considerations in, 1289–1290 indications for, 1290 lateral femoral cutaneous nerve, 1293 obturator nerve, 1293–1294, 1294f sciatic nerve, 1290–1292, 1291f ulltrasound technique of, 1290 range of motion of, 1003, 1004t root vs. nerve lesions in, 48t Low-power lasers, 939 Ludington test, for bicipital tendinitis, 354, 354f Lumbar diskography interpretation of, 137–138 procedure in, 137 sample procedure note in, 137 technique of, 124–126, 124f, 125f, 126f, 127f Lumbar dorsal root ganglionotomy, 1340–1345 anatomy in, 1341, 1341f benign pulsed treatment in, 1343 complications of, 1344 efficacy of, 1344–1345, 1344t history in, 1340–1341 indications for, 1341–1342 lower impedance in, 1343 postprocedure advice and, 1343–1344 proximity between needle tip and nerve in, 1343 target identification in, 1342–1343 technique of, 1342–1343, 1342f Lumbar epidural nerve block, 1205–1213. See also Epidural nerve block, lumbar Lumbar facet block, 1221–1229 anatomic aspects of, 1223 complications of, 1227–1229 contraindications to, 1222t diagnostic, 1221–1222, 1222t drugs for, 1227 historical considerations in, 1221 indications for, 1221, 1222t protocol for, 86, 87f technique of, 1223–1227 intra-articular injections in, 1223–1224, 1224f, 1225f medial branch, 1224–1227, 1226f, 1226t, 1227f, 1228f therapeutic, 1223
Lumbar facet joints anatomy of, 716, 717f, 1223 pain in. See Low back pain; Lumbar facet syndrome Lumbar facet syndrome, 56, 716–721 anatomic features in, 716, 717f clinical features of, 719 diagnosis of, intra-articular blocks in, 717–719, 718f, 719t pain characteristics of, in normal volunteers, 716–717, 717f pathology of, 720 prevalence of, 719–720 treatment of, 720–721 intra-articular steroids in, 720 radiofrequency lesioning in, 1335–1340. See also Lumbar medial branch radiofrequency radiofrequency neurotomy in, 720–721, 721f Lumbar medial branch radiofrequency, 1335–1340 anatomy in, 1336, 1341f complications of, 1339 efficacy of, 1339–1340, 1341t history in, 1335–1336 indications for, 1337 pain in, 1336–1337, 1337f postprocedure advice and, 1339 technique of, 1337–1339, 1339f, 1340f Lumbar nerve root block, fluoroscopicallyguided, 88–89, 89f Lumbar radicular pain, 55, 55t Lumbar radiculopathy, 55, 707–715 diagnostic tests for, 711–712 differential diagnosis of, 712, 713t epidural fibrosis and, 1258–1259 etiology of, 708–709 historical considerations in, 707, 708f, 709f imaging studies of, 711–712 Lasègue test for, 707, 708f nerve root involvement in, diagnostic features of, 713t neurophysiologic studies of, 712 physical examination in, 711, 711f signs and symptoms of, 709–710, 710t straight leg raising test for, 710, 710t treatment of, 712–714 conservative, 712–713 interventional techniques in, 713 side effects and complications in, 714 surgical, 713–714 Lumbar spine osteoarthritis of, 700, 700f osteomyelitis of, 695–696, 696f radiography of, 77–78, 77f, 78f, 79f, 80f stenosis of, 56, 56t structure and function of, 751, 751f Lumbar spondylolisthesis, 56 Lumbar sympathetic ganglion, anatomy of, 222, 222f Lumbar sympathetic nerve block, 1230–1236 anatomic aspects of, 1231 complications of, 223, 1235 contraindications to, 1231 differential, 156t drugs for, 1235 evaluation of, 1235 for acute/postoperative pain, 222–223, 222f historical considerations in, 1230 indications for, 1230–1231 interpretation of, 1235–1236 responses to, 1235–1236 technique of, 1231–1235 classic or traditional, 1231–1233, 1232f, 1233f lateral, 2f, 1233–1234, 1233f, 1234f, 1235f Lumbopelvic stability, assessment of, 777, 778f Lumbosacral plexus neuropathy, 382 Lumbosacral spine metastatic lesions of, 696–697, 697f morning stiffness of, 698–699, 699f strain in, 699–700 Lung(s). See also Pulmonary. Respiratory entries effects of thoracic epidural nerve block on, 1180 Lung abscess, 654, 654f Lung cancer, chest pain in, 656–658, 656f Lyme disease, 65, 66f, 67f knee pain due to, 839, 839f laboratory tests for, 65
Lymphangioleiomyomatosis, 651–652 Lymphatics, epidural, 1129 Lymphocytes, 59 Lymphocytosis, 59 Lysis, of epidural adhesions, 1138–1141, 1258–1272. See also Epidural adhesiolysis
M
Magnesium block, 22 Magnesium imbalance, 70–71 Magnesium oxide, for acute arachnoiditis, 748 Magnesium sulfate for medication overuse headache, 461t for post-thoracotomy pain, 667 Magnetic field therapy, 939 Magnetic resonance angiography (MRA), 106 in headache, 251 cluster, 442 migraine, 425 Magnetic resonance imaging (MRI), 106–116 advances in, 106 advantages of, 106 contraindications to, 107 in arachnoiditis, 745–746, 745f, 746f in brachial plexopathy, 537f, 539 in cervical dystonia, 561 in cervical radiculopathy, 526 in headache, 107, 251 migraine, 425 in iliopsoas bursitis, 818, 818f in median nerve entrapment, 610, 610f in neuropathic pain, 204–205 in olecranon bursitis, 602, 603f in palliative radiation therapy, 313, 313f in peripheral neuropathy, 266 in pregnancy, 778 in subdeltoid bursitis, 582, 583f in Tietze's syndrome, 634–635, 635f in ulnar nerve entrapment, 606–607, 608f musculoskeletal, 106–107 neurologic, 107 of Baker's cyst, 853–854, 854f, 855f of bone marrow, 110–111 edematous lesions in, 110–111 degenerative conditions associated with, 111 reflex sympathetic dystrophy causing, 111, 113f vascular causes of, 111, 112f of cartilage, 114 of coccyx, 801, 802f of female pelvis, 689, 690f of glomus tumor, 629, 629f of ligaments, 113–114, 114f of muscles, 114–115, 115f of nerves, 114–115 of osteoarthritis, 389–390, 389f, 390f of quadriceps expansion syndrome, 856, 858f of rotator cuff disorders, 566, 568f, 575, 576f of spine, 107–109 anular tears in, 108, 110f intervertebral disk disease in, 107–108, 109f lesions in, 554, 554f stenosis in, 109, 111f of tendons, 112–113 of thoracic spine, 646, 647f of vertebral compression fractures, 115–116, 116f, 1377–1378, 1378f principles of, 106 Magnetic resonance myelography, 140, 140f Malingering chronic pain and, 953 occupational back pain and, 725, 732 Mandibular nerve anatomy of, 1069f, 1070f, 00145:s0044 irritative neuropathy of, 1372, 1372f Mandibular nerve block. See also Trigeminal nerve block coronoid approach to, 1076–1078, 1076f, 1077f, 1078f mental, 1079–1080, 1079f Manual healing, 936t Manual therapy, for lumbar radiculopathy, 713 Maprotiline, for tension-type headache, 434t Marginal zone (lamina I) neurons, 12–13, 12t, 13f Marijuana use, detection of, 73–74 Massage therapy for neuropathic pain, 211 for tension-type headache, 435
Masseteric nerve, 1070 Mastoiditis, 498, 499f Maxillary cholesterol granuloma, 500, 500f Maxillary nerve, anatomy of, 1069–1070, 1069f, 1070f Maxillary nerve block. See also Trigeminal nerve block coronoid approach to, 1076–1078, 1076f, 1077f, 1078f infraorbital, 1078–1079, 1079f Maxillary sinusitis, 498–500, 500f McGill Pain Questionnaire (MPQ), 3, 194, 195f short-form, 194–196, 196f, 197f McGregor lines, 546, 546f McMurray's test, for torn meniscus, 841, 842f Mechanical instability, in failed back surgery syndrome, 768 Mechanical spine pain, cryoanalgesia for, 1370 Meckel's cave, 1069, 1069f Meclofenamate, for tension-type headache, 433t Meclofenamic acid, for cancer pain, 305t Medial branch block, for cervical facet syndrome diagnostic, 518, 518f therapeutic, 519 Medial branch neurotomy, for cervical facet syndrome, 520 Medial collateral ligament integrity of, valgus stress test for, 840, 840f magnetic resonance imaging of, 113–114, 114f Medial collateral ligament syndrome, 364–365, 364f, 365f Medial epicondylitis (golfer's elbow), 598–600, 599f, 600f vs. cubital tunnel syndrome, 607–608, 1161, 1164f Median cutaneous nerve, anatomy of, 1153– 1154, 1154f Median nerve, anatomy of, 1157, 1158f, 1160f Median nerve block at elbow, 1157–1159, 1157f, 1158f, 1160f at wrist, 1165–1168, 1166f, 1167f, 1168f cutaneous and intercostobrachial, 1153–1154, 1154f, 1155f Median nerve entrapment by ligament of Struthers, 610, 1159 electrodiagnosis of, 184 in anterior interosseous syndrome, 611–613. See also Anterior interosseous syndrome in carpal tunnel syndrome, 620–621. See also Carpal tunnel syndrome in pronator teres syndrome, 609–611. See also Pronator teres syndrome Mediastinal tumors, 657–658 Medical history, in peripheral neuropathy, 261–262, 262t Medication history, in pain management, 39–40, 41t Medication overuse, definition of, 453–454 Medication overuse headache, 453–463. See also Headache classification of, 454–455 clinical evaluation of, 458 clinical features of, 457–458 diagnostic criteria for, 454, 454t history in, 458 International Headache Society definition of, 453 management of, 459–460 bridge (transition) therapies in, 460–461, 461t education in, 460 in withdrawal, 461–462 initial visit in, 460 long-term care needs in, 462 psychologic support in, 461, 462f treatment plan design in, 460 mechanisms of, 456–457 medications associated with, 454, 454t cause or consequence, 455–456 probable, 453 psychologic evaluation of, 458–459 assessment tools in, 459 role of analgesics in, 455 Medication scheduling, regular, for burn pain, 238 Meditation, 968, 968t. See also Relaxation technique(s) in MBSR program, 973, 974
Index 1431 Medulloblastoma, metastatic, 504f Mefenamic acid for cancer pain, 305t for tension-type headache, 433t pharmacology of, 887t Melatonin, for cluster headache, 451 Meloxicam, pharmacology of, 887t Memorial Delirium Assessment Scale (MDAS), 338 Memorial Pain Assessment Card, 337 Meningioma, spinal, 546–547 Meningitis, bacterial, headache in, 252, 254–255 Meniscus, torn, McMurray's test for, 841, 842f Menopausal osteoarthritis, 386 Mental nerve, irritative neuropathy of, 1372 Mental status, assessment of, 43, 43t, 44t Meperidine, 895t, 906 chemical structure of, 896f for cancer pain, 305–306, 306t dosage of, 331t Mepivacaine, 931t, 932t Meralgia paresthetica, 381–382, 382f causes of, 821, 822f, 1243t clinical presentation of, 821, 822f, 823f diagnosis of, 821 differential diagnosis of, 00108:p0020, 1243t femoral cutaneous nerve block for, 1242– 1244, 1243f, 1244f treatment of, 821–823, 823f Mercury poisoning, screening for, 74 Mesothelioma, malignant, 657, 657f Metacarpal nerve block, 1171, 1172f Metacarpophalangeal joint, arthritis of, 618–619, 618f Metallic foreign body, in cornea, 484, 484f Metastases bone. See Bone metastases palliative radiation therapy for of brain, 317–318 of liver, 317 vertebral augmentation in, 1386–1387 Metatarsalgia clinical presentation of, 866, 867f etiology of, 866, 867t Metatarsophalangeal joints, 860–861 Metaxalone, 925t, 926 for tension-type headache, 433t Methadone, 895t, 908 for cancer pain, 305–307, 306t for phantom pain, 298 Methocarbamol, 925t, 926 for tension-type headache, 433t Methotrexate for giant cell arteritis, 481 for rheumatoid arthritis, 401 Methylnaltrexone, 911–912 Methylphenidate for cancer-related fatigue, 340 for opioid-induced sedation, 342 Methylprednisolone. See also Bupivacaine/ methylprednisolone injections for acute arachnoiditis, 748 for anterior interosseous syndrome, 612 for cancer pain, 309 for carpal tunnel syndrome, 359, 359f, 621, 621f for cervical plexus block, 1099 for cubital bursitis, 605, 605f for de Quervain's tenosynovitis, 622–623, 623f for foot and ankle arthritis, 861 for fractured ribs, 638 for genitofemoral neuralgia, 691, 691f for giant cell arteritis, 411 for golfer's elbow, 599 for herniated disk, 1181 for intercostal neuralgia, 641 for meralgia paresthetica, 821–823, 823f for olecranon bursitis, 603, 604f for piriformis syndrome, 792 for post-thoracotomy pain syndrome, 639–640 for systemic lupus erythematosus, 405 for Tietze's syndrome, 635 Methysergide, for cluster headache, 449 Metoclopramide for migraine headache, 425–426 for nausea, 341, 341f Mexiletine for facial complex regional pain syndrome, 512 for mononeuritis multiplex, 671–672 for neuropathic pain, 210–211
Microdiskectomy, for lumbar radiculopathy, 714 Microvascular decompression for trigeminal neuralgia, 469–470 of glossopharyngeal nerve root, 1084–1085, 1085f Microwavable heating pads, 980–981, 981f Microwave diathermy, 984 Midazolam, intravenous, for diskography, 123 Middle ear, painful conditions of, 497–498, 498f, 499f Midtarsal joint, 860 Migraine headache, 420–427. See also Headache aura in, 422t, 423, 423t persistent, 424 symptoms of, 423 basilar-type, 424–425, 424t central sensitization and, 421 chronic, 424, 424t definition of, 454–455 diagnostic criteria for, 454, 454t vs. tension-type headache, 431 classification of, 422t clinical examples of, 422–423 clinical presentation of, 422–425, 422t definition of, 432 demographics of, 39t hemiplegic, 423 clinical example of, 423–424, 424t historical perspective on, 420–421 imaging studies for, 425 in status migrainosus, 424, 424t male-to-female ratio in, 422 pain in, 38 patent foramen ovale and, 421–422 pathogenesis of, 421 pathophysiology of, 422 premonitory symptoms of, 422, 422t prevention of, 426 retinal, 422t, 424, 424t seizures triggered by, 424 transformed, 432 treatment of, 425–427 biofeedback in, 956 nonpharmacologic, 427 osteopathic manipulative therapy in, 1007 yoga in, 970 vs. cluster headache, 445, 445t without aura, 422t diagnostic criteria of, 422t Migrainous neuralgia, 436–437. See also Cluster headache Mind-body control, 936t Mindfulness Based Stress Reduction (MBSR) program, 969, 973–975, 974t Minimally invasive access, and failed back surgery syndrome, 768 Mini-Mental State Examination (MMSE), 43, 44t, 338 Miosis, opioid-induced, 896 Mirror therapy, for neuropathic pain, 211–212 Mirror visual feedback therapy, for complex regional pain syndrome, 286 Mirror-image pain (allochiria), 8 Mitochondrial myopathy, inherited, 414 Mobilization, for sacroiliac joint dysfunction, 761 Modafinil, for cancer-related fatigue, 340 Modified superman exercises, 991–992, 992f Monkey hand, 533–534 Monoamine oxidase (MAO) inhibitors, 917–918 common, 917–918, 918f dietary restrictions with, 917t drug interactions with, 918t prophylactic, for migraine headache, 426 Mononeuritis multiplex, 669–672, 670f, 670t Mononeuropathy classification of, 261t electrodiagnosis of, 183–184 Morning stiffness, of lumbosacral spine, 698–699, 699f Morphine, 895t, 901–903 administration of, 902 chemical structure of, 218f, 893f clinical uses of, 902–903 for arachnoiditis, infusion of, 750 for cancer pain, 305–306, 306t, 307 dosage of, 331t for phantom pain, 298–299 mechanism of action of, 28 medicinal use of, 890
1432 Index Morphine (Continued) metabolism of, 902, 903f preparations of, 902–903 spinal administration of. See Spinal opioids Morphogenetic singularity theory, and acupuncture, 1021 Morton's interdigital neuroma, 866–868, 867f, 868f Motor skills, abnormal, in complex regional pain syndrome, 277–279 Motor system, examination of, 46, 46t Motor unit, 179 anatomy of, 177–178, 177f physiology of, 179, 180f Mouth ulcers, in systemic lupus erythematosus, 403, 404f Movement-related pain, 943–944 Moxibustion, in Chinese medicine, 1024 Mu (µ) opioid receptors, 892, 892t, 904f Multi-detector row computed tomography, 96. See also Computed tomography (CT) Multidimensional nature, of cancer pain, assessment of, 338–343 Multidimensional rating scales, in pain assessment, 194–199 Multidisciplinary pain treatment programs, 713 Multimodal therapy, comprehensive, for chronic pain, 950–952 Multiple myeloma, 69 vertebral augmentation in, 1386–1387 Multiple sclerosis, demographics of, 39t Muscle(s) abdominal, contraction of, 674, 676f examination of, 46, 46t magnetic resonance imaging of, 114–115, 115f Muscle discrimination, in biofeedback, 960 Muscle fibers, in motor unit, 177–178, 178f Muscle groups, targeted abbreviated, 972t 18 steps for tensing, 972t Muscle potentials in nerve conduction, 178 production of, 177–178, 177f Muscle relaxants, 924–928. See also specific agent abuse of, potential for, 925 clinical efficacy of, 924–925 commonly used, 925–926, 925t for chronic arachnoiditis, 749 for lumbar radiculopathy, 712 for tension-type headache, 433–434, 433t impeding biofeedback, 962 mechanism of action of, 924 pharmacokinetics of, 924, 925t side effects of, 925 Muscle relaxation, progressive, 968. See also Relaxation technique(s) for burn pain, 238 technique of, 972, 972t Muscle scanning, in biofeedback, 960 Muscle spasm/spasticity, drug therapy for, 926–928 Muscle strength/strengthening for rotator cuff disorders, 576 grading of, 46t Muscle tension headache, 428. See also Tension-type headache Muscle tone, testing of, 46 Muscle weakness in complex regional pain syndrome, 274 knee pain with, 838 Muscle-sparing thoracotomy, 665 Muscular rigidity, opioid-induced, 896 Musculoskeletal pain chronic, 371. See also Fibromyalgia transcutaneous electrical nerve stimulation for, 996 Musculoskeletal system changes of, during pregnancy, 775–776 disorders of, water-based exercises for, 989–990 Music therapy, 937 Mycobacterium tuberculosis infection, of spine, 738–739, 741f Myelography, 139–140, 140f in brachial plexopathy, 539 Myelopathy, cervical, 541–557. See also Cervical myelopathy Myeloscopy. See Spinal canal endoscopy
Myelotomy, for cancer pain, 334–335 Myofascial pain, 776 Myofascial prolotherapy, 1029, 1032–1033, 1033f. See also Prolotherapy Myopathy, painful, electrodiagnosis of, 185, 185t Myringitis, 497
N
Nabumetone, pharmacology of, 887t Nail(s), examination of, in peripheral neuropathy, 265, 265t Nail growth, abnormal, in complex regional pain syndrome, 274 Nalbuphine, 895t, 910 chemical structure of, 910f Naloxone, 911–912 chemical structure of, 911f for respiratory depression, opioid-induced, 308 Naltrexone, 911–912 Naproxen, 882 for cancer pain, 305t for tension-type headache, 433t pharmacology of, 887t Naratriptan for cluster headache, 450 for medication overuse headache, 461, 461t Nasal discharge, in cluster headache, 439 Nasal pain, 495t, 498–500 Nasal tumors, malignant, 500, 500f Nasociliary nerve, 1069 Nasopharyngeal carcinoma, with spread to cavernous sinus, 491, 491f Nasopharyngoma, 500 Natural killer (NK) cells, 59 Nausea and vomiting cancer-related, palliative care for, 340–341, 340t, 341f chronic, management of, 341, 341f etiology of, 340, 340t opioid-induced, 308, 341, 895–896 ondansetron for, 341 Nd:YAG laser, 1397–1398, 1398f. See also Laser diskectomy. Laser therapy results with, 1405–1406 Neck. See also Cervical entries Neck distraction test, for cervical radiculopathy, 525, 526t Neck pain atlanto-occipital nerve block for, 1047–1049, 1049f, 1050f cervical facet joints and, 1116 in cervical facet syndrome, 516 in cervical myelopathy, 549 in cervical radiculopathy, 524–525, 525t prolotherapy for, 1041–1042, 1041f, 1042f Needle electrodes, in electromyography, 176–177, 177f findings of, 179–180, 179f, 180f, 181f Neer impingement test, 573, 573f, 586 Neoprene sleeves, in management of osteoarthritis, 392 Nephrolithiasis, vs. orchialgia, 794–795, 795t Nephropathy, contrast-induced, epidurography and, 143 Nerve(s). See also named nerve dysfunction of, mechanisms of, 1029, 1029f, 1030f magnetic resonance imaging of, 114–115 Nerve block(s). See also specific nerve block for details diagnostic, 144–149, 145t accuracy of, 147 appropriate use of, 146–147, 146t celiac plexus, 149 cervical facet, 148 clinical rationale for, 144–146, 145f, 146f for cancer pain, 320, 320t historical imperative for, 144–146, 145f in lumbar facet syndrome, 717–719, 718f, 719t intercostal nerve, 148 neuroaxial, 147–148 occipital nerve, 148 selective nerve root, 149 specific, 147–149 stellate ganglion, 148 differential, 150–161 anatomic approach to, 156–157, 156t brachial plexus, 155
Nerve block(s) (Continued) celiac plexus, 156t controversies surrounding, 157–160, 158f conventional sequential spinal, 151–153 disadvantages of, 153 interpretation of, 152–153, 153t modified, 153–154, 153t advantages of, 154 procedure for, 151–152, 152t critical blocking length and, 157, 158f decremental, 158–159, 158f diagnostic utility of, 159–160 epidural, 154–155 fiber size and, 150–151, 151t frequency-dependent, 158–159, 158f internodal intervals and, 157, 158f lumbar paravertebral sympathetic, 156t pharmacologic approach to, 150–156, 151f, 151t results of, 160, 160t role of, 160–161, 160t stellate ganglion, 156t superior hypogastric plexus, 156t thoracic paravertebral sympathetic, 156t for acute/postoperative pain, 219–227 celiac plexus, 221–222, 221f epidural nerve, 223–225, 223f, 224f intercostal nerve, 225–226, 226f lumbar sympathetic, 222–223, 222f somatic, 223–227, 226t sphenopalatine ganglion, 219–220, 220f stellate ganglion, 220, 221f sympathetic, 219–223 trigeminal nerve, 225, 00024:t0055 for cancer pain, 309–310, 310t, 319–323, 320t, 330. See also under specific nerve block for glossopharyngeal neuralgia, 474–475, 474f, 475f for herpes zoster, 269, 270f for mononeuritis multiplex, 672 for phantom pain, 299 prognostic, for cancer pain, 320–321 regional for burn pain, 234–235 for cancer pain, 321 indications for, 320t role of, 319 for phantom pain, 297 for postmastectomy pain, 663–664 Nerve conduction, physiology of, 178 Nerve conduction studies, 180–182, 181f. See also Electromyography, diagnostic electrodes in, 176–177, 177f F wave in, 180–182 H-reflex in, 182 in brachial plexopathy, 536–538, 538t in peripheral neuropathy motor, 266 sensory, 265–266 Nerve conduction velocity formula for, 180 measurement of, 180–182, 181f Nerve fibers. See also Afferent(s); Axon(s) classification of, 10, 11t, 151t size of conduction velocity and, 151t differential nerve blocks and, 150–156, 151f, 151t sensitivity to local anesthetics and, 150–151, 151t type A beta classification of, 10, 11t properties of, 11 delta classification of, 10, 11t properties of, 11 type C classification of, 10, 11t properties of, 10–12, 11f Nerve injury hyperalgesia and, 24–27. See also Pain processing system, in nerve injury inflammatory conditions in, 27 pain in. See Neuropathic pain Seddon's classification of, 532–533, 532f Nerve root block, selective diagnostic, 149 fluoroscopically-guided, 88–89, 89f
Nerve root compression, of cervical region, 524, 525t. See also Cervical radiculopathy Nerve root cysts, in failed back surgery syndrome, 767, 767f Nerve root trauma, after automated percutaneous diskectomy, 1396 Nerve sheath tumors, femoral neuropathy due to, 826 Nerve stimulation, in continuous and pulsed radiofrequency mode, 1332–1333 Nerve stimulator, for cervical plexus block, 1097, 1098f Neural constriction injury, chronic, neurofascial prolotherapy for, 1030 Neural flossing exercises, 00169:f0175, 1268 Neural trauma, after cervical epidural nerve block, 00153:s0180 Neuralgia. See at specific site and type Neuralgic amyotrophy. See also Parsonage-Turner syndrome hereditary, 536 Neuralgiform headache attacks, short-lasting unilateral, with conjunctival injection and tearing, 444–445 Neurapraxia, 182, 532–533, 532f Neurilemmoma, 546–547 Neuritis brachial, 380–381, 381f optic, 486–488, 487f, 488f Neuroadenolysis, of pituitary, 1326–1330. See also Pituitary neuroadenolysis Neuroaxial hemorrhage, after spinal cord stimulation, 1316–1317 Neuroaxial nerve blocks, diagnostic, 147–148 Neurodestructive procedures, for glossopharyngeal neuralgia, 475 Neuroendocrine tumors, scintigraphic imaging for, 93–94, 94f Neurofascial prolotherapy, 1029, 1033–1035. See also Prolotherapy born out of clinical observations, 1029–1030 chronic constriction injury and, 1030 needles used in, 1034, 1034f response of, 1034–1035, 1035f sensory nerve vulnerability at site of, 1029–1030, 1029f, 1030f use of, 1034, 1034f Neurofibroma, 546–547 of brachial plexus, 533t, 536, 537f Neurogenic inflammation, 1012–1013, 1012f, 1030 bystander disease from, correction of, 1031, 1031f concept related to stopping, 1030–1031, 1031f in complex regional pain syndrome, 277, 278f Neurohumoral mechanisms, of acupuncture, 1020–1021 Neurologic examination, 42t cranial nerve assessment in, 43–46, 44t, 45f, 46f deep tendon reflexes in, 48–49, 48t, 49f gait in, 49 in peripheral neuropathy, 264–265, 265t mental status assessment in, 43, 43t, 44t motor assessment in, 46, 46t sensory assessment in, 47–48, 47f, 48t Neurologic trauma, after spinal cord stimulation direct, 1318–1319 indirect, 1319 Neurolytic blockade, 324–328. See also Nerve block(s). specific nerve block agent(s) for, 325–327, 325t, 326t alcohol, 325–327 ammonium compounds, 327 clostridial neurotoxin, 327 glycerol, 327 hypertonic solutions, 327 phenol, 325 vanilloids, 327 complications of, 328 for cancer pain, 311, 324–328 future considerations for, 328 history of, 324 limitations of, 327–328 locations and applications of, 324–325 of stellate ganglion chemical, 1112, 1112f efficacy of, 1112, 1112f
Index 1433 Neurolytic blockade (Continued) radiofrequency, 1112, 1113f efficacy of, 1115 patient selection for, 324 subarachnoid, 1214–1220. See also Subarachnoid neurolytic block suprascapular nerve, technique of, 1177 with local anesthetic, 1187 with radiofrequency lesioning, 1190 Neuroma, 24. See also Pain processing system, in nerve injury cryoanalgesia for, 1366 dorsal root ganglion and, 26 Morton's, 866–868, 867f, 868f Neuromatrix action patterns of, 6–7 body-self, 5 conceptual reasons for, 5–6 neurosignature of, 4–5 phantom limbs and, 4–7, 5f Neuronal hyperactivity, 7–8 Neurons dorsal horn, 12–14 anatomic localization of, 12–13, 13f functional properties of, 14 in nerve injury, reorganization of, 26–27 in tissue injury, 21–22, 21f, 22f nociceptive-specific, 14 wide dynamic range, 14, 14f in tissue injury, 21–22, 21f Neuropathic pain, 202–212, 338 adjunctive medications for, 210–211 anticonvulsants for, 209–210, 920 antidepressants for, 210 complementary strategies for, 211 conditions associated with, 202 definition of, 202–203 diagnosis of, 208–209 examples of, 206–208 functional brain imaging in, 204–205 genetic predisposition to, 205–206 history of, 208 in arachnoiditis, 744 in cancer patients, 333 in sickle cell disease, 247 interventional strategies for, 211 management of, 209–212 mirror therapy for, 211–212 opioids for, 210, 943 physical examination in, 208–209 physical therapy for, 211 postmastectomy, 660. See also Postmastectomy pain processing of, 203–204, 203f, 204f psychologic therapies for, 209 psychological comorbidity associated with, 206 radiation therapy for, 316–317 topical analgesics for, 210 transcutaneous electrical nerve stimulation for, 996 Neuropathic Pain Scale, 197–199, 199f Neuropathy(ies). See also specific neuropathy clinical and laboratory features of, 68t immune-mediated, 66–67 nonmalignant inflammatory sensory, 67 nontraumatic, electrodiagnosis of, 183 painful, 374–383, 375t clinical evaluation of, 374–375 peripheral. See Peripheral neuropathy screening for, 65–67 small-fiber, 67 traumatic, electrodiagnosis of, 182–183 uncommon, electrodiagnosis of, 184–185 Neuroplasticity of ascending spinal tracts, 17 pain and, 7–8 Neuropraxia, 1029 clinical presentations explainable by, 1031–1032 Neurostimulation. See also Spinal cord stimuilation; Transcutaneous electrical nerve stimulation (TENS) equipment for, manufacturers of, 00174:p0340, 1306t for cancer pain, 311 for postmastectomy pain, 663 Neurostimulator device, complications of, 1317t, 1319–1321, 1320f, 1320t
Neurostimulator lead(s), in spinal cord stimulation locations of, 1304t migration of, 1317t, 1319–1320, 1320f, 1320t permanent placement of, 1307 types of, 1304, 1304t, 1305f Neurosurgery cordotomy in, 334, 334f dorsal rhizotomy in, 335 dorsal root entry zone lesioning in, 333–334, 334f for cancer pain, 311, 333–335 patient selection and, 333 hypophysectomy in, 335 myelotomy in, 334–335 Neurotmesis, 182–183, 532–533, 532f Neurotomy medial branch, for cervical facet syndrome, 520 radiofrequency for lumbar facet syndrome, 720–721, 721f for occipital neuralgia, 1067 Neutropenia, definition of, 59 Nitric oxide, in tissue injury, 22 Nitroglycerin for post-thoracotomy pain, 667 triggering cluster headache, 440 Nitrous oxide, inhaled, for burn pain, 234 N-methyl-D-aspartate (NMDA), 22, 23f N-methyl-D-aspartate (NMDA) receptor, in pain modulation, 31, 32f N-methyl-D-aspartate (NMDA) receptor antagonists for complex regional pain syndrome, 285 for neuropathic pain, 211 for phantom pain, 298 mechanism of action of, 30, 30f Nociception, 302. See also Pain processing system afferent transmitter systems in, pharmacology of, 17–18, 18f amplification of, neural mechanisms for, 1013–1015 psychology and, 1016 suppression of, neural mechanisms for, 1015–1016 Nociceptive pain, somatic, 338 Nociceptive reflex, in chronic tension-type headache, 429 Nociceptive signals, transmission and regulation of, 1013 Nociceptors, 1011–1016 A-delta, 1011 C, 1011 c-polymodal, 11, 12 deep vs. cutaneous, 1013 function of, 1011–1012 in inflammation, 1012–1013, 1012f sensitization of function of, 1012, 1012f spinal cord terminations of, 1013 Nonabused drugs, in pain history, 41t Nonendoscopic laser fiber diskectomy (modified Choy technique), 1403–1404, 1404f Nonimplantable infusion pump, for arachnoiditis, 749–750 Noninfectious mass, fibrotic, after spinal cord stimulation, 1318–1319 Non-narcotic agents, in pain history, 41t Non-neuronal cells in nerve injury, 26 in tissue injury, 24, 25f Nonopioid analgesics, for burn pain, 234 Non-small cell lung cancer, 656 Nonsteroidal anti-inflammatory drugs (NSAIDs). See also specific agent, e.g., Aspirin analgesic effects of, 884–885 anti-inflammatory effects of, 885 characteristics of, 885–886, 885f for acute/postoperative pain, 217–218, 217f selection of, 217, 217t for cancer pain, 304, 305t for complex regional pain syndrome, 283 for giant cell arteritis, 480 for lumbar radiculopathy, 712 for migraine headache, 426 for osteoarthritis, 393–394 for osteoporosis, 705 for plantar fasciitis, 874 for rheumatoid arthritis, 401 for rotator cuff disorders, 576
1434 Index Nonsteroidal anti-inflammatory drugs (NSAIDs) (Continued) for systemic lupus erythematosus, 405 for tension-type headache, 00047:f0030, 433–434 for trochanteric bursitis, 816 indications for, 886 mechanism of action of, 29 peripheral, 29 spinal, 29 over-the-counter, 879–882 overview of, 878–879, 879f pharmacokinetics of, 886 selection of, 886 comparative pharmacology in, 887t guidelines in, 889t side effects of, 217–218, 886–888, 889t Nontraumatic neuropathy, electrodiagnosis of, 183 Nortriptyline, 915, 915f for acute arachnoiditis, 748 for intercostal neuralgia, 640–641 for mononeuritis multiplex, 671 for postmastectomy pain, 663t for post-thoracotomy pain syndrome, 639 for proctalgia fugax, 805 for tension-type headache, 434t for thoracic radiculopathy, 646–647 Nose. See Nasal. Naso- entries Nosebleed (epistaxis), sphenopalatine ganglion block causing, 220 Nuclear medicine imaging. See Scintigraphy Nucleoplasty, for lumbar radiculopathy, 714 Nucleus proprius (lamina III, IV, V) neurons, 12t, 13 characteristics of, 14, 14f Nucleus pulposus. See also Intervertebral disk anatomy of, 118–119, 118f, 119f herniated, in failed back surgery syndrome, 768, 768f Numbness after celiac plexus block, 1202 in peripheral neuropathy, 261t Numeric rating scale, in pain assessment, 193f, 194 Nutriceuticals, for osteoarthritis, 394 Nutrition, 936t evaluation of, in peripheral neuropathy, 262t Nutritional counseling, for neuropathic pain, 211
O
Obesity meralgia paresthetica and, 821, 822f osteoarthritis associated with, 395 water-based exercises in, 990 O'Brien active compression test, 574–575 Obstetric pain, hypnosis for, 965 technique of, 966 Obturator canal, 829, 830f Obturator hernia, 830–831 Obturator nerve anatomy of, 829, 829f, 1245, 1246f sensory testing of, 829, 830f Obturator nerve block, 1245–1247, 1293–1294, 1294f anatomic aspects of, 1245, 1246f complications of, 1247 for acute pain, 1245 for chronic pain, 1245–1246 for spasticity, 1246 indications for, 1245–1246 technique of, 1246–1247 direct, 1246–1247, 1246f indirect, 1247 ultrasound-guided, 1247, 1247f Obturator neuropathy, 829–831, 829f, 830f, 830t Occipital artery, palpation of, for occipital nerve block, 1059, 1060f Occipital headache, 503–505, 1063–1065 after cervical plexus block, 1101 Occipital nerve, 503 anatomy of, 1059, 1060f, 1062–1063, 1063f needle tip proximity to, 1059, 1060f, 1061f third, and headache, 1063–1065 Occipital nerve block, 1062–1067 anatomic aspects of, 1059, 1060f anatomic considerations in, 1062–1063, 1063f diagnostic, 148
Occipital nerve block (Continued) for cluster headache, 450 for occipital neuralgia, 503, 504–505, 505f indications for, 1059 rationale for, 1065 side effects and complications of, 1059–1060, 1061f technique of, 1059, 1060f, 1061f, 1065–1067, 1066f Occipital neuralgia complications of, 505 differential diagnosis of, 503 radiofrequency techniques for, 1067 signs and symptoms of, 503, 504f tests for, 503, 504f treatment of, 504–505, 505f vs. trigeminal neuralgia, 466 Occupational back pain, 722–736. See also Low back pain acute, 722, 723f analgesics for, 724 attribution of, 730–731, 731t certification for, 726–727 chronic, 728–730 diagnosis of, 729–730 medical treatment for, 729 precision treatment for, 730 psychosocial treatment for, 728t, 729 compensation for, 731–732 confounding factors in, 733–734 extraneous, 722, 723f euphemistic, 725–726 evidence of, 727–728, 728t imaging studies for, 723 innuendoes and, 732–733 light duties and, 725 malingering and, 725, 732 medical management of, 722–726 modification of work practices and, 727 negotiations in, 725 overview of, 722, 723f prevention of, 733 red flag indicators in, 723, 723f return to work in, 724, 725 workplace intervention in, 724 Occupational therapy for bone pain, 704 for complex regional pain syndrome, 286 for mononeuritis multiplex, 672 Occupations osteoarthritis associated with, 395 peripheral neuropathy associated with, 263, 263t Octreotide, for cluster headache, 448 Ocular lesions, in giant cell arteritis, 476–477 Ocular/periocular pain, 482–493 anatomic aspects of, 482 causes of, 483–488 from corneal abrasions, 484, 484f from styes, 483, 483f in conjunctivitis, 484–485, 484f in glaucoma, 485–486, 485f, 485t, 486f in optic neuritis, 486–488, 487f, 488f in uveitis, 486, 487f referred, 488–493 in carotid-cavernous fistulas, 491, 492f in cavernous sinus aneurysms, 490–491, 490f in cavernous sinus thrombosis, 492 in cavernous sinus tumors, 491, 491f in cluster headache, 488–489, 489f in herpes zoster infections, 492–493, 492f in Tolosa-Hunt syndrome, 489 Oculomotor nerve (III) disease states of, 375–376 evaluation of, 44t palsies associated with, 376, 377, 377f, 377t Office of alternative medicine, 936. See also Alternative medicine Olecranon bursitis, 601–603, 602f, 603f, 604f Olfactory nerve (I), evaluation of, 44t Ondansetron for cancer-related nausea, 340 for opioid-induced emesis, 341 One-legged stork test, for sacroiliac joint disorders, 760 Operant techniques for burn pain, 238–239 for chronic pain, 949–950
Ophthalmic nerve, anatomy of, 1069, 1069f Ophthalmic nerve block, 1078, 1078f. See also Trigeminal nerve block Opioid(s), 890–912. See also specific agent, e.g., Morphine absorption of, 898 abuse of, screening for, 73, 74 addiction to, 898, 898f vs. dependence, 308–309 agonist-antagonist, 909–911, 910f, 911f antagonist, 911–912, 911f antitussive effects of, 895, 896t classification of, 892–893, 893f, 894f cross-tolerance to, 897 dependence on, vs. addiction, 308–309 distribution of, 901 dosing guidelines for, 218–219 duration of effect of, 218–219 excretion of, 901 for acute/postoperative pain, 218–219, 218f for arachnoiditis, infusion of, 750 for burn pain, 233–234 for cancer pain, 304–309 administration of, 304–307, 306t, 308t checklist for, 346, 348t spinal, 310–311 selection of, 304–307, 306t side effects of, 307–308 tolerance to, 308 for complex regional pain syndrome, 283 for herpes zoster, 269–270 for mononeuritis multiplex, 671 for neuropathic pain, 210 intrathecal administration of, 211 for osteoporosis, 705 for phantom pain, 298–299 for postmastectomy pain, 662 half-life values for, 899t hyperalgesia and, 897–898 in pain history, 41t mechanism of action of, 00003:p0225, 893–895, 895f peripheral, 29 spinal, 28–29, 29f vs. supraspinal systems, 29 supraspinal, 28f, 00003:p0230 vs. spinal systems, 29 metabolism of, 901 nausea and vomiting due to, 341 overdosing of, in failed back surgery syndrome, 764 pharmacodynamics of, 895–897 pharmacokinetics of, 898–901, 899t physical dependence on, 898, 899t physiologic effects of cardiovascular, 896 central nervous system, 895–896 cutaneous, 897 gastrointestinal, 896–897 genitourinary, 897 immunologic, 897 neuroendocrine, 897 respiratory, 896 uterine, 897 potencies of, 218, 895, 895t pseudoaddiction to, 898 route of administration of, 219, 307, 308t, 898, 900f inhalational, 900 intranasal, 900 iontophoresis, 901 neuraxial, 901 oral, 898 rectal, 900 subcutaneous, 900 transdermal, 900–901, 900f semisynthetic, 893t, 904–905 chemical structure of, 894f side effects of in cancer patients, 307–308 strategies for limiting, 943, 943t with spinal and supraspinal administration, 33 sites of action of, 00003:p0205 spinal. See Spinal opioids synthetic, 893t, 906–909 chemical structure of, 894f tolerance to, 308, 897 toxicity of, 218 withdrawal from, signs and symptoms of, 899t
Opioid peptides, endogenous, 891 Opioid receptors, 891–892, 892t Opiophobia, 898 Opium as source for morphine, 893 historical considerations in, 890–891, 891f medicinal use of, 890 Optic disc atrophy of, 45, 46f cupping of, in glaucoma, 485, 486f edema of, in optic neuritis, 487–488, 487f enlarged, 45, 46f examination of, 45, 45f myopic degeneration of, 45, 45f Optic nerve (II), evaluation of, 44t Optic nerve drusen, 45, 45f Optic neuritis, 486–488, 487f, 488f Orchialgia, 793–797 chronic, definition of, 793 diagnosis of, 795–796, 795t differential diagnosis of, 794–795, 795t historical considerations in, 793 pathophysiology of, 793–794, 794f treatment of conservative, 796–797, 796f surgical, 797 Orchidectomy, for orchialgia, 797 Orchitis, self-palpation, 795 Organomegaly, in peripheral neuropathy, 265 Orphenadrine, 925t, 926 for tension-type headache, 433t Orthopedic trauma, CT scan of, 97–98, 98f Orthotic devices for osteoarthritis, 391t, 392, 393f for plantar fasciitis, 874 for rheumatoid arthritis, 402 Os odontoideum, with instability, 547–548, 548f Osmolal gap, 70 Osmolality, 70 Ossification of posterior longitudinal ligament (OPLL), 76, 76f, 544, 544f classification of, 544, 545f Osteitis pubis, 82, 788–790, 789f, 790f treatment of, 788–789, 790f vs. iliopsoas bursitis, 819, 819t Osteoarthritis, 384–395 Bouchard nodes in, 386, 386f calcium-containing crystals in, 390 diagnosis of, 387–391, 388t differential diagnosis of, 388t, 390–391 epidemiologic studies on, 384, 385f generalized, 386 Heberden nodes in, 386 historical perspective on, 384 magnetic resonance imaging of, 389–390, 389f, 390f management of, 391–395, 391t, 392t barriers to, 395 biomechanical approaches to, 392, 393f education and empowerment in, 392 exercise in, 392 issues in, 391–392, 392t medical, 392–394 surgical, 394–395 therapeutic options in, 391, 391t weight reduction in, 392 menopausal, 386 of hand, 81, 386, 386f of hip, 81, 82f, 386 of knee, 82–83, 83f, 385, 385f, 386f of shoulder, 566–569 diagnosis of, 566 differential diagnosis of, 566–567 imaging studies of, 566, 567f, 568f treatment of, 567, 569f of spine, 385 lumbar, 700, 700f magnetic resonance imaging of, 107 of sternoclavicular joint, 643, 644f of wrist, 81 pain in, 386–387 placebo effect in, 394 prevention of, 395 barriers to, 395 radiographic studies of, 388–389, 388t, 389f risk factors for, 395 scintigraphy of, 389 signs and symptoms of, 385 ultrasonography of, 389
Index 1435 Osteoarthritis (Continued) vs. iliopsoas bursitis, 818–819, 819t vs. rheumatoid arthritis, 399–400 Osteochondritis dissecans, of elbow, 79, 80f Osteochondromatosis, synovial, 83, 83f Osteochondrosis, intervertebral, 107 Osteoid osteoma, CT scan of, 99, 101f Osteolysis, of distal clavicle, 79 Osteomyelitis, vertebral, 695–696, 696f Osteonecrosis aseptic vertebral, 78, 80f magnetic resonance imaging of, 111, 112f of hip, 81, 83f subchondral, after laser diskectomy, 1406–1407 Osteopathic manipulative therapy, 998–1008 biotensegrity in, 1002–1003 choice of modality in, 1004–1005 clinical applications of, 1006–1008 for ankle sprains, 1007 for fibromyalgia, 1007–1008 for low back pain, 1006–1007 for migraine cephalgia, 1007 for scoliosis, 1007 for whiplash, 1007 gait analysis in, 1003 historical considerations in, 998–999, 999f, 999t history in, 1000 motion pattern grading in, 1002 nociceptive model and, 999–1000 obstetric application of, 1008 pharmaceuticals and, 1006 physical examination in, 1000 post-patient encounter recommendations in, 1005–1006 postural evaluation in, 1000–1001, 1001f, 1001t prone evaluation in, 1004 ranges of motion in, 1001–1002, 1002f lower extremity, 1003, 1004t upper extremity, 1003, 1004t scapulothoracic motion in, 1003–1004 seated evaluation in, 1003 somatic dysfunction and, 999–1000 standing evaluation in, 1003 structural examination in, 1000–1004, 1001f, 1001t, 1002f, 1004t supine evaluation in, 1004 TART examination in, 999t, 00136:s0120, 1000 tissue texture changes and, evaluation of, 00136:s0120, 999t Osteopathic medicine, principles of, 998, 999t Osteoporosis, 701–706 assessment of, issues with, 702–703, 702t, 703f hip fractures from, 701 prevalence of, 701–702, 702t treatment of, 703–706 better pain relief in, 705–706 nonopioids in, 704–705 nonpharmacologic, 703–704, 704f opioids in, 705 pharmacologic, 704–705 vertebral compression fractures in, 78, 1376 studies of, 1386 treatment options for, 1377t vitamin D deficiency and, 701 Osteotomy, for osteoarthritis, 391t, 394 Otalgia, 494–498. See also Ear pain Otitis externa, 495, 497f Otitis media, 497–498, 498f Outpatients, sickle cell pain management of, 247 Overflow pain, in glossopharyngeal neuralgia, 471 Overuse injuries, 350, 351t. See also Sports injury(ies). specific injury rotator cuff disorders and, 570 Oxaprozin, pharmacology of, 887t Oxycodone, 895t, 905 chemical structure of, 218f, 894f, 904f for cancer pain, 305–306, 306t, 307 Oxygen therapy, for cluster headache, 446–447 Oxymorphone, 905 chemical structure of, 894f, 904f
P
P38 mitogen activated protein kinase C, in tissue injury, 23 Pace test, for piriformis syndrome, 792 Paced respiration breathing, 971
Pain. See also at anatomic site, e.g., Neck pain acute. See Acute pain after celiac plexus block, 1202 and neuroplasticity, 7–8 and psychopathology, 8 burn. See Burn pain cancer. See Cancer pain chronic. See Chronic pain colicky, 699 cranial nerve palsies associated with, 376, 377f, 377t definition of, 50, 191, 1016 determinants of, 3–4, 4f diagnostic approach to, 51–52, 52t factors influencing, 144, 145t gate control theory of, 3 history of. See Pain history management of. See specific therapy mechanisms of, conceptual models of, 2–3, 3f mirror-image (allochiria), 8 multiple determinants of, 8–9 neural blockade for, 144–149, 150–161. See also Nerve block(s) neuromatrix theory of, 4–7, 5f neuronal hyperactivity and, 7–8 neuropathic. See Neuropathic pain nociceptive, 50 somatic, 338 phantom. See Phantom pain/sensation physical examination and. See Physical examination postmastectomy, 660–664, 661f, 662t, 663t postoperative. See Postoperative pain preoperative. See Preoperative pain quality of experiences of, 5–6 referred patterns of from lumbar facet joints, 716–717, 717f to eye, 52 to eye, 488–493. See also Ocular/periocular pain, referred somatic, 699, 710t nociceptive, 338 subjective nature of, 191–192 sympathetically maintained, 273, 279–280, 279f throbbing, 699 visceral, 338 radiation therapy for, 317 Pain assessment Brief Pain Inventory in, 196–197, 198f choice of scale in, 199–201 Edmonton Classification System in, 338, 339f in elderly, 200f, 200t, 201, 201t JCAHO standards for, 193–201, 193t LANSS Pain Scale in, 199, 199f McGill Pain Questionnaire in, 3, 194, 195f short-form, 194–196, 196f, 197f multidimensional rating scales in, 194–199 patient selection for, 199 Neuropathic Pain Scale in, 197–199, 199f numeric rating scale in, 193f, 194 objective, 192–193 single-dimension scales in, 193–194 patient selection for, 201 subjective, 191–192 verbal descriptor scale in, 193f, 194 verbal numeric scale in, 194 visual analog scale in, 193–194, 193f Pain Assessment in Advanced Dementia Scale (PAINAD), 200t, 201 Pain disorders, biofeedback for, 955 efficacy levels in, 956t Pain history, 36–42 associated factors in, 38, 39t character in, 38 chronicity in, 37–38 duration and frequency in, 38 general aspects of, 38–39 in 20th century, 2–3 interview in, 40–42 location in, 37, 37f medication history in, 39–40, 41t mode of onset in, 37 pain litany in, 37–38 severity in, 38 Pain mapping, conscious, 1370–1371 Pain modulation, 31–34 spinal excitatory systems in, 31, 32f spinal systems in, 33 supraspinal systems in, 33–34
1436 Index Pain pathways, 703, 704f ascending, 203, 203f descending, 204, 204f sclerotogenous, 53f, 55 Pain patterns, 50–56 case studies of, 51, 52 diagnostic approach to, 51–52, 52t referred, 52 from lumbar facet joints, 716–717, 717f to eye, 52 spatial, 51 spinal, 52–56, 53f, 55t, 00006:t0030, 56t temporal, 51 Pain Pentagon, 704, 704f Pain processing system activation of, 19–20, 20f afferent line labeling in, 17 afferents in. See also Afferent(s) primary, 10–12, 11f, 11t anatomy of, 10–18 ascending pathways in, 14–15 plasticity of, 17 distinct pathways in, 17 dorsal horn neurons in, 12–14, 13f, 14f dynamics of, 19–140 frequency encoding in, 17 functional overview of, 16–17 in nerve injury, 24–27 afferent sensitivity changes in, 26 afferent sprouting in, 26 dorsal horn reorganization in, 26–27 dorsal root ganglion cell cross-talk in, 26 dynorphin in, 27 evoked hyperpathia in, 26–27 glutamate release in, 26 loss of GABAergic/glycemic control in, 26 morphologic correlates of, 24 non-neuronal cells in, 26 peripheral and central activity generation in, 24–25, 25f psychophysics of, 24 spontaneous, 24–26 sympathetic input in, 27, 27f in tissue injury, 20–24 afferent response properties of, 20, 20f alogenic agents in, 20–21, 21t bulbospinal systems in, 23, 24f central facilitation in, 22–24 central sensitization in, 21–22 dorsal horn response properties of, 21–22, 21f, 22f glutamate receptors in, 22, 23f lipid mediators in, 22, 23f nitric oxide in, 22 non-neuronal cells in, 24, 25f peripheral afferent terminal and, 20 peripheral sensitization in, 20–21, 21t phosphorylating enzymes in, 23 psychophysics of, 20 nociceptive-specific pathway in, 14 pharmacologic agents modifying, 27–30 alpha2-adrenergic agonists, 30, 30f intravenous local anesthetics, 30, 30f N-methyl-D-aspartate receptor antagonists, 30 nonsteroidal anti-inflammatory drugs, 29 opioids, 27–29, 28f, 29f spinal dorsal horn in, 12, 12t, 13f supraspinal projections in, 15–16, 15f, 16f wide dynamic range neurons in, 14, 14f Pain state, spontaneous, 24–26, 25f Painful crisis, in sickle cell disease, 244–245 Palliative care of cancer patient, 336–348, 337t anger in, 345 assessment in, 337–345 cognitive, 343–345, 343f, 344f, 344t instruments for, 338–339 communication in, 345 community issues and adjunct treatments in, 345 family involvement in, 345 for anxiety, 343 for appetite disturbances, 342 for depression, 342–343 for drowsiness, 342 for dyspnea, 341–342 for fatigue, 339–340 for nausea, 340–341, 340t, 341f for sleep disturbances, 342
Palliative care (Continued) for well-being, 343 interventional procedures in, 346, 347f management principles in, 346, 346t, 347f psychological support and, 345 radiation therapy in, 312–318. See also Radiation therapy, palliative WHO definition of, 336–337 Palpation, of knee, 839, 840f Pamidronate, for complex regional pain syndrome, 285 Pancoast tumor, 656–657 radiation therapy for, 317, 317f vs. cervical radiculopathy, 527 with infiltration of brachial plexus, 1142–1144, 1143f Pancoast-Tobias syndrome, 656–657, 657f Pancreatic cancer CT scan of, 686, 686f palliative radiation therapy for, 317 Pancreatic pseudocyst, 682, 683f, 685–686, 685f Pancreatitis acute, 72, 682–684, 683f, 683t, 684f celiac plexus block for, 683–684, 684f thoracic epidural nerve block for, 1182 chronic, 72, 684–686, 684t, 685f, 686f Panner's disease, 80 Papilledema advanced, 45, 45f early, 45, 45f Paracetamol, for osteoarthritis, 393 Paraffin baths, 981, 981f Parapharyngeal space, pleomorphic adenoma of, 500, 501f Paraplegia, after celiac plexus block, 1202–1203 Parathyroid hormone (PTH), 70 Paravertebral nerve block. See also Intercostal nerve block for post-thoracotomy pain, 666 Paresthesia, in postmastectomy pain, 662t Parotid gland, adenoid cystic carcinoma of, 378–379, 379f Paroxetine, 916 Paroxysmal hemicrania, 444 Pars interarticularis, defects in, 751, 752f, 753t, 754t. See also Spondylolisthesis; Spondylolysis Parsonage-Turner syndrome, 380–381, 381f brachial plexopathy in, 536, 537f, 538f Passive straight leg raising test, for sacroiliac joint disorders, 760 Patellar taping, in management of osteoarthritis, 392, 393f Patellar tendinopathy, vs. suprapatellar bursitis, 844, 845f Patent foramen ovale cluster headache and, 442 migraine and, 421–422 Patient-controlled analgesia (PCA), 219 for post-thoracotomy pain, 667 Patrick Fabere's test, 777, 777f Pectoralis minor syndrome, 534–535 Pelvic pain differential diagnosis of, 776, 776t in pregnancy, 775–780. See also Pregnancy, low back pain in management of, limitations in, 945, 945t postpartum, 780 Pelvic pain provocation test, posterior (thigh thrust), 777, 777f Pelvic plexus block, for orchalgia, 796–797 Pelvic rock test, for sacroiliac joint disorders, 1285, 1285f Pelvic tilt, for sacroiliac joint disorders, 762 Pelvis bony, 757, 758f female, magnetic resonance imaging of, 689, 690f fracture of, CT scan of, 98, 98f ligaments of, 757, 758f radiography of, 81–82 Pentazocine, 909–910 Peptide release, in tissue injury, 21t Percutaneous balloon compression, for trigeminal neuralgia, 468–469 Percutaneous disk decompression, for lumbar radiculopathy, 713 Percutaneous diskectomy automated, 1393–1396
Percutaneous diskectomy (Continued) anatomic aspects of, 1393 complications of, 1395–1396, 1396f indications for, 1393, 1394f technique of, 1393–1395, 1394f, 1395f laser, 1397–1407. See also Laser diskectomy Percutaneous fusion techniques, 1408–1414. See also Facet joint fusion Percutaneous glycerol retrogasserian rhizotomy, for trigeminal neuralgia, 468 Pericranial muscles, involvement of, in tension-type headache, 429, 430f Peridural hematoma, in failed back surgery syndrome, 766 Perineal pain, cryoanalgesia for, 1370 Peripheral nerve blocks for lower extremity, 1289–1298. See also Lower extremity, peripheral nerve blocks for for upper extremity, 1151–1173. See also Upper extremity, peripheral nerve blocks for Peripheral nerve stimulation, 1300–1302 anatomic aspects of, 1301 complications of, 1302 indications for, 1300 technique of, 1301–1302, 1301f, 1302f Peripheral neuropathy, 260–267 classification of anatomic, 260, 261t temporal, 261, 262t CT scan in, 266 eye examination in, 265 foot examination in, 263–264, 264f history of, 260–265 family, 262–263 medical and surgical, 261–262, 262t social, 263, 263t magnetic resonance imaging in, 266 neurologic examination in, 264–265, 265t neurophysiologic testing in, 265–266 organomegaly in, 265 pain in, 261t physical examination in, 263–265, 263t, 264f, 265t review of systems in, 263 skin/hair/nail examination in, 265, 265t treatment of, 266–267, 266t, 267t verbal descriptors of, 260, 261t, 262f vs. cervical radiculopathy, 527 Peripheral vascular insufficiency, transcutaneous electrical nerve stimulation for, 996 Peritoneal penetration, after ilioinguinaliliohypogastic nerve block, 1240–1241 Periumbilical ecchymosis, in acute pancreatitis, 682, 684f Peroneal nerve common, electrodiagnosis of, 184 injury to, cryoanalgesia for, 1371 neuralgia secondary to irritation of, 1371 Peroneal nerve block deep, 1297 peripheral, 1297 Personality traits in chronic pain, 949 in cluster headache, 440–441 Pes anserine bursitis, 848–850, 849f treatment of, 849–850, 850f Petrosal nerve, resection of, for cluster headache, 451–452, 451t Phalen test, for carpal tunnel syndrome, 358, 358f, 620, 621f Phantom pain/sensation, 292–300 calcitonin for, 297 diagnostic testing for, 295 differential diagnosis of, 295–296 disability from, 293–294 epidemiology of, 292–293 epidural anesthesia for, 296–297 etiology of, 294–295 historical considerations in, 292, 293f incidence of, 292–293 neuromatrix and, 4–7, 5f physical examination in, 295 prevention of, 296 regional anesthesia for, 297 risk factors for, 293–294 signs and symptoms of, 295, 295f treatment of, 296–297
Phantom pain/sensation (Continued) acupuncture in, 300 drug therapy in, 297–299 electroconvulsive therapy in, 300 guided imagery in, 970–971 nerve blocks in, 299 neuromodulation in, 299–300 nonsurgical techniques in, 300 physical therapy in, 300 psychological therapies in, 300 side effects and complications in, 300 stump revision in, 300 Phenanthrene alkaloids, 893t, 901–903. See also specific agent, e.g., Morphine Phenelzine, 917–918, 918f for migraine prophylaxis, 426 Phenol in neurolytic blockade, 325, 325t subarachnoid neurolytic block with, 1218–1219, 1218f Phenylbutazone, for cancer pain, 305t Phenytoin, 919–920, 920f dosing guidelines for, 920 side effects of, 919, 920t, 921f Phosphorus imbalance, 70–71 Phosphorylation, in tissue injury, 23 Photophobia, in cluster headache, 440 Phrenic nerve anatomy of, 1088, 1090f inadvertent blockade of, in cervical plexus block, 1101 Phrenic nerve block, 1088–1090 anatomic aspects of, 1088 bilateral, 1101 complications of, 1089–1090 indications for, 1088, 1089t, 1090f technique of, 1088–1089, 1090f Physiatric approach, to cancer pain, 311 Physical dependence, definition of, 898 Physical examination, 42–49 deep tendon reflexes in, 48–49, 48t, 49f gait in, 49 general aspects of, 43 mental status assessment in, 43, 43t, 44t motor assessment in, 46, 46t neurologic assessment in, 42t sensory assessment in, 47–48, 47f, 48t Physical therapy for bone pain, 704 for complex regional pain syndrome, 286 for low back pain, during pregnancy, 779 for mononeuritis multiplex, 672 for neuropathic pain, 211 for phantom pain, 300 for piriformis syndrome, 792 for plantar fasciitis, 874 for post-thoracotomy pain, 668 for tension-type headache, 435 Physician training, in diskography, 122 Piedallu's test, 760 Pincer effect, of spinal cord compression, 543, 543f Piper Fatigue Self-Report Scale, 340 Piriformis muscle, anatomy of, 791, 792f Piriformis syndrome, 712, 791–792, 792f Piroxicam, for cancer pain, 305t Pituitary macroadenoma, 491, 491f Pituitary neuroadenolysis, 1326–1330 anatomic aspects of, 1326–1330 complications of, 1330, 1330t contraindications to, 1326, 1327t history of, 1326 indications for, 1326, 1327t pain relief after mechanisms of, 1330 success of, 1330 postoperative care after, 1329–1330 preoperative preparation for, 1327 results of, 1330 technique of, 1327–1329, 1327f, 1328f, 1329f Plantar fascia, anatomy of, 872, 873f Plantar fasciitis, 369–370, 369f, 370f, 872–874, 873f Platelet(s), 60 Platelet count, 60 Pleomorphic adenoma, of parapharyngeal space, 500, 501f Pleura, innervation of, 649
Index 1437 Pleural effusion after celiac plexus block, 1203 chylous, 651–652 in mesothelioma, 657 radiography of, 645f Pleural puncture, after thoracic epidural nerve block, 1184 Pleurisy from adjacent pulmonary infection, 654, 654f from systemic inflammatory conditions, 655 Plexopathy, electrodiagnosis of, 185 Pneumonia, 654, 654f Pneumothorax, 655, 655f, 655t after celiac plexus block, 1203 after intercostal nerve block, 1187, 1189–1190 after suprascapular nerve block, 1178 in pulmonary Langerhans cell histiocytosis, 652 Podagra, 71 Polyarteritis nodosa, 63 Polyarthralgia, knee pain with, 838 Polychondritis, 495, 497f Polymerase chain reaction assay, for HIV infection, 64 Polymethylmethacrylate (PMMA) fluoroscopically-guided injection of, 89, 90f preparation and delivery of, in vertebral augmentation, 1382–1383, 1383f Polymyalgia rheumatica, 409–410, 413–415, 414t, 415t giant cell arteritis and, 413, 415, 478 Polymyositis, 408–409 Polyneuropathy classification of, 261t electrodiagnosis of, 176f, 183 Popeye deformity, of biceps tendon, 354, 354f Popliteal block, 1294 Positive reinforcement, for burn pain, 238–239 Posterior cruciate ligament anatomy of, 834–835, 836f integrity of, posterior drawer test for, 841, 841f Posterior drawer test, 841, 841f Posterior interosseous syndrome, electrodiagnosis of, 184 Posterior pelvic pain provocation test (thigh thrust), 777, 777f Postherniorrhaphy pain, cryoanalgesia for, 1365 Postherpetic neuralgia, 207, 269f thoracic epidural nerve block for, 1181 Postmastectomy pain syndrome, 660–664 definition of, 660–661 differential diagnosis of, 661–662 historical considerations in, 660, 661f sensory abnormalities in, 662t signs and symptoms of, 660–661 testing for, 661 treatment of, 662–663 Postoperative pain cryoanalgesia for, 1363–1365 in burn patients, 229–230, 230f management of, 233 management of, 216–227 hypnosis in, 964 technique of, 965 narcotic analgesics in, 218–219, 218f neural blockade in, 219–227, 220f, 221f, 222f, 223f, 224f, 225f, 226f, 226t. See also Nerve block(s), for acute/ postoperative pain nonsteroidal anti-inflammatory drugs in, 217–218, 217f, 217t prophylactic measures in, 216 Postsympathectomy syndrome, 1114 treatment of, 1114 Post-thoracotomy pain, cryoanalgesia for, 1363–1364, 1364f Post-thoracotomy pain syndrome, 638–640, 639f, 655, 656f, 665–668 anatomic aspects of, 665 causes of, 638t clinical presentation of, 666 differential diagnosis of, 666 epidemiology of, 665–666 management of drug therapy in, 667 in acute phase, 666–667 in chronic phase, 667–668 interventional procedures in, 667–668, 668f physical therapy in, 668 thoracic epidural nerve block in, 666
Post-thoracotomy pain syndrome (Continued) pathogenesis of, 665 predictive and preventive factors in, 666 Post-traumatic neuralgia vs. complex regional pain syndrome I, 282–283 vs. complex regional pain syndrome II, 291 Post-traumatic stress disorder in cancer patients, 342–343 neuropathic pain and, 206 Posture, osteopathic evaluation of, 1000–1001, 1001f, 1001t Posture enhancement, for sacroiliac joint disorders, 762 Potassium channels, 00003:s0130 Potassium ion release, in tissue injury, 21t Pott's disease, 738–739, 741f Power spectrum, of electromyography, 957 Pramipexole, for cluster headache, 450 Precision therapy, for occupational back pain, 730 Prednisolone for giant cell arteritis, 481, 481t for polymyalgia rheumatica, 415, 415t Prednisone for carpal tunnel syndrome, 621 for cluster headache, 448, 489 for complex regional pain syndrome, 285 for giant cell arteritis, 255–256, 411 for medication overuse headache, 461, 461t for mononeuritis multiplex, 672 for polymyalgia rheumatica, 410 for systemic lupus erythematosus, 405 Pregabalin, 923, 923f for acute arachnoiditis, 748 for mononeuritis multiplex, 671 Pregnancy femoral neuropathy in, 826 low back pain in, 775–780 and labor and delivery, 780 clinical history of, 776 disabling, 776 imaging studies of, 778–779 interventional injections for, 780 medical therapy for, 779–780 physical examination of, 777, 777f, 778f physical therapy for, 779 resolution of, 780 musculoskeletal changes during, 775–776 osteopathic manipulative therapy in, 1008 pelvic pain in, 775 radiation exposure during, 104–105 Preoperative pain, management of, hypnosis in, 964 technique of, 965 Prepatellar bursitis (housemaid's knee), 365–366, 365f, 845–847, 845f, 846f treatment of, 846, 847f Pretrigeminal neuralgia, 465. See also Trigeminal neuralgia Prevertebral fascia, 1103 Priapism, in sickle cell disease, 246 Procaine hydrochloride, chemical structure of, 145f Procedural pain, in burn patients, 229–230, 230f management of, 232–233 Procedure(s), unplanned, burn patients and, 241 Proctalgia fugax, 804–806, 805f, 806f vs. coccydynia, 801 Proctitis, vs. proctalgia fugax, 804 Prodrome, in migraine headache, 422, 422t Progressive muscle relaxation, 968. See also Relaxation technique(s) for burn pain, 238 technique of, 972, 972t Prolotherapy, 1027–1044 advantages of, 1032, 1032t definition of, 1027, 1032t enthesofascial/intra-articular, 1027–1028, 1032 for elbow pain, 1042–1043, 1042f for foot pain, 1035, 1036f for hip pain, 1040–1041, 1040f for knee pain, 1037, 1037f, 1038f for lower abdomen pain, 1040–1041, 1040f for lower leg pain anterior, 1035–1036, 1036f medial, 1036–1037, 1036f, 1037f for neck pain, 1041–1042, 1041f, 1042f for shoulder pain, 1041–1042, 1041f, 1042f
1438 Index Prolotherapy (Continued) for thigh pain anterior, 1040–1041, 1040f posterior and gluteal regions, 1037–1040, 1038f, 1039f for wrist pain, 1043–1044, 1043f myofascial, 1029, 1032–1033, 1033f neurofascial, 1029, 1033–1035 born out of clinical observations, 1029–1030 chronic constriction injury and, 1030 needles used in, 1034, 1034f response of, 1034–1035, 1035f sensory nerve vulnerability at site of, 1029–1030, 1029f, 1030f use of, 1034, 1034f types of, 1027–1044 comparisons between, 1032, 1032t Pronator teres syndrome, 609–611, 609f, 610f, 611f, 1157f, 1159, 1160f electrodiagnosis of, 184 positive test for, 609–610, 610f Propionic acids, 881–882, 887t. See also specific agent, e.g., Ibuprofen Propoxyphene, 908–909 chemical structure of, 908f for cancer pain, 306t Propranolol, for postoperative dural sac deformities, 785 Prostadynia, vs. proctalgia fugax, 804 Prostaglandin synthesis, analgesic effects of NSAIDs and, 884–885 Prostate-specific antigen (PSA), 63–64 Protective screens, during radiation procedures, 104 Proteinase release, in tissue injury, 21t Proteins, serum, assays for, 67–69, 69f Prothrombin time (PT), 60 Protriptyline for postmastectomy pain, 663t for tension-type headache, 434t Provider credentialing, for acupuncture, 1026 Provocation diskography, 123 Proxicam, chemical structure of, 217f Proximal interphalangeal joint, arthritis of, 618–619, 618f Pruritus, opioid-induced, 897 Pseudoaddiction, to opioids, 898 Pseudoarthrosis in failed back surgery syndrome, 769, 769f in spondylolysis, 752 Pseudocyst, pancreatic, 682, 683f, 685–686, 685f Pseudomeningocele, 781–782, 782f, 783f in failed back surgery syndrome, 770, 770f treatment of, 785 Pseudopapilledema, 45, 45f Pseudotumor cerebri, headache in, 253, 256 Psychiatric disorder(s), chronic pain and, 952–953 Psychogenic headache, 428. See also Tension-type headache Psychologic testing tools, for spinal cord stimulation, 1306, 1306t Psychological comorbidity, associated with neuropathic pain, 206 Psychological counseling, for chronic arachnoiditis, 749 Psychological factors. See also Anxiety; Depression in cancer patients, management of, 311 in chronic pain, 947–953 in cluster headache, 440–441 in complex regional pain syndrome, 275 in pain perception, 1016 in palliative care, 345 Psychopathology, pain and, 8 Psychophysics of nerve injury, 24 of tissue injury, 20 Psychophysiology, 955 Psychostimulants, for cancer-related fatigue, 340 Psychotherapy for complex regional pain syndrome, 287 for neuropathic pain, 209 for occupational back pain, 726, 728t, 729 for phantom pain, 300 for vulvodynia, 800 Pterygoid nerve, external, 1070 Ptosis, 376 Pubic symphysis palpation, 777
Pubic symphysis test, 760 Pulmonary. See also Lung entries Pulmonary embolism, 653–654, 654f Pulmonary hypertension, 653 Pulmonary infections, pleurisy from, 654, 654f Pulmonary Langerhans cell histiocytosis, 652 Pulsating magnetic field therapy (PMFT), 939 Pulse therapy, with corticosteroids, for neuropathic pain, 211 Pursed-lip breathing, 971
Q
Qi, in Chinese medicine, 1020 Qi gong, in Chinese medicine, 1024 Quadriceps expansion syndrome, 856–859, 857f, 858f, 859f Quadriceps muscle, anatomy of, 835 Quadriceps tendon, anatomy of, 856, 857f Quantitative sensory testing, 182 in peripheral neuropathy, 266 Quantitative sudomotor axon reflex test (Q-SART), 182 Quinine sulfate, for muscle spasms, 928 Quota system, in burn pain management, 238
R
Racz technique, for epidural adhesiolysis, 1138–1141, 1258–1272. See also Epidrual adhesiolysis Radial nerve anatomy of, 614, 1151–1152, 1152f, 1155f, 1156f, 1157 electrodiagnosis of, 184 Radial nerve block at elbow, 1154–1157, 1155f, 1156f, 1157f at humerus, 1151–1153, 1152f, 1153f at wrist, 1162–1165, 1164f, 1165f Radial tunnel syndrome, 613–614, 613f, 614f vs. tennis elbow, 613–614, 614f, 1153, 1153f Radiation absorbed dose of, 102 effective dose of, 102, 103t exposure to, during pregnancy, 104–105 ionizing, 312 fetal exposure to, 778 harmful effects of, 102 patient protection during, 103 staff protection during, 103–104 system for limitation of, 102 Radiation therapy brachial plexopathy due to, 536, 536t palliative, 312–318 bisphosphonates with, 316 cost-effectiveness of, 318 for bone pain, 312 for brachial plexus involvement, 317, 317f for brain metastases, 317–318 for celiac plexus involvement, 317 for neuropathic pain, 316–317 for spinal cord compression, 317 for trigeminal neuralgia, 318 for visceral pain, 317 hemibody, 316 history of, 312 imaging studies for, 313, 313f indications for, 312 optimal prescription dose in, 313, 314t radiopharmaceuticals in, 316 technique of, 313–316, 313f, 314t Radicular pain cervical, 55, 55t, 117–118 features of, 710t lumbar, 55, 55t, 117–118, 708 lumbosacral, 710 signs and symptoms of, 709–710 vs. somatic referred pain, 710t Radiculitis, vs. orchialgia, 794–795, 795t Radiculopathy cervical, 522–528. See also Cervical radiculopathy definition of, 117–118 electrodiagnosis of, 185 lumbar, 707–715. See also Lumbar radiculopathy spinal, 53f, 55, 55t. See also under specific part of spine thoracic, 646–648, 647f vs. spinal stenosis, 56t
Radiofrequency ablation for post-thoracotomy pain, 667 for sacroiliac joint disorders, 762 Radiofrequency current continuous, 1332, 1333–1334, 1333f, 1334f monitoring of, 1333 pulsed, 1332, 1334–1335 of suprascapular nerve, 1177–1178 used in medicine, 00178:p0025 Radiofrequency generator, 1332–1333, 1332f Radiofrequency lesioning, 1331–1360 clinical applications of, 1335–1360 continuous, 1333–1334, 1333f, 1334f continuous impedance monitoring in, 1332 for cervical facet syndrome, 1345–1357, 1345t anatomy in, 1345–1346, 1346f complications of, 1352 efficacy of, 1352 history in, 1345 indications for, 1346–1347 patient selection for, 1346, 1347f technique of, 1347–1357 posterolateral approach in, 1348–1352, 1351f prone approach in, 1347, 1348f, 1349f, 1350f, 1351f for cervicogenic headache, 1357–1360, 1358t anatomy in, 1358, 1358f efficacy of, 1360 history in, 1357–1358 indications for, 1358–1359 technique of, 1359–1360, 1359f for lumbar dorsal root ganglion, 1340–1345 anatomy in, 1341, 1341f benign pulsed treatment in, 1343 complications of, 1344 efficacy of, 1344–1345, 1344t history in, 1340–1341 indications for, 1341–1342 lower impedance in, 1343 postprocedure advice and, 1343–1344 proximity between needle tip and nerve in, 1343 target identification in, 1342–1343 technique of, 1342–1343, 1342f for lumbar facet syndrome, 1335–1340 anatomy in, 1336, 1341f complications of, 1339 efficacy of, 1339–1340, 1341t history in, 1335–1336 indications for, 1337 pain in, 1336–1337, 1337f postprocedure advice and, 1339 technique of, 1337–1339, 1339f, 1340f intercostal nerve block with, 1188–1190 anatomic aspects of, 1188, 1190f complications of, 1189–1190 indications for, 1188 technique of, 1188, 1190f nerve stimulation in, 1332–1333 pulsed, 1334–1335 temperature monitoring in, 1333 types of, 1333–1335, 1333f voltage monitoring in, 1333, 00178:t0010 Radiofrequency neurolysis, of stellate ganglion, 1112, 1113f efficacy of, 1115 Radiofrequency neurotomy for lumbar facet syndrome, 720–721, 721f for occipital neuralgia, 1067 Radiofrequency (retrogasserian) rhizotomy, for trigeminal neuralgia, 469 Radiofrequency thermocoagulation and pulsed lesioning, after sphenopalatine ganglion block, 1057 for cluster headache, 452 Radiofrequency units, in spinal cord stimulation, 1305 Radiography, 75–84 computed, 75 in arachnoiditis, 745–746, 746f in brachial plexopathy, 539 in cervical dystonia, 561 in intercostal neuralgia, 640 in lumbar osteomyelitis, 696, 696f in olecranon bursitis, 602, 603f in osteoarthritis, 388–389, 388t, 389f in palliative radiation therapy, 313, 313f in rheumatoid arthritis, 399, 399f, 400f
Radiography (Continued) in suprascapular nerve block technique, 1175–1176, 1176f, 1177f of ankle, 84 of cervical spine, 75–76, 76f of chondroma, in costosternal junction, 640, 640f of elbow, 79–80, 80f of foot, 84 of hand, 80–81 of hip, 81–82, 82f, 83f of knee, 82–83, 83f of lumbar spine, 77–78, 77f, 78f, 79f, 80f of lumbosacral metastatic lesions, 697, 697f of pars interarticularis, 752–753, 753f of pelvis, 81–82 of rotator cuff disorders, 575 of shoulder, 78–79, 80f osteoarthritic, 566, 567f of spondylolysis, 752–754, 753f, 754t of thoracic spine, 77, 77f of thymoma, 643, 643f of wrist, 80–81 traditional, 75 Radioisotope scanning. See Scintigraphy Radiopharmaceuticals, in palliative radiation therapy, 316 Radiosurgery, gamma knife for cluster headache, 452 for trigeminal neuralgia, 469 Raeder's syndrome, vs. trigeminal neuralgia, 466–467 Ramsay-Hunt syndrome, 268, 494, 496f Ranawat's lines, 546, 546f Range of motion, of shoulder, 572 Rapidly adapting stretch receptors (RARs), in respiratory system, 650, 650f, 658, 659f Rash erythematous malar, in systemic lupus erythematosus, 403, 403f in dermatomyositis, 408, 408f, 409f in herpes zoster, 268 knee pain with, 838 Raynaud's disease, biofeedback for, 956–957 Raynaud's phenomenon, biofeedback for, 956–957 Reappraisal, in burn pain management, 239–240 Rebound headache. See also Headache analgesic, mechanisms of, 456, 457f Reboxetine, 917, 917f Rectal cancer, vs. proctalgia fugax, 804, 806, 806f Rectal dysfunction, in arachnoiditis, 747 Rectal examination, in sacroiliac joint disorders, 760–761 Recurrent laryngeal nerve, inadvertent blockade of, in cervical plexus block, 1101 “Red back pain,”, 726 Red blood cell indices, 58 Referred pain patterns of from lumbar facet joints, 716–717, 717f to eye, 52 to eye, 488–493. See also Ocular/periocular pain, referred Reflex(es) autonomic, in peripheral neuropathy, 266 cough, 658 deep tendon, examination of, 48–49, 48t, 49f H (Hoffmann), 182 Hering-Breuer, 650 nociceptive, in chronic tension-type headache, 429 pathologic in cervical myelopathy, 550 in cervical radiculopathy, 525, 525t somatovisceral, 998 viscerosomatic, 998 Reflex sympathetic dystrophy. See Complex regional pain syndrome Refraction, definition of, 988 Regional anesthesia. See also Nerve block(s) for burn pain, 234–235 for cancer pain, 321 continuous, 321 indications for, 320t role of, 319 for phantom pain, 297 for postmastectomy pain, 663–664
Index 1439 Regular medication scheduling, for burn pain, 238 Rehabilitation aquatic, 987. See also Hydrotherapy for brachial plexopathy, 539–540 for cervical facet syndrome, 518–519 Reinforcement, positive, for burn pain, 238–239 Relaxation, cue-controlled, 973 Relaxation response, 967 Relaxation technique(s), 938, 967–975. See also Alternative medicine anxiety in, 00130:p545, 975 autogenic training, 968–969 technique of, 971 for acute/postoperative pain, 216 for burn pain, 237–238 guided imagery, 969 technique of, 971 historical perspectives of, 968–969 in biofeedback. See also Biofeedback electromyography-assisted, 957 skin conductance-assisted, 957 skin temperature-assisted, 958–959 indications for, 969–971 meditation, 968, 968t progressive muscle relaxation, 968 technique of, 972, 972t, 973t regimen for, 972–975, 973t relaxed breathing, 971 side effects of, 975 techniques of, 971–975 yoga, 969, 969t Relaxation training regimen, 972–975, 973t Mindfulness Based Stress Reduction program in, 973–975, 974t Relaxation-induced anxiety, 975 in biofeedback, 961–962 Relaxed breathing, 971 Relaxin, increased levels of, during pregnancy, 776 Remifentanil, 907 Renal function tests, 69–70 Renal transplantation, femoral neuropathy after, 826–827 Resisted abduction release test, for trochanteric bursitis, 361, 362f Resisted hip adduction test, for iliopsoas bursitis, 817, 818f Respiratory dysfunction chest pain in, 649–659. See also Chest pain opioid-induced, 896 tolerance to, 308 Respiratory innervation, sensory, 649–650 Resurfacing procedures, for osteoarthritis, 394 Retinal migraine, 422t, 424, 424t. See also Migraine headache Retinal vein, central, occlusion of, 45, 46f Retroachilleal bursitis, 865 Retrocalcaneal bursitis, 865 Retrocollis, 559–560 muscles involved in, 562t Retropharyngeal space abscess, 500, 502f Reverse Hill-Sachs lesions, 575 Reverse Phalen maneuver, 620 Reye's syndrome, aspirin and, 880, 881 Rhenium-188, in palliative radiation therapy, 316 Rheumatic pain, progressive muscle relaxation for, 969 Rheumatoid arthritis, 396–402 Baker's cyst in, 398, 398f clinical classification criteria for, 397t demographics of, 39t differential diagnosis of, 397t, 399–400, 400f involving cervical spine, 546, 546f, 547f, 547t juvenile, 396–397 aspirin dosing guidelines for, 880 laboratory findings in, 398–399 laboratory tests for, 63 late-onset, vs. polymyalgia rheumatica, 414 radiographic findings in, 399, 399f, 400f rheumatoid factor in, 398, 399 signs and symptoms of, 397–398, 397f, 398f treatment of, 400–402 anti-inflammatory agents in, 401 assistive devices in, 402 disease-modifying drugs in, 401 heat and cold therapy in, 402 immunosuppressive drugs in, 401–402 orthotics in, 402 surgical, 402
Rheumatoid arthritis (Continued) vs. systemic lupus erythematosus, 404 water-based exercises for, 990 Rheumatoid factor (RF), 63, 398, 399 Rhizotomy dorsal, for cancer pain, 335 percutaneous glycerol, for trigeminal neuralgia, 468 radiofrequency, for trigeminal neuralgia, 469 Rib(s) cartilage abnormalities of in costosternal syndrome, 632, 633f in Tietze's syndrome, 634 fractures of, 636–638, 637f intercostal nerve block for, 638, 638f thoracic epidural nerve block for, 1181 treatment of, 658 slipping, pain in, 677–679, 678f Right upper quadrant syndrome, in sickle cell disease, 246 Rigid-scope endoscopic laser diskectomy, 1404–1405, 1405f Romberg's sign, 49 Ropivacaine chemistry of, 930–931, 931f, 931t for post-thoracotomy pain, 666 pharmacokinetics of, 932t Rotator cuff, anatomy of, 352, 353f Rotator cuff disorders, 352–354, 353f, 570–578 angiofibroblastic hyperplasia in, 570–571 calcific tendinosis in, 79, 80f clinical presentation of, 571–575 diagnosis of, 575 extrinsic vs. intrinsic mechanisms of, 570–571 historical considerations in, 570–571, 571f history in, 571 magnetic resonance imaging of, 566, 568f, 575, 576f overuse syndromes and, 570 physical examination in, 571–575, 572f, 573f, 574f radiographic studies of, 575 treatment of, 576–577 indications for, 576 nonoperative, 576–577 surgical, 577, 577f, 578f ultrasonography of, 575, 575f Rucksack (backpack) paralysis, 535
S
“S” allele, of 5-HTTLPR gene, 205 Sacral canal anatomy of, 1250, 1251f contents of, 1250, 1251f Sacral hiatus anatomy of, 1250 localization of, in caudal epidural nerve block, 1252–1253, 1252f, 1253f, 1254f Sacroiliac joint anatomy of, 757–758, 758f dysfunction of, 759 movement of, 758–759 normal, 79f radiographic anatomy of, 1285–1286, 1286f Sacroiliac joint disorders, 1285–1288 anatomic aspects of, 1285–1286, 1286f evaluation of, 760–761 pain in, 759–760, 759f pelvic rock test for, 1285, 1285f radiographic studies of, 1285, 1286f treatment of, 761–762 education in, 761 injection technique in, 761–762, 762f, 1286–1288, 1286f, 1287f fluoroscopically-guided, 87–88, 88f mobilization in, 761 modalities in, 761–762 posture enhancement in, 762 radiofrequency ablation in, 762 strengthening exercises in, 762 surgical, 762 Sacroiliac ligament palpation, long dorsal, 777 Sacroiliac syndrome, 712 Sacroiliitis, 78, 79f Sacrum, anatomy of, 1250, 1250f Saddle embolus, imaging of, 653, 654f
1440 Index Salicylate(s), 879–881. See also Aspirin characteristics of, 885–886, 885f comparative pharmacology of, 887t sodium, 881 Salmonella infection, of spine, 737 Salsalate, for cancer pain, 305t Samarium-153, in palliative radiation therapy, 316 Saphenous nerve anatomy of, 827, 828f neuralgia secondary to irritation of, 1371 Saphenous nerve block, 1297 Saphenous neuropathy, 827–828, 828f, 828t Sarcoidosis, 652–653, 653f Scalene interval, 534–535 Scalene interval syndrome, 534–535 Scalp, discoid lupus of, 403, 403f Scalp acupuncture, 1023–1024. See also Acupuncture Scapular pain, differential diagnosis of, 590–591 Scapulocostal syndrome, 588–592 anatomic aspects of, 589–590, 590f, 590t complications of, 592 differential diagnosis of, 590–591, 591f historical considerations in, 588 pain patterns in, 588, 589f signs and symptoms of, 588–589, 589f, 590f treatment of, 591–592, 591f trigger points in, 588, 589f Scapulothoracic articulation, layers of, 589–590, 590t Scheuermann's disease, 77 Schmorl's nodes, 77, 108 Schwannoma, 546–547 of brachial plexus, 533t, 536 Sciatic nerve constriction of, 1029, 1029f electrodiagnosis of, 184 Sciatic nerve block, 1290–1292, 1291f Sciatic scoliosis, 707 Sciatica, vs. sacroiliac joint pain, 776 Scintigraphy, 91–94 diagnostic, 91, 92f in complex regional pain syndrome, 281, 282f in palliative radiation therapy, 313, 313f of osteoarthritis, 389 of pars fracture, 753, 753t, 754t therapeutic, 91–94 for neuroendocrine tumors, 93–94, 94f for painful arthropathy, 93, 93f for painful bone metastases, 92–93, 93f Scleroderma, 405–408 differential diagnosis of, 407, 407f laboratory findings in, 407 signs and symptoms of, 405–407, 405f, 406f treatment of, 407–408 Scoliosis osteopathic manipulative therapy for, 1007 sciatic, 707 Scottie dog sign in lumbar facet block, 1224, 1225f in spinal cryoablation, 1367–1368, 1368f, 1369 in spondylolysis, 752–753, 753f Scraping, in Chinese medicine, 1024 Scrotitis, vs. orchialgia, 795 Seated flexion test, for sacroiliac joint disorders, 760 Second-degree burns, 229, 230f Sedation, for burn pain, 234 Seddon's classification, of nerve injury, 532–533, 532f Seizures, migraine-triggered, 424 Selective nerve root block diagnostic, 149 fluoroscopically-guided, 88–89, 89f Selective serotonin reuptake inhibitors (SSRIs), 915–916 absorption and metabolism of, 916 abuse potential of, 916 common, 916, 916f for osteoporosis, 705 for proctalgia fugax, 805 mechanism of action of, 916 overdosage of, 916 side effects of, 916 withdrawal of, 916 Selective tolerance, to opioids, 897 Self-manipulation, for sacroiliac joint dysfunction, 761
Sensitization, in tissue injury central, 21–22 peripheral, 20–21, 21t Sensor placement for electromyography-assisted relaxation, 957 for skin conductance-assisted relaxation, 957 Sensory disturbance, in cervical myelopathy, 550 Sensory innervation of eye, 482–483, 483f of respiratory system, 649–650 Sensory nerve action potential (SNAP), 536–538 Sensory nerve vulnerability, neurofascial prolotherapy and, 1029–1030, 1029f, 1030f Sensory ring electrodes, in electromyography, 176–177, 177f Sensory system, examination of, 47–48, 47f, 48t Sensory testing, quantitative, 182 Septic olecranon bursitis, 602, 603f Seroma, after spinal cord stimulation, 1317t, 1319, 1319f Sertraline, 916 Serum osmolality, 70 Serum proteins, assays for, 67–69, 69f Sesamoiditis, 368–369, 369f Setting schedules, in burn pain management, 240 Sexual dysfunction, in arachnoiditis, 747 Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT), 444–445 Short-wave diathermy, 983, 984f Shoulder. See also Acromioclavicular joint osteoarthritis of, 566–569 diagnosis of, 566 differential diagnosis of, 566–567 imaging studies of, 566, 567f, 568f treatment of, 567, 569f painful causes of, 566–567, 568t prolotherapy for, 1041–1042, 1041f, 1042f range of motion and, 566, 566f radiography of, 78–79, 80f rotator cuff disorders of. See Rotator cuff disorders visual inspection of, 571–572, 572f Shrug sign, 572–573, 573f Sickle cell anemia, 243, 244t Sickle cell crisis, 244–245 Sickle cell disease, 243–248 acute pain syndromes in, 244–246, 245t chest pain in, 656 chronic pain syndromes in, 245t, 246–247 historical perspective on, 243, 244t management of hypnosis in, 965 in day unit, 247–248 in emergency department, 248 in hospital, 248 in outpatient setting, 247 nonpharmacologic, 247 pharmacologic, 247 preventive therapy in, 248 pathophysiology of, 243–248, 245f screening for, 59 Sickle cell pain syndromes, 243. See also Sickle cell disease acute, 244–246, 245t chronic, 245t, 246–247 types of, 244, 244t Sickle hemoglobin (Hb S), 59, 243 Sigma (σ) opioid receptor, 892t Simian hand, 533–534 Single-dimension scales, in pain assessment, 193–194 Singultus. See Hiccups Sinusitis, 495t, 498–500, 500f Skier's position to relieve iliohypogastric neuralgia pain, 689 to relieve ilioinguinal neuralgia pain, 687, 688f Skin examination of, in peripheral neuropathy, 265, 265t opioid effects on, 897 Skin conductance-assisted biofeedback, 957 Skin temperature, measurement of, in complex regional pain syndrome, 281–282, 283f Skin temperature-assisted biofeedback, 958–959 Sleep disturbances cancer-related, palliative care for, 342 neuropathic pain and, 206
Slipping rib syndrome, pain in, 677–679, 678f Slowly adapting stretch receptors, in respiratory system, 650, 650f, 658, 659f Sluder's neuralgia, 482–483, 1054 Small cell lung cancer, 656 Smoking, triggering cluster headache, 441 Snapping hip syndrome, 817 Social history, in peripheral neuropathy, 263, 263t Sodium channel(s), 00003:s0120 voltage-gated, 931 Sodium channel blockers, for complex regional pain syndrome, 284 Soft tissue restoration, balance of growth and disrepair factors in, 1027, 1028f. See also Prolotherapy Solutions, for differential spinal nerve blocks, 151–152, 152t, 153, 153t Somatic nerve blocks, for acute/postoperative pain, 223–227, 226t Somatic pain, 699 nociceptive, 338 vs. radicular pain, 710t Somatosensory abnormalities, in complex regional pain syndrome, 275–276, 276f Somatosensory evoked potentials (SEPs), 189–190, 189f in brachial plexopathy, 538, 539t Somatovisceral reflexes, 998 Spasticity, obturator nerve block for, 1246 Specific heat, in hydrotherapy, 988 Speed test, for biceps tendinitis, 585, 586f Spermatic nerve block, for orchalgia, 796 Spermatic plexus, 793 Spermatocele, 795 Sphenopalatine ganglion anatomy of, 219, 1055 pathophysiology of, 1054–1055 Sphenopalatine ganglion block, 1054–1058 complications of, 220, 1058 diagnostic studies and, 1054–1055 evidence for use of, 1055, 1056t for acute/postoperative pain, 219–220, 220f historical significance of, 1054 indications for and contraindications to, 1054 infrazygomatic approach to, 1056–1057, 1057f intranasal approach to, 1056 precautions in, 1055 radiofrequency thermocoagulation and pulsed lesioning in, 1057 techniques of, 1056–1057 Spinal abscess, epidural, 547, 548f Spinal accessory nerve (XI), evaluation of, 44t Spinal anesthesia, with opioids. See Spinal opioids Spinal canal anatomy of, 168 measurement of, 543, 543f narrowing of, causes of, 541–542, 542f Spinal canal endoscopy, 162–174 abnormal findings in, 172, 173f anatomic aspects of, 168–169 caudal approach to, 167–168 consensus paper on, 166 contraindications to, 167t definition of, 166 epidural adhesions lysis in, 167–168 epidural images in, 171–172 historical considerations in, 162–166, 163f in arachnoiditis, 745 indications for, 166–167, 167t normal findings in, 171–172, 173f paramedian approach to, 169 postprocedure management of, 171 preparation for, 169 side effects and complications of, 172 step-by-step procedure in, 169–171, 170f terminology used in, 166 Spinal cord anatomy of, 168 ischemia of, 544 pathologic change in, 541–542, 542f Spinal cord compression causes of, 542–548 pincer effect of, 543, 543f tumor-induced, radiation therapy for, 317 Spinal cord injury, complex regional pain syndrome II after, 290–291 Spinal cord stenosis, after spinal cord stimulation, 1318
Spinal cord stimulation, 1303–1310 anatomic aspects of, 1304, 1304f, 1304t complication(s) of, 1308, 1316–1323, 1317t bleeding, 1319 neuroaxial, 1316–1317 device, 1319–1321, 1320f, 1320t generator/reservoir site other, 1320 pain at, 1319 infectious, 1308, 1317–1318, 1317f, 1318f intrathecal agent, 1321 intrathecal catheter, 1321 lead migration, 1319–1320, 1320f, 1320t loss of appropriate stimulation, 1319–1320, 1320f, 1320t neurologic direct, 1318–1319 indirect, 1319 overview of, 1316 seroma, 1319, 1319f cost effectiveness of, 1309–1310 electrodes for, selection of, 1305 equipment for, 1304–1305, 1305f, 1306t for angina, 1309 for arachnoiditis, 749 for complex regional pain syndrome, 286, 1309 for failed back surgery syndrome, 1308–1309 for ischemia, 1309 for neuropathic pain, 211 for phantom pain, 299–300 for postmastectomy pain, 663 future directions for, 1310 history of, 1303 implanted pulsed generator in, types of, 1305, 1305f lead implantation in migration after, 1319–1320, 1320f, 1320t permanent, 1307 mechanism of action of, 1303, 1304t outcomes of, 1308–1309 patient selection for, 1306, 1306t principles of, 1310, 1310t programming in, 1307–1308 psychologic testing for, 1306, 1306t risk assessment in, 1321–1322 risk reduction strategies in, 1322–1323 surgical technique of, 1306–1307 technical considerations in, 1304–1305 thoracic, 1182 trial period for, 1306–1307, 1307f Spinal dorsal horn, 12 afferent projections in, 12 anatomy of, 12, 12t, 13f neurons of, 12–14 anatomic localization of, 12–13, 13f functional properties of, 14 nociceptive-specific, 14 wide dynamic range, 14, 14f Spinal excitatory systems, in pain modulation, 31, 32f Spinal fusion complications of. See Failed back surgery syndrome for cervical facet syndrome, 520 for failed back surgery syndrome, 774 rationalization for, 765 Spinal manipulative therapy, 1009–1018. See also Alternative medicine and pain, 1016–1018 mechanism 1: direct effect on pain generation, 1016–1017 mechanism 2: activation of on pain suppression mechanisms, 1017 mechanism 3: effect on motor output, 1017–1018 mechanism 4: effect on higher centers of processing, 1018 for neurogenic inflammation, 1012–1013, 1012f introduction to, 1009–1010 nociception and, 1011–1016. See also Nociceptors Spinal nerve block, differential conventional sequential, 151–153 disadvantages of, 153 interpretation of, 152–153, 153t modified, 153–154, 153t advantages of, 154
Index 1441 Spinal nerve block, differential conventional sequential (Continued) observations after, 152t preparation of solutions for, 152t, 153t procedure for, 151–152, 152t Spinal nerve tumors, in cervical radiculopathy, 524 Spinal opioids choice of drug in, 330–331 costs of, 1313 delivery systems for, 1311–1315. See also Implantable drug delivery systems dosage of, 331, 331t for arachnoiditis, 750 for cancer pain, 310–311 problems associated with, 1313 indications for, 330 intermittent bolus vs. continuous infusion of, 331 patient selection for, 330, 1311–1313 patient's support system for, 1313 preimplantation trial for, 1312, 1312t patient's ability to assess results of, 1312–1313, 1312t route of administration of, 331 side effects of, 331, 332t, 1312 Spinal pain cryoanalgesia for, 1366–1369, 1367f, 1368f, 1369f, 1370 patterns of, 52–56, 53f, 55t, 00006:t0030, 56t Spinal procedure(s), fluoroscopically-guided, 75–76 facet joint block, 85–87, 87f sacroiliac joint injection, 87–88, 88f selective nerve root block, 88–89, 89f vertebroplasty, 89–90, 90f Spinal radiculopathies, 53f, 55, 55t Spinal stenosis central, 712 in failed back surgery syndrome, 769, 770f magnetic resonance imaging of, 109, 111f Spinal systems, in pain modulation, 33 Spinal tracts, ascending anatomy of, 14–15 plasticity of, 17 Spine. See also CervicalLumbar; Lumbosacral. SpinalThoracic. Vertebral entries CT scan of, 98–99, 99f, 100f, 101f infections of, 737–742 innervation of, 1010–1011, 1010f magnetic resonance imaging of, 107–109 anular tears in, 108, 110f intervertebral disk disease in, 107–108, 109f stenosis in, 109, 111f osteoarthritis of, 385 tumors of, 546–547 Spinomesencephalic projections, in pain processing system, 15–16, 15f Spinoparabrachial projections, in pain processing system, 15, 16f Spinoreticulothalamic projections, in pain processing system, 15, 15f Spinothalamic projections, in pain processing system, 16, 16f Spiritual healing, 937–938 Spirochetal diseases. See also specific disease laboratory tests for, 64–65, 65f, 66f, 67f Splanchnic nerve(s), anatomy of, 1192, 1193f Splanchnic nerve block, 1200, 1200f. See also Celiac plexus nerve block definition of, 1192 Splenic infarction, in sickle cell disease, 246 Splenic sequestration crisis, in sickle cell disease, 246 Splinting, for trigger finger, 626 Spondylitis infective, 737–742, 737f, 738f, 739f, 740f, 741f, 742f definition of, 737 in children, 737–738 nonpyogenic, 738, 741f, 742f pyogenic, 737, 740f signs and symptoms of, 739–742 testing for, 742 treatment of, 742 tuberculous, 738–739, 741f Spondyloarthropathy, destructive, 548 Spondylolisthesis, 751, 752f, 755–756, 755f classification of, 755, 755t grading of, 78, 78f, 755, 756f
Spondylolisthesis (Continued) in failed back surgery syndrome, 769, 769f, 770f lumbar, 56 pain in, 756 treatment of, 756 Spondylolysis, 751–755 diagnosis of, 752–754, 753f, 753t, 754t genetic factors in, 752 pain in, 754–755, 754t pathology of, 752 prevalence of, in athletes, 752, 752t treatment of, 755 Spondylosis cervical, 542–544, 542f dynamic mechanical factors in, 543–544, 543f, 544f ischemic factors in, 544 static mechanical factors in, 543, 543f lumbar, 700, 700f radiography of, 77, 77f Spontaneous muscle activity, in electromyography, 179, 179f Sports injury(ies), 350–370 Achilles bursitis, 367–368, 368f adductor tendinitis, 363–364, 363f, 364f bicipital tendinitis, 354–356, 354f, 355f, 356f carpal tunnel syndrome, 357–359, 357f, 358f, 359f de Quervain's tenosynovitis, 359–361, 360f, 361f deltoid ligament strain, 366–367, 366f lateral epicondylitis (tennis elbow), 356–357, 356f, 357f medial collateral ligament syndrome, 364–365, 364f, 365f plantar fasciitis, 369–370, 369f, 370f prepatellar bursitis (housemaid's knee), 365–366, 365f rotator cuff disorders, 352–354, 353f sesamoiditis, 368–369, 369f supraspinatus tendinitis, 351–352, 351f, 352f trochanteric bursitis, 361–363, 361f, 362f types of, 350, 351t Sprains ankle, osteopathic manipulative therapy for, 1007 magnetic resonance imaging of, 113–114 Spurling neck compression test, for cervical radiculopathy, 525, 526t Squamous cell carcinoma, of sinuses, 500 Stabilizing exercises, for low back pain, in pregnancy, 779 Staff changeover, in burn pain management, 241 Staff protection, during radiation procedures, 103–104 Stance phase, in gait analysis, 1003 Staphylococcus aureus infection, of spine, 737 Status migrainosus, in migraine headache, 424, 424t Stellate ganglion anatomy of, 220 chemical neurolysis of, 1112, 1112f efficacy of, 1115 radiofrequency neurolysis of, 1112, 1113f efficacy of, 1115 Stellate ganglion block, 1103–1115 agents for, 1105–1106 complications of, 220, 1112–1114 contraindications to, 1105 diagnostic, 148 differential, 156t efficacy of, 1115 equipment for, 1105–1106 for acute/postoperative pain, 220, 221f for facial complex regional pain syndrome diagnostic, 506, 507f, 508f therapeutic, 512–513 for herpes zoster, 269, 1104–1105 for intractable angina, 1104 for long Q-T syndrome, 1105 for post-traumatic syndrome, 1104 for vasculopathies, 1104 for visual acuity, 1105 indications for, 1104–1105, 1105t neurolytic chemical, 1112, 1112f radiofrequency, 1112, 1113f
1442 Index Stellate ganglion block (Continued) patient preparation for, 1105–1106 technique of, 1106–1111 C7 anterior approach in, 1107 fluoroscopic, 1107, 1107f, 1108f new, 1107–1110, 1109f paratracheal approach in, 1106–1107, 1106f ultrasonographic, 1110–1111, 1110f, 1111f in-plane approach in, 1111 needle insertion approach in, 1111 nerve localization in, 1111 Stenosis. See at anatomic site Sterile techniques, for diskography, 123 Sternalis muscle, anatomy of, 636 Sternalis syndrome, 635–636, 636f, 637f Sternoclavicular joint abnormalities of, radiography of, 645f anatomy of, 643–644 osteoarthritis of, 643, 644f Sternoclavicular joint syndrome, 643–644, 643f, 644f Sternum, osseous anatomy of, 642, 642f Steroids. See specific agent Still's disease, 396–397 Stimulating electrodes, in electromyography, 176–177, 177f Stimulator sciatic nerve, placement of, 1301, 1301f, 1302, 1302f ulnar nerve, placement of, 1301, 1301f Stingers, 534, 535f. See also Brachial plexopathy Straight leg raising test active, 777, 778f for lumbar radiculopathy, 710, 710t for sacroiliac joint disorders, 760 Strain(s), deltoid ligament, 366–367, 366f Strengthening exercises, for sacroiliac joint disorders, 762 Stress fractures, femoral, vs. iliopsoas bursitis, 819, 819t Stretching exercises, for rotator cuff disorders, 576 Stroke complex regional pain syndrome II after, 290 headache in, 251–252, 251f, 253–254 water-based exercises after, 990 Strontium-89, in palliative radiation therapy, 316 Stump pain, 292. See also Phantom pain/ sensation prevalence of, 293 Stump revision, for phantom pain, 300 Stye (hordeolum), 483, 483f Sub-Achilles bursitis, 865 Subacromial spur, arthroscopic decompression for, 577, 577f Subarachnoid hemorrhage, headache in, 251–252, 251f, 254, 254f Subarachnoid neurolytic block, 1214–1220 complications of, 1219–1220, 1219f, 1220f criteria for, 1214 informed consent for, 1214 success rates for, 1219–1220 technique of, 1215–1216, 1215f, 1216f with alcohol, 1216–1218, 1217f with phenol, 1218–1219, 1218f Subaxial subluxation, in rheumatoid arthritis, 546, 547f Subcostal nerve, 1185 Subcutaneous calcaneal bursitis, 865 Subdeltoid bursitis, 582–584, 583f treatment of, 582–584, 583f Subdural puncture, inadvertent, in cervical epidural nerve block, 1136 Subluxation, in rheumatoid arthritis atlantoaxial, 546, 546f subaxial, 546, 547f vertical, 546, 546f Substantia gelatinosa (lamina II) neurons, 12t, 13 Subtalar joint, 860 Subtendinous bursitis, 865 Suction blisters, in cold-type complex regional pain syndrome, 277 Sudomotor axon reflex test, quantitative, 182 Sufentanil, 907 transdermal formulation of, 901 Suffering, 302, 945 Suicide headache, 436, 439. See also Cluster headache
Sulfasalazine, for rheumatoid arthritis, 401 Sulindac for cancer pain, 305t pharmacology of, 887t Sumatriptan, for cluster headache, 447 Superior gluteal neuralgia, cryoanalgesia for, 1371 Superior hypogastric plexus, anatomy of, 793, 794f Superior hypogastric plexus block, differential, 156t Superior sulcus tumor. See Pancoast tumor Supine sculling exercises, 991–992, 992f Supraclavicular brachial plexus block, 1145–1148. See also Brachial plexus block indications for, 1145 side effects and complications of, 1147–1148 technique of, 1146–1147, 1146f, 1147f Supraorbital nerve, irritative neuropathy of, 1371, 1372f Suprapatellar bursitis, 843–845, 844f, 845f treatment of, 844–845, 845f Suprapatellar pouch cyst, noncommunicating, 844f Suprascapular nerve anatomy of, 591f entrapment of, 591 pulsed radiofrequency of, 1177–1178 Suprascapular nerve block, 1174–1178 anatomic aspects of, 1175, 1175f complications of, 1178 drugs for, 1174 efficacy of, 1178 equipment for, 1174 historical considerations in, 1174 indications for and contraindications to, 1174 neurolytic, technique of, 1177 patient preparation and positioning for, 1174–1175 technique of, 1175–1177 blind, 1175, 1175f radiographic, 1175–1176, 1176f, 1177f ultrasound, 1176–1177, 1177f, 1178f with pulsed radiofrequency, 1177–1178 Supraspinal projections, in pain processing system, 15–16, 15f, 16f Supraspinal systems, in pain modulation, 33–34 Supraspinatus tendinitis, 351–352, 351f, 352f Sural nerve block, 1297 Surface electrodes, in electromyography, 176–177, 177f Surgical history, in peripheral neuropathy, 261–262, 262t Surgical interventions. See also specific procedure, e.g., Diskectomy arthroscopic, for rotator cuff disorders, 577, 577f, 578f at wrong level, and failed back surgery syndrome, 770–771 endoscopic, for carpal tunnel syndrome, 621 excessive, and failed back surgery syndrome, 765 for piriformis syndrome, 792 for plantar fasciitis, 874 for vulvodynia, 800 in cervical myelopathy anterior approach to, 555–556, 556t indications for, 555 posterior approach to, 556–557, 556t in cervical radiculopathy, 528 in cluster headache, 451–452, 451t thoracic epidural nerve block for, 1181 Swan-neck deformity in rheumatoid arthritis, 399, 399f of finger, 618, 618f Swing phase, in gait analysis, 1003 Sympathectomy, for complex regional pain syndrome, 286 Sympathetic nerve blocks for acute/postoperative pain, 219–223 for cancer pain, 310 for complex regional pain syndrome, 285 for herpes zoster, 269 for neuropathic pain, 211 lumbar, 1230–1236. See also Lumbar sympathetic nerve block Sympathetic nervous system (SNS) cervical, anatomy of, 1103, 1104f, 1105f in nerve injury, 27, 27f lumbar, anatomy of, 1231
Sympathetically maintained pain, in complex regional pain syndrome, 273, 279–280, 279f Syndrome of inappropriate antidiuretic hormone (SIADH) secretion, 61 Synovectomy, radionuclide, for painful arthropathy, 93, 93f Synovial fluid analysis, in rheumatoid arthritis, 399 Synovial osteochondromatosis, 83, 83f Syphilis, laboratory tests for, 64–65 Systemic illness, in peripheral neuropathy, 262t Systemic lupus erythematosus, 402–405 differential diagnosis of, 404–405 extra-articular manifestations of, 403–404, 404f, 404t laboratory findings in, 404 laboratory tests for, 61–63, 63t signs and symptoms of, 402–404, 403f, 404f treatment of, 405 vs. rheumatoid arthritis, 400 Systemic sclerosis, 405. See also Scleroderma
T
T cells, 59, 64 Tachycardia, opioid-induced, 896, 896f Tactile allodynia, 12 Tadalafil, for complex regional pain syndrome, 285 Tai chi, 1024 Tailor's bunion (bunionette), 870f, 871 Talocrural joint, 860 Tapentadol, 909 Targeted muscle groups abbreviated, 972t 18 steps for tensing, 972t Tarsal tunnel syndrome, 382–383 TART examination, in osteopathic medicine, 999t, 00136:s0120, 1000 Tear(s), rotator cuff. See Rotator cuff disorders Telangiectases, in scleroderma, 405–406, 406f Temperature monitoring, in radiofrequency lesioning, 1333 Temporal arteritis. See Giant cell arteritis Temporal artery, in giant cell arteritis, 476, 477f biopsy of, 478, 478t Temporomandibular joint disorders biofeedback for, 957 vs. tension-type headache, 432–433 vs. trigeminal neuralgia, 38 Tendinitis Achilles, 863–864, 863f, 864f adductor, 363–364, 363f, 364f biceps, 354–356, 354f, 355f, 356f, 585–587. See also Biceps tendinitis in scleroderma, 406 rotator cuff. See Rotator cuff disorders supraspinatus, 351–352, 351f, 352f vs. orchialgia, 794–795, 795t Tendinopathy, 112 rotator cuff. See Rotator cuff disorders Tendinosis, calcific, of shoulder, 79, 80f Tendon(s). See also named tendon degeneration of. See Tendinopathy magnetic resonance imaging of, 112–113 of ankle, 860, 862f Tennis elbow (lateral epicondylitis), 356–357, 356f, 357f, 594–597, 595f differential diagnosis of, 594 signs and symptoms of, 594, 596f testing for, 594, 596f treatment of, 594–596, 597f vs. radial tunnel syndrome, 613–614, 614f, 1153, 1153f Tenosynovitis de Quervain's, 81, 359–361, 360f, 361f, 622–623, 623f definition of, 112–113 extensor, 618 flexor, 618 Tension-type headache, 428–435. See also Headache chronic, 429 definition of, 454 nociceptive reflex in, 429 clinical features of, 428–431, 429t diagnostic testing in, 430, 431, 431t differential diagnosis of, 431–433, 431t historical considerations in, 428–431 muscle involvement in, 429, 430f
Tension-type headache (Continued) physical findings in, 430, 430f, 431f postural mechanical factors in, 430 treatment of, 433–435, 433t antidepressants in, 434, 434t biofeedback in, 956 botulinum neurotoxin in, 435, 435t massage therapy in, 435 muscle relaxants in, 433–434, 433t nonpharmacologic, 434–435 NSAIDs in, 00047:f0030, 433–434 physical therapy in, 435 yoga in, 970 vs. migraine headache, 431 vs. temporomandibular joint syndrome, 432–433 Testicular denervation, for orchalgia, 797 Testicular innervation, 793, 794f Testicular pain, 793–797. See also Orchialgia Testicular torsion, 795, 795t Thalidomide, for cancer-related fatigue, 340 Thebaine, 903 Therapeutic approach, to cancer pain, 303–304 Thermal biofeedback, 956–957, 959 Thermistors, 959 Thermoluminescent dosimeters, during radiation procedures, 104 Thigh pain, prolotherapy for in anterior region, 1040–1041, 1040f in posterior and gluteal regions, 1037–1040, 1038f, 1039f Thigh thrust (posterior pelvic pain provocation test), 777, 777f Third-degree burns, 229, 230f Thomas test, for iliopsoas bursitis, 817 Thompson test, for Achilles tendon rupture, 864–865 Thoracic diskectomy, laser, 1405. See also Laser diskectomy Thoracic diskography, technique of, 129–131, 130f, 131f, 132f Thoracic epidural anesthesia (TEA), for post-thoracotomy pain, 666 Thoracic epidural nerve block, 1179–1184. See also Epidural nerve block, thoracic Thoracic facet block, protocol for, 86, 87f Thoracic inlet syndrome, 534–535 Thoracic nerve root block, fluoroscopicallyguided, 88 Thoracic outlet syndrome, 534–535, 535f vs. cervical radiculopathy, 527 Thoracic radiculopathy, 646–648, 647f Thoracic spine magnetic resonance imaging of, 646, 647f radiography of, 77, 77f Thoracic sympathetic nerve block, differential, 156t Thoracoscopic surgery, video-assisted, 665 Thoracotomy chest pain after, 655, 655f. See also Postthoracotomy pain syndrome surgical approaches to, 665 Thought stopping, in burn pain management, 239 Three-D technique, of epidural adhesiolysis, 1266–1267, 1269f, 1270f, 00169:f0140, 00169:f0145, 00169:f0150, 00169:f0155, 00169:f0160, 00169:f0165, 00169:f0170 Throat pain, 495t, 500–502, 502f Throbbing pain, 699 Thromboangiitis obliterans, demographics of, 39t Thrombocytosis, 60 Thrombosis, cavernous sinus, 492 Thumb, trigger, 626–627 Thyroid function tests, 63 Thyroid-stimulating hormone (TSH), 63 Thyroxine (T4), 63 Tiagabine, 922–923, 922f Tibial nerve hour-glass deformity of, 1029, 1030f posterior, electrodiagnosis of, 184 Tibial nerve block, posterior, 1297 Tic convulsif, 465. See also Trigeminal neuralgia Tic douloureux, 38, 465. See also Trigeminal neuralgia Tick bites, knee pain due to, 839 Tic-like neuritides of fifth cranial nerve, vs. trigeminal neuralgia, 466 Tietze's syndrome, 634–635, 634f, 635f
Index 1443 Tinel's sign in carpal tunnel syndrome, 358, 358f, 620, 621f in iliohypogastric neuralgia, 690 in ilioinguinal neuralgia, 687, 1237 in meralgia paresthetica, 821 in pronator syndrome, 609–610 Tissue injury, nociception in, 20–24. See also Pain processing system, in tissue injury Tizanidine, 925t, 926 for cluster headache, 450 for neuropathic pain, 210–211 for tension-type headache, 433t Tolerance, to opioids, 897 Tolmetin for cancer pain, 305t for tension-type headache, 433t pharmacology of, 887t Tolosa-Hunt syndrome, 377–378, 378f ocular/periocular pain in, 489 vs. cluster headache, 445–446 Topical analgesics, for neuropathic pain, 210 Topical creams, for osteoarthritis, 393 Topiramate, 922, 922f for cluster headache, 449 for migraine prophylaxis, 426–427 for mononeuritis multiplex, 671 Torsion, testicular, 795, 795t Torticollis in cervical dystonia, 558. See also Cervical dystonia muscles involved in, 562t Total iron-binding capacity (TIBC), 58–59 Total joint replacement for osteoarthritis, 391t, 394 for rheumatoid arthritis, 402 referral for, 394–395 Tourniquet use, femoral neuropathy after, 826 Toxicity ethanol, after celiac plexus block, 1203 local anesthetic, 931t, 932–933, 932f, 933f after caudal epidural nerve block, 1256 narcotic analgesic, 218 Toxicology, 74 Traction for lumbar radiculopathy, 713 for sacroiliac joint disorders, 761 Tramadol, 909 for neuropathic pain, 210 for osteoporosis, 705 for phantom pain, 298 Tranquility, opioid-induced, 895 Tranquilizers, for herpes zoster, 270 Transcutaneous electrical nerve stimulation (TENS), 939, 995–997. See also Alternative medicine; Neurostimulation apparatus for, 996, 997f contraindications to, 997, 997t for lumbar radiculopathy, 713 for orchalgia, 796 for phantom pain, 299 for postmastectomy pain, 663 for post-thoracotomy pain, 667 indications for, 996, 996t scientific basis of, 995–996 technique of, 997 Transient ischemic attack (TIA), headache in, 251 Transmitters ascending projection, 18 primary afferent, 17–18, 18f Transplantation, renal, femoral neuropathy after, 826–827 Trauma. See also specific trauma, e.g., Fracture(s) brachial plexopathy due to, 534–535, 534f, 535f chest wall, 658, 658f cough-induced, 653 femoral neuropathy due to, 826 knee pain due to, 837 neural, after cervical epidural nerve block, 00153:s0180 neurologic, after spinal cord stimulation direct, 1318–1319 indirect, 1319 neuropathic, electrodiagnosis of, 182–183 orthopedic, CT scan of, 97–98, 98f spinal cord, complex regional pain syndrome II after, 290–291 sports, 350, 351t. See also Sports injury(ies). specific injury visceral, after celiac plexus block, 1203
Trazodone, 914f, 915 Tremor, physiologic, in complex regional pain syndrome, 277–278 Trendelenburg sign, in trochanteric bursitis, 814 Trendelenburg's test, modified, 777, 778f Treponema pallidum, in syphilis, 64 Trial period, for spinal cord stimulation, 1306–1307, 1307f Triamcinolone for herniated disk, 1181 for trochanteric bursitis, 815–816 Tricyclic antidepressants. See Antidepressants, tricyclic Trigeminal nerve (V) anatomy of, 225, 1069, 1069f, 1070f, 1075–1076 evaluation of, 44t herpes zoster involving, 269, 270f vs. trigeminal neuralgia, 466 mandibular division of, 1075f, 1076, 1076f neural blockade of coronoid approach to, 1076–1078, 1076f, 1077f, 1078f mental, 1079–1080, 1079f maxillary division of, 1075f, 1076, 1076f neural blockade of coronoid approach to, 1076–1078, 1076f, 1077f, 1078f infraorbital, 1078–1079, 1079f ophthalmic division of, 1075–1076, 1075f neural blockade of, 1078, 1078f sensory distribution of, 37f surgical intervention involving, for cluster headache, 451, 451t tic-like neuritides of, vs. trigeminal neuralgia, 466 Trigeminal nerve block, 1074–1080 anatomic aspects of, 1075–1076, 1075f, 1076f complications of, 225, 1080 contraindications to, 1074 for acute/postoperative pain, 225, 00024:t0055 indications for, 1074, 1075t selective of mandibular nerve, 1079–1080, 1079f of maxillary nerve, 1078–1079, 1079f of ophthalmic nerve, 1078, 1078f technique of, via coronoid approach, 1076–1078, 1076f, 1077f, 1078f Trigeminal neuralgia, 464–470 clinical presentation of, 465 demographics of, 39t diagnosis of, 465 differential diagnosis of, 465–467 historical considerations in, 464 intermittent, 465 pain in, 37, 37f tic convulsif in, 465 tic douloureux in, 465 treatment of, 467–470 complications and pitfalls in, 470 gamma knife radiosurgery in, 469 medical, 467–468 microvascular decompression in, 469–470 percutaneous procedures in, 468–469 radiation therapy in, 318 surgical, 468 trigger zones in, 465 vs. atypical facial pain, 467, 467b vs. cluster headache, 445 vs. geniculate neuralgia, 466 vs. glossopharyngeal neuralgia, 465–466 vs. herpetic/postherpetic neuralgia of cervical dorsal root ganglia, 466 of trigeminal nerve, 466 vs. occipital neuralgia, 466 vs. Raeder's syndrome, 466–467 vs. temporomandibular joint dysfunction, 38 vs. tic-like neuritides, 466 vs. trigeminal neuropathy, 378–379, 379f with cluster headache, 465 Trigeminal neuropathy, vs. trigeminal neuralgia, 378–379, 379f Trigger finger, 626–627, 627f Trigger point(s) in scapulocostal syndrome, 588, 589f in sternalis syndrome, 635, 636f Trigger point injections for cancer pain, 321 for post-thoracotomy pain, 667
1444 Index Trigger thumb, 626–627 Trimipramine, for tension-type headache, 434t Triptans, for migraine headache, 425 Trochanter, greater, bursae associated with, 813, 814f Trochanteric bursitis, 361–363, 361f, 362f, 813–816 clinical presentation of, 814 diagnosis of, 814–815 differential diagnosis of, 815, 815t etiology of, 813, 814f historical considerations in, 813 treatment of, 815–816, 815t complications and pitfalls in, 816 Trochlear nerve (IV), evaluation of, 44t Tuberculosis, spinal, magnetic resonance imaging of, 647f Tuboplasty, femoral neuropathy after, 826 Tuck sign, 618 Tui na, in Chinese medicine, 1024 Tumor(s). See at anatomic site;specific tumor Tumor necrosis factor-α, in herniated disk, 1401 Turner's sign, in acute pancreatitis, 682, 684f Tympanic membrane, infection of, 497
U
Ulcerative colitis, relaxation techniques for, 970 Ulcers leg, in sickle cell disease, 246–247 mouth, in systemic lupus erythematosus, 403, 404f Ulnar nerve anatomy of, 1160–1161, 1163f, 1168–1169, 1170f compression of, 606, 607f corticosteroid injection of, 608, 608f electrodiagnosis of, 184 Ulnar nerve block at elbow, 609, 1159–1162, 1161f, 1162f, 1163f, 1164f at wrist, 1168–1171, 1169f, 1170f, 1171f, 1172f Ulnar nerve entrapment, at elbow, 606–609, 607f, 608f Ulnar tunnel syndrome, 1171, 1171f, 1172f vs. cervical radiculopathy, 1171 Ulnocarpal impaction syndrome, 81 Ultrasonography of Baker's cyst, 853–854, 854f of iliopsoas bursitis, 818, 818f of lateral femoral cutaneous nerve, 821–823, 823f of osteoarthritis, 389 of plantar fasciitis, 873, 873f of quadriceps expansion syndrome, 856, 859f of rotator cuff disorders, 575, 575f therapeutic heat production in, 983 indications for, 979t Ultrasound-guided technique of celiac plexus block, 1201, 1201f of femoral nerve block, 1292–1293, 1292f of ilioinguinal-iliohypogastric nerve block w, 1239–1240, 1241f of lateral femoral cutaneous nerve block, 1293 of nerve blocks at ankle, 1297 at knee, 1296, 1296f peripheral, 1290 of obturator nerve block, 1247, 1247f, 1294, 1294f of sciatic nerve block, 1291, 1291f, 1294f of stellate ganglion block, 1110–1111, 1110f, 1111f efficacy of, 1115 in-plane approach to, 1111 needle insertion approach to, 1111 nerve localization for, 1111 of suprascapular nerve block, 1176–1177, 1177f, 1178f Unilateral neuralgiform headache attacks, short-lasting, with conjunctival injection and tearing, 444–445 Upper extremity. See also specific part peripheral nerve blocks for, 1151–1173 median nerve
Upper extremity (Continued) at elbow, 1157–1159, 1157f, 1158f, 1160f at wrist, 1165–1168, 1166f, 1167f, 1168f cutaneous and intercostobrachial, 1153–1154, 1154f, 1155f metacarpal and digital, 1171–1173, 1172f radial nerve at elbow, 1154–1157, 1155f, 1156f, 1157f at humerus, 1151–1153, 1152f, 1153f at wrist, 1162–1165, 1164f, 1165f ulnar nerve at elbow, 1159–1162, 1161f, 1162f, 1163f, 1164f at wrist, 1168–1171, 1169f, 1170f, 1171f, 1172f range of motion of, 1003, 1004t root vs. nerve lesions in, 48t Urea, 69 Uric acid, measurement of, 71 Urinary incontinence after caudal epidural nerve block, 1256–1257 after cervical epidural nerve block, 1137 in arachnoiditis, 747 Urinary retention after caudal epidural nerve block, 1256–1257 after cervical epidural nerve block, 1137 Urinary tract infection, definition of, 71 Urine drug test, 73 Urine osmolality, 70 Urine retention, opioid-induced, 897 Uterine contractions, opioid effects on, 897 Uveitis, 486, 487f
V
Vagus nerve (X) anatomy of, 1086, 1087f evaluation of, 44t Vagus nerve block, 1086–1087, 1087f Valgus stress test for medial collateral ligament integrity, 840, 840f for medial collateral ligament syndrome, 364–365, 365f Valproic acid, for cluster headache, 449 Van Dursen's standing flexion test, 760 Vanilloids. See also specific agent, e.g., Capsaicin in neurolytic blockade, 325t, 327 Varicocele, 795 Varus stress test, for lateral collateral ligament integrity, 840, 841f Vascular insufficiency, peripheral, transcutaneous electrical nerve stimulation for, 996 Vasculitis, laboratory tests for, 61–63, 62f, 62t, 63t Vasculopathy(ies), stellate ganglion block for, 1104 Vasoconstriction, in complex regional pain syndrome, 276, 277 Venlafaxine, 917, 917f for facial complex regional pain syndrome, 512 Ventral funicular projection systems, 14 Verapamil for cluster headache, 448 for migraine prophylaxis, 426 Verbal Analog Pain Scale, 337 Verbal descriptor scale, in pain assessment, 193f, 194 Verbal numeric scale (VNS), in pain assessment, 194 Vertebral fractures compression, 78, 1375–1387 biconcave, 1377 CT scan of, 1378, 1379f evaluation of, 1377–1379, 1378f, 1379f, 1379t kyphoplasty for, 1381–1382, 1381f, 1382f outcomes of, 1386 PMMA preparation and delivery in, 1382–1383, 1383f vs. vertebroplasty, 1384t magnetic resonance imaging of, 115–116, 116f, 1377–1378, 1378f nonosteoporotic, 1376–1377 osteoporotic, 1376 studies of, 1386 treatment options for, 1377t
Vertebral fractures (Continued) pathophysiology of, 1376–1377 prevention of, 1377, 1377t vertebral augmentation for complications of, 1383–1384 contraindications to, 1383–1384, 1383t in patients with multiple myeloma and metastases, 1386–1387 outcomes of, 1384–1387, 1384t techniques of, 1379–1387, 1380f, 1381f vertebroplasty for, 1379–1387, 1380f, 1381f outcomes of, 1385–1386 PMMA preparation and delivery in, 1382–1383 vs. kyphoplasty, 1384t wedge, 1377 thoracic epidural nerve block for, 1181 Vertebral osteomyelitis, 695–696, 696f Vertebral osteonecrosis, aseptic, 78, 80f Vertebral pain, 52–55 local, 697–698, 698f Vertebroplasty, 1379–1387, 1380f, 1381f complications and contraindications to, 1383–1384, 1383t fluoroscopically-guided, 89–90, 90f outcomes of, 1385–1386 PMMA preparation and delivery in, 1382–1383 vs. kyphoplasty, 1384t Vertical subluxation, in rheumatoid arthritis, 546, 546f Vestibulectomy, vs. biofeedback, 956 Vestibulitis, vulvar, 798 Video-assisted thoracoscopic surgery (VATS), 665 Virtual reality, in burn pain management, 237, 237f Visceral pain, 338 in low back, 699 in lungs, 649–650, 650f radiation therapy for, 317 transcutaneous electrical nerve stimulation for, 996 Visceral trauma, after celiac plexus block, 1203 Viscerosomatic reflexes, 998 Viscosity, definition of, 988 Visual acuity, stellate ganglion block for, 1105 Visual Analog Pain Scale, 193–194, 193f, 337 Visual disturbances, in giant cell arteritis, 476–477 Visual evoked potentials (VEPs), 187–188, 188f Vitamin B12 deficiency, 65 Vitamin D, for osteoporosis, 705 Vitamin D deficiency, 70 osteoporosis and, 701 Vitamin K deficiency, 72 Volar aspect, of hand, 616 Voltage monitoring, in radiofrequency lesioning, 1333, 00178:t0010 Voluntary muscle activity, in electromyography, 179–180, 180f Vomiting. See Nausea and vomiting Vulvar vestibulitis, 798 Vulvodynia, 798–800 anatomic aspects of, 798, 799f clinical presentation of, 798 diagnosis of, 798–799, 799t treatment of, 799–800, 800f
W
Waddell's sign, 321–322, 725–726, 732 Waldman knee squeeze test, for adductor tendinitis, 363, 364f Walking, gait assessment in, 49 Wall crunch exercises, 991–992, 992f Wall sit exercises, 991–992, 991f Wallenberg's syndrome, 512 Warning signs, in x-ray room, 104 Water heating pads, circulating, 980, 980f Water walking forward/backward exercises, 991–992, 991f Water-based exercises, 989–993, 991f, 992f, 993f. See also Hydrotherapy Watson stress test, for carpometacarpal arthritis, 358–359, 359f Waveforms, in electromyography, 179 Weakness in cervical myelopathy, 550 in cervical radiculopathy, 525
Weakness (Continued) in peripheral neuropathy, 261t muscle, in complex regional pain syndrome, 274 Weaver's bottom, 808 Webs, arachnoid, 783, 784f Wedge fractures, 1377 Weight gain during pregnancy, 775–776 knee pain with, 838–839 meralgia paresthetica and, 821, 822f Weight loss in management of osteoarthritis, 391t, 392 knee pain with, 838–839 low back pain and, 695–696 Well-being, of cancer patient, palliative care for, 343 Wertheim and Rovenstine's method, of cervical plexus block, 1097–1098, 1099f Whiplash cervical facet syndrome and, 517 osteopathic manipulative therapy for, 1007 Whirlpool baths, 993–994. See also Hydrotherapy iced, 985 White blood cell (WBC) count, 59 Wide dynamic range neurons, 14, 14f in tissue injury, 21–22, 21f Wind-up, 31 Withdrawal, in medication overuse headache, 461–462
Index 1445 Women cluster headache in, 441 migraine headache in, 422, 441 Work, return to, occupational back pain and, 724, 725 Working environment, modification of, for rotator cuff disorders, 576–577 Workplace intervention, in occupational back pain, 724 World Health Organization (WHO) analgesic ladder, for cancer pain management, 330, 330f, 346, 347f, 655f, 656 World Health Organization (WHO) definition, of palliative care, 336–337 Worst (first) syndrome, 37–38 Wound care, in burn pain management, 240, 241–242 Wound infections, after spinal cord stimulation, 1317t, 1319 Wrist anatomy of, 616, 617f arthritis of, 616–618 median nerve block at, 1165–1168, 1166f, 1167f, 1168f median nerve entrapment at. See Carpal tunnel syndrome osteoarthritis of, 81 painful differential diagnosis of, 616, 617t prolotherapy for, 1043–1044, 1043f radial nerve block at, 1162–1165, 1164f, 1165f
Wrist (Continued) radiography of, 80–81 ulnar nerve block at, 1168–1171, 1169f, 1170f, 1171f, 1172f
X
Xiphisternal joint, anatomy of, 642 Xiphisternal syndrome, 641–643, 641f, 642f, 643f Xiphodynia, 641 Xiphoid process, anatomy of, 642, 642f X-ray(s), 75. See also Radiography X-ray machines, radiation protection accessories of, 103
Y
“Yellow back pain,”, 726 Yergason test for biceps tendinitis, 585, 586f for bicipital tendinitis, 354–355, 355f Yin-yang theory, 1020, 1020f Yoga, 969, 969t. See also Relaxation technique(s) in MBSR program, 973–974, 974t
Z
Zagapophyseal joints. See Facet joints Zinc oxide ointment, for herpes zoster, 271 Zinc protoporphyrin, 74 Zolmitriptan, for cluster headache, 447 Zoster sine herpete, 268. See also Herpes zoster
