An imprint of Elsevier Inc. 2008, Elsevier Inc. All rights reserved. First published 2008 No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the Publishers. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department, 1600 John F. Kennedy Boulevard, Suite 1800, Philadelphia, PA 19103-2899, USA: phone: (+1) 215 239 3804; fax: (+1) 215 239 3805; or, e-mail:
[email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting ‘Support and contact’ and then ‘Copyright and Permission’. ISBN-13: 978-0-7216-2872-1 British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging in Publication Data A catalog record for this book is available from the Library of Congress Notice Medical knowledge is constantly changing. Standard safety precautions must be followed, but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the Publisher nor the author_assume any liability for any injury and/or damage to persons or property arising from this publication. The Publisher Printed in the USA Last digit is the print number: 9 8 7 6 5 4 3 2 1
Commissioning Editors: Susan Pioli, Dolores Meloni Project Development Manager: Joanne Scott Editorial Assistants: Sarah Penny, Gregory De Roeck Project Manager: Alan Nicholson Design Direction: Charles Gray Illustration Manager: Gillian Richards Illustrators: Ethan Danielson, Oxford Illustrators Marketing Managers (UK/USA): Verity Kerkhoff, Kathleen Neely
List of Contributors
Arjang Abbasi DO Attending Physician Interventional Pain Management and Spine Rehabilitation Long Island Spine Specialists Commack NY USA Elsayed Abdel-Moty PhD Research Associate Professor Department of Neurological Surgery The Rosomoff Comprehensive Pain and Rehabilitation Center Miami Beach FL USA Salahadin Abdi MD, PhD Professor of Clinical Anesthesiology Chief, Division of Pain Medicine University of Miami Pain Center LM Miller School of Medicine Miami FL USA David R. Adin DO Spine and Sports Fellow Department of Physiatry Hospital for Special Surgery New York NY USA Sang-Ho Ahn MD, PhD Associate Professor of Rehabilitation Medicine and Spine Center Yeungnam University College of Medicine Daegu Republic of Korea Venu Akuthota MD Director The Spine Center and Associate Professor Department of Rehabilitation Medicine University of Colorado School of Medicine Aurora CO USA William A. Ante MD Attending Physiatrist Physical Medicine and Rehabilitation Tri-State Orthopaedic Surgeons, Inc. Evansville IN USA
Alvin K. Antony MD, FABPM&R, FABPM Director, Physiatry and Pain Management Advanced Centers for Orthopedic Surgery and Sports Medicine Clinical Instructor, Department of PM&R Johns Hopkins University Medical Center Baltimore MD USA Charles N. Aprill MD Clinical Professor Physical Medicine and Rehabilitation Interventional Spine Specialists Louisiana State University Health Science Center Kenner LA USA Madhuri Are MD, BA Assistant Professor, Cancer Pain Management Department of Anesthesiology and Pain Medicine MD Anderson Cancer Center University of Texas Houston TX USA Joshua D. Auerbach MD Resident Department of Orthopaedic Surgery University of Pennsylvania Philadelphia PA USA Giancarlo Barolat MD Director and CEO The Barolat Institute Lone Tree CO USA Katrien Bartholomeeusen PT MSc Manual Therapy, Dip ManipTher, MSc Sport PT Head of Private Practice for Manipulative PT and Sports PT Faculty of Physical Education and Physiotherapy Lier Belgium
Lisa M. Bartoli DO, MS, FAAPMR Adjunct Clinical Assistant Professor Head Team Physician USA Rugby Women’s National Team Center for Health and Healing Department of Orthopedics Beth Israel Medical Center New York NY USA Bonnie Lee Bermas MD Associate Rheumatologist Robert B. Brigham Arthritis Center Brigham and Women’s Hospital Boston MA USA Sarjoo M. Bhagia MD, MSc (Orth) Interventional Physiatrist Department of Orthopedics and Rehabilitation Miller Orthopaedic Clinic Charlotte NC USA Amit S. Bhargava MD, MS Physician Interventional Spine, EMG, Arthritis, Pain and Sports Medicine Physical Medicine and Rehabilitation Owings Mills MD USA Atul L. Bhat MD Clinical Instructor Department of Physical Medicine and Rehabilitation Tufts University School of Medicine Nashua NH USA Klaus Birnbaum Priv.-Doz. Physician Orthopädie Hennef Hennef Germany Nikolai Bogduk BSc(Med), MBBS, PhD, MD, DSc, Dip Anat, MMed (Pain Management) FAFRM, FAFMM, FFDM (ANZCA) Conjoint Professor of Pain Medicine Department of Clinical Research The Newcastle Bone and Joint Institute University of Newcastle Newcastle Australia
Donatella Bonaiuti MD Physiatrist Chief of Rehabilitation Medicine Department S. Gerardo Hospital Milan Italy Guiseppe Bonaldi MD Director, Neuroradiology Department Department of Neuroradiology Riuniti Hospital Bergamo Italy Joanne Borg-Stein MD Assistant Professor of Physical Medicine and Rehabilitation Department of Physical Medicine and Rehabilitation, Harvard Medical School Medical Director, Spaulding Wellesley Rehabilitation Center Wellesley MA USA Kenneth P. Botwin MD Fellowship Director Florida Spine Institute Clearwater FL USA Craig D. Brigham MD Physician OrthoCarolina Charlotte NC USA Oleg Bronov MD Clinical Instructor in Radiology Department of Radiology/Neuroradiology Division University of Pennsylvania Medical Center Philadelphia PA USA Lee Ann Brown DO Physical Medicine and Rehabilitation Florida Spine Institute Clearwater FL USA
ix
List of Contributors Mark D. Brown MD, PhD Professor and Emeritus Chairman Department of Orthopaedics and Rehabilitation University of Miami School of Medicine Miami FL USA Thomas N. Bryce MD Assistant Professor Department of Rehabilitation Medicine Mount Sinai Medical Center New York NY USA Allen W. Burton MD Associate Professor Department of Anesthesiology and Pain Medicine University of Texas MD Anderson Cancer Center Houston TX USA John A. Carrino MD, MPH Assistant Professor of Radiology Harvard Medical School Department of Radiology Brigham and Women’s Hopsital Boston MA USA Bojun Chen MD, PhD Clinical Instructor Department of Rehabilitation Medicine Mount Sinai Medical Center New York NY USA Yung Chuan Chen MD Physical Medicine and Rehabilitation Specialist, Pain Physician, Physiatrist Physical Medicine and Rehabilitation Spinal Diagnostics and Treatment Center Daly City CA USA Cynthia Chin MD Associate Professor of Clinical Radiology Department of Radiology University of California, San Francisco San Francisco CA USA Kingsley R. Chin MD Assistant Professor of Orthopaedic Surgery Division of Spine Surgery Hospital of the University of Pennsylvania Philadelphia PA USA
x
Larry H. Chou MD Medical Director, Sports and Spine Rehabilitation Division Premier Orthopaedic and Sports Medicine Associates, LTD Clinical Associate Professor of Physical Medicine and Rehabilitation University of Pennsylvania Health System Philadelphia PA USA David W. Chow MD Medical Director California Spine Center Walnut Creek CA USA Yung Chuan Chen MD Physical Medicine and Rehabilitation Specialist, Pain Physician Physical Medicine and Rehabilitation Spinal Diagnostics and Treatment Center Daly City CA USA Gianluca Cinotti MD Registrar Orthopaedic Surgery Clinical Orthopedics Universita of Rome Italy Steven P. Cohen MD Associate Professor Department of Anesthesiology and Critical Care Medicine John Hopkins School of Medicine Baltimore MD USA Paul Cooke MD, FABPM&R Assistant Attending Physiatrist Hospital for Special Surgery Attending Physician, The Medical Center of Princeton Princeton, NJ USA Anthony R. Cucuzzella MD Medical Staff Christiana Care Health System Christiana Spine Center Newark NJ USA Richard J. Daniels MD Staff Interventional Radiologist University Hospital Pennsylvania Philadelphia PA USA Kenny S. David MS(Orth) Consultant Department of Orthopaedic Surgery Christian Medical College Vellore India
Gregory Day FRACS (Orth) Associate Professor Department of Surgery School of Medicine Bond University Queensland Australia
Omar El-Abd MD Clinical Instructor, Interventional Physiatrist Spaulding Rehabilitation Hospital Harvard Medical School Wellesley MA USA
Miles Day MD, FIPP, DABPM Associate Professor Department of Anesthesiology and Pain Medicine Texas Tech University Health Sciences Center Lubbock TX USA
Mark I. Ellen MD, FAAPM&R Medical Director and Section Chief Physical Medicine and Rehabilitation Service Birmingham Veterans Administration Medical Center Birmingham AL USA
Rick B. Delamarter MD Medical Director The Spine Institute Santa Monica CA USA
Dawn M. Elliott PhD Associate Professor Department of Orthopaedic Surgery and Department of Bioengineering University of Pennsylvania Philadelphia PA USA
Michael J. DePalma MD Associate Professor Director, VCU Spine Center Physical Medicine and Rehabilitation Virginia Commonwealth University Richmond VA USA Richard Derby MD Medical Director Spinal Diagnostics and Treatment Center Adjunct Clinical Associate Professor Division of Physical Medicine and Rehabilitation Stanford University Medical Center Daly City CA USA Timothy R. Dillingham MD, MS Professor and Chairman Dept of Physical Medicine and Rehabilitation The Medical College of Wisconsin Brookfield WI USA Carol A. Dolinskas MD, FACR Clinical Associate Professor of Radiology University of Pennsylvania Philadelphia PA USA Jonathan A. Drezner MD Associate Professor, Team Physician Associate Director, Sports Medicine Fellowship Department of Family Medicine Hall Health Sports Medicine University of Washington Seattle WA USA Thomas Edrich MD, PhD Instructor of Anesthesia Department of Anesthesiology Brigham and Women’s Hospital Boston MA USA
Clifford R. Everett MD, MPH Assistant Professor of Orthopaedics Physical Medicine and Rehabilitation Department of Orthopaedics University of Rochester Rochester NY USA Amir H. Fayyazi Assistant Professor Department of Orthopedics Institute for Spine Care Syracuse NY USA Claudio A. Feler MD, FACS Semmes-Murphey Neurologic and Spine Institute Associate Professor Department of Neurosurgery University of Tennessee Health Science Center Memphis TN USA Julius Fernandez MD Semmes-Murphey Neurologic and Spine Institute Assistant Professor Department of Neurosurgery University of Tennessee Health Science Center Memphis TN USA Robert Ferrari MD, FRCPC, FACP Clinical Professor University of Alberta Hospital Edmonton AB Canada Jeffrey S. Fischgrund MD Attending Orthopaedic Surgeon William Beaumont Hospital Royal Oak MI USA
List of Contributors David A. Fishbain MD, BSc (Hon), MSc, FAPA Professor of Psychiatry and Adjunct Professor of Neurological Surgery University of Miami Rosomoff Pain Center Miami Beach FL USA Colleen M. Fitzgerald MD Medical Director, Women’s Health Rehabilitation Rehabilitation Institute of Chicago Assistant Professor Physical Medicine and Rehabilitation Northwestern University Feinberg School of Medicine Chicago IL USA Yizhar Floman MD Professor of Orthopedic Surgery Israel Spine Center Assuta Hospital Tel Aviv Israel Edward J. Fox MD Assistant Professor of Orthopaedic Surgery Division of Orthopaedic Oncology Hospital of the University of Pennsylvania Philadelphia PA USA Michael B. Furman MD, MS Clinical Assistant Professor Department of Physical Medicine and Rehabilitation Temple University School of Medicine Philadelphia PA USA Rollin M. Gallagher MD, MPH, DABPM Director of Pain Management Department of Anesthesiology Philadelphia Veterans Affairs Medical Center Philadelphia PA USA Steven R. Garfin MD Professor and Chair Department of Orthopedics University of California San Diego San Diego CA USA Timothy A. Garvey MD Staff Surgeon Twin Cities Spine Center Minneapolis MN USA
Robert J. Gatchel PhD, ABPP Professor and Chairman Department of Psychology College of Science, University of Texas at Arlington Arlington TX USA Peter Gerner MD Assistant Professor of Anesthesiology Department of Anesthesiology Brigham and Women’s Hospital Boston MA USA Peter C. Gerszten MD, MPH, FACS Associate Professor of Neurological Surgery Department of Neurological Surgery Presbyterian University Hospital Pittsburgh PA USA Russell V. Gilchrist DO Assistant Professor Department of Physical Medicine and Rehabilitation University of Pittsburgh Medical Center Pittsburgh PA USA Robert S. Gotlin DO, FAAPMR Director, Orthopaedic and Sports Rehabilitation Assistant Professor, Rehabilitation Medicine Albert Einstein College of Medicine at Yeshiva University Department of Orthopaedic Surgery Continuum Center for Health and Healing New York NY USA M. Sean Grady MD Professor and Chairman Department of Neurosurgery University of Pennsylvania School of Medicine Philadelphia PA USA Richard D. Guyer MD Associate Clinical Professor Department of Orthopedics University of Texas PlanoTX USA Andrew J. Haig MD, FAAEM, FAAPMR Associate Professor Physical Medicine and Rehabilitation and Orthopedic Surgery University of Michigan Ann Arbor MI USA
Stephen Hanks MD Assistant Professor of Clinical Orthopaedic Surgery Department of Orthopaedic Surgery University of Arizona Health Sciences Center Pittsburgh PA USA Matthew Hannibal MD Orthopedic Surgeon San Francisco Orthopedic Surgeons San Francisco CA USA Mouchir Harb MD Attending Physician Spring Valley Hospital Las Vegas NV USA Donal F. Harney MD, Dip Pain Med, CARCSI, FCARCSI Department of Anesthesiology Pain Management and Research Center University Hospital Maastricht Maastricht The Netherlands Mark A. Harrast MD Clinical Associate Professor of Rehabilitation Medicine and Orthopaedics and Sports Medicine University of Washington Seattle WA USA Syed Anees Hasan MD Spine Fellow Penn Spine Center, HUP University of Pennsylvania Health System Philadelphia PA USA Sara Ruth Sanne Haspeslagh, MD, FIPP Anesthesiologist, Pain Specialist Department of Anesthesiology AZ Sint-Augustinus Hospital Wilrijk Belgium James Heavner PhD, DVM Professor Department of Anesthesiology Texas Tech University Health Sciences Center Lubbock TX United States Johannes Hellinger MD Professor of Orthopaedics, Spine Surgeon Department of Orthopaedics Isar Klinik Munich Munich Germany
Stefan Hellinger MD Orthopaedic Surgeon, Spine Surgeon Department of Orthopaedics Isar Klinik Munich Munich Germany Steven Helper MD Physiatrist Penn Spine Fellow University of Pennsylvania Philadelphia PA USA Harry N. Herkowitz MD Chairman Department of Orthopaedic Surgery William Beaumont Hospital Royal Oak MI USA Harish S. Hosalkar, MD, MBMS(Orth), FCPS (Orth), DNB (Orth) Pediatric Orthopedic Surgeon Department of Orthopedic Surgery University of Pennsylvania Philadelphia PA USA Kenneth Hsu MD Attending Orthopaedic Surgeon Spine Center St. Mary’s Hospital and Medical Center San Francisco CA USA Raymond D. Hubbard MD Pre-doctoral Fellow Department of Bioengineering University of Pennsylvania Philadelphia PA USA Christopher W. Huston MD Consultant to Phoenix Suns, Mercury and Arizona Rattlers The Orthopedic Clinic Association Phoenix AZ USA Victor W. Isaac MD, FAAPMR Associate Director Center for Spine, Joint and Neuromuscular Rehabilitation Brentwood TN USA Zacharia Isaac MD Instructor Physical Medicine and Rehabilitation Harvard Medical School Chestnut Hill MA USA
xi
List of Contributors James D. Kang MD Professor of Orthopaedic and Neurological Surgery Department of Orthopaedic Surgery University of Pittsburgh School of Medicine Pittsburgh PA USA
Daniel H. Kim MD, FACS Assistant Clinical Professor Department of Orthopaedic Surgery The Boston Spine Group Boston MA USA
Joseph M. Lane MD Professor Orthopaedic Surgeon Orthopaedic Surgery Hospital for Special Surgery New York NY USA
Brinda S. Kantha DO Attending Physician New Jersey Institute of Minimally Invasive Spine Surgery West Orange NJ USA
David H. Kim MD Assistant Clinical Professor Department of Orthopaedic Surgery Tufts University Medical School New England Baptist Hospital The Boston Spine Group Boston MA USA
Hoang N. Le MD Clinical Instructor in Neurosurgery Department of Neurosurgery Stanford Medical Center Palo Alto CA USA
Frederick S. Kaplan MD Isaac and Rose Nassau Professor of Orthopaedic Molecular Medicine Department of Orthopaedic Surgery University of Pennsylvania School of Medicine Philadelphia PA USA
Mark A. Knaub MD Assistant Professor of Orthopaedics and Rehabilitation Penn State Milton S. Hershey Medical Center Penn State College of Medicine Hershey PA USA
Jaro Karppinen MD, PhD, BSc Professor of Physical and Rehabilitation Medicine Department of Occupational Medicine Finnish Institute of Occupational Health Oulu Helsinki Finland
Brian J. Krabak MD, MBA Clinical Associate Professor Department of Rehabilitation Medicine University of Washington Seattle WA USA
Yoshiharu Kawaguchi MD, PhD Assistant Professor Department of Orthopaedic Surgery Toyama Medical and Pharmaceutical University Toyama Japan Christina Kerger Hynes MD Attending Physician, Women’s Health Rehabilitation Rehabilitation Institute of Chicago Instructor, Physical Medicine and Rehabilitation Northwestern University Feinberg School of Medicine Chicago IL USA Byung-Jo Kim MD, PhD Associate Professor of Neurology Department of Neurology Korea University College of Medicine Seongbuk-Gu Seoul Korea Choll W. Kim MD, PhD Assistant Professor, Minimally Invasive Orthopaedic Surgery Department of Orthopaedic Surgery University of California San Diego CA USA xii
Elliot S. Krames MD Medical Director Department of Anesthesiology Pacific Pain Treatment Centers San Francisco CA USA
Kathryn E. Lee Pre-doctoral Fellow Department of Bioengineering University of Pennsylvania Philadelphia PA USA Sang-Heon Lee MD, PhD Physiatrist Research Physician Spinal Diagnostics and Treatment Center Daly City CA USA David A. Lenrow MD, JD Vice Chair of Clinical Affairs Associate Professor Department of Physical Medicine and Rehabilitation Hospital of the University of Pennsylvania Philadephia PA USA
Per O. J. Kristiansson MD, PhD Associate Professor of General Practice Department of Public Health and Caring Sciences Uppsala University Uppsala Sweden
Paul H. Lento MD Assistant Professor, Northwestern Medical School and Attending Physician, Center for Spine, Sports and Occupational Rehabilitation Rehabilitation Institute of Chicago Chicago IL USA
Jukka-Pekka Kouri MD Specialist in Physical Medicine and Rehabilitation Pain Specialist Helsinki Finland
Isador H. Lieberman BSc, MD, MBA, FRCS(C) Professor of Surgery Spine Institute Cleveland Clinic Cleveland OH USA
Richard D. Lackman MD, FACS Associate Professor and Chairman Department of Orthopaedic Surgery Hospital of the University of Pennsylvania Philadelphia PA USA Francis P. Lagattuta MD Fellowship Director LAGS Spine and Sportscare Medical Center, Inc. Santa Maria CA USA
Julie T. Lin Assistant Professor Department of Rehabilitation Medicine Weill Medical College of Cornell University New York NY USA Jason S. Lipetz MD Assistant Professor Department of Rehabilitation Medicine Albert Einstein College of Medicine East Meadow NY USA
Donald Liss MD Assistant Clinical Professor of Rehabilitation Medicine Columbia University College of Physicians and Surgeons New York NY and Attending Physician The Physical Medicine and Rehabilitation Center Englewood NJ USA Howard Liss MD Assistant Clinical Professor of Rehabilitation Medicine Columbia University College of Physicians and Surgeons New York NY and Attending Physician The Physical Medicine and Rehabilitation Center Englewood NJ USA Steven M. Lobel MD Fellow Georgia Pain Physicians Training Program Atlanta GA USA Carmen E López-Acevedo MD Associate Professor Department of Physical Medicine, Rehabilitation and Sports Medicine University of Puerto Rico School of Medicine San Juan Puerto Rico Susan M. Lord BMedSc, BMed, PhD, FANZCA, FFPMANZCA Staff Specialist, Pain Medicine Division of Anaesthesia, Intensive Care & Pain Management John Hunter Hospital New Lambton Heights NSW Australia William W. Lu PhD, MHKIE Associate Professor Department of Orthopaedics and Traumatology The University of Hong Kong Hong Kong China Keith D. K. Luk Professor of Orthopaedic Surgery Department of Orthopedic Surgery Duchess of Kent Children’s Hospital University of Hong Kong Hong Kong China Gregory E. Lutz MD Physiatrist-in-Chief Hospital for Special Surgery New York NY USA
List of Contributors Jean-Yves Maigne MD Head, Department of Physical Medicine Hôtel-Dieu Hospital Paris France
Ian Bruce McPhee FRACS (ortho) Associate Professor Orthopaedics Division of Orthopaedics The University of Queensland Queensland Australia
Gerard A. Malanga MD Director, New Jersey Sports Institute New Jersey Medical School West Orange NJ USA
Samir Mehta MD Resident Department of Orthopaedic Surgery University of Pennsylvania Philadelphia PA USA
Julie Marley PT, Dip MDT Physical Therapist Spine Center Christiana Spine Center Newark NJ USA Richard Materson MD Clinical Professor, Physical Medicine and Rehabilitation Baylor College of Medicine and University of Texas Medical School and Chairman of the Board, Institute for Religion and Health Texas Medical Center Houston TX USA Christopher J. Mattern MD Orthopaedic Resident Hospital for Special Surgery New York NY USA Eric A.K. Mayer MD Physician Productive Rehabilitation Institute of Dallas for Ergonomics Dallas TX USA Tom G. Mayer MD Medical Director, Productive Rehabilitation Institute of Dassas for Ergonomics Clinical Professor of Orthopedic Surgery University of Texas Southwestern Medical Center Dallas TX USA Frank McCabe MPT Cert. MDT Physical Therapist Physical Therapy Wallace, Glick and McCabe Physical Therapy and Fitness Montgomery PA USA Colleen McLaughlin BSRT Radiology Technologist Penn Spine Center University of Pennsylvania Health System Philadelphia PA USA
Renée S. Melfi MD Physician Physical Medicine and Rehabilitation Orthopaedic Associates of Central New York Syracuse NY USA Thomas Metkus BS Associate Professor Department of Neurosurgery University of Pennsylvania School of Medicine Philadelphia PA USA Mathew Michaels MD Consultant Georgia Pain Physicians, PC Atlanta GA USA William F. Micheo MD Chairman and Professor Department of Physical Medicine, Rehabilitation and Sports Medicine University of Puerto Rico School of Medicine San Juan USA
Michael Ray Moore MD Clinical Assistant Professor of Surgery The Bone and Joint Center The University of North Dakota School of Medicine and Health Sciences Bismarck ND USA Michael H. Moskowitz MD MPH Assistant Clinical Professor Anesthesiology and Pain Medicine University of California Davis Sacramento CA and Bay Area Pain Medical Associates Mill Valley CA USA S. Ali Mostoufi MD Interventional Physiatrist MGH Spine Center MGH Pain Clinic Boston MA USA Scott F. Nadler DO Formerly, Professor Physical Medicine and Rehabilitation Randolph NJ USA Stefano Negrini MD Scientific Director Italian Scientific Spine Institute (ISICO) Milan Italy Markus Niederwanger MD Fellow Georgia Pain Physicians Training Program Atlanta GA USA
Evan R. Minkoff DO Physician Desert Pain and Rehabilitation Associates Palm Desert CA USA
Conor W. O’Neill MD Comprehensive Spine Diagnostics Medical Group, Inc Daly City CA USA
Peter J. Moley MD Assistant Attending Physiatrist HSS Affiliated Physician’s Office Old Greenwich CT USA
Donna D. Ohnmeiss Dr.Med President Texas Back Institute Research Foundation Plano TX USA
Marco Monticone MD Researcher Italian Scientific Spine Institute Milan Italy Gul Moonis MD Assistant Professor of Radiology Department of Radiology/Neuroradilgy Division University of Pennsylvania Medical Center Philadelphia PA USA
Raymond W.J.G Ostelo PhD, PT Doctor of Epidemiology Institute for Research in Extramural Medicine (EMGO) Institute VU Medical Centre Amsterdam The Netherlands Jeffrey Ostrowski PT Physical Therapist Excel Physical Therapy Philadelphia PA USA
Ashley Lewis Park MD, FACP Clinical Assistant Professor of Medicine Department of Internal Medicine Division of Rehabilitation University of Tennesee College of Medicine Staff Physician, Campbell Orthopaedic Clinic Germantown TN USA Vikram Parmar MD Physician Opelousas General Health System Opelousas LA USA Rajeev K. Patel MD Assistant Professor Orthopaedics Department of Orthopaedics University Orthopaedic Associates Pittsford NY USA Andrew Perry MD Orthopaedic Resident University of California San Diego San Diego CA USA Frank M. Phillips MD Professor of Orthopaedic Surgery Rush University Medical Center Chicago IL USA Robert J. Pignolo MD, PhD Assistant Professor of Medicine Department of Medicine Division of Geriatric Medicine University of Pennsylvania School of Medicine Philadelphia PA USA Christopher T. Plastaras MD Assistant Professor Physical Medicine and Rehabilitation Feinberg Northwestern School of Medicine Chicago IL USA Franco Postacchini MD Professor of Orthopaedic Surgery Clinical Orthopedics University of Rome ‘La Sapienza’ Rome Italy Roberto Postacchini MD Professor of Orthopaedic Surgery Clinica Ortopedica University of Rome ‘La Sapienza’ Rome Italy Ben B. Pradhan MD, MSE Director of Clinical Research The Spine Institute Santa Monica CA USA xiii
List of Contributors Joshua P. Prager MD, MS, DABPM Director Department of Anesthesiology and Internal Medicine UCLA Pain Medicine Center Los Angeles CA USA Heidi Prather DO Associate Professor Chief, Section of Physical Medicine and Rehabilitation Department of Orthopedics Washington University School of Medicine St Louis MO USA Adriana S. Prawak DO Attending Physician and Partner Sports and Spine Rehabilitation Division Premier Orthopaedic and Sports Medicine Associates, LTD Havertown PA USA Joel M. Press MD Attending Physician Spine and Sports Rehabilitation Center, Rehabilitation Institute of Chicago and Associate Professor Department of Physical Medicine and Rehabilitation Northwestern University Feinberg School of Medicine Chicago IL USA G. X. Qiu MD Professor of Orthopaedic Surgery Department of Orthopaedic Surgery Peking Union Medical College Hospital Beijing PR China Gabor B. Racz MD, DABA, FIPP, ABMP, ABIPP Professor and Chair Department of Anesthesiology and Pain Management Texas Tech University Lubbock TX USA Kristjan T. Ragnarsson MD Professor and Chairman Department of Rehabilitation Medicine Mount Sinai Medical Center New York NY USA Raj D. Rao MD Director of Spine Surgery Department of Orthopedic Surgery Medical College of Wisconsin Milwaukee WI USA
xiv
Ryan S. Reeves MD Medical Director, Spine Team Texas Attending Physiatrist, Spine Team Texas Southlake TX USA
Terry C. Sawchuk MD Adjunct Professor Intermountain Spine Institute University of Utah Salt Lake City UT USA
Ramnik Singh MD Attending Physician Institute for Spinal Disorders Cedars-Sinai Medical Center Los Angeles CA USA
Luke Rigolosi MD Physical Medicine and Rehabilitation New Jersey Medical School University of Medicine and Dentistry of New Jersey University Hospital Newark NJ USA
Jerome Schofferman MD Director of Research and Education Spine Care Medical Group San Francisco Spine Institute Daly City CA USA
Clayton D Skaggs DC Associate Professor of Research Logan University Adjunct Instructor Department of Obstetrics Washington University St Louis MO USA
James Schuster MD, PhD Assistant Professor Department of Neurosurgery The Hospital of the University of Pennsylvania Philadelphia PA USA
Jan Slezak MD Medical Director of Northeast Pain Research Center Interventional Spine Medicine Barrington NH USA
Eric D. Schwartz Associate Professor of Radiology Department of Radiology/Neuroradiology Division University of Pittsburgh Medical Center Pittsburgh PA USA
Curtis W. Slipman MD Director, Penn Spine Center Associate Professor of Physical Medicine and Rehabilitation University of Pennsylvania Health System Philadelphia PA USA
Rinoo Vasant Shah MD, DABPMR, DABPMR (Pain), DABPM Assistant Professor Department of Anesthesiology Guthrie Clinic Horseheads NY USA
Wesley L. Smeal MD Attending Physician, Spine and Sports Rehabilitation Center Rehabilitation Institute of Chicago Instructor, Department of Physical Medicine and Rehabilitation Northwestern University – Feinberg School of Medicine Chicago IL USA
Hubert L. Rosomoff MD, DMedSc, FAAPM Medical Director The Rosomoff Comprehensive Pain and Rehabilitation Center Miami Jewish Home and Hospital at Douglas Gardens Miami Beach FL USA Renee Steele Rosomoff RN, BSN, MBA Program Director The Rosomoff Comprehensive Pain and Rehabilitation Center Miami Beach FL USA Sarah M. Rothman Pre-doctoral Fellow Department of Bioengineering University of Pennsylvania Philadelphia PA USA Anthony S. Russell MA, MBBChir, FRCP, FRCPC, FACP Professor of Medicine University of Alberta Edmonton AB Canada Bjorn Rydevik MD, PhD Professor of Orthopaedic Surgery Department of Orthopaedics Salgrenska University Hospital Gothenburg Sweden Durgadas Sakalkale MD Clinical Instructor Department of Orthopaedics and Rehabilitation Yale University School of Medicine New Haven CT USA Robert Savarese DO Physician Jacksonville Orthopedic Institute Jacksonville FL USA
Parag Sheth MD Assistant Professor of Medicine Department of Rehabilitation Medicine Mount Sinai School of Medicine New York NY USA Frederick A. Simeone MD, FACS Emeritus Professor of Neurosurgery University of Pennsylvania School of Medicine Philadelphia PA USA Alexander C. Simotas MD Assistant Professor of Rehabilitation Medicine Physical and Rehabilitative Medicine Weill Medical College of Cornell University New York NY USA Gurkirpal Singh BS, MBBS, MD Adjunct Clinical Professor of Medicine Division of Gastroenterology and Hepatology Stanford University School of Medicine Stanford CA USA
Jennifer L. Solomon MD Clinical Instructor Physical Medicine and Rehabilitation Weill Medical College of Cornell University New York NY USA Hillel M. Sommer MD, FRCPC, CSPQ, Dip. Sport Med Associate Professor Physical Medicine and Rehabilitation University of Manitoba Winnipeg MB Canada Brad Sorosky MD Clinical Instructor Department of Physical Medicine and Rehabilitation Northwestern Feinberg School of Medicine Chicago IL USA
List of Contributors Daniel Southern MD Danbury Orthopedic Associates Danbury CT USA Gwendolyn A. Sowa MD, PhD Assistant Professor of Physical Medicine and Rehabilitation Center for Sports, Spine and Occupational Rehabilitation Pittsburgh PA USA Milan P. Stojanovic PhD Director, Interventional Pain Program HMS Anaesthesia Massachusetts General Hospital Boston MA USA William J. Sullivan MD Assistant Professor Department of Physical Medicine and Rehabilitation University of Colorado at Denver and Health Sciences Centre Aurora CO USA Gul Koknel Talu MD Associate Professor of Anesthesiology Department of Algology Medical Faculty of Istanbul University Istanbul Turkey Andrea Tarquinio RN Head Nurse Penn Spine Center Hospital of the University of Pennsylvania Philadelphia PA USA Philip Tasca MD Assistant Clinical Professor of Rehabilitation Medicine Columbia University Medical Center New York NY and Interventional Physiatrist The Physical Medicine and Rehabilitation Center, PA Englewood NJ USA Santhosh A. Thomas DO, FAAPM&R Medical Director, Spine Center Co-Director, Medical Spine Fellowship Cleveland Clinic Foundation Westlake OH USA Issada Thongtrangan MD Department of Neurosurgery Stanford University Medical Center Palo Alto CA USA
Carlos F. Tirado MD Clinical Research Fellow in Addiction University of Pennsylvania Treatment Research Centre Philadelphia PA USA John E. Tobey MD Clinical Instructor, Department of Physical Medicine and Rehabilitation University of Colorado Health Sciences Center Boulder CO USA
Christophe Van de Wiele MD, PhD Department of Nuclear Medicine University Hospital Gent Gent Belgium
Douglas S. Won MD Attending Spine Surgeon Southwest Spine Institute Irving TX USA
Maarten van Kleef Head of Department of Anesthesiology and Pain Management Pain Management and Research Center University Hospital Maastricht Maastricht The Netherlands
Kirkham Wood MD Associate Professor Department of Orthopaedics Massachusetts General Hospital Boston MA USA
Daisuke Togawa MD, PhD Adjunct Staff Spine Centre Hakodate Central General Hospital Hakodate City Hokkaido Japan
Jan Van Zundert MD, PhD, FIPP Head of Multidisciplinary Pain Centre Anesthesiologist, Department of Anesthesiology, Pain Management and Research Centre, University Hospital Maastricht Maastricht The Netherlands
Jesse T. Torbert MD, MS Orthopaedic Tumour Post-Doctoral Research Fellow Pennsylvania Hospital Philadelphia PA USA
Kamen Vlassakov MD Director, Division of Orthopaedic and Regional Anesthesia Brigham and Women’s Hospital Boston MA USA
Carlo Trevisan MD Medical Specialist Surgeon in Orthopedics Clinical Orthopedics University of Milan–Bicocca Monza Italy John J. Triano DC, PhD, FCCS(C) Director Chiropractic Division Texas Back Institute Plano TX USA Mark D. Tyburski MD Physiatrist Department of Physical Medicine and Rehabilitation Spine Clinic Roseville CA USA Mohammad N. Uddin MD Pain Management Physician APAC Centers for Pain Management Chicago IL USA Alexander Vaccaro MD, FACS Professor and Co-chief, Spine Division Department of Orthopaedic Surgery Rothman Institute Philadelphia PA USA Vijay B. Vad MD Assistant Professor Department of Rehabilitation Medicine Weill Medical College of Cornell University New York NY USA
John B. Weigele MD, PhD Assistant Professor of Radiology Department of Radiology Hospital of the University of Pennsylvania Philadelphia PA USA William C. Welch MD Chief of Neurosurgery, Pennsylvania Hospital Professor of Neurosurgery Clinical Practices of the University of Pennsylvenia University of Pennsylvania Health System Philadelphia PA USA C. Y. Wen MMedSc MBBS Department of Orthopaedics and Traumatology Clinical Science Building Prince of Wales Hospital Hong Kong China Robert E. Windsor MD FAAPMR FAAPM FAAEM President Georgia Pain Physicians, PC Atlanta GA USA
Chandra S Yerramalli PhD Department of Orthopaedic Surgery McKay Orthopaedic Research Laboratory University of Pennsylvania Philadelphia PA USA Anthony T. Yeung MD Orthopedic Surgeon Arizona Institute for Minimally Invasive Spine Care Arizona Orthopedic Surgeons Phoenix AZ USA Christopher Alan Yeung MD Voluntary Clinical Instructor Department of Orthopedic Surgery University of California San Diego School of Medicine Phoenix AZ USA Way Yin MD Medical Director Spinal Diagnostics; Interventional Pain Management Interventional Medical Associates of Bellingham, PC Bellingham WA USA Faisel M. Zaman MD, FAAPMR&ABPM Interventional Physiatrist Intermountain Spine Institute Affiliate Faculty, University of Utah Division of Physical Medicine and Rehabilitation Salt Lake City UT USA James F. Zucherman MD Medical Director Orthopedic Spine Surgeon St Mary’s Spine Center San Francisco CA USA
Beth A. Winklestein PhD Assistant Professor of Bioengineering and Neurosurgery Department of Bioengineering University of Pennsylvania Philadelphia PA USA xv
Preface
Two decades ago, the notion that the variety of disciplines that practice spine care would universally embrace the concept of a comprehensive algorithmic approach was an anathema. While this methodical, stepwise approach had been practiced by the spine surgical community the other specialties treating patients with spinal disorders have had a haphazard orientation. Some disciplines offered a singular technique, which was used to treat all painful conditions, while others used ‘a little of this, and a little of that’. As the years passed, a variety of influences have irrevocably changed the perspective that conservative care cannot be appropriately integrated with the surgical approach. Among the propelling factors have been cohort and randomized studies of patients undergoing medical rehabilitation and interventional spine care; an explosion in the number of physicians who practice interventional spine/pain medicine; education of the lay community, which has been accelerated by the internet, and their desire to pursue the least aggressive treatment available; and malpractice lawsuits predicated on surgery having been performed without adequate conservative treatment. This book represents the culmination of the growth and development of the diagnosis and treatment of patients with spinal pain. Indeed, the composition of editors underscores the importance this integrated approach has taken. Our focus has been to write about algorithmic approaches for a variety of conditions. A basic premise and a central theme of this text is that certain disorders require immediate surgery, but most
can be managed with medications, therapy and possibly injection or other percutaneous procedures. We want the reader to understand when surgery can be delayed, when it should be avoided, and when it is required. It is also our hope that this text will provide a stepwise approach for those patients that have disorders that fall under the former two situations. Some of our algorithms are universally accepted, while others represent the idiosyncratic approach of the author. In fact, there are several instances in which the same problem is attacked in a different way by two authors. Since the science of medical rehabilitation and interventional spine care is evolving, it is no surprise that spine practitioners may have different views regarding which tests to request, the order of diagnostic and treatment interventions and which therapeutic alternatives are best. However, within that expected and reasonable diversity of opinion a central belief should be conveyed to the reader. Patients deserve the least aggressive care feasible, but the alternatives must be chosen by the individual spine practitioners’ interpretation of the literature and their clinical experience. When this is accomplished, an algorithmic approach can be offered that adequately balances the potential outcomes and known side effects or complications. As our understanding of painful spinal disorders evolves we should expect that most patients with a particular disorder will be treated in a similar fashion and we believe this textbook places us closer to this penultimate goal. Curtis W. Slipman 2007
xvii
Acknowledgments
The development and production of a textbook of this scope is an enormous task and requires the assistance of numerous individuals. My appreciative comments begin with my residency at Columbia Presbyterian Medical Center and its residency director, Erwin Gonzalez. During the past 24 years he has served as a mentor and enthusiastic supporter. In 1992 when I was recruited to develop the Penn Spine Center, it was Alfred Fishman who had the vision, political prowess and guidance to insure that interventional physiatry would thrive in an academic setting. Concurrently, Ron Wisneski, whose tenure of chief of orthopedic spine surgery temporarily overlapped with my presence at The University of Pennsylvania, helped formulate the idea of an algorithmic approach to neck and back pain. Since my arrival at Penn an exponential growth in my education of spine care occurred. Richard Herzog provided the foundation and nuances for the interpretation of radiological studies, Ron Wisneski and Ed Vresilovic shared the surgical perspective and were open to learning and employing a Physiatric perspective. Of course there were and remain many physicians with whom I have practiced that have a played a key role in my understanding of spinal disorders. Among them are Lori Loevner, Evan Siegelman, Robert Grossman, Murray Dalinka, Robert Hurst, Paul Marcotte, David Lenrow, Fred Kaplan, Mark Ellen, Larry Chou, Dawn Elliot, and Beth Winklestein. Several physicians who practiced outside of Penn were instrumental in the growth of the Penn Spine Center and in my spine education including Fred Simeone and Giancarlo Barolat. Perhaps the single most valuable contribution to my understanding of spine care comes from the Penn Spine Center Fellows; Elliot Sterenfeld, Chris Huston, David DeDanious, Randy Palmitier, Jason Lipetz, Howard
Jackson, Zac Isaac, Atul Bhat, Russell Gilchrist, Mike Frey, Phil Tasca, Sarjoo Bhaggia, Omar el Abd, Michael DePalma, Raj Patel, David Chow, Frank Bender, Carl Shin, Amit Bhargava, Aleya Salem, Victor Isaac, Faisel Zaman, Serge Menkin, Steven Helper, and Paul Singh. Their enthusiasm, intellect and hard work have created the opportunity to see a large volume of patients, conduct research and refine my views on interventional spine care. There have been a few individuals who as medical students shared their time, enthusiasm and intellect who deserve recognition, Larry Chou, Chris Plastaras, Alfred Campbell, Catherine Loveland-Jones and Jason Berke. My current chairman, Richard Salcido, and a number of staff members at the Penn Spine Center were particularly supportive of the time and effort I needed to devote to the writing and editing of this text including Andrea Tarquinio, Colleen McLaughlin and Lynette Rundgren. The editorial staff at Elsevier, Joanne Scott, Amy Head, Cecilia Murphy, Susan Pioli, Dolores Meloni and Rolla Couchman deserve enormous thanks for their dedication, attention to detail and perseverance. Without their effort and guidance this book would not exist. I want to thank the physicians who have been the pioneers and leaders in interventional spine for the last two decades. These individuals created the opportunity all of us are now enjoying. Join me in extending appreciative thoughts to Scott Nadler, Rick Derby, Nic Bogduk, Jeff Saal, Stan Herring, Joel Press, Charles Aprill, Guisseppe Bonaldi, Paul Dreyfus, and Stu Weinstein. Finally a deep heartfelt thanks to the co-editors of this text, Rick Derby, Fred Simeone, Tom Mayer, David Lenrow, Kingsley Chin, Salahadin Abdi and Larry Chou. Their input has been invaluable and their energy irreplaceable. Curtis W. Slipman 2007
xix
To Jared
PART 1
GENERAL PRINCIPLES
Section 1
Introduction
CHAPTER
Past, Present, and Future of Interventional Physiatry
1
Richard Materson
THE PAST One might inquire what a history and philosophical chapter is doing in an evidence-based clinical textbook. Interventional spine procedures by physiatrists at first glance seem simply to be an outgrowth of physical medicine, a clinical right turn justified by new information similar to other changes in medical practice such as interventional cardiology. But the role of the practitioner is so fundamentally changed from previous roles that a deeper inquiry is invited. How do such striking ‘about-faces’ occur in medicine? What and who promotes these changes and how are they accomplished? After all, a hospital-based practitioner can’t simply announce one day that he or she is going to have entry to a surgical suite or intervention room and do new procedures. The author is grateful to the many early members of the Physiatric Association of Spine Sport and Occupational Rehabilitation (PASSOR) who were willing to e-mail to the author their observations regarding how they became involved is this movement, who influenced them, and in which directions they believe we are evolving. Most of organized medicine, including its Boards, Academies and educational hierarchy, justify their existence by including words such as ‘in the public interest …’ in their constitution or bylaws preamble. None should believe that such baser needs such as ego, power, control, and economic well-being and keeping a practice away from ‘the other guy’ do not play a role as well. The trick to good organizational management and maintenance of the voluntary system of medical accreditation is to be sure the balance favors public good a great deal more than the practitioner benefit. The development of interventional physiatry represents a model study of how change is reasonably brought about in medical practice. If one reviews the history of the practice of medicine in the United States since Flexner’s report,1 the complex story of organized medicine is found to be the string in the supersaturated sugar solution (the great mix of knowledge, attitudes, and practices) allowing the formation of rock candy (the roles of the various medical and surgical specialties). An approach through organized medical channels is the ‘way’ to get desired changes. Change does not occur quickly, nor particularly smoothly; however, the system seems to work. Perseverance pays. Such has been the case for interventional physiatry. Osler in medicine, and Halstead and others in surgery are names known by every internist and surgeon. These pioneers opined that 4 years of matriculation through even the best medical school curriculum was inadequate to teach the volume and complexity of knowledge, skills, and behaviors required to properly care for patients with significant illness. Postgraduate medical education at the bedside was required, and the development of a capacity for life-long professional learning. During the first 20 years of the twentieth century there was no such thing as a physical medicine and rehabilitation doctor. World
War One, however, produced sufficient casualties, many with musculoskeletal injuries, that would become chronic and which seemed to improve when treated with physical modalities including hydrotherapy and therapeutic exercise and newly harnessed portions of the electromagnetic spectrum. With the lead of the American Medical Association in the 1915–21 time frame, a group of physical modality experts were called together to see how more physicians might learn about and put to use these procedures. The AMA Board of Trustees approved this group, called the American Congress of Physical Therapy, in September 1921. It was not to be the start of a new specialty, but rather a task force to enhance knowledge and skills. It consisted of physicians from medicine, most of whom were attached to academic centers and who had studied and advocated for these methods. The AMA had previously and subsequently stimulated and assisted the creation of the American College of Surgeons (ACS) and the American College of Physicians (ACP) and several surgical and medical specialty organizations. With the American Association of Medical Colleges (AAMC) and the Association of Teaching Hospitals, the AMA, ACP, and ACS, the idea of credentialing individuals who were willing to subject themselves to additional postgraduate education, training, and experience and who were willing to put their knowledge and skills to a test, thereby identifying properly trained ‘specialists’ for the public. The medical schools came under the supervision of the Liaison Council for Medical Education (LCME), the residencies under residency review committees (RRCs) appointed jointly by the AMA section councils and specialty societies and supervised by the Accreditation Council on Graduate Medical Education (ACGME) and the American Board of Medical Specialties (ABMS), continuing education led by the Council on Medical Specialty Societies (CMSS). The various liaison groups had representation from practitioners, academicians, hospitals, boards, and medical and surgical academies. When federal dollars became prominent in support of medical education and practice, government representatives were added, but control was always in the hands of physician volunteers who were either elected by or appointed by their peers to represent them. In its earliest days practitioners of physical medicine often shared an interest in the newly developed area of ionizing radiation. In 1923, the American College of Radiology and Physiotherapy became the first physical medicine society. As radiology established itself as a separate discipline, the organization’s name was changed to drop radiology; however, the first journal was titled the Archives of Physical Therapy, X-ray and Radium. In 1930, the organization became the American Congress of Physical Therapy and in 1945, as the practice of physical therapy became its own discipline, the name changed to the American Congress of Physical Medicine. By 1954, the World War Two-developed team concept of care, espoused by Howard Rusk and George Deaver, caused another name change to Physical Medicine 1
Part 1: General Principles
and Rehabilitation. By 1967, the ‘team concept of rehabilitation’ devotees were of sufficient number to cause the name to change to the American Congress of Rehabilitation Medicine. Their journal became the Archives of Physical Medicine and Rehabilitation. Upon action from an AMA advisory council on medical specialties, on June 6, 1947, eleven physiatrists became the first American Board of Physical Medicine with Krusen as its first chairman and Zeiter as vice-chairman. A few physiatrists were ‘grandfathered’ and a total of 103 became the first listed Board Diplomats. In 1949 the board name was changed to the American Board of Physical Medicine and Rehabilitation following the trend towards rehabilitation. The group that was to become the American Academy of Physical Medicine and Rehabilitation (PM&R) began in 1938–39 as an invitation-only membership of 42 physical therapy physicians with an intent of limiting membership to 100 physicians. After 1952, all Diplomats of the American Board of Physical Medicine and Rehabilitation were invited to become members. In 1957, a conference was held to determine the proper roles of the Academy versus the American Congress. The Congress was to control the journal, to provide interdisciplinary rehabilitation education, and to reach out to nonphysiatrist physicians interested in the field. The Academy was to bring their member physiatrists into closer collaboration with other physician peers and concentrate on physiatric education and policy. The Academy was to represent the field in the AMA House of Delegates. Later, after considerable negotiation, the Archives of PM&R ownership were split by the Congress with the Academy for a purchase price of ‘$1.00 and considerations.’ Editorial Boards represented each organization under an editor-in-chief. As the Academy grew, and as the various allied professions became more independent with policy interests different at times from physicians, physiatric membership in the Congress declined. Several attempts were made to work out ways to stay allied and share a common central office but a split was inevitable. The Congress now is independent of the Academy, smaller in membership and has refocused itself to interdisciplinary rehabilitation research. The Council of Academic Societies (CAS) of the Association of American Medical Colleges in 1967 rejected the American Academy of Physical Medicine and Rehabilitation as too broadly based to be a constituent member but at the same time recognized the newly formed Association of Academic Physiatrists (AAP) to represent undergraduate and graduate medical education interests and academic policy. The history of the specialty of Physical Medicine and Rehabilitation is covered in detail elsewhere and should be reviewed for a more complete story.2–6 Elkins, Knapp, Bennett, Bierman, Kovacs, Molander, Coulter, Zeiter, Krusen Ewerhardt and others were among the originators of the field followed by Rusk, Deaver, Johnson, Lehman, Kottke, Stillwell and many more than can be mentioned here. Review will be rewarding to observe how a small group of dedicated physicians gave much volunteer time and attention to the multiple facets necessary for growth of a medical specialty. One should appreciate that what began as a ‘physical medicine’oriented body of knowledge transitioned to a medical rehabilitation orientation over time. Physical medicine was never ‘lost;’ it was simply less visible with the overriding mass appeal of rehabilitation as popularized by Rusk.7 New York philanthropist Bernard Baruch played a major role in stimulating development of 12 departments that matriculated nearly 60 early physiatric pioneers. Baruch convinced President Truman of the field’s contribution to the war and postwar effort. The President ordered military medical authorities to embrace the field. Civilian interest followed. Large infusions of federal dollars from the Medicare program followed. During the DeBakey era, heart disease and stroke held the top-tiered research support position. This funding resulted in increased medical rehabilitation demands and 2
funding at a time of virtual nonfunding for musculoskeletal disorders and research. These currents influenced the practitioners and their representatives in the American Academy of Physical Medicine and Rehabilitation. Those physicians with a more physical medicine orientation often complained of inadequate attention and resource sharing in the Academy. In general, the physical medicine oriented physiatrists gravitated towards care of more acute neuro-musculo-skeletal disorders including ever more ubiquitous spine related pain. In the military, the training programs focused on physical medicine, with rehabilitation to occur in the Veterans Administration system. In this setting, and in the growing private musculoskeletal practice setting, the physiatrist saw acute patients and often provided full diagnostic and therapeutic care, referring to other specialties as was appropriate. This conflicted with the rehabilitation model in which practitioners were describing their domain as ‘the third phase of medicine after preventive medicine and acute care.’ In the latter paradigm, the physiatrist did not have access to the patient except upon referral from a physician or surgeon who were the primary practitioners. In preparation of this chapter, a call was sent to founding PASSOR members to identify the influences upon them to become members. Perhaps the most frequently cited was the desire to become a primary practitioner for musculoskeletal patients. They were influenced by orthopedists such as James Cyriax, Arthur White, John Fromoyer, Malcolm Pope, W.H. Kirkaldy-Willis, and Alf Nachemson and sometimes encouraged to become ‘nonoperative orthopedists’ in lieu of physiatrists. They were also influenced by independent minded physiatrists whose credentials in physical medicine were rich and who were expert in use of modalities and therapeutic exercise, clinical kinesiology, and the newly developing field of electrodiagnostic medicine such as V. Lieberson, Carl Granger, Justus Lehman, Ernest Johnson, Myron Laban, Erwin Gonzalez, Ian MacLean, Joe Honet and others. Henry Betts was identified as a facilitator sympathetic to growth in this arena. Newer generations of PASSOR members were greatly influenced by Jeffrey and Joel Saal and their associate Stan Herring. These physiatrists were often themselves sportsmen whose interests gravitated in this direction. To this group add those physiatrists whose practices included large numbers of injured workmen. Many of these patients suffered spine-related pain disorders. The musculoskeletal physiatrists included also those who followed the work of Janet Travell and Dave Simons in dealing with the clinical entity of myofascial pain syndrome and those whose interests gravitated to arthritis and related disorders. Many of these physicians tended to feel that the Archives of Physical Medicine and Rehabilitation, especially those issues sponsored by the American Congress of Rehabilitation Medicine, did not adequately represent their spine and musculoskeletal interests and did not believe the Archives was well regarded by spine and sports peers in medicine. The policy issues facing the main field of rehabilitation, which were primarily government regulatory-related, were of little concern to the physical medicine practitioner who was not practicing in rehabilitation facilities but was more often office or clinic based. Furthermore, the educational offerings of the Academy were felt to slight the need for both basic and advanced material from the musculoskeletal area, especially spine and sport, and not to pay adequate attention to the office practice needs of these physiatrists. The earliest and common practice model, which continues today, was for the physiatrist to associate with an orthopedist or orthopedic group practice, becoming the member who did not perform surgery, but attended to diagnostics and postoperative care. Government and insurance bodies tended to ‘bundle’ preoperative care, surgery, and limited postoperative care into one standard surgical fee. The surgeon now had a financial incentive to pass on care to another specialist. Furthermoe, additional members in a group practice made investment in practice-owned diagnostic
Section 1: Introduction
imaging equipment and laboratories inviting and increased the frequency of use of the equipment. As physiatrists became competent in interventional spine procedures, more struck out on their own or became part of single-specialty (physiatric spine medicine) practice groups. Several academic programs became involved. Orthopedists and family practitioners laid claim to sports medicine, although several physiatrists have become professional and school team physicians and are highly regarded for their work. Physiatrists have become increasingly attractive to insurers and re-insurers as the physicians of choice for industrial musculoskeletal injuries and post-trauma soft tissue injuries. These physicians offer thorough history and physical examination, astute diagnostic capabilities, nonsurgical (read less expensive) remediative and rehabilitative care, ability to collaborate when surgery is indicated, and disability evaluation and management all in one place. The capacity to perform electromyography and diagnostic and therapeutic blocks in carefully selected patients was an added benefit. During the 1980s the Academy of PM&R attempted to address these musculoskeletal and related issues by permitting the development of special interest groups (SIGs) which became responsible for developing education appropriate to their interest and promoting policy concerns to Academy Board attention. During the annual meeting, the Academy met the first part of a week, the Congress the second part, with the middle weekday for supposed integrated blend. Time and organizational collaboration was inadequate to meet the needs of either party and disenchantment grew. There was even consideration of development of a new group outside of the Academy of PM&R to represent the interests of these musculoskeletal-oriented physiatrists. At the same time, the Academy Board, and in fact much of organized medicine, was involved in a great debate regarding subspecialization and the credentialing of subspecialists. To the degree that groups identified special added competence, the issues of territoriality appeared, i.e. limitation to one kind of practitioner or open to members of vorious Boards of Specialty. Added to this were issues of curriculum content definition and development of a critical mass of expert educators and clinical facilities to achieve the educational standards. Would specialization prevent the general Diplomat from practice in the defined area? Would that in effect drive out competition and be inflationary? Would subspecialty educational offerings be available to all (generally making the offerings entry level) or be at advanced level, good for the specialist but beyond benefit to the generalist? Would an added credential become a requirement for hospitals and certifying organizations to allow privileges or access to practitioners or for courts to recognize expertise? The Academy (and medicine) resolved these issues differently in various areas such as pediatric rehabilitation, electrodiagnostic medicine, spinal cord injury, and head injury rehabilitation. There was waxing and waning of support for the musculoskeletal specialization at the Academy Board level depending on the relative representation of rehabilitation primary versus physical medicine primary practitioners on the Board. Quick fixes allowing SIGs greater access to program content met with resistance from program committee members who felt their control and ability to meet their responsibilities challenged. At the same time, division over ownership and editorial control of the Archives of PM&R raged on at a time when the two organizations were growing ever more apart in their aspirations and needs. In 1983, the Richard and Hinda Rosenthal Foundation indicated its wish to identify physiatrists less than 50 years of age who would be outstanding leaders in the clinical nonoperative care of low back pain. An AAPM&R Rosenthal Lectureship was created with Myron M. LaBan, MD, as the first recipient and Jeffery A Saal, MD, as the
second. Both of these physiatrists were strongly identified with the movement to enhance the place of spine, sports and occupational rehabilitation in the field. The Rosenthal award served not only to recognize outstanding and innovative practitioners such as the two mentioned and those Rosenthal awardees who followed, but indicated real interest on the part of the many physiatrists who overflowed the meeting rooms to hear these lectures. The Academy leadership had to be impressed with the quality of the presentations and the professionalism of those who were listening. This was not simply some start-up group of malcontents, but rather a real wave of practitioners with like clinical interests. Jeff Saal, MD, became the first physician at Stanford University to begin facet and image-guided epidural spinal injections. By 1987, he, together with his brother Joel and associate Stanley Herring, MD, began to teach two-day spinal injection courses which attracted a larger number of applicants than could be accommodated. This type of course was integrated into Academy offerings. Short courses were recognized to be inadequate to gain competency but served as an introduction and facilitated the need for curricular design and Fellowship development. In 1989, the Saal brothers again made a major contribution to understanding the rationale for antiinflammatory use in disc disease by describing disc disease treatment with epidural steroids and stabilization exercises and elaborating on the inflammatory enzymes involved (PLA2). This attracted great additional interest in interventional physiatry. The new data were particularly welcome in an era of ‘low back losers’ and Nachemsen’s articles regarding the great divergence of surgical rates between the United States and Sweden and describing the long-term natural course of disc disease. By now the journal Spine was becoming well recognized as a place to publish spine-related material. From 1983, a succession of Academy of PM&R Presidents (Grant, Kraft, LaBan, Materson, Gonzalez, MacLean) were particularly impressed with the need to reach out to their colleagues, pressing this movement, and were themselves interested in musculoskeletal medicine practice. Drs Opitz, de Lateur, Christopher, and Demopoulos were interspersed with these others and, while personally more rehabilitation medicine oriented or balanced, paved the way for ascendancy of this area from a SIG to a higher-level entity within the Academy.
THE PRESENT With the urging of LaBan, Honet and Gonzalez, Saal and others, the concept of making this group an official body of the Academy with the ability to raise dues, put on educational offerings, and self-govern became real with the official creation of the Physiatric Association of Spine, Sports and Industrial Rehabilitation (PASSOR) in 1993 with Jeff Saal, MD, as its first president. A three-year probationary period for new councils was defined in the Academy Bylaws. PASSOR Founding members and Charter members are listed in Table 1.1 and Table 1.2. The Founding members in particular all played important roles in getting the organization established, supported the educational programs and special courses as organizers and faculty, took leadership in the definition of a Fellowship curriculum, contributed to definitions for proper billing and procedure codes for this subspecialty, and represented the subspecialty to outside organizations and journals. They also contributed to the writing of the PASSOR Constitution and Bylaws. Worried that feisty PASSOR leaders might lead a movement to ‘jump ship’ from the Academy if their needs were not immediately met, the then Academy president appointed Joe Honet and Dick Materson, former Academy presidents, to an Advisory Board for PASSOR and Myron LaBan as a Board Liaison. Their job was to see that ‘cooler heads’ prevailed and that PASSOR was given good information on the best strategies to assure its needs were met. As an 3
Part 1: General Principles
Table 1.1: PASSOR Founding Members
Table 1.2: PASSOR Charter Members
Jeffrey A. Saal, MD, Founding Chairman
Terence P. Braden, III, DO
Richard P. Bonfiglio, MD
Mark Steven Carducci, DO
Robert S. Gamburg, MD
James P. Foydel, MD
Steve R. Geiringer, MD
Michael Fredericson, MD
Erwin G. Gonzalez, MD
Kenneth W. Gentilezza, MD
Peter A. Grant, MD
Michael C. Geraci, Jr., MD
Andrew J. Haig, MD
Jerel H. Glassman, MPH, DO
Stanley A. Herring, MD
Richard A. Goldberg, DO
Gerald P. Keane, MD
Robert S. Gotlin, DO
Francis P. Lagattuta, MD
Robert Iskowitz, MD
Edward R. Laskowski, MD
John Keun-Sang Lee, MD
Joel M. Press, MD
Aaron M. Levine, MD
Joel S. Saal, MD
Howard I. Levy, MD
Curtis W. Slipman, MD
Donald Liss, MD
Barry S. Smith, MD
Howard Liss, MD William James Pesce, DO Bernard M. Portner, MD
attendee at a majority of the subsequent board meetings, this author will testify as to the maturity, wisdom, professionalism, and dedication of the founding officers and those leaders who have followed to this date. With Jeff Saal, MD, as Founding President of PASSOR and Erwin Gonzalez his successor, administration of PASSOR and its transition to a fully functioning academic organization proceeded at a remarkable pace, withstanding the trials and tribulations of meeting the individual desires of its well ego-defined Board personalities. A dues structure was necessary in order to put on programs, develop and disseminate academic and marketing materials, enhance membership, promote research, and reward visiting faculty for contributions. An initial dues of US$300 per member per annum was agreed upon to which would be added the revenues from the successful and oversubscribed cadaver courses on injection techniques (now named the PASSOR Spinal Procedures Workshop Series) and annual meetings fees. Disputes regarding the size of the economic commitment of membership and its effect on both PASSOR membership and Academy membership numbers, and access of PASSOR materials and educational events to non-PASSOR Academy members caused animated debate but were resolved. AAPM&R Bylaws stated Councils could self-govern; however, all policy and procedure were required to be consistent with Academy policy and subject to their overall approval. The PASSOR Board controlled finances, but dues were collected and finances reviewed and approved at Academy Board levels. Subsequent PASSOR presidents (see Table 1.3, PASSOR past presidents) each identified major areas of emphasis for their presidential years. As frequently happens in similar organizations, discussion began to consider lengthening the presidential term to 2 years to allow task completion, as presidents discovered the tasks were great and the time short. (A single-year term prevailed, encouraging presidential efficiency). As PASSOR members demonstrated their ability to plan and conduct highly valued educational offerings for the annual AAPM&R session, they were allocated additional program time and responsibility, evolving towards greater control of all musculoskeletal offerings. Aside from standard lectures and symposia, clinical demonstrations were scheduled and some (such as joint examination) videotaped for future use. Topics were purposefully varied so that sports 4
Stephen R. Ribaudo, MD Robert D. Rondinelli, MD, PhD Sridhar V. Vasudevan, MD John C. Vidoloff, MD
medicine and industrial medicine topics could be interspersed with those dealing with the spine (which was always highlighted by the Rosenthal Lecture presentation). Typical of similar organizations, a committee structure was seen as desirable. Committees dealing with Constitution and Bylaws; Nominations and Membership were first, followed by Education and Program, Research, Marketing and Communication, Medical Practice, and Information Systems. Unlike too many other organizational committees, PASSOR members served faithfully and enthusiastically, with appropriate and timely reports requiring careful management of board meetings to remain on course and on time. The presidents rose to the occasion so that motions were acted upon, either being
Table 1.3: PASSOR Past Presidents Jeffrey A. Saal, MD
1993–1994
Erwin G. Gonzalez, MD
1994–1995
Joel S. Saal, MD
1995–1996
Joel M. Press, MD
1996–1997
Robert E. Windsor, MD
1997–1998
Andrew J. Cole, MD
1998–1999
Barry S. Smith, MD
1999–2000
Gerard A. Malanga, MD
2000–2001
William F. Micheo, MD
2001–2002
Bruce E. Becker, MD
2002–2003
Section 1: Introduction
approved, disapproved, or tabled, and with meaningful but limited debate encouraged. This was carried out efficiently and with good humor, with a minimum of bruised egos, which can be a part of such undertakings. A review of the board meeting minutes, minutes of telephone conferences, annual meetings, and reports to members demonstrate a continued thread of progress of important PASSOR business. This was facilitated by outstanding administrative support in the person of Dawn M. Levreau, staff liaison assigned by Academy Executive Director Ronald A. Henrichs, CAE. Ms. Levreau was an Illinois State University graduate with a BS in economics and a minor in Speech Communication who began work at the Academy in April, 1994. Her educational background, and 12 years of experience in association management, made her an invaluable contributor to PASSOR growth. Those who serve in volunteer medical organization roles recognize just how important good staffing is to an organization’s success. Board and Committee and Task Force packets were prepared in orderly fashion, agendas planned, meetings, speakers, meeting and exhibit space planned and carried out with flexibility and positive attitude. The Academy board, other councils, committees, and staff developed a pride in their work with PASSOR and sparked member enthusiasm with benefits. Rarely do members speak up when things go well in organizations; rather, their loud protests are heard if someone is perceived to ‘muck up.’ In PASSOR’s history, praise for leadership and staff assistance has been a constant. PASSOR members became interested in defining a model musculoskeletal curriculum and muscuoskeletal physical examination competencies for use in Fellowships and generally in postgraduate PM&R training programs. Evidence of a generally unsatisfactory low level of history taking and physical examination skills observed at Fellowship entry has propelled this into a major project. Plans to educate the instructors, identified in collaboration with the Association for Academic Physiatrists, were seen as a precursor to organizing curricula and instructional materials. A traveling Fellowship was proposed and is being explored so that a Fellow might gain from the varied strengths of more than one teaching program. So as not to tread on prerogatives of credentialing bodies, RRC, and Boards, these materials were seen as approaches or guidelines rather than requirements for certification. Since fellowships were not formally defined, Dr. Slipman, in his capacity of Chair of the Education Committee of PASSOR, developed the concept that a single credible reference source was necessary for residents who wished to seek elective fellowships of value. Together with committee member Terry Sawchuk he produced the first resident’s Fellowship Guide. Rob Windsor subsequently recognized the need to differentiate between Fellowships PASSOR recognized and those which it did not. Modest criteria for PASSOR recognition were set but the idea was set in motion that all Fellowships were not created equal. More recently, Jason Lipetz, in his role as Education Committee Chair, further raised the bar, as the entry requirement includes scholarly criteria (publications and scientific presentations). These materials were developed and disseminated and have become a valuable resource for trainees. PASSOR promulgated its criteria for Fellowship Directors and model curricular content of fellowships. Programs could voluntarily supply information for the guide but PASSOR found itself incapable of policing the accuracy of the data even if it were desirable to do this. Nevertheless, the guide has been highly valued by residents exploring such programs and informal truth-telling networks developed by resident’s ‘circuits’ complemented the guides. Issues of practice privileges at hospitals and institutions began to develop, with some physiatrists denied privileges. This spurred investigation of formal subspecialization credentials through the RRCs, the Boards, and the ABMS. Subspecialization is a complex issue as previously alluded to in this chapter dealing with
curriculum, capacity, means of credentialing, and its effect on others and the public. Further pursuit by PASSOR members is active, especially in the sports medicine arena. Confusion over the meaning of, pronunciation of, and marketing usefulness of the term physiatrist has come up recurrently. A ‘naming’ organization was hired to study the issue and present choices for new name consideration and adoption. Observations of member’s practices and member interviews and polls were carried out with no real consensus. Older members preferred to stay with ‘physiatrist,’ younger members wished a name change. ‘Externist,’ ‘orthomyologist,’ ‘orthologist’ and others were discussed. The name was to apply to muscuolskeletal-interested physiatrists, not replace ‘physiatrist.’ The PASSOR board agreed that 90% of the members should favor a change and polls were taken. Response was never adequate to be determinative, and in the interim, marketing could not be delayed. With time and exposure, more members seemed to be comfortable with ‘physiatrist.’ The AAPM&R Board decided to dip into reserves and launch a major marketing program for the field. After considerable discussion the PASSOR Board decided also to invade reserves and make a major financial and creativity contribution to the effort. The Academy Marketing and Communication staff was geared up for the effort and PASSOR members made outstanding contributions to brochure development, newspaper inserts, speaker bureaus, and development of desktop office marketing materials aimed at patients, medical colleagues, insurance companies, and adjusters. A USA Today insert was highly regarded. The program was a remarkable success. The PASSOR goal was to identify the physiatrist as the physician of choice (experts) for functional musculoskeletal rehabilitation. Drs K Ragnarsson and Joel Press played major roles. Education has always been a mainstay of PASSOR. Officers and members generously gave of their time to produce AAPM&R annual meeting muscuoskeletal programs and demonstrations. Mid-year advanced-level courses were offered with varied success in attracting attendance despite the high order of materials and lecturers. An exception was the PASSOR Spinal Procedures Workshops Series that was sufficiently popular to be offered at or about the time of the Annual AAPM&R meeting and at mid-year on a regional basis. Joel Press started the idea of a special bibliography with a sports topic while he chaired the first education committee. The work continued through Curtis Slipman’s chair of the committee and the two served as the editors of the final product. Following Brian A Casazza, MD, and Jason Lipetz and others, the medical education committee saw to the development of bibliographies regarding major musculoskeletal topics including Lower Extremity, Lumbar Spine, and Cervical Spine as the initial three. All Fellowship Chairs are to review and contribute to these documents. The bibliographies were placed in the PASSOR website as the new millennium brought PASSOR to the cyber-education age. Musculoskeletal and EMG case studies were added after the pioneering contributions of Ian C. MacLean, MD, to make the EMG case studies available for this methodology. These continue to be contributed by Jason Lipetz, MD, and his medical education committee members who have also attempted to add a cyber journal club to the offerings. The Fellowship Guide and other references were also made available online. Informally, PASSOR members contributed to the Academy’s cyclic Study Guide sections promulgated through the Academy of PM&R’s Medical Education Committee (MEC). They also contributed to the Resident and Practitioner Self-Assessment materials published by the Academy’s MEC subcommittee on self-assessment (SAE-R and SAE-P). Earlier, some papers authored by PASSOR members were developed and distributed as educational mini- monographs; however, this has been discontinued. PASSOR Educational Guidelines for the 5
Part 1: General Principles
Performance of Spinal Injection Procedures was produced and additional education guides are planned. Promulgation of ‘practice guidelines’ was considered and rejected for a myriad of reasons including copyright and legal issues as well as an inability to keep such papers current. Collaboration with the information steering function of the Agency for Health Care Research and Quality (AHRQ – formally the Agency for Health Care Policy Research [AHCPR] of the Department of Health and Human Services) and other organizations such as the American Association of Electrodiagnostic Medicine and The American Academy of Neurology was considered more appropriate for practice guidelines. Several coalitions of spine and musculoskeletal societies developed including the National Association of Spine Societies (NASS), the Council of Spine Societies (COSS), and the Joint Commission on Sports Medicine. PASSOR members regularly contributed in ever increasing numbers to the peer-reviewed medical literature in the Archives of Physical Medicine and Rehabilitation and other journals. After considerable investigation and debate a formal affiliation with and sponsorship of the Clinical Journal of Sports Medicine began with Stuart Weinstein, MD, as Senior Editor. However this affiliation was dropped at the end of the first contract term in 2003. PASSOR paid the subscription price for its members during the contract. The PASSOR Spinal Procedure Workshop Series and the musculoskeletal and sports education courses were the paradigm of PASSOR members giving extraordinarily generously of their time and personal
expertise to take learners through a well-devised curriculum and practical clinical demonstrations and experience. These courses were organized and carried out by PASSOR members with the capable assistance of Academy staff. Professional meetings companies expert in the delicate arrangements for such courses helped arrange the cadaver courses. Space does not permit listing all of these outstanding educators; however, a few are mentioned here: Curtis Slipman, Jeff and Joel Saal, Robert Windsor, Andrew Haig, Andrew Cole, Gerard Malanga, William Micheo, Francis Lagattuta, Paul Dreyfuss, Jeffrey Young, Stanley Herring, Stuart Weinstein, Scott Nadler, Heidi Prather, Jeff Pavell, Anthony Cucuzzella, Bruce Becker, Joel Press, Michael Furman, David Bagnall, Jay Smith, Sheila Dugan, Barry Smith, Ann Zeni, Venu Akuthota, Lori Wasserburger, Kurt Hoppe, Susan Dreyer, Terry Sawchuk, Frederick McAdam, Erwin Gonzalez, Jerrold Rosenberg, Krystal Chambers, Christopher Huston, Edward Rachlin, James Atchison, and Joseph Feinberg. Research was recognized as the key to successful incorporation of this subspecialty into accepted practice. This needed to be evidencebased, primarily clinical, research. PASSOR elected to support the newly reformatted Foundation for Physical Medicine with a significant donation from reserves and personal commitment to a challenge grant by all Board members. PASSOR tightened its criteria for award of the Rosenthal Awardees (Table 1.4 – Rosenthal Lecturers). Recently, the Saal Family Foundation has announced its sponsorship of spine research. A PASSOR Research Grant Award for US$10 000
Table 1.4: Richard and Hinda Rosenthal Foundation Lecturers The Richard and Hinda Rosenthal Foundation Lecture is presented by a young physiatrist who has demonstrated noteworthy advancement in the nonsurgical care of low back pain. This prestigious lectureship was established through the generosity of the Richard and Hinda Rosenthal Foundation. Lecturer
Year
Rosenthal Lecture Title
Scott F. Nadler, DO
2003
Core Strength: What is it all about?
Stuart M. Weinstein, MD
2001
The 21st Century Physiatrist: Seasoned Veteran or Rookie Sensation. Cancelled due to 9/11
Joseph D. Fortin, DO
2000
Interventional Physiatry: The ‘Cardiology’ Approach to Musculoskeletal Medicine
Curtis W. Slipman, MD
1999
Controlling Our Future: Managing the Dilemmas Facing Physiatry
Susan J. Dreyer, MD
1998
The Forgotten Spinal Epidemics: Osteoporosis
Andrew J. Cole, MD
1997
Education and Mentoring: Physiatric Core Values
Paul H. Dreyfuss, MD
1996
Diagnosis Driven Spine Care in the 21st Century
Joel M. Press, MD
1995
The Future of Physiatric Low Back Care
Andrew J. Haig, MD
1994
New Job for an Old Test: Needle Electromyography of the Paraspinal Muscles
James Rainville, MD
1993
Uncoupling Pain and Impairment – Maximizing the Potential of Chronic Low Back Pain in Patients
Maury Ellenberg, MD
1992
Radiculopathy Secondary to Disc Herniation: Does it Require Surgery?
Nicolas E. Walsh, MD
1991
Research Design in Low Back Pain
Joel S. Saal, MD
1990
The Biochemistry and Pathophysiology of Lumbar Degenerative Disc Disease: A Rationale for Non-Operative Care
Stanley A. Herring, MD
1989
Stanley A. Herring, MD The Physiatrist as the Primary Spine Care Specialist, Implications for Training and Education
Avital Fast, MD
1988
Low Back Pain in Pregnancy
Irina Barkan, MD
1987
Lumbar Outlet Syndrome and Myofascial Back Syndrome: Diagnosis and Treatment
Patricia E. Wongsam, MD
1986
Biomechanics of the Lumbar Spine: Some Recent Advances
Jeffery A. Saal, MD
1985
Advances in Conservative Care in the Lumbar Spine: Correlation of SNR Block and Clinical EMG Findings
Myron M. LaBan, MD
1983
Vesper’s Curse’ Night Pain – The Bank of Hypnosis
Note that Dr. Nadler passed away in December 2004.
6
Section 1: Introduction
Table 1.5: PASSOR Research Grant Recipients 2004
Jay Smith, MD
Electromyographic Activity in the Immobilized Shoulder Girdle Musculature during Ipsilateral and Contralateral Upper Limb Motions
2003
Julie Lin, MD
Functional Impact of the Posture Training Support in Elderly Osteoporotic Patients
2002
Michael Fredericson, MD
The Effect of Running on Bone Density and Bone Structure in Elite Athletes
2001
Heidi Prather, DO
Vertebral Compression Fractures Related to Cancer Patients and Treatment with Vertebroplasty
2000
Anne I. Zeni, DO PT
Does Athletic Amenorrhea Induce Cardiovascular Changes?
1999
Gregory E. Lutz, MD
The Biomechanical and Histological Analysis of Intradisc Electrothermal Therapy on Interventional Discs
1998
Thierry H.M. Dahan, MD
Double blind randomized clinical trial examining the efficacy of modified Bupivacaine suprascapular nerve blocks in the treatment of chronic refractory painful subacromial impingement syndrome
‘seed money’ Research Award was created. (See Table 1.5 for awardees and topics.) Organizations Awards highlight PASSOR values. Aside from the Presidential awards, Research Grant Award, and Rosenthal Lectureships, the PASSOR Board created the PASSOR Distinguished Clinician Award to honor members who have achieved distinction on the basis of their outstanding performance in musculoskeletal patient care, their scholarly level of teaching, and who have contributed significantly to the advancement of the specialty through participation in PASSOR activities (see Table 1.6 – Distinguished Clinician Awardees). A Distinguished PASSOR Member Award was also created to honor PASSOR members who have provided invaluable services to the specialty through participation in PASSOR activities (see Table 1.7). These awards were to be directed to members who were not serving on the Board in the three years prior to the award.
THE FUTURE PASSOR has had a recent strategic plan which redefines its mission, goals, and objectives and which seeks to reintegrate PASSOR into the mainstream of the Academy of PM&R. This would eliminate distinct dues or meeting fees and necessitate creative ways to maintain funding and momentum. It remains to be seen if this is not simply another change in the flow of organizational makeup and if the good will and resources necessary to meet the needs of all members is present. A number of members have opined that simply being a nonoperative orthopedist eschews the valuable education, training, and experience of general physiatrist rehabilitation training. The proper value of team care and methodologies, and attention to psychosocial, vocational and disablement issues for selected patients
Table 1.6: PASSOR Distinguished Clinician Award Recipients The PASSOR Distinguished Clinician Award honors PASSOR members who have achieved distinction on the basis of their outstanding performance in musculoskeletal patient care, their scholarly level of teaching, and have contributed significantly to the advancement of the specialty through participation in PASSOR activities.
must be appreciated and not shunned. Some members opine that there is often no need for ancillary assistance when a skilled physiatrist can ‘provide it all,’ and state that physical therapists, chiropractors, and others do not truly represent competition if physiatrists are good at all that they lay claim to be good at. This author is in agreement with colleague Bernie Portner, MD,8 who observes, ‘… that much of what is done today is way off mark. There is, in the book on the History of Medicine, a chapter entitled ‘blood letting, the four humors, the hypothymic syndrome and other nonsensical, yet commonly held, tomfoolery of days gone by …’ and then gives his personal opinion of some of today’s practices. Each of us could make a list of those things that we do which may not be adequately supported by evidence-based research, or which appear to have greater physician emollient benefit than good patent outcome. Often, procedures are promulgated with much greater enthusiasm than for which evidence of their long-term success exists. Polls of spines surgeons have indicated that financial incentives alone for doing added procedures, not careful medical individualization, have made laminectomy without fusion relatively rare. We must support and utilize evidence-based medical literature, starting with this textbook, and look for carefully done outcomes research. Despite the requirement for resource constraint considerations and cost–benefit analysis, as a profession we must guard against primarily economic-driven clinical decision-making, or the public will demand diminishment of medical autonomy and substitution of creativity-stifling regulation. To this end, NIH, NIDRR, and other recognized funders of research (including private endowments) must support bona fide musculoskeletal clinical and research models. Regarding progress in academia, Curtis Slipman founded the first interdisciplinary academic spine program at the university of Pennsylvania in 1992 at a time when physiatrists were being blocked by anesthesia and orthopedics. His program included direct participation of ortho spine, neurosurg spine, and radiology, and all saw patients in the same facility, and created the first academic
Table 1.7: Distinguished PASSOR Member Award Recipients
2003
PASSOR members who have provided invaluable service to the specialty through participation in PASSOR activities.
Francis P. Lagattuta, MD
2002
Erwin G. Gonzalez, MD
2002
Paul H. Dreyfuss, MD
2001
Jeffrey A. Saal, MD
2001
Jeffrey L. Young, MD
2000
Robert E. Windsor, MD
2000
Robert E. Windsor, MD
7
Part 1: General Principles
interventional physiatric fellowship in 1993. Slipman’s emphasis had also been on developing leaders of interventional physiatry that could go on to develop academic programs with top-notch fellowships. He has been able to place a group of incredibly productive young physiatrists in academic centers. These physiatrists include: Zacharia Isaac at Harvard, Omar el Abd at Harvard, Jason Lipetz at Einstein in NY, Michael dePalma at the Medical College of Virginia, Raj Patel at the University of Rochester, David deDanious at the Medical College of Wisconsin, Russell Gilchrist at the University of Pittsburgh, and Amit Bhargavia at the University of Maryland. The University of Michigan program was founded by Andrew Haig, MD, and emphasized the critical importance of research to this field. Another prediction that has been observed to be coming true is that young women physiatrists who were themselves athletes during their school years have become attracted to this arena and see opportunity in the hands-on approach to interventional spine treatment, and welcome the opportunity to contribute to the medical literature dealing specifically with women’s issues Physiatry will continue to evolve as science warrants and practitioners are willing. Organizations such as PASSOR, collaborating with organized medicine, will facilitate the needed changes as new young
8
leaders act today to create the history of tomorrow. Congratulations colleagues, you’ve produced an enviable history.
References 1.
Flexner A. Medical education in the United States and Canada: A report to the Carnegie Foundation for the advancement of teaching. Bulletin No 4. New York: Carnegie Foundation for the Advancement of Teaching; 1910.
2.
Materson R. Introduction. In: Grabois M, Garrison S, Hart K, Lehmkuhl D, eds. Physical medicine and rehabilitation. The complete approach. Malden, Mass: Blackwell Science; 2000:1–16.
3.
Kottke F, Knapp ME. The development of physiatry before 1950. Arch Phys Med Rehab 1988; 69:4–14.
4.
Krusen FH. Historical development in physical medicine and rehabilitation during the last forty years. Arch Phys Med Rehab 1969; 50:1–5.
5.
Martin GM, Opitz J, eds. The first 50 years: The American Board of Physical Medicine and Rehabilitation. Arch Phys Med Rehab 1997; 78(supp 2):1–68.
6.
Opitz J, ed. Fifty years of physiatry; the forging of the chain. Arch Phys Med Rehab 1988; 69: 1–3.
7.
Rusk HA. A world to care for. New York: Random House; 1972.
8.
Porner B. e-mail communication to Materson. May 2004.
PART 1
GENERAL PRINCIPLES
Section 1
Introduction
CHAPTER
Epidemiology
2
David A. Lenrow
INTRODUCTION Epidemiology is the branch of medicine that deals with the study of the causes, distribution, and control of disease in populations.1 Epidemiology of spine pain provides insight into the scope of the problem and allows us to evaluate the impact of various treatment methods and preventative strategies. Without reliable epidemiologic data it is impossible to evaluate treatment or prevention with any accuracy. In reviewing the literature on the epidemiology of spine pain, it quickly becomes evident that there are significant gaps in our knowledge which require sound evidence-based medicine for resolution. Until we have reproducible data with set criteria for spine pain, in general and specific populations, we will be unable to accurately define its natural history or the benefit of selected treatments. Historically, the medical profession has held a variety of opinions on the cause of spine pain with associated treatments. This led to the teaching of treatments without any clear scientific evidence and has propagated potentially ineffectual approaches to ill-defined causes of spine problems. The long history of opinion-based clinical medicine and medical education is coming to a close. In this era of evidencebased medicine it is essential to determine the epidemiology of spine problems so we can proceed to focusing on effective treatment and prevention. Understanding the epidemiology of spine pain will establish the extent of the problem in the population, and its natural history. The next level of studies should be aimed at determining the relationship between specific factors, both external and internal, which are associated with spine pain. It is likely that this will vary with specific etiologies of spine pain, so the studies of causation will be intimately linked with research aimed at determining the pain generators in specific syndromes. Only when we have reached this level of understanding will researchers be able to systematically develop methods of treatment and prevention which elevate the care of these patients from opinion-based to evidence-based medicine. The terms often used in studying the effect of spine pain on populations are incidence and prevalence. Prevalence is the percentage of a population that is affected with a particular disease or symptoms at a given time or during a specific set time interval. There are many factors contributing to prevalence including, but not limited to, the number of new cases, the duration of symptoms, and individuals with spine pain moving in or out of the study population.2 The determination of prevalence only requires sampling at one time point. A cross-section of the population of interest should be sampled to ensure that the data will be generalizable to the population as a whole. The study population must reflect the population to which the information will be applied or the information will have little or no utility. Point prevalence is thought to be fairly accurate when obtained in surveys, whereas prevalence over long periods of time or an individual’s lifetime is often less accurate. Memory fades with time, particularly if pain has resolved.
Incidence is the rate of occurrence of spine pain or a specific subset of spine pain in the population being studied. Incidence is always in relation to a defined period of time. It refers to new episodes or occurrences. To determine incidence in a specific population it is necessary to sample an appropriate cross-section of the population when they are symptom free and then to follow them for occurrence of symptoms over a specific time period. Prevalence and incidence of spine pain allow us to better define the scope of the problem. They also allow for the formulation of theories of etiology by analysis of associated factors. They do not determine causation.3 The estimates of costs to society further define the problem and include economic, medical, and disability-related costs.
CHALLENGES The collection of epidemiologic data on spine pain presents difficulties on several levels. The inclusion criteria for an episode of spine pain vary. Without clear and standardized criteria for an episode of spine pain, or a specific syndrome, it is not possible to generalize or combine the data from studies. An example is an attempt to compare point prevalence across studies that define episodes of spine pain as having a duration of at least 2 weeks to studies which count any episode of spine pain, even fleeting pain. These studies are not comparable and the information in each is at best only generalizable to the specific population of the study. Consistency among studies with clearly defined criteria for an episode of spine pain would allow for comparison and pooling of data. Fleeting, transient, mild neck pain should not be evaluated in the same category as severe, intense, disabling, chronic neck pain. The study should include the question used and how it was administered. The length of the particular questions used and the method of administration can alter the responses obtained. The prevalence period must be defined. Only the same prevalence periods should be compared. Point prevalence represents the most reliable information to obtain in survey studies since memory is not required. The longer the recall period the more this is apt to be affected by memory.4 This can cause errors in both directions. Memory may fade with time or events may be remembered as occurring more recently than they actually occurred.5,6 Point prevalence avoids this issue. Self-reporting of spine pain has been criticized for being subjective and not as reliable as direct observation or examination. With pain, and specifically spine pain, there is no objective test to determine the existence of symptomatic pain. When assessing the outcomes of a treatment, we rely substantially on our patients’ reported symptoms, and perhaps in research that is also our best tool with the least misperception. What has been called a weakness of many studies may be its strength. 9
Part 1: General Principles
Generalizability of the information from a study population is frequently the goal. To allow for the extrapolation of findings from the sampled population to the larger population requires that the sample population be representative of the group as a whole. It is essential that the study population be a random sample of the target population. It is important to define the population prior to sampling so the outcome is relevant. It is time to standardize the methodology of performing epidemiologic studies for spine pain. We need widespread use of standardized scales for data collection, appropriate population samples and valid, reliable outcome measures. If the measures used have not been validated, the data are of questionable value at best.
Scope of the problem Spine pain is nearly ubiquitous in industrial societies. It is among the most common medical problems in developed countries. It is present in rural workers and in sedentary through heavy-duty occupations. In the majority of cases causation remains muddled. The often repeated causal factors including obesity, heavy work, leg length discrepancy, and others have not been proven. The data for low back pain vary but the lifetime prevalence in industrial nations is high, 50–85% or greater.7,8 The annual incidence is approximately 5% with some reports up to 15%.8 Back pain accounted for 15 million physician visits in 1990 in the US.9 It is a major factor in lost work days and the first or second most common cause of disability.10 In people under 45 year of age it is the most common cause of disability in the US.10 The societal costs are enormous. The prognosis for a single episode of back pain is excellent, with 90–95% of acute episodes resolving fully. Resolution of symptoms usually occurs within 3 months. The patients who do not recover are often noted to be the major cost in disability and medical care. It is becoming evident that there is a significant recurrence rate for acute back pain with an associated progression to chronic pain. With surveys, participants have been found to forget up to 25% of episodes of back pain for which they sought medical attention, making recurrence rates difficult to determine. The epidemiology of neck pain is much less often the target of studies, but it appears to be nearly as prevalent as back pain.
History Back pain has been present since the earliest of recorded time. In the Edwin Smith papyrus circa 1500 BCE there is a description of back pain, including the examination and diagnosis. Neanderthal skeletons and Egyptian mummies revealed degenerative spine changes. Hypocrites (460–370 BC) noted that back pain with sciatic pain lasted about 40 days and affected men 40–60 years old.11 Historically, chronic back pain was not thought to be secondary to injury until the mid nineteenth century. This was the time of the industrial revolution and the building of the railways. It was called railway spine and thought to be related to work, or even travel on the railroad, even if there was no identifiable injury.12 This led to the acceptance of spine pain as an occupational injury.
STATISTICS
North America
Europe
National Health and Nutrition Examination Survey-CDC (NHANES 1999–2000) found the prevalence of low back pain (LBP) within the past 3 months to be 37.44% with a sample size of 4880.24 Neck pain over the previous 3 months lasting at least 1 day revealed a prevalence of 18.46%. Deyo analyzed the NHANES II data (1976–1980) with a survey population of 27 801 and found a lifetime prevalence in the US of LBP of 13.8% and prevalence in the previous year of 10.3%.25 In the Deyo study an episode of LBP was defined as lasting at least 2 weeks.
In Britain, a study in the general population with 4515 respondents from three general practices determined the prevalence of neck and back pain.13 An episode of spine pain was defined as lasting at least 1 week in duration. The 1-month prevalence of all spinal pain was 29%. The prevalence for back pain was 24.5% for women and 21.3% for men. For neck pain the prevalence was 16.5% for women and 10.7% for men. Of the total spine pain, 40% was disabling. 10
A British study with 12 907 respondents to a survey found a 1-year prevalence of 34% and a weekly prevalence of 20% for neck pain.14 Of the total respondents, 11% reported neck pain within the past year that interfered with their normal activities. An episode was defined as pain lasting 1 day or longer. In one of the few prospective studies the lifetime and annual prevalence of low back pain in the UK was 59% and 42%, respectively.15 This was a mailed survey with 1455 respondents. An incidence rate of 4% was found. Age was associated with increased prevalence. An episode of back pain was defined as lasting longer than 1 day and not associated with menstrual cycle, pregnancy, or febrile illness. Guez, in a Swedish study of 4392 adults, found an 18% prevalence of chronic neck pain with continuous pain lasting longer than 6 months.16 Of the subjects with neck pain, 30% had a history of trauma. No data were reported on the interval between trauma and neck pain. The definition of neck injury was injury that was severe enough to lead to a physician visit. In another Swedish population study with 6000 respondents, 48% of men and 38% of women reported neck pain on a self-administered questionnaire.17 The prevalence as a whole was 43% with women having a significantly higher prevalence than men. Chronic neck pain defined as lasting greater than 6 months was reported in 22% of women and 16% of men. A history of head or neck trauma was present in 25% of the subjects who developed chronic neck pain. Linton, in a Swedish study, surveyed 3000 persons and found a 2-year prevalence of 73% for low back pain.18 Of these, 17% utilized sick time and another 14% had been off work but did not use sick time. In the Mini-Finland Health Survey 8000 people were interviewed and examined.19 Lifetime prevalence of neck pain was 71%. Chronic neck pain was diagnosed in 9.5% of the men and 13.5% of the women. An association was found between neck pain and history of injury and mental and physical stress at work. In a survey study of 10 000 Norwegians, the 1-year prevalence rate of neck pain was 34.4%.20 Neck pain lasting for more than 6 months had a prevalence of 13.8%. In a telephone survey of 1964 participants in Catalonia, Spain, the 6-month prevalence of low back pain was 50.9%.21 Back pain was more common in women, manual workers and less-educated respondents. Back pain limited the daily activities in 36.7% and was responsible for time off work in 17% and disability pension in 6.5%. In a Belgian study of 618 blue collar workers in the steel industry, lifetime prevalence was 66%, 1-year prevalence was 53%, and 1-week prevalence was 25%.22 An episode was any ‘problem in the low back.’ Most of these episodes were mild and categorized as fatigue or common low back pain. Only 17% sought medical advice and only 11% were limited in their occupational or domestic activities. In the Netherlands in a survey with 3664 respondents, low back pain had a prevalence of 26.9% and neck pain 20.6%. Low back pain was the most common musculoskeletal pain and neck pain was the third most common.23
Section 1: Introduction
Canada has been the site for many epidemiologic studies for both lumbar and cervical ailments. Cassidy et al., with 1131 respondents to a mailed survey in Saskatchewan, found 28.4% point prevalence and 84.1% lifetime prevalence of back pain.26 The 6-month prevalence was graded into five intensities and disability categories. This was an attempt to stratify the prevalence so that transient nondisabling pain could be differentiated from disabling back pain. Low intensity/ low disability back pain accounted for 48.9% of the population that had back pain in the previous 6 months. High intensity/high disability back pain was reported by 10.7% of this population. The remaining 12.3% of the subjects in the 6-month prevalence group reported high intensity/low disability back pain. Women were twice as likely as men to report severe disabling back pain; low intensity was equal between genders. The authors conclude that general prevalence is not terribly useful information since the majority of responders who had episodes of back pain had low intensity/nondisabling episodes of back pain. Cote et al. looked at the prevalence of neck pain in the same random survey of the Saskatchewan population.27 The lifetime prevalence of neck pain was 66.7% and point prevalence was 22.2%. Neck pain was defined as any pain between the occiput and third thoracic vertebrae as detailed on a mannequin diagram. Subjects were stratified by intensity of pain and disability in a fashion similar to the study on back pain. Women experienced more neck pain than men in all severity groups. Women had a 58.8% 6-month prevalence and men had a 47.2% 6-month prevalence. The 6-month prevalence of low intensity/low disability neck pain was 39.75% and 10.1% for high intensity/low disability neck pain. A total of 4.6% of the surveyed population reported highly disabling neck pain for the previous 6-month period. Interestingly, low intensity/low disability neck pain was found to decrease with age. High disability neck pain was more prevalent in women than in men. Kopec et al., in a longitudinal study of households in 10 provinces in Canada, were able to determine the incidence of back pain.10 The interval of the two surveys was 2 years and the sample size was 11 063 subjects age 18 years or older. An episode of back pain was defined as lasting longer than or equal to 6 months in duration or expected duration. The 2-year incidence in females was 9.0% and in males was 8.1%. Of note is that this was a self-administered survey but the question was ‘Have you been diagnosed by a health professional with back problems, excluding arthritis?’ One could envision several potential biases of this longitudinal prospective study. The question asked is not defined in terms of intensity but only duration. The duration maybe 6 months or longer or in the alternative be expected to last 6 months or longer. This opinion on expected duration is that of the subjects. The diagnosis of back problems by health professionals is being self-reported by the subject and not by health professionals or their records. The validity of this second-hand information is unclear. George, in another Canadian survey with 1131 respondents, showed an 8% 6-month incidence of clinically significant low back pain by the Chronic Pain Questionnaire.28 The prevalence of low back pain in North America, as elsewhere, varies by study. In an attempt to reconcile the variability and determine reliable prevalence rates a methodological review of the literature was performed to identify acceptable studies and compare prevalence rates.29 They found 13 studies from 1981–1998 methodologically acceptable, but with variable assessments and definitions of an episode of back pain. The range of point prevalence in the studies varied from 4.4% to 33.0%. One-year prevalence rates ranged from 3.9 to 63%. The explanation for the variability is partially blamed on the differing durations of back pain required to constitute a reportable episode.
Asia In a cross-sectional study of garment workers, battery/kiln workers, and teachers in Shanghai, People’s Republic of China, the overall yearly prevalence of back pain was 50%.30 The number of subjects in this study was 383. This was self-reported back pain with symptoms lasting a minimum 24 hours. Garment workers had the highest yearly prevalence of 74% while teachers had a prevalence of 40%. The 7-day prevalence was 45% for garment workers and 22% for teachers. The different occupations were thought to account for the variation in prevalence. In a study of 800 workers in Russia, the lifetime prevalence was 48.2%, point prevalence was 11.5%, and the 1-year prevalence was 31.5%. The vast majority (88.2%) had pain for less then 2 weeks. Only 1.8% had pain for longer than 12 weeks.31
Low-income countries Studies to determine statistics for spine pain in low-income countries are much less common than in wealthy industrialized nations. The literature on back pain is primarily from high-income countries accounting for less then 15% of the world population. In an attempt to test the hypothesis that in low-income countries, since physical labor is more common, back pain should have a higher prevalence, a systematic review of the literature for lowincome countries was performed.5 The point prevalence was the benchmark and used for comparison. Interestingly, high-income countries had 2–4 times the point prevalence found in rural, lowincome countries. The variation within both the high-income and low-income groups was twofold. This large disparity within categories of countries puts the methodology and therefore strength of the study into question. Notwithstanding the methodologic issues, manual labor does not appear to correlate with back pain. Perhaps physical activity is protective or even serves as treatment. This study in a general way lends evidentiary support to exercise as a treatment modality. Harlow found a 29.8% prevalence of low back pain, a 38.3% prevalence of upper back pain, and a 26.4% prevalence of neck pain in women in Tijuana, Mexico. 32 In a study in urban Zimbabwe of 10 839 respondents, back pain was the second most disabling condition after headaches.33 Omokhodion, in 840 Southwest Nigerian office workers, found a 12-month prevalence of low back pain of 38% and point prevalence of 20%.34 The overall rate of disability was 5.6%. In a cross-sectional study in rural Tibet with n=499, the point prevalence of low back pain was 34.1%, the 12-month prevalence was 41.9%. 35 Subjects also reported functional disability related to their pain. In rural China 36 the prevalence was found to be 12.1% and in Nepal 37 18.4% for low back pain. Sharma reported that 23% of patients seen for medical care in outdoor rural India were seen for back pain.38 The information from rural nations may be helpful in our understanding of the factors important in developing spine pain and its prevention. The prevalence and incidence of spine pain is a large problem internationally regardless of compensation systems and culture. The variability both in the same populations and across populations is substantial. Even with this large variation in prevalence and methodology the statistics remain staggering. Before we hypothesize on why these variations are found, both in different groups of subjects and in time, we must determine the value of the data we are comparing. The methodology and generalizability of the individual studies must be sound and comparable before there is any value in formulating reasons for the differences noted. 11
Part 1: General Principles
COST The cost of back pain to various societies is hard to quantify. This is due to the lack of central data collection and variation in methodology. Extrapolating data from worker’s compensation claims in the US and then projecting to the population as a whole reveals staggering costs.39 In 1988 the estimate was 22.4 million cases of back pain with 149.1 million lost work days. This loss of workdays alone is estimated to cost more than US$13.3 billion. This does not take into account health care, personal expenses, and insurance costs. Estimates of total cost in the US range from US$50 to US$100 billion per year. A Swedish study found that 6% of sufferers accounted for over 50% of the costs.18 In Australia the cost is estimated at US$10 billion per year with a lifetime prevalence of 80%.40 In the Netherlands back pain is the most common cause of lost days at work and disability. In 1991 the direct costs of medical care for back pain in the Netherlands was US$367.6 million and the indirect costs were US$4.6 billion.41 In a 2003 study in the US, back pain was the second most common pain condition resulting in lost time from work after headache.42 Out of the total work force, 3.2% lost time from work as a result of back pain. Pain-related loss of productive work time cost an estimated US$61.2 billion. The majority was because of decreased productivity while at work and not due to absence from work.
FACTORS The cause of most episodes of spine pain is uncertain. The purported risk factors are numerous. Heavy lifting, particularly on a repetitive basis, has often been suggested as an inciting event. Age, gender, and psychological distress have all been implicated, but not consistently. Cigarette smoking and obesity have been related to back pain in some studies.43–46 Socioeconomic status has been identified as a risk factor in some studies43,47 but not all studies.10 Before leaping from associated factors to causation and postulated mechanisms, we must have better data for prevalence and incidence so the significance of these potentially inconsequential associations can be adequately evaluated. Cote et al. analyzed the Saskatchewan Health and Back Pain Survey data to determine the factors associated with neck pain and disability.48 In the sample population, 15.9% reported prior neck injury in a motor vehicle accident. This history and headaches were strongly associated with all grades of neck pain. Subjects with cardiovascular or digestive problems had a higher 6-month prevalence of disabling neck pain but not milder neck pain. There was an association between low back pain and neck pain. The Mini-Finland Health Survey found chronic neck pain strongly associated with back pain and shoulder disorders, but only weakly associated with osteoarthritis, cardiovascular, and mental disorders.19 Trauma to the neck or low back was associated with chronic neck pain. Kopec et al., in a prospective study, tried to identify factors in the development of back pain in the general population.10 General health and psychosocial factors were important in both sexes. Other factors in men were age, usual activity pattern, lack of gardening, and height. For women the other factors were self-reported arthritis or rheumatism and a history of psychological trauma. If a woman has none of these identified factors her risk of developing back pain in a 2-year period is 6%. For a woman who has activity restriction, has been diagnosed with arthritis or rheumatism, has two or more traumatic events in childhood, and reports a high level of personal stress, her risk of developing back pain is 32% in a 2-year period. General health was a strong predictor of back pain in a study in the UK by Croft et al.49 They studied 2715 individuals from two general
12
practices in Manchester. The relative risk was 1.5 for men and 2.2 for women who had poor general health.
Weight Weight has often been cited as a risk factor in spine pain, most often in low back pain. Webb found an association between obesity and back pain with disability but not with neck pain or low-intensity back pain.13 Kopec et al. found no significance but weight was close to significant as a factor in women.10 Croft found weight to be a significant factor for women but not men.49 Gyntelberg, in a study of Danish men, found an association between height and low back pain but not weight.50
Occupation In a British survey with 12 907 respondents, no association for neck pain was found for lifting, vibratory tool use, or professional driving.14 There was an association found with above-the-shoulder activity for >1 hr/day. Stronger associations were found with tiredness or frequent stress. Occupations with the highest prevalence were, in descending order; construction workers, nurses, armed services members, and the unemployed. No association was found between physical workload, postures, or exposure to vibration and low back pain in steel workers.22 In a study in the Netherlands, scaffolders had a 60% 12-month back pain prevalence.51 Supervisors had similar rates for back pain and perceived disability but less severe back pain and lower absence rates than scaffolders. Ehrlich opines that most spine pain is not related to work activities but may be related to psychosocial factors.52 Job dissatisfaction, stress, the system of compensation, and hiring a lawyer are all reported to decrease return-to-work rates. Hadler states how back pain is dealt with determines if it is disabling or not; secondary gain such as workers’ compensation increases the morbidity.53
Secondary gain There is a long-standing controversy regarding the role of secondary gain in spine pain and disability. Disability from spine pain was not a significant problem until the industrial revolution. Cassidy et al. analyzed the effect of compensation on whiplash injury in Saskatchewan.54 On January 1, 1995, the tort compensation system for traffic injuries was changed to a no-fault system eliminating recovery for pain and suffering. This provided natural data collection points. It is important to note that Saskatchewan was the only insurer for motor vehicle injuries in the Province and all residents benefit from state health insurance. For the last 6 months of the tort claim system the 6-month cumulative incidence was 417 per 100 000 persons compared to 302 and 296 per 100 000 in the first and second 6-month periods of the no-fault system. This equates to a 28% decrease in claims for whiplash injury. The time from the date of injury to claim closure decreased from 409 days to 194 days in the same time interval. During this same period there was an increase in the number of vehicle-damage claims and distance driven.
Psychological The development of back pain has often been associated with psychological factors.55–57 In the Manchester study, psychological factors were found to be predictive of low back pain.57 This was a prospective study of 4501 surveyed subjects. Subjects with no back pain but high scores for psychological distress were more likely to develop back pain than individuals with low scores.
Section 1: Introduction
Perez found an association prospectively between psychological factors and back pain in healthy workers.56 The only factors related to back pain in that study were age, depression, and general stress. Kopec et al. found general stress to be a factor in men and personal stress (a subset of general stress) a factor in women, as well as a history of psychological trauma in women.10 In a Finnish study, an association between depression and neck and back pain was found in both men and women.58 Power, in a British cohort study looking at early life variables, found psychological distress at age 23 to be the strongest predictor of low back pain.59 This doubled the risk of back pain later in life. In rural India 67%, of patients seen for low back pain had psychosocial issues, and 38% were dissatisfied with their current job.38
Smoking Smoking has be implicated as a factor in developing spine pain.45,59 The Manchester study,49 Kopec et al.10 and Guez et al.16 among others did not find an association between spine pain and smoking. In a systematic review of the literature for 1976–1997 an association between smoking and non-specific back pain was found.45 The results revealed an association between smoking and back pain in men in 18 of 26 studies and in 18 of 20 studies in women. It is not clear if smoking preceded back pain or if there is a close relationship. The finding of a positive association does not imply causation.
Age The highest prevalence of low back pain occurs between 40 and 60 years of age. Kopec et al., in one of the few studies looking at incidence and age, showed a peak incidence at 45–64 years of age.10 Rates of back pain seem to increase during adult life until age 65 and then they decrease. Predicting back pain by knowing the causation and associated factors would allow for an intelligent, scientific approach to prevention. The data currently available are often contradictory and difficult to explain. In one study, gardening is associated with a lower risk of low back pain.10 In other studies sports and nonoccupational home improvement increased the risk.49 Is gardening really associated with lower incidence of back pain or do people prone to back pain not garden? We must ask the right questions to determine the association between risk factors and the development of spine pain. Perhaps these are just chance associations. Without precise methodology, reproducibility, and multiple studies in agreement, the true associated factors remain uncertain and true causation beyond our reach.
respondents reporting persistent annual low back pain.15 Acute episodes recurred and in some patients turned into chronic, constant pain.
DISABILITY Spine pain is a major cause of disability. It has been estimated that 1% of the population is disabled by back pain. It is the leading cause of disability in the US for the population under 45 years old and the second cause for those 45–65 years old.46 Back pain accounts for approximately one-fourth of worker’s compensation claims in the US. In a survey of 30 074 respondents 5256 subjects, or about 17.5%, self-reported back pain lasting at least 1 week.39 Construction workers in males and nurses aides in females had the highest prevalence rates of 22.6% and 18.8%, respectively. Subjects reported missing work or changing jobs in 12.1% of those with reported pain. Extrapolating this to national estimates yields staggering numbers of cases of back pain and lost work days. There is little known about the extent of the disability spine pain produces in less-industrialized nations. In Nigerian office workers, only 5% of those surveyed reported lost days due to back pain, with a mean of 4.7 days per year.34 The incidence of back pain was similar to that in industrialized nations but the absence from work was not as significant. The history of spine pain and disability helps illuminate some of the factors that transform spine pain, as an accepted part of life, into a disabling condition. Allan and Waddell review the history of back pain and disability.11 There was very little written about spine pain causing disability until the industrial revolution. Early reports of spine disability in railway workers led to much more frequent spine disability in the early twentieth century. This was coupled with the concept of compensation for work-related injury. During WWI the US draft board rejected recruits that had static problems of the spine to avoid backache. Recruits still developed backache, but could be made fit for service by special training battalions. This suggested that back pain might be a fitness problem and not a medical problem. In the British armed forces there was a fivefold increase in withdrawal from duty for back pain between WWI and WWII. In Britain in 1911 and the US in 1949, workers were covered for injury by Workman’s Compensation Insurance. As the breadth of compensation increased so did the extent of disability for back pain. The author’s concluded that disability is not a natural sequelae of back pain, but is secondary to how we compensate, manage, and treat patients with these aliments.
CONCLUSION RECURRENCE The traditional notion that the great majority of episodes of nonspecific back pain resolve has come under scrutiny. There is good evidence that a substantial fraction of back problems have recurrent symptoms. Miedema found that 28% of patients with an episode of back pain, for which they consulted their physician, went on to develop chronic back pain.41 Only 1 in 5 people with back pain consult their physician. In a review of the literature the 1-year recurrence rate for low back pain was 20–44%.8 Lifetime recurrence rates were up to 72%. These studies were prospective studies for occupational back pain. Nurses and drivers had the highest recurrence rates while white collar workers had the lowest recurrence rates. In general, men had higher rates of recurrence than women. In a longitudinal cross-sectional study in the UK there was a 59% lifetime prevalence, with 42% of those
Spine pain is a widely prevalent condition. Spine disorders account for a tremendous cost both in lost productivity and medical care to industrial societies. Back pain is one of the top two reasons persons seek medical care, superceded only at times by respiratory infection. The prevalence is variable across studies but there is no standardized methodology to study spine pain. Definitions of spine problems vary greatly as do methods of obtaining data. These variables make it impossible to compare statistics across studies even if the populations were identical. Spine pain is not a specific disease or one etiology of pain, which makes it difficult to address. It is most often of non-specific cause, or more accurately an as yet unidentified cause. The rate of surgery varies by regions and by country with up to a 15fold variation within the US. The use of various treatments including COX-2 antiinflamatory drugs, spinal injections, IDET and percutaneous discectomies, just to name a few treatments, vary greatly by geographic area. Treatment trends have changed throughout the history
13
Part 1: General Principles
of medicine. The factors driving these shifts are, unfortunately, not always scientific in basis or in the patient’s best interest. This is perhaps driven more in the US by reimbursement trends and patients desire for specific treatments. The lay press and insurance industry fuel this, and not necessarily scientific evidence. Once these treatment modalities become common and patients ask for them, it is very difficult to study their effectiveness. The first step to evidence-based medicine in the treatment of spine pain is the collection of valid, consistent, epidemiologic data. This will serve as the foundation on which to build rational treatment in the future. The study of the epidemiology of spine pain is essential to understanding the scope of the problem, factors implicated in causation, and the natural history. The next step is to control causative factors or comorbid conditions with possible etiologic associations, to see if the incidence of these conditions can be altered. Basing our treatment of spine disorders on poor epidemiologic studies amounts to opinionbased medicine rather than rational treatment with evidence as its foundation. The charge to this generation of researchers and medical professionals is to base treatment on scientific evidence. To do so, we must first focus on accurate epidemiology with consistent definitions of episodes of spine pain and durations that are significant.
References 1. Pickett JP, et al. The american heritage dictionary of the English language. 4th edn. Boston: Houghton Mifflin Company; 2000. 2. Looney P, Stratford P. The prevalence of low back pain in adults: A methodological review of the literature. Physical Therapy April 1999; 79(4):384. 3. Spitzer WO. In: Troidl H, Spitzer WO, McPeek B, et al. eds. Principles and practice of research: Strategies for surgical investigators. New York: Springer-Verlag; 1986. 4. Leboiuf-yde C, Lauritsen JM. The prevalence of low back pain in the literature: A structured review of 26 Nordic studies from 1954 to 1993. Spine 1995; 20:2112– 2118. 5. Volinn E. The epidemiology of low back pain in the rest of the world: A review of surveys in low and middle-income countries. Spine 1997; 22:1747–1754. 6. Carey TS, Garrett J, Jackman A, et al. Reporting of acute low back pain in a telephone interview: Identification of potential biases. Spine 1995; 20:787–790.
20. Bovim G, Schrader H, Sand T. Neck pain in the general population. Spine 1994; 19:1307–9. 21. Bassols A, Bosch F, Campillo M, et al. Back pain in the general population of Catalonia (Spain). Prevalence, characteristics and therapeutic behavior. Gac Sanit 2003; 17(2):97–107. 22. Masset D, Malchaire J. Low back pain, epidemiologic aspects and work-related factors in the steel industry. Spine 1994: 19(2):143–146. 23. Picavet HSJ, Schouten JSAG. Musculoskeletal pain in the Netherlands: prevalences, consequences and risk groups, the DMC3-study. Pain 2003; 102:167–178. 24. http://www.cdc.gov/nchs/about/major/nhanes/frequency/mpq.htm 25. Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low back pain and its related medical care in the United States. Spine 1987; 12:264–268. 26. Cassidy JD, Carroll LJ, Cote P. The Saskatchewan health and back pain survey: The prevalence of low back pain and related disability in Saskatchewan adults. Spine 1998; 23(17):1860–1866. 27. Cote P, Cassidy JD, Carroll L. The Saskatchewan health and back pain survey: The prevalence of neck pain and related disability in Saskatchewan Adults. Spine 1998; 23(15):1689–1698. 28. George C. The six-month incidence of clinically significant low back pain in the Saskatchewan adult population. Spine 2002; 27(16):1778–1782. 29. Loney PL, Stratford PW. The prevalence of low back pain in adults: A methodological review of the literature. Physical Therapy 1999; 79:384–396. 30. Jin K, Sorock GS, Courtney TK. Prevalence of low back pain in three occupational groups in Shanghai, People’s Republic of China. J Safety Res 2004; 35:23–28. 31. Toroptsova N, Benevolenskaya L, Karyakin A, et al. Cross-sectional study of low back pain among workers at an industrial enterprise in Russia. Spine 1995; 20(3):328–332. 32. Harlow SD, Becceril LA, Scholten JN, et al. The prevalence of musculoskeletal complaints among women in Tijuana, Mexico: sociodemographic and occupational risk factors. Int J Occup Environ Health 1999; 5(4):267–275. 33. Jelsma J, Mielke J, Powell G, et al. Disability in an urban black community in Zimbabwe. Disabil Rehabil 2002; 24:851–859. 34. Omokhodion FO, Sanya AO. Risk factors for low back pain among office workers in Ibadan, Southwest Nigeria. Occup Med (Lond) 2003; 53(4):287–289. 35. Hoy D, Toole MJ, Morgan D, et al. Low back pain in rural Tibet. Lancet 2003; 362(9353):225–226.
7. Anderson GBJ. Epidemiology of low back pain. Acta Orthop Scand 1998; 69(suppl):28–31.
36. Wigley RD, Zhang NC, Zeng QY, et al. Rheumatic disease in China: ILAR-China Study comparing the prevalence of rheumatic symptoms in northern and southern rural populations. J Rheumatol 1994; 21:1484–1490.
8. Andersson GBJ. Epidemiological features of chronic low-back pain. Lancet 1999; 354:581–585.
37. Anderson RT. An orthopedic ethnography in rural Nepal. Med Anthropol 1984; 8:46–58.
9. Hart GL, Deyo RA, Cherkin DC. Physician office visits for low back pain. Spine 1995; 20:11–19.
38. Sharma SC, Singh R, Sharma AK, et al. Incidence of low back pain in work age adults in rural North India. Indian J Med Sci 2003; 57(4):145–147.
10. Kopec JA, Sayre EC, Esdaile JM. Predictors of back pain in a general population cohort. Spine 2003; 29:70–78.
39. Guo HR, Tanaka S, Cameron LL, et al. Back pain among workers in the United States: national estimates and workers at high risk. Am J Industrial Med 1995; 28:591–602.
11. Allan DB, Waddell G. An historical perspective on low back pain and disability. Acta Orthop Scand 1989; 60(Suppl 234):1–23. 12. Harrington R. On the tracks of trauma: railway spine reconsidered. Soc Hist Med. 2003 Aug 16(2):209–223. 13. Webb RT, Lunt M, Urwin M, et al. Prevalence and predictors of intense, chronic, and disabling neck and back pain in the UK general population. Spine 2003; 28:1195–1202. 14. Palmer KT, Walker-Bone K, Griffin MJ, et al. Prevalence and occupational associations of neck pain in the British population. Scand J Work Environ Health 2001; 27:49–56. 15. Waxman R, Tennant A, Helliwell P. A prospective follow-up study of low back pain in the community. Spine: 2000; 25(16):2085–2090. 16. Guez M, Hildingsson C, Stegmayr B, et al. Chronic neck pain of traumatic and nontraumatic origin: a population-based study. Acta Orthop Scand 2003; 74:576–579. 17. Guez M, Hildingsson C, Nilsson M, et al. The prevalence of neck pain: A population-based study from northern Sweden. Acta Orthop Scand 2002; 73:455–459. 18. Linton SJ, Ryberg M. Do epidemiological results replicate? The prevalence and health-economic consequences of neck and back pain in the general population. Eur J Pain 2000; 4(4):347–354.
14
19. Makela M, Heliovaara M, Sievers K, et al. Prevalence, determinants and consequences of chronic neck pain in Finland. Am J Epidemiol 1991; 134:1356–1367.
40. Frymoyer JW, Cats-Baril WL. An overview of the incidences and costs of low back pain. Orthop Clin North Am 1991; 22:263–271. 41. Miedema A, Chorus AM, Wevers CW, et al. Chronicity of back problems during working life. Spine 1998; 23(18):2021–2028. 42. Stewart WF, Ricci JA, Chee E, et al. Lost productive time and cost due to common pain conditions in the US workforce. JAMA 2003: 290(18):2443–2454. 43. Burdorf A, Sorock G. Positive and negative evidence of risk factors for back disorders. Scand J Work Environ Health 1977; 23:243–256. 44. Skovron ML. Epidemiology of low back pain. Baillieres Clin Rheumatol 1992; 6:559–573. 45. Goldberg MS, Scott SC, Mayo NE, et al. A review of the association between cigarette smoking and the development of nonspecific back pain and related outcomes. Spine 2000; 25:995–1014. 46. Frank JW, Kerr MS, Brooker AS, et al. Disability resulting from occupational low back pain: I. What do we know about primary prevention? A review of the scientific evidence on prevention before disability begins. Spine 1996; 21:2908–2917. 47. Houtman IL, Bongers PM, Smulders P, et al. Psychosocial stressors at work and musculoskeletal problems. Scand J Work Environ Health 1994; 20:139–145.
Section 1: Introduction 48. Cote P, Cassidy D, Carroll L. The factors associated with neck pain and its related disability in the Saskatchewan population. Spine 2000; 25(9):1109–1117. 49. Croft PR, Papageorgiou AC, Thomas E, et al. Short-term physical risk factors for new episodes of low back pain: Prospective evidence from the South Manchester Back Pain Study. Spine 1999; 24:1559–1561. 50. Gyntelberg F. One-year incidence of low back pain among male residents of Copenhagen aged 40–59. Dan Med Bull 1974; 21:30–36. 51. Elders L, Heinrich J, Burdorf A. Risk factors for sickness absence because of low back pain among scaffolders: A 3-year follow-up study. 2003; 28(12):1340–1346.
54. Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating compensation for pain and suffering on the outcome of insurance claims for whiplash injury. N Engl J Med 2000; 342:1179–1186. 55. Bigos S, Battie MC, Spengler DM, et al. A prospective study of work perceptions and psychological factors affecting the report of back injury. Spine 1991; 16:1–6. 56. Perez CE. Chronic back problems among workers. Health Rep 2000; 12:42. 57. Croft PR, Papageorgiou AC, Ferry S, et al. Psychologic distress and low back pain: evidence from a prospective study in the general population. Spine 1995; 20:2731–2737.
52. Ehrlich GE. Back pain. J Rheumatol 2003; 30 (suppl 67):26–31.
58. Rajala U, Keinanen-Kiukaanniemi S, Uusimaki A, et al. Musculoskeletal pains and depression in middle-aged Finnish population. Pain 1995; 61:451–457.
53. Hadler NM. Occupational musculoskeletal disorders. Philadelphia: Lippincott Williams and Wilkins; 1999.
59. Power C, Frank J, Hertzman C, et al. Predictors of low back pain onset in a prospective British Study. Am J Public Health 2001; 91:1671–1678.
15
PART 1
GENERAL PRINCIPLES
Section 2
Spinal Pain
CHAPTER
Inflammatory Basis of Spinal Pain
3
James D. Kang and Stephen Hanks
INTRODUCTION Low back pain with or without radiculopathy continues to be a significant clinical entity causing major disability in patients. However, the etiology of low back pain and the exact pathophysiology remains elusive. Intervertebral disc degeneration has been implicated as one of the key factors associated with low back pain. The intervertebral disc continues to be a structure of great interest because its degeneration or failure may influence a variety of structures in processes believed to play a role in low back pain. There has been a large body of recent work focusing on the interaction between biomechanics and the biochemistry of disc degeneration and their seemingly coupled interaction. Low back pain is undoubtedly one of the largest health problems affecting society, both individually and as a whole. It is the second most common reason listed for a doctor’s office visit and the lifetime prevalence is estimated at 91%. Of the total Workmen’s Compensation expenditure nationwide, it accounts for somewhere between 70% and 90%. It is the second leading cause of disability worldwide and its incidence is increasing disproportionately to the population growth and other disabling conditions. For these important reasons, characterizing the underlying causes of low back pain has become more important in the scientific literature in the last 7–10 years.
THE INTERVERTEBRAL DISC The intervertebral disc has many functions including stabilization of the spine by attaching vertebral bodies together and allowing movement between these bodies giving the spine its flexibility. With the facet joints, the spine bears the entire compressive load to which the trunk of the body is exposed. Discs within the lumbar spine are exposed to three times or more the weight of the trunk while in the sitting position and this number can double during certain activities such as jumping, lifting out of position, or trauma. Changes within the disc as humans age affects the ability of the spine to respond to the loads to which it is subjected.
Disc structure The intervertebral disc is composed of four concentrically arranged layers including (1) the outer anulus fibrosus, (2) the fibrocartilaginous inner anulus fibrosus, (3) the transition zone between the anulus fibrosus and the nucleus pulposus, and (4) the nucleus pulposus. The outer anulus is composed of approximately ninety collagen sheaths bonded together in concentric laminated bands within which the fibers are arranged in the helicoid manner. These sheaths are oriented at about 30° to the disc plane and at about 120° therefore in alternate bands. This orientation is important
in resisting the high pressure of the nucleus, as well as maintaining stability against rotational forces. Cutting all fibers of the same orientation, while preserving fibers of the other direction, results in a greater increase in the axial rotation of the isolated motion segments than does removal of both facet joints. The inner anulus fibers attach directly to the cartilaginous endplate whereas the outer fibers attach directly to the vertebral body via Sharpey’s fibers. The nucleus pulposus is centrally located and consists of a relatively random network of collagen and hydrated proteoglycans. The lumbar nucleus occupies 30–50% of the total disc area in cross-section. Water content varies from 70% to 90%, is highest at birth, and decreases with advances in age as the concentration of proteoglycans also decreases. The intervertebral disc is composed of a collection of macromolecules that include mostly collagen and proteoglycan. The matrix of the outer anulus consists of approximately 80% of type I collagens and small amounts of type V collagen. Inside the outer anulus, the concentrations of type II collagen and proteoglycan become progressively greater toward the center of the disc as the concentration of type I collagen decreases. Inside the nucleus, the concentration of type II collagen approaches 80% while type I is absent. Type II fibers are more hydrophilic than type I fibers and therefore are 25% more hydrated. Most of the data on the mechanical behavior of discs have been obtained from in vitro studies of spine specimens obtained at autopsy. There is evidence that the hydration in discs changes quickly after death, including transfer of water from the outer to inner anulus, and this may affect testing results in research using cadavers. The presence of degenerative discs, as mentioned, is nearly universal as humans age. All disc tissue ages from birth to death, with the most marked changes occurring in the nucleus pulposus where the proteoglycan concentration, water content, and the number of viable cells all decrease. These changes are accompanied by fragmentation of the aggregating proteoglycans. Although all discs eventually show these same changes, the rate at which they show them varies not only from person to person, but within discs from the same individual.
Disc biomechanics In general, tissue failure occurs because the loads to which they are exposed as stresses generated exceed the strength of the tissue. These can be tensile, compressive, or shear forces contributing to the damage. Stokes and Greenapple demonstrated strains of 6–10% during extremes of flexion and axial rotation in lumbar disc fibers.1 The strains were greater in the posterolateral areas than in the anterior regions. While pure axial compression, even in testing at very high loads, does not cause herniation of the nucleus pulposus, cyclic loading can cause annular tears that may eventually lead to disc herniation. Discs are known to exhibit creep, relaxation, and hysteresis. In these studies, the amount of hysteresis was shown to increase with 17
Part 1: General Principles
load and decrease with age. These studies also demonstrate that nondegenerative discs creep less slowly than degenerative discs. This may indicate that there is less physiologic elasticity in degenerative discs. Finite element analysis has effectively modeled the functional spinal unit (FSU). It has been shown that in compression the load is transferred from one vertebra to another through the endplates via the nucleus pulposus and the anulus fibrosus. The application of a load causes pressure to develop within the disc, pushing fibers out and away from the center of the disc. Rupture of the annular fibers was seen posterolaterally in the innermost layer during progressive failure analysis in compression and in shear loads at various rotations. The rupture progressed toward the periphery, with increased loads up to the maximum used in the analysis. These structural changes to the disc and functional spinal unit can be readily seen with modern imaging techniques. However, mechanical phenomena or biomechanical changes are inadequate to explain some of the clinical observations made in the patients who have low back pain or radiculopathy. These include clinical improvement after treatment with powerful antiinflammatory medications, clinical improvement in the absence of a change in the pathologic anatomy of the disc, and the lack of correlation between symptoms or neurologic signs and the size of the disc herniation.
INFLAMMATION Acute inflammation is a response of living tissue to damage and it has three functions. The inflammatory exudates formed carry protein and fluid in cells from blood vessels to the damaged area to mediate local defenses. It also helps eliminate any infective agent that is present in the area, and helps break down damaged tissue, facilitating its removal from the site of the damage. Acute inflammation may result from physical damage, chemical substances, microorganisms, or other agents. The response results in changes in local blood flow and increased permeability of blood vessels that facilitates the escape of proinflammatory cells from the blood into the tissues. These changes are essentially the same whatever the cause and wherever the site. Usually, acute inflammation is a short-lasting process. However, the length of the process is probably dependent on the inciting cause. Hypersensitivity reactions are another cause of acute inflammation, as are physical agents such as tissue damage from trauma, ultraviolet or ionizing radiation, burns, or frostbite. Irritants and corrosive chemicals can cause inflammation and tissue necrosis. Lack of oxygen or necrosis is another mechanism by which acute inflammation can propagate. In this particular cause, the reduction of oxygen and nutrients resulting from inadequate blood flow or infarction is a potent inflammatory stimulus. Celsus described the four principal effects of acute inflammation nearly 2000 years ago (Table 3.1). These include redness from acute dilatation of small blood vessels within the area. Heat, or warmth, is usually seen only in the peripheral parts of the body such as the skin. It is also due to the increased blood flow or hyperemia through the
Table 3.1: Celsus’s original description of the characteristic signs of inflammation Erythema (rubor) Warmth (calor) Pain (dolor) (Loss of function was added by Virchow)
18
region from vascular dilatation. Swelling results from edema which is the accumulation of fluid in the extravascular space and from the physical mass of the inflammatory cells migrating to the area. Pain is one of the best-known features of acute inflammation and it results partly from the stretching and distortion of tissues due to the edema in the area. Chemical mediators of acute inflammation including bradykinin, the prostaglandins, and serotonin are also known to induce pain. Loss of function is a well-known consequence of inflammation added by Virchow to the list originated by Celsus. Movement of an inflamed area is consciously and reflexively inhibited by pain, while severe swelling or local muscle spasm may limit movement of the area. The acute inflammatory response involves three changes or processes. Changes in the vessel size and flow, increased vascular permeability and the formation of the fluid exudate, and migration or de-margination of polymorphonuclear leukocytes (PML) into the extravascular space are characteristic processes of acute inflammation. Briefly, these early stages involve small blood vessels adjacent to the area of the tissue damage, which become dilated with increased blood flow. As blood flow begins to slow, the endothelial cells swell and partially retract so that they form a leaky continuum within the blood vessel. The vessels become leaky, which permits the passage of water, salts, and small proteins into the damaged area. One of the main proteins to leak out during this period is fibrinogen. Circulating PMLs initially adhere to the swollen endothelial cells and then migrate through these channels created by the retracted endothelial cells and through the basement membrane, passing into the area of tissue damage. Later on, blood monocytes (macrophages) migrate in a similar way. The microcirculation consists of a network of small capillaries that lie between the arterioles. These microcapillaries initially experience an increased blood flow following the initial phase of arteriolar constriction, which is transient. Blood flow to the injured area may increase up to tenfold during this time, but then blood flow begins to slow down, allowing the leukocytes to de-marginate into the area. The slowing of this blood flow, which follows the phase of hyperemia, is due to increased vascular permeability and allows plasma to escape into the tissues while blood cells stay within the blood vessels. Blood viscosity is therefore relatively increased as the percentage of red cells relative to white cells and other proteins increases. The increased vascular permeability increases capillary hydrostatic pressure as well as allowing the escape of plasma proteins in the extravascular space. Instead of the usual return of fluid into the vascular space, however, proteins act to increase the colloid osmotic pressure in the extravascular space. Consequently, more fluid leaves the vessel than comes back and the net escape of protein rich fluid is called exudation. Experimental work has demonstrated three patterns of increased vascular permeability. There is an immediate response that is transient, lasting 30–60 minutes, mediated by histamine acting on the endothelium directly. A delayed response starts 2–3 hours after injury and may last for up to 8 hours. This is mediated by factors synthesized by local cells such as bradykinin or factors from the complement cascade, or those released from dead neutrophils in the exudate. A third response that can be prolonged for more than 24 hours is seen if there is a direct necrosis of the endothelium. In the later stages of acute inflammation where movement of neutrophils becomes important, experimental evidence has shown purposeful migration of neutrophils along a concentration gradient. This movement appears to be mediated by substances known as chemotactic factors diffusing from the area of damage. The main neutrophil chemotactic factors are C5a, LTB4, and bacterial components. These factors, when bound to the receptor on the surface of a neutrophil, activate secondary messenger systems stimulating increased cytosolic calcium with the assembly of cytoskeletal specializations that are involved in their ability to move.
Section 2: Spinal Pain
The spread of the inflammatory response following injury to a small area of tissue suggests that chemical substances are released from the injured tissues spreading out to uninjured areas. These chemicals are called endogenous mediators and contribute to the vasodilatation, de-margination of neutrophils, chemotaxis, and increased vascular permeability. Chemical mediators released from the cells include histamine, which is probably the best-known chemical mediator in acute inflammation. It causes vascular dilatation in the immediate transient phase of increased vascular permeability. This substance is stored in mast cells, basophils and eosinophils, as well as platelets. Histamine released from those sites is stimulated by complement components C3a and C5a, and by lysosomal proteins released from neutrophils. Lysosomal compounds are released from neutrophils and include cationic proteins that may increase vascular permeability and neutral proteases, which may activate complement. Prostaglandins are a group of long-chain fatty acids derived from arachidonic acid and synthesized by many cell types. Some prostaglandins potentiate the increase in vascular permeability caused by other compounds. Part of the antiinflammatory activity of drugs such as aspirin and nonsteroidal antiinflammatory drugs (NSAIDs) is attributable to inhibition of one of the enzymes involved in prostaglandin synthesis. Leukotrienes are also synthesized from arachidonic acid, especially in neutrophils, and appear to have vasoactive properties. SRS-A (slow-reacting substance of anaphylaxis) involved in type I hypersensitivity is a mixture of leukotrienes. Serotonin (5-hydroxytryptamine) is present in high concentration in mast cells and platelets and is a potent vasoconstrictor. Lymphokines are a family of chemical messengers released by lymphocytes. Aside from their major role in type IV sensitivity, lymphokines also have vasoactive or chemotactic properties. Within the plasma are four enzymatic cascade systems including the complement system, the kinins, the coagulation factors, and the fibrinolytic system, which are interrelated and produce various inflammatory mediators. The complement system is a cascade system of enzymatic proteins and can be activated during the acute inflammatory reaction in various ways. In tissue necrosis, enzymes capable of activating complement are released from dying cells. During infection, the formation of antigen–antibody complexes can activate complement via the classical pathway, while endotoxins of Gram-negative bacteria activate complement via the alternative pathway. Products of the kinin, coagulation, and fibrinolytic systems can also activate complement. The products of complement activation that are most important in acute inflammation include C5a, which is chemotactic for neutrophils, increases vascular permeability, and releases histamine from mast cells. C3a has similar properties to those of C5a, but is less active. C5, 6, and 7 are all chemotactic for neutrophils and, in combination with 8 and 9, have additional cytolytic activity. Finally, C4b, C2a, and C3b are all important in the opsonization of bacteria, which facilitates phagocytosis by macrophages. The kinin system includes the kinins, which are peptides of 9 to 11 amino acids that are important in increasing vascular permeability. The most important of these is bradykinin. The kinin system is activated by coagulation factor XII. Bradykinin is also an important chemical mediator of pain, which is a cardinal feature of acute inflammation. Within the coagulation system, factor XII, once it has been activated by contact with extracellular materials, will activate the coagulation, kinin, and fibrinolytic systems directly. This system is responsible for the conversion of soluble fibrinogen into fibrin, which is the major component of the acute inflammatory exudate. These fibrin degradation products result from the lysis of fibrin in the presence of plasmin. Within the fibrinolytic system, the fibrin degradation products have effects on local vascular permeability.
The PML is the characteristic cell in acute inflammation. Its ability to move in a response to a concentration gradient of chemotactic factors has been well demonstrated and is mediated by cytosolic calcium. Neutrophils are able to bind to bacterial components via their Fc receptor and are able to phagocytose various particles or organisms and partially liquefy them with toxic compounds contained within lysosomes. Following tissue damage or loss from any cause, including damage due to the inflammatory process, there may be resolution, regeneration, or repair. All of these processes may occur in the same tissue or begin as soon as there is significant tissue damage. Healing does not wait for inflammation or other mechanisms to subside, but usually takes place concurrently. The outcome depends on which of these three processes predominate and on a number of factors. Resolution tends to occur when there is little tissue destruction as well as a limited period of inflammation and short, successful treatment. Regeneration occurs when lost tissue is replaced by a proliferation of cells of the same type reconstructing the normal architecture. Regeneration proceeds based on cell type, and cells are usually classified into three groups based on their ability to regenerate. Labile cells are those that are normally associated with high rate of loss and replacement and therefore have a high capacity for regeneration. Stable cells do not normally proliferate to a significant extent but can be stimulated to do so after they have been damaged. Permanent cells are unable to divide after their initial development and therefore cannot regenerate when lost (i.e. neurons). Tissue architecture is also important. Simple structures are easier to reconstruct following damage than complex ones. An imperfect attempt at regeneration can have important clinical consequences such as the cirrhosis that results after damage to the liver and the resulting abnormal nodular architecture from the repair. This process is also dependent on the amount of tissue loss. There must be cells left in the area to regenerate, as well as a reasonable volume to regenerate prior to scar formation. In repair, the process results in formation of a fibrous scar from the granulation tissue. Following the acute inflammation and phagocytosis of necrotic debris and other foreign material, blood vessels proliferate and fibroblasts assemble at the edge of the damaged area. As the endothelial cells and fibroblasts grow into the damaged area, vascularization also proceeds. Fibroblasts continue to proliferate, producing collagen and giving the tissue mechanical strength; eventually a scar consisting of dense collagen results. Factors influencing healing include the rate of healing, the presence of foreign material or of continuing inflammation, inadequate blood supply, abnormal motion, or certain medications that inhibit this process. Systemically, the healing process becomes less effective and slower with increasing age. Nutritional deficiencies play an important role as well as metabolic diseases such as renal failure or diabetes mellitus. Some patients with ongoing malignancies are actually in a catabolic state and unable to heal even simple wounds. Additionally, corticosteroids are important systemic inhibitors of wound healing.
The process of inflammation Inflammation is a complex, stereotypical reaction of the body in response to damage of cells in vascularized tissues. In avascular tissue such as the normal cornea or within the disc space, true inflammation does not occur. The cardinal signs of inflammation presented earlier, including redness, swelling, heat, pain and deranged function, have been known for thousands of years. The inflammatory response can be divided temporally into hyperacute, acute, subacute, and chronic inflammation. The response can be based on the degree of tissue damage, such as superficial or profound, or on 19
Part 1: General Principles
the immunopathological mechanisms such as allergic, or inflammation mediated by cytotoxic antibodies, or inflammation mediated by immune complexes, or delayed-type hypersensitivity reactions. As presented earlier, the development of inflammatory reactions is controlled by cytokines, by products of the plasma enzyme systems (complement, the coagulation system, the kinin and fibrinolytic pathways), by lipid mediators (prostaglandins and leukotrienes) released from different cells, and by vasoactive mediators released from mast cells, basophils, and platelets. These inflammatory mediators controlling different types of reactions differ from one another. Fast-acting mediators such as the vasoactive amines and the products of the kinin system modulate the immediate response. Later, newly synthesized mediators such as leukotrienes are involved in the accumulation and activation of other cells. Once the leukocytes have arrived at the site of inflammation, they release mediators that control the later accumulation and activation of other cells. However, it is important to realize that in inflammatory reactions initiated by the immune system the ultimate control is exerted by the antigen itself, in the same way as it controls the immune response itself. For this reason, the cellular accumulation at the site of a chronic infection or in an autoimmune reaction is quite different from that at sites where the antigenic stimulus is rapidly cleared. Inflammation can become chronic. In certain settings, the acute process, characterized by neutrophil infiltration and edema, gives way to a predominance of mononuclear phagocytes and lymphocytes. This probably occurs to some degree with the normal healing process that becomes exaggerated and chronic when there is an effective elimination of foreign material as in some infections, or introduction of foreign bodies, or deposition of crystals, or persistent inflammatory product secretions such as disc herniations.
Inflammatory cells Mast cells and basophils Mast cells and basophils play a central role in inflammation and immediate allergic reactions. They are able to release potent inflammatory mediators such as histamine, proteases, chemotactic factors, cytokines, and metabolites of arachidonic acid that act on the vasculature, smooth muscle, connective tissue, mucous glands, and inflammatory cells. Mast cells settle in the connective tissue and usually are not circulating in the bloodstream. Basophils are the smaller circulating granulocytes that settle into the tissues upon stimulation. Both these types of cells contain special cytoplasmic granules which store these mediators of inflammation. The release of these mediators is known as degranulation and can be induced by physical destruction such as mechanical trauma, or chemical substances such as proteases, or endogenous mediators including tissue proteases or cationic proteins derived from eosinophils and neutrophils, or immune mechanisms which may be IgE dependent or IgE independent. Neutral proteases, which account for the vast majority of the granule protein, serve as markers of mast cells and different types of mast cells. The newly generated mediators, often absent in resting mast cells, are typically produced during IgE-mediated activation and consist of arachidonic acid metabolites, principally leukotriene C4 (LPC4), and prostaglandin D2 (PGD2), and cytokines. Of particular interest in humans is the production of tumor necrosis factor (TNF-αγ, IL-4, IL-5, and IL-6). In the cytoplasm of both mastocytes and macrophages are special granules called lipid bodies where metabolism of arachidonic acid occurs and where their products, including leukotrienes, may be stored.
20
Eosinophils Eosinophils are terminally differentiated end-stage leukocytes that reside predominantly in submucosal tissue and are recruited at the sites of specific immune reactions including allergic diseases. Like other granulocytes, they possess a polymorphous nucleus, although with only two lobes and no nucleus. The eosinophil cytoplasm contains large ellipsoid granules. Recently, it has been recognized that eosinophils are capable of elaborating cytokines that include those with potential growth factor activities and those with potential roles in acute and chronic inflammatory responses. Cytokines produced by human eosinophils that have activity in acute and chronic inflammatory responses include IL-1α, IL-6, IL-8, TNF-α, and both transforming growth factors TGF-α and TGF-β. In addition to the acute release of protein, cytokine, and lipid mediators of inflammation, eosinophils likely contribute to chronic inflammation including the development of fibrosis. Additional roles for the eosinophil modulating extracellular matrix deposition and remodeling are suggested by studies of normal wound healing. During dermal wound healing, eosinophils infiltrate into the wound site and sequentially express TGF-α early and TGF-β later during wound healing.
Neutrophils Neutrophils, also known as polymorphonuclear leukocytes, represent 50–60% of the total circulating leukocytes and constitute the first line of defense. Once an inflammatory response is initiated, neutrophils are the first cells to be recruited. Neutrophils contain granules which contain antimicrobial or cytotoxic substances, neutral proteinases, acid hydrolases, and a pool of cytoplasmic membrane receptors. The granules contain, in addition to other substances, serine proteases such as elastase and cathepsin-G, which hydrolyze protein in cell envelopes. Substrates of granulocyte elastase include collagen crosslinks and proteoglycans, as well as elastin components of blood vessels, ligaments, and cartilage. Cathepsin-G cleaves cartilage proteoglycans while granulocyte collagenases are active against type I, and to a lesser degree type III collagen from bone, cartilage, and tendon. Collagen breakdown products have chemotactic activity for neutrophils, monocytes, and fibroblasts. Although neutrophils are essential to host defense, they have also been implicated in the pathology of many chronic inflammatory conditions and ischemia– reperfusion injury. This may be triggered by substances released from damaged host cells or as a consequence of superoxide generation through xanthine oxidase. Neutrophils, macrophages, endothelial, and other cells produce two types of free radicals. The first type is represented by reactive oxygen intermediates that are formed in neutrophils by the activity of NADPH oxidase. The second type includes reactive nitrogen intermediates such as nitric oxide. Reactive nitrogen intermediates have been of some interest in low back-associated pain. These are sometimes called reactive oxynitrogen intermediates. The pathway by which they are originated is an oxidative process in which short-lived nitric oxide is derived from the guanidino nitrogen in the conversion of L-arginine to L-citrulline. This reaction is catalyzed by nitric oxide synthase (NOS) and, like the respiratory burst, it involves oxygen uptake. Three distinct isoforms of nitric oxide synthase representing three distinct gene products have been isolated and purified. The three isoforms vary considerably in their subcellular location, structure, kinetics, regulation, and hence functional roles. Two of the enzymes are constantly present and termed constitutive NOS (cNOS). The endothelial cNOS is mostly membrane bound and formed only in endothelial cells. The neuronal cNOS was identified in cytosol or central and peripheral neurons. The third isoform is an
Section 2: Spinal Pain
inducible form that is not present in resting cells. Cytokines are a potent stimulus for iNOS production or suppression. Those with an apparent stimulating effect include IFN-γ, IL-1, IL-6, TGF-α, GMCSF, and PAF (platelet activating factor) while suppression has been observed by IL-4, IL-8, IL-10, TGF-β, PDGF (platelet derived growth factor), and MDF (macrophage deactivating factor). Cytokines are basic regulators of all neutrophil functions. Many of them, including somatesthetic growth factors and pyogens, have shown to be potent neutrophil priming agents. Neutrophils are also capable of de novo synthesis and secretion of small amounts of some cytokines including IL-1, IL-6, IL-8, TNF-α and GM-CSF. Bioactive lipids originate mainly from arachidonic acid which is an abundant constituent of neutrophil membranes. Arachidonic acid is metabolized to prostaglandins, leukotrienes, and lipoxins. LTB4 is a strong neutrophil chemoattractant that may play a role in the priming process. Vasoactive leukotrienes LTC4, LTB4, and LTE4 increase microvascular permeability and may contribute to ischemia–reperfusion injury. In contrast to leukotrienes, prostaglandins suppress most neutrophil functions, possibly through their ability to elevate intracellular cyclic AMP.
Macrophages Macrophages can be divided into normal and inflammatory macrophages. A macrophage population in a particular tissue may be maintained by three mechanisms: the influx of monocytes from the circulating blood, local proliferation, and biologic turnover. Under normal steady-state conditions, the renewal of tissue macrophages occurs through local proliferation of progenitor cells and not by monocyte influx. Inflammatory macrophages are present in various exudates. Very specific markers such as peroxidase activity may characterize them and, since they are derived exclusively from monocytes, they share similar properties. Macrophages are generally a population of ubiquitously distributed mononuclear phagocytes responsible for numerous homeostatic, immunologic, and inflammatory processes. Their wide tissue distribution make these cells well suited to provide an immediate defense against foreign elements prior to leukocyte immigration. Macrophages display a wide range of functional and morphologic phenotypes. The term activated macrophages is reserved for macrophages possessing specifically increased functional activity. There are two stages of macrophage activation. The first is a prime stage in which macrophages exhibit enhanced MHC class II expression, antigen presentation, and oxygen consumption, but reduced proliferation. The agent that primes macrophages for activation is IFN-γ, a product of stimulated TH1 and TH0 cells. Other factors including IFN-α, IFN-β, IL-3, M-CSF, GM-CSF, and TNF-α can also prime macrophages for select functions. Primed macrophages respond to secondary stimuli to become fully activated, the stage defined by their inability to proliferate, high oxygen consumption, killing of facultative and intercellular parasites, tumor cell lysis and maximal secretion of the mediators in inflammation including TNF-α, PGE2, IL-1, IL-6, and reactive oxygen species of nitric oxide production by iNOS. Macrophages are important producers of arachidonic acid and its metabolites. Upon phagocytosis, macrophages release up to 50% of their arachidonic acid for membranous esterified glycerol phospholipid. It is immediately metabolized into different types of prostanoids. From them, prostaglandins, especially PGE2 and prostacyclin (PGI2), are characterized as proinflammatory agents. They induce vasodilation, act synergetically with complement components C5a and LTB4, and mediate myalgia response to IL-1. In combination with
bradykinin and histamine, they contribute to edema and pain induction. Thromboxane (TXA2) is considered an inflammatory mediator that facilitates platelet aggregation and triggers vasoconstriction. Neovascularization is an important component of inflammatory reactions and subsequent repair and remodeling processes. Some diseases such as arthritis are maintained by persistent neovascularization. Macrophages are very important to this process. The angiogenic activity of macrophages is associated with their secretory activity in an active state. Macrophages become angiogenic when exposed to low oxygen conditions or to wound-like concentrations of lactate, pyruvate, or hydrogen ions. They can also be activated by cytokines such as IFN-γ, GM-CSF, PAF, or MCP (monocyte chemoattractant protein).
Mediators of inflammation In addition to the previously mentioned cell types, there are several chemical mediators of inflammation. There is considerable redundancy of these mediators. The most important vasoactive mediators stored in mast cells and basophil granules are histamine and serotonin. These are both also present in human platelets. Histamine has diverse functions including dilation of small vessels, locally increased vascular permeability by endothelial cell contraction, chemotaxis for eosinophils, and blocking of key T-lymphocyte function. Serotonin is also capable of increasing vascular permeability, dilating capillaries, and producing contractions of nonvascular smooth muscle.
Lipid mediators The major constituents of cell membranes are phospholipids. Cellular phospholipase, especially phospholipase A2 and C, are activated during inflammation and degrade phospholipids to arachidonic acid. Arachidonic acid has a short half-life and can be metabolized by two major routes, the cyclooxygenase and the lipoxygenase pathways. The cyclooxygenase pathway produces prostaglandins, prostacyclins, and thromboxanes. The lipoxygenase pathway produces either leukotrienes or lipoxins. The prostaglandins are a family of lipid-soluble hormone-like molecules produced by different cell types in the body. For example, macrophages and monocytes are large producers of both PGE2 and PGF2. Neutrophils produce moderate amounts of PGE2, and mast cells produce PGD2. PGE2 enhances vascular permeability, is pyrogenic, and increases sensitivity to pain. Prostaglandins must be synthesized and released in response to an appropriate stimulus and do not exist free in tissues. Thromboxin A2 is produced by monocytes and macrophages as well as platelets. It causes platelets to aggregate and vasoconstriction. These effects are somewhat opposed by the action of prostacyclin which is a potent vasodilator. Leukotrienes LTD4 and 5-hydroxyeicosatetranoate (5-HETE) cause the chemotaxis and chemokinesis of several cell types including neutrophils. They are spasmogenic and cause contraction of smooth muscle and have effects on mucous secretion. Lipoxins LXA4 and LXB4 stimulate changes in microcirculation.
Products of the complement system Complement is a complex system containing more than 30 different glycoproteins present in the serum in the form of components, factors, or other regulators, and on the surface of different cells in the form of receptors. The components of the classical pathway are numbered 1–9 and in prefix by the letter ‘C.’ All these pathways use C5–C9
21
Part 1: General Principles
that form the membrane attack complex (MAC). Activation of each of the components results from the proteolytic cleavage event in a cascade mechanism. The complement system influences the activity of numerous cells, tissues, and physiologic mechanism of the body. The result of cytotoxic complement reaction may be beneficial or harmful to the body. The complement system is a potent mechanism for initiating and amplifying inflammation. This is mediated through fragments of complement components. Tissue injury following ischemic infarction may also cause complement activation and abundant deposition of membrane attack complex may be readily seen in tissue following ischemic injury.
Cytokines mediating inflammatory functions Cytokines are soluble glycoproteins that act nonenzymatically through specific receptors to regulate cell functions. Cytokines make up the fourth major class of soluble intercellular signaling molecules with neurotransmitters, endocrine hormones, and autocoids. Cytokines are synthesized, stored, and transported by many different cell types. Lymphokines are cytokines that are secreted mainly by activated T lymphocytes and monokines are produced by activated macrophages and monocytes. In order to unify the terminology of these factors, the term interleukin was accepted. Besides the term expressing their origin, cytokines can also be named according to their function as are interferons and others. Cytokines are directly responsible for the temporal amplitude and duration of the immune response as well as tissue remodeling. Individual cytokines can have widely varying responses and functions depending on cell type, concentration, and the synergistic or modulating effects of other cytokines. The information that an individual cytokine conveys depends on a pattern of regulators to which a cell is exposed and not on just a single cytokine. There is no doubt that cytokines contribute to the signs, symptoms, and pathology of inflammatory, infectious, autoimmune, and malignant diseases. TNF-α is an excellent example. Locally, it has important regulatory and antitumor activities but when TNF-α circulates in higher concentrations it may be involved in the pathogenesis of endotoxic shock, cachexia, and other serious diseases. Inflammation is dependent on both pro- and antiinflammatory cytokines. Proinflammatory cytokines are produced predominantly by activated macrophages and are involved in the upregulation of inflammatory reactions. Antiinflammatory cytokines belong to the T-cell-derived cytokines and are involved in the downregulation of inflammatory reactions. The central role in inflammatory responses involves IL-1 and TNFα. Antagonists to IL-1 (IL-1ra) and TNF-α may become important clinically in the treatment of some rheumatologic conditions such as ankylosing spondylitis and rheumatoid arthritis. IL-1 and TNF-α with IL-6 serve as endogenous pyrogens. The upregulation of inflammatory reactions is also performed by IL-11, IFN-α, IFN-β, and especially by the members of the chemokines superfamily. On the other hand, antiinflammatory cytokines (IL-4, IL-10, and IL-13) are responsible for the downregulation of the inflammatory response. The production of most lymphokines and monokines such as IL-1, IL-6, and TNF-α is also inhibited by TGF-β. However, TGF-β has a number of proinflammatory activities including chemoattractant effects on neutrophils, T lymphocytes, and nonactivated monocytes. TGF-β has been demonstrated to have in vivo immunosuppressive and antiinflammatory effects, as well as proinflammatory and selected immunoenhancing activities. When administered systemically, TGF-β acts as an inhibitor, but if given locally it can promote inflammation. Generally, TGF-β stimulates neovascularization and the proliferation and activities of connective tissue cells, and is a pivotal factor in scar formation and wound healing. But TGF-β has antiproliferative effects on most 22
other cells including epithelial cells, endothelial cells, smooth muscle cells, myeloid, erythroid, and lymphoid cells.
Chemokines Chemokines represent a superfamily of chemotactic cytokines acting as initiators and potentiators of antiinflammatory reactions. They are active over a high concentration range, and are produced by a wide variety of cell types. Exogenous irritants and endogenous mediators such as IL-1, TNF-α, PDGF and IFN-γ induce the production of chemokines, and because they bind to specific cell surface receptors they are considered second-order cytokines. Additionally, most chemokine molecules share structural similarities and function, and are attractants for many different types of cells.
BIOCHEMISTRY OF DISC DEGENERATION The biochemical events that occur with intervertebral disc degeneration and, in particular, the role of biochemical mediators of inflammation and tissue degradation, have received more attention in the literature over the last 10 years. Matrix metalloproteinases (MMPs), prostaglandin E2 (PGE2), and a variety of cytokines have been shown to play a role in the degradation of articular cartilage. Nitric oxide is another mediator. The clinical presentation of acute lumbar radiculopathy is most often attributed to a compressed lumbar nerve root by a herniated intervertebral disc. It is well-known and something of a paradox that some patients with large herniations have no radicular symptoms and, in contrast, some patients with no evidence of disc herniations have severe radiculopathy. While the mechanics of nerve root compression undoubtedly play a role in the pain, it probably only partially explains the exact pathophysiology of the radiculopathy.
MMPs, cytokines, and nitrous oxide Matrix metalloproteinases (MMPs) are thought to be responsible for the turnover of the extracellular matrix within the nucleus pulposus and anulus fibrosus. Their activity is controlled on at least three levels. First, they are upregulated by cytokines such as interleukin-1 via gene expression, and also by TNF-αγ. Next, MMPs are latent in their proform, requiring activation prior to reaching their full degradative potential. And lastly, MMPs are inhibited in connective tissue by a number of TIMPs (tissue inhibitors of metalloproteinases). MMPs come in several different varieties. The most commonly investigated ones in terms of intervertebral disc degeneration have been MMP2 (gelatinase-α) and MMP3 (stromelysin). Kang investigated stromelysin production as well as production of nitric oxide IL-6 and PGE2, comparing 18 herniated lumbar discs with 8 control discs obtained from patients undergoing anterior surgery for scoliosis and burst fractures.2 Kang examined gelatinase, stromelysin, as well as collagenase activity. His group found a nearly sixfold increase in gelatinase among the herniated disc samples compared to the controls. Collagenase production was absent in the control subjects and nonsignificantly elevated in the herniated discs. Caseinase (or stromelysin – MMP3) showed an approximately fourfold increase in the herniated samples compared with the control discs. This early finding and the activity of MMPs in herniated disc samples was interesting, especially in the case of caseinase (stromelysin) which is known to degrade the core protein of cartilage proteoglycans. The progressive loss of these proteoglycans within the nucleus pulposus is believed to be one of the central reasons behind its desiccation and failure to retain its water content. The high levels found in the herniated discs probably repre-
Section 2: Spinal Pain
sent the levels found in the degenerative discs compared to the lower level of MMP activity in the normal discs. It is likely that the smaller or lower activity of the MMPs in the normal discs reflects a basal amount of MMP activity responsible for ongoing remodeling of the disc architecture. The high MMP production in the herniated discs is likely a result of the increased inflammatory mediators produced within the discs or in the immediate area of the discs because of the inflammation. IL-1 is known to have a positive modulating response on the MMPs. In the presence of a high IL-1 concentration and a low or relatively low TIMP concentration, the degradative enzymes may be expected to flourish. In a follow-up study to this article, Kang et al. reported on the effect of interleukin-1β on control and herniated discs using samples from the lumbar and cervical spine.3 They showed significantly elevated MMP production in the form of gelatinase and stromelysin by normal nondegenerated disc specimens after the addition of IL-1β. The basal levels of gelatinase and stromelysin were already increased in the lumbar and cervical degenerative disc specimens and the addition of IL-1β to these cultures did not significantly increase them. Collagenase activity was not detected. An interesting control in this last study was the use of L-NMA (nmonomethyl-L-arginine) to block endogenously produced NO. Cells were cultured (control and diseased) in the presence of L-NMA in order to study the effects of endogenously produced nitrous oxide on the other mediators. When L-NMA was added to the nondegenerate control specimens that had been stimulated with IL-1β, the production of gelatinase was significantly decreased, but not the production of stromelysin. When this same effect was studied in herniated lumbar discs that were stimulated with IL-lβ, both gelatinase and stromelysin were significantly reduced. Interestingly, the same study done on the herniated cervical discs stimulated with IL-1β had no significant effect on gelatinase or stromelysin.3 Several other authors have studied MMPs and their association with intervertebral disc degeneration. Fujita et al. studied autopsy specimens of degenerative discs.4 They first discovered serine elastases with high activity in the endplate and nucleus pulposus of degenerative discs. Another group using a monoclonal antibody against MMP3, found the MMP3-positive cell ratio was significantly correlated with the magnetic resonance imaging grade of intervertebral disc degeneration. The MMP3-positive cell ratio observed in prolapsed lumbar
intervertebral discs was significantly higher than in nonprolapsed discs. The same study used an anti-TIMP1 monoclonal antibody to demonstrate the normal presence of MMP3 and TIMP1 together in the degenerative intervertebral discs and hypothesized that an imbalance between MMP3 and TIMP may induce degeneration. IL-1 is a known mediator of mesenchymal cells and probably has a central role in disc degeneration. It is one of the key inflammatory mediators and it has been found in mononuclear cells responding to disc herniations. The studies on human disc tissue have had difficulty demonstrating IL-1β in the intervertebral disc tissues, but when disc cells were stimulated with lipopolysaccharide, elevated levels of IL1β were found. Both MMP2 (gelatinase) and MMP3 (stromelysin) respond to IL-1. In an experiment using ovine disc cells, Shen et al. demonstrated the ability of IL-1 to enhance the in vitro production of MMP2 and MMP3 by cells of the nucleus pulposus.5 However, the active form of MMP3 predominated over the active form of MMP2 in this model of IL-1 activation. This suggests that, in the presence of IL-1 as an inflammatory mediator, MMP3 may be more intimately involved with ongoing intervertebral disc degeneration than is MMP2. Therefore, the MMPs appear to be key factors in disc degeneration (Fig. 3.1). 3. They are the active form of the enzymes that they produce, and are capable of degrading constituents of the extracellular matrix and basement membrane at physiologic pH values. Substrates for these MMPs are present in abundance in the disc: collagens II and III are substrates for MMP1, MMP8 and MMP13, as well as their proteoglycans and other minor collagens which are substrates for MMP2 and MMP9. Compared with healthy discs, degenerative discs have been noted to have higher activities of not only MMP3 and MMP7, but also TIMP1. MMP3 activity has been correlated to the size of osteophytes present in disc degeneration. Inhibitors of MMPs have been found in low levels and are constitutively expressed. TIMP2 appears to be released by most cell types within the discs, whereas TIMP1 appears to be exclusively overexpressed in discs with degenerative disease. These expressions of MMPs and TIMPs have also been measured in spines with presumed abnormal biomechanical loading characteristics such as those with scoliosis. Handa et al. showed that proteoglycans and inhibitors of MMPs were produced in increased amounts under hydrostatic conditions when loads were increased to within a normal range.6 Taking these loads to abnormally high pressures resulted in decreased proteoglycan production and an increased production of MMP3.
Resident chondrocytes
TNF-α
Macrophage infiltration of disc tissue
Neurovascularization
Nerve conduction velocity reduction
Factories for production of inflammatory mediators (TNF-α, IL-1, IL-6, NO)
Nerve ingrowth
Nerve sensitization DRG sensitization
Back pain
Radiculopathy
Nitric oxide
↓
MCP-1 IL-8
MMP3/TIMP
Matrix degradation response to abnormal loading
Disc degeneration
↓
Upregulation
MMP-7 TNF-α
IL-1 (Many sources)
MMP2/MMP3
Nitric oxide
Matrix degradation
Nerve effects
Back pain
IL-6/PGE2
Radiculopathy
Fig. 3.1 MMPs as key factors in disc degeneration. 23
Part 1: General Principles
Much of the work involving the study of MMP activation and measurement has been done using tissue obtained from patients operated on for herniated discs. Therefore, many of these publications include the fact that the assay was done on disc tissue that had been presumably exposed to some type of a burst of inflammation after exposure to the epidural space. It has been proposed that patients with herniated, sequestered, or noncontained herniations may have a more severe inflammatory reaction and pain response. Nygaard et al. looked at 37 patients undergoing surgery for lumbar disc herniation.7 They divided the patients into those who had a bulging disc, a contained or incomplete herniation, or a noncontained or sequestered free disc fragment. Unfortunately, they were unable to recruit enough patients with bulging discs to investigate this phenomenon statistically. In looking at the two groups with the largest number of patients, including the contained herniation group which had 25 members and the noncontained herniation group which had 9 members, there was a significant difference in the mean concentrations of LTB4, with the noncontained group having almost double the concentration versus the contained herniation group. As well, thromboxane B2 was significantly higher in the noncontained versus the contained herniation group. Although the measured concentration of these two proinflammatory cytokines was lower in the bulging disc, their numbers were too small to be included in the statistical analysis. This study seems to support the theory that there are different inflammatory characteristics of different degrees of disc herniations. One of the other paradoxes in the delineation of an inflammatory response for disc herniation has to do with the atypical cellular response when compared to inflammation occurring at other places in the body. Neutrophils are the sine qua non of acute inflammation; however, they have really only been found in noncontained or sequestered disc fragments where neovascularization may be occurring. Most of the cellular elements that have been identified and are proposed to be the source or factories for most of the inflammatory cytokines are macrophages. Gronblad,8 Nojara,9 Yasuma,10 and Haro11 have identified macrophages as well as vascular proliferation in the granulation tissue of herniated discs. Haro additionally found that inflammatory cells were more abundant in the noncontained group of disc herniations than in the contained group. Inflammatory cells are known to act in an autocrine or paracrine type fashion with regard to their effect on resident cells in the inflammatory process. This must also be true for the degenerative disc. The intervertebral disc, which is normally nourished through diffusion, can become neovascularized to some extent after exposure to the epidural space. These discs display granulation tissue with macrophage and T-lymphocyte infiltration not observed in healthy discs. Haro et al. have proposed that the natural resorption of a herniated disc appears to occur by a vascularization-mediated process and is correlated with macrophage infiltration. It is also known that chondrocytes replace proteoglycans within the nucleus pulposus and these cells have been proposed to play a very important role in the inflammatory process in regards to production of abnormal types of collagen as well as MMPs and TIMPs in response to abnormal loading characteristics. Haro et al. reported their results in a co-culture system of chondrocytes and macrophages and demonstrated a marked upregulation of MMP3 by disc chondrocytes with the addition of macrophages to the culture system. This resulted in eventual resorption of the disc through macrophage action. They further used MMP-null mice to determine that the production of MMP3 by the chondrocytes was required for macrophage infiltration in disc resorption. In a more recent study, this same group has shown that the production of MMP7 by macrophages was found to be required for infiltration into disc tissue through a mechanism involving the release of soluble TNF-α.12 24
The support for macrophage-mediated cellular response in herniated disc tissue is also supported by another study by Haro. While macrophage invasion appears to accompany and participate in the inflammatory response, the likely end to this is reabsorption of the herniated disc tissue. Groups have proposed neovascularization of these disc tissues as the means by which this happens. Previous studies have shown that resorption may be mediated by neovascularization as measured through Gd-DTPA MRI. Komori showed that the tendency of these herniated disc tissues to spontaneously resorb was proportional to the degree of Gd-DTPA enhancement, which suggests that the resorption was mediated by a vascular event.13 Haro and his group have shown that, in an in vitro co-culture system they have used previously, an increase in macrophage VEGF protein (vascular endothelial growth factor) and mRNA expression was observed after they exposed disc tissue to the co-culture.14 They found TNF-α was required for induction of VEGF protein and conclude that this may be one mechanism for resorption for herniated disc tissue. Further evidence for the involvement of the macrophage and its importance is shown in the paper by Burke et al.15 This group studied the production of monocyte chemoattractant protein-1 (MCP1) and interleukin-8 (IL-8) by intervertebral discs removed after surgery. Burke found that MCP1 and IL-8 were detected in both the control and herniated disc specimens and that the noncontained herniated samples contained higher levels of these chemokines than those with an intact anulus. They proposed that the MCP1 production attracts the macrophages while IL-8 may influence the angiogenesis or the neovascularization that is seen in these samples. Although the stimulus for MCP1 in this in vitro experiment was not investigated and is as yet unknown, this may represent a physiologic mechanism for initiation of macrophage infiltration after disc prolapse and the process of disc resorption. IL-8 was also strongly influenced by the noncontained morphology of these samples. In addition to the angiogenic properties of IL-8, it is also chemotactic for T cells that have been identified in the chronic inflammatory filtrate around disc herniations. In addition to TNF activation of or paracrine/autocrine effects governing MMP production, TNF-αγ has long been regarded to be a key player in mediating the sensitization of nerve roots by material from the nucleus pulposus, and other effects such as edema, intervascular coagulation, reduction in blood flow, and the splitting of myelin. TNF-αγ is known to be released from the chondrocyte resident cells in the nucleus pulposus. In a local application of TNF-αγ, it induced a reduction in nerve conduction velocity in a porcine experiment done by Aoki et al.16 In this study, applications of interleukin-1β and interferon-γ induced a very small reduction of nerve velocity compared with epidural fat. In a follow-up study to this, Olmarker and Rydevik demonstrated that local blockers to TNF-αγ prevented the reduction of nerve conduction velocity and seemed to limit the nerve fiber injury and intercapillary thrombus formation, as well as the intraneural edema seen in the absence of the inhibitor.17 These authors have suggested that TNF-αγ inhibitors may be important therapeutically in the future. Presently, synthesis of TNF-αγ can be blocked with systemic corticosteroids, IL-10, TGF-βγ or by other drugs such as chlorpromazine, pentoxifylline, or ciclosporin. However, these drugs are non-specific inhibitors and may result in side effects that would be undesirable. Presently, there are anti-TNF agents being used in the treatment of rheumatoid arthritis. The first of these, infliximab (Remicade), was quickly followed by etanercept (Enbrel). Recently, a monoclonal antibody against TNF-αγ, adalimumab (Humira), has been released. These agents are not presently approved for treatment of sciatic pain, but have given sufferers of rheumatoid arthritis a further dimension for their treatment. Another potent inflammatory mediator that is also induced by TNF-αγ is nitric oxide. Nitric oxide is a particularly interesting
Section 2: Spinal Pain
Table 3.2: Temporal relationships in disc degeneration Pre-adolescence
Adolescence
Early Adulthood
Middle Adulthood
Late Adulthood
Matrix remodeling for ‘slow growth’
Highest period of weightbearing linear growth
Continued matrix imbalance
Continued structural imbalances
Structural loss of height stable
No inflammogenic changes
Matrix remodeling imbalances
Collagen isotype switch ↑chondrocyte nests
Chronic and acute on chronic inflammation
In vivo collapse and autofusion or
Loss of proteoglycan
Inflammogenic events (e.g. injury, abnormal motion)
Desiccation and breakdown of anulus
In vivo collapse with facet joint incompetence and instability
Onset of early degeneration
Structural changes – loss of height
compound in that it has been shown to act in various ways depending on the tissues that in which it resides. In bone, mechanical stress affects intracellular cyclic AMP, calcium, and PGE2 levels, as well as having effects on matrix synthesis. It has been demonstrated that nitric oxide is a key mediator of these processes. Articular chondrocytes have been shown to produce large amounts of nitric oxide. As described in the preceding sections introducing the inflammatory process, nitric oxide is produced in several forms including the inducible form that is present in chondrocytes. Kang et al. first showed the spontaneous production of nitric oxide from human lumbar discs and that this production was higher in herniated discs than normals.2 In a follow-up study, Kang et al. examined the effects of IL-1β on normal and herniated disc tissue. They found that the addition of IL-1βγ caused a significant increase in the production of nitric oxide as well as IL-6 and PGE2.3 While these inflammatory mediators were sharply increased in both normal and herniated disc tissue, the interesting point to this paper was that MMP production did not change in the herniation disc material, while the normal disc showed a sharp increase in the production of MMPs. It is also noted by this group that endogenously produced nitric oxide had a large inhibitory effect on IL-6.
PUTTING IT ALL TOGETHER The inflammatory basis for intervertebral disc degeneration likely begins at or around the time of puberty when linear growth accelerates. It is possible that the rapid growth rate seen during this time outstrips the ability of the intervertebral disc to remodel effectively, leading to imbalances in MMP and TIMP concentrations. This may be further enhanced by increased diffusional demands for nutrition and a less than desirable pH balance within the disc (Table 3.2). As the process continues, changes in collagen isotype and loss of proteoglycan support occur and nests of chondrocytes replace normally aggregating proteoglycans. These chondrocytes likely become the factories for continued MMP and TIMP production as well as the source for inflammatory mediators. As the changes progress outward toward the disc anulus and involve the ability of the disc to respond to loads, chondrocyte proliferation continues and collagen fragmentation secondary to abnormal loading initiates an inflammatory response within the disc. As the process continues toward the periphery, the anulus begins to fail under the increased stiffness of the FSU and the inflammatory cascade promulgates. Macrophages are recruited and produce multiple inflammatory mediators. Granulation tissue around the disc containing these cells is a source for continuing inflammation
Changes contributing to DJD or stenosis
as well as the neovascularization that both potentiates the response and serves as a nidus for nerve invasion of the outer anulus. Inflammatory mediators such as bradykinin, nitric oxide, and TNF-αγ may directly affect local nerves having effects on conduction velocity and sensitizing nerve endings to normally benign motion. As well, the effect on perineural vascularity and edema is pronounced in the presence of these mediators. These proinflammatory contributors may help explain the previously mentioned paradox concerning a lack of evidence supporting compression per se in causing spinal nerve pain. Researchers continue to unravel the temporal relationships as well as new ways of treating this common entity. Solution of the a priori ‘first cause’ for degenerative disc disease will probably await our ability to genetically replace damaged discs. Such research is ongoing in several centers and deserves support.
References 1. Stokes I, Greenapple DM. Measurement of surface deformation of soft tissue. J Biomech 1985; 18:107. 2. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21(3):271–277. 3. Kang JD, Stefanovic-Racic M, McIntyre LA, et al. Toward a biochemical understanding of human intervertebral disc degeneration and herniation: contributions of nitric oxide, interleukins, prostaglandin E2, and matrix metalloproteinases. Spine 1997; 22(10):1065–1073. 4. Fujita K, Nakagawa T, Hirabayashi K, et al. Neutral proteinases in human intervertebral disc: role in degeneration and probable origin. Spine 1993;1 8(13):1766–1773. 5. Shen B, Melrose J, Ghosh P, et al. Induction of matrix metalloproteinase-2 and -3 activity in ovine nucleus aragose gel culture by interleukin-1β: a potential pathway of disc degeneration. Eur Spine J 2003; 12:66–75. 6. Handa T, Ishihara H, Ohshima H, et al. Effects of hydrostatic pressure on matrix synthesis and matrix metalloproteinase production in the human lumbar intervertebral disc. Spine 1997; 22(10):1085–1091. 7. Nygaard ØP, Mellgren SI, Østerud B. The inflammatory properties of contained and noncontained lumbar disc herniation. Spine 1997; 22(21):2484–2488. 8. Gronblad M, Virri J, Ronkko S, et al. Type (group II) phospholipase A2 and inflammatory cells in macroscopically normal, degenerated, and herniated human lumbar disc tissues. Spine 1996; 21(22):2531–2538. 9. Nojara. Marseilles: ISSLS Presentation; 1993. 10. Yasuma T, Arai K, Yamauchi Y. The histology of lumbar intervertebral disc herniation. The significance of small blood vessels in the extruded tissue. Spine 1993; 18(13):1761–1765. 11. Haro H, Shinomiya K, Komori H, et al. Upregulated expression of chemokines in herniated nucleus pulposus resorption. Spine 1996; 21:1647–1652.
25
Part 1: General Principles 12. Haro H, Crawford HC, Fingleton B, et al. Matrix metalloproteinase-7-dependent release of tumor necrosis-αγ in a model of herniated disc resorption. J Clin Invest 2000; 105(2):143–150. 13. Komori H, Okawa A, Haro H, et al. Contrast-enhanced magnetic resonance imaging in conservative management lumbar disc herniation. Spine 1998; 23(1):67–73. 14. Haro H, Kato T, Komori H, et al. Vascular endothelial growth factor (VEGF)-induced angiogenesis in herniated disc resorption. J Orthop Res 2002; 20(3):409–415. 15. Burke JG, Watson RWG, McCormack D, et al. Spontaneous production of monocyte chemoattractant protein-1 and interleukin-8 by the human lumbar intervertebral disc. Spine 2002; 27(13):1402–1407. 16. Aoki Y, Rydevik B, Kikuchi S, et al. Local application of disc-related cytokines on spinal nerve roots. Spine 2002; 27(15):1614–1617.
Franson RC, Saal, JS, Saal JA. Human disc phospholipase A2 is inflammatory. Spine 1992; 17(6S):S129–S132. Freemont AJ, Peacock TE, Goupille P, et al. Nerve ingrowth into diseased intervertebral disc in chronic back pain. Lancet 1997; 350(9072):178–181. Freemont AJ, Watkins A, Maitre CL, et al. Current understanding of cellular and molecular events in intervertebral disc degeneration: implications for therapy. J Pathol 2002; 196(4):374–379. Gaetani P, Rodriguez y Baena R, Riva C, et al. Collagenase-1 and stromelysin distribution in fresh human herniated intervertebral disc: a possible link to the in vivo inflammatory reactions. Neurol Res 1999; 21(7):677–681.
17. Olmarker K, Rydevik B. Selective inhibition of tumor necrosis factor-α prevents nucleus pulposus-induced thrombus formation, intraneural edema, and reduction of nerve conduction velocity. Spine 2001; 26(8):863–869.
Goupille P, Jayson MIV, Valat JP, et al. Matrix metalloproteinases: the clue to intervertebral disc degeneration. Spine 1998; 23(14):1612–1626.
Further reading
Grabowski PS, Wright PK, Van’t Hof RJ, et al. Immunolocalization of inducible nitric oxide synthase in synovium and cartilage in rheumatoid arthritis and osteoarthritis. Br J Rheumatol 1997; 36:651–655.
Adams MA, Hutton WC. 1981 Volvo Award in Basic Science. Prolapsed intervertebral disc. A hyperflexion injury. Spine 1982; 7(3):184–191. Ahn SH, Cho YW, Ahn MW, et al. mRNA expression of cytokines and chemokines in herniated lumbar intervertebral discs. Spine 2002; 27(9):911–917.
Goupille P, Jayson MIV, Valat JP, et al. The role of inflammation in disk herniation-associated radiculopathy. Semin Arthritis Rheum 1998; 28(1):60–71.
Grange L, Gaudin P, Trocme C, et al. Intervertebral disk degeneration and herniation: the role of metalloproteinases and cytokines. Joint Bone Spine 2001; 68(6): 547–553.
An HS, Thonar EJ-MA, Masuda K. Biological repair of intervertebral disc. Spine 2003; 28(15):S86–S92.
Habtemariam A, Gronblad M, Virri J, et al. A comparative immunohistochemical study of inflammatory cells in acute-stage and chronic-stage disc herniations. Spine 1998; 23(20):2159–2165.
Baggiolini M, Dewald B, Moser B. Interleukin-8 and related chemotactic cytokines-CXC and CC chemokines. Adv Immunol 1994; 55:97–179.
Hashizume H, Kawakami M, Nishi H, et al. Histochemical demonstration of nitric oxide in herniated lumbar discs. Spine 1997; 22(10):1080–1084.
Brisby H, Byröd G, Olmarker K, et al. Nitric oxide as a mediator of nucleus pulposusinduced effects on spinal nerve roots. J Orthop Res 2000; 18(5):815–820.
Häuselmann HJ, Oppliger L, Michel BA, et al. FEBS Letts 1994; 352:361–364.
Burke JG, Watson RWG, McCormack D, et al. Intervertebral discs which cause low back pain secrete high levels of proinflammatory mediators. J Bone Joint Surg Br 2002; 84(2):196–201. Burke JG, Watson RWG, Conhyea D, et al. Human nucleus pulposus can respond to a pro-inflammatory stimulus. Spine 2003; 28(24):2685–2693. Caron JP, Fernandes JC, Martel-Pelletier J, et al. Chondroprotective effect of intraarticular injections of interleukin-1 receptor antagonist in experimental osteoarthritis. Suppression of collagenase-1 expression. Arthritis Rheum 1996; 39(9): 1535–1544.
Horwitz AL, Hance AJ, Crystal RG. Granulocyte collagenase: selective digestion of type I relative to type III collagen. Proc Natl Acad Sci USA 1977; 74(3):897–901. Igarashi T, Kikuchi S, Shubayev V, et al. 2000 Volvo Award Winner in Basic Science Studies. Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Spine 2000; 25(23):2975–2980. Kääpä E, Han X, Holm S, et al. Collagen synthesis and types I, III, IV, and VI collagens in an animal model of disc degeneration. Spine 1995; 20(1):59–66. Kanemoto M, Hakuda S, Komiya Y, et al. Immunohistochemical study of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 human intervertebral discs. Spine 1996; 21(1):1–8.
Collier S, Ghosh P. The role of plasminogen in interleukin-1 mediated cartilage degradation. J Rheumatol 1988; 15(7):1129–1137.
Kanerva A, Kommonen B, Gronblad M, et al. Inflammatory cells in experimental intervertebral disc injury. Spine 1997; 22(23):2711–2715.
Cooper RG, Freemont AJ, Hoyland JA, et al. Herniated intervertebral disc-associated periradicular fibrosis and vascular abnormalities occur without inflammatory cell infiltration. Spine 1995; 20(5):591–598.
Koch H, Reinecke JA, Meijer H, et al. Spontaneous secretion of interleukin 1 receptor antagonist (IL-1Ra) by cells isolated from herniated lumbar discal tissue after discectomy. Cytokine 1998; 10(9):703–705.
Coppes MH, Marani E, Thomeer RTWM, et al. Innervation of ‘painful’ lumbar discs. Spine 1997; 22(20):2342–2350.
Kokkonen SM, Kurunlahti M, Tervonen O, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine. Spine 2002; 27(20):2273–2278.
Dayer JM, de Rochemonteix B, Burrus B, et al. Human recombinant interleukin-1 stimulates collagenase and prostaglandin E2 production by human synovial cells. J Clin Invest 1986; 77:645–648.
Lefebvre V, Peeters-Joris C, Vaes G. Modulation by interleukin 1 and tumor necrosis factor-α of production of collagenase, tissue inhibitor of metalloproteinases and collagen types in differentiated and dedifferentiated articular chondrocytes. Biochim Biophys Acta 1990; 1052:366–378.
Dean DD, Martel-Pelletier J, Pelletier JP, et al. Evidence for metalloproteinase and metalloproteinase inhibitor imbalance in human osteoarthritic cartilage. J Clin Invest 1989; 84:678–685. DiPasquale G, Caccese R, Pasternak R, et al. Proteoglycan- and collagen-degrading enzymes from human interleukin 1-stimulated chondrocytes from several species: proteoglycanase and collagenase inhibitors as potentially new disease-modifying antiarthritic agents (42416). Proc Soc Exp Biol Med 1986; 183(2):262–267.
26
Fox SW, Chambers TJ, Chow JW. Nitric oxide is an early mediator of the increase in bone formation by mechanical stimulation. Am J Physiol 1996; 270:E955–E960.
Liu GZ, Ishihara H, Osada R, et al. Nitric oxide mediates the change of proteoglycan synthesis in the human lumbar intervertebral disc in response to hydrostatic pressure. Spine 2001; 26(2):134–141. Liu J, Roughley PJ, Mort JS. Identification of human intervertebral disc stromelysis and its involvement in matrix degradation. J Orthop Res 1991; 9(4):568–575.
Doers TM, Kang JD. The biomechanics and biochemistry of disc degeneration. Curr Opin Orthop 1999; 10:117–121.
Lotz M, Guerne PA. Interleukin-6 induces the synthesis of tissue inhibitor of metalloproteinases-1/erythroid potentiating activity (TIMP-1/EPA). J Biol Chem 1991; 266(4):2017–2020.
Doita M, Kanatani T, Ozaki T, et al. Influence of macrophage infiltration of herniated disc tissue on the production of matrix metalloproteinases leading to disc resorption. Spine 2001; 26(14):1522–1527.
Maroudas A, Stockwell A, Nachemson A, et al. Factors involved in the nutrition of the human lumbar intervertebral disc: cellularity and diffusion of glucose in vitro. J Anat 1975; 120(1):113–130.
Edwards DR, Murphy G, Reynolds JJ, et al. Transforming growth factor beta modulates the expression of collagenase and metalloproteinase inhibitor. EMBO J 1987; 6(7):1899–1904.
Martel-Pelletier J, McCollum R, Fujimoto N, et al. Excess of metalloproteases over tissue inhibitor of metalloprotease may contribute to cartilage degradation in osteoarthritis and rheumatoid arthritis. Lab Invest 1994; 79(6):807–815.
Evans CH, Watkins SC, Stefanovic-Racic M. Nitric oxide and cartilage metabolism. Methods Enzymol 1996; 269:75–88.
Matrisian LM. Metalloproteinases and their inhibitor in matrix remodeling. Trends Genet 1990; 6(4):121–125.
Eyre DR, Muir H. Types I and II collagens in intervertebral disc. Interchanging radial distributions in anulus fibrosus. Biochem J 1976; 157:267–270.
Meachim G, Cornah MS. Fine structure of juvenile human nucleus pulposus. J Anat 1970; 107(2):337–350.
Eyre DR, Muir H. Quantitative analysis of types I and II collagens in human intervertebral discs at various ages. Biochim Biophys Acta 1977; 492:29–42.
Melrose J, Ghosh J, Taylor TKF. Neutral proteinases of the human intervertebral disc. Biochim Biophys Acta 1987; 923:483–495.
Section 2: Spinal Pain Melrose J, Ghosh J, Taylor TKF, et al. The serine proteinase inhibitory proteins of the human intervertebral disc: their isolation, characterization and variation with aging and degeneration. Matrix 1992; 12:456–470.
Roberts S, Menage J, Duance V, et al. 1991 Volvo Award in Basic Sciences. Collagen types around the cells of the intervertebral disc and cartilage end plate: an immunolocalization study. Spine 1991; 16(9):1030–1038.
Miyamoto H, Saura R, Harada T, et al. The role of cyclooxygenase-2 and inflammatory cytokines in pain induction of herniated lumbar intervertebral disc. Kobe J Med Sci 2000; 46:13–28.
Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15(7):674–678.
Mort JS, Dodge GR, Roughley PJ, et al. Direct evidence for active metalloproteinases mediating matrix degradation in interleukin 1-stimulated human articular cartilage. Matrix 1993; 13:95–102. Nagano T, Yonenobu K, Miyamoto S, et al. Distribution of the basic fibroblast growth factor and its receptor gene expression in normal and degenerated rat intervertebral discs. Spine 1995; 20(18):1972–1978.
Sakurai H, Kohsaka H, Liu MF, et al. Nitric oxide production and inducible nitric oxide synthase expression in inflammatory arthritides. J Clin Invest 1995; 96:2357– 2363. Sedowofia KA, Tomlinson IW, Weiss JB, et al. Collagenolytic enzyme systems in human intervertebral disc. Their control, mechanism, and their possible role in the initiation of biomechanical failure. Spine 1982; 7(3):213–222.
Ng SCS, Weiss JB, Quennel R, et al. Abnormal connective tissue degrading enzyme patterns in prolapsed intervertebral discs. Spine 1986; 11(7):695–701.
Shinmei M, Kikuchi T, Yamagishi M, et al. The role of interleukin-1 on proteoglycan metabolism of rabbit anulus fibrosus cells cultured in vitro. Spine 1988; 13(11):1284– 1290.
Olmarker K, Larsson K. Tumor necrosis factor alpha and nucleus pulposus-induced nerve root injury. Spine 1998; 23(23):2538–2544.
Specchia N, Pagnotta A, Toesca A, et al. Cytokines and growth factors in the protruded intervertebral disc of the lumbar spine. Eur Spine J 2002; 11(2):145–151.
Özaktay AC, Cavanaugh JM, Asik I, et al. Dorsal root sensitivity to interleukin-1 beta, interleukin-6 and tumor necrosis factor in rats. Eur Spine J 2002; 11(5): 467–475.
Stadler J, Stefanovic-Racic M, Billiar TR, et al. Articular chondrocytes synthesize nitric oxide in response to cytokines and lipopolysaccharide. J Immunol 1991; 147:3915– 3920.
Park JB, Kim KW, Han CW, et al. Expression of Fas receptor on disc cells in herniated lumbar disc tissue. Spine 2001; 26(2):142–146. Park JB, Chang H, Kim YS. The pattern of interleukin-12 and T-helper types 1 and 2 cytokine expression in herniated lumbar disc tissue. Spine 2002; 27(19):2125–2128. Pearce RH, Mathieson JM, Mort JS, et al. Effect of age on the abundance and fragmentation of link protein of the human intervertebral disc. J Orthop Res 1989; 7(6):861–867. Pendás AM, Knäuper V, Puente XS, et al. Identification and characterization of a novel human matrix metalloproteinase with unique structural characteristics, chromosomal location, and tissue distribution. J Biol Chem 1997; 272(7):4281–4286.
Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine 1996; 21(2):218–224. Tengblad A, Pearce RH, Grimmer BJ. Demonstration of link protein in proteoglycan aggregates from human intervertebral disc. Biochem J 1984; 222(1):85–92. Tolonen J, Grönblad M, Virri J, et al. Oncoprotein c-Fos and c-Jun immunopositive cells and cell clusters in herniated intervertebral disc tissue. Eur Spine J 2002; 11(5):452–458. Willburger RE, Wittenberg RH. Prostaglandin release from lumbar disc and facet joint tissue. Spine 1994; 19(18):2068–2070.
27
PART 1
GENERAL PRINCIPLES
Section 2
Spinal Pain
CHAPTER
Transduction, Transmission and Perception of Pain
4
Sarah M. Rothman, Raymond D. Hubbard, Kathryn E. Lee and Beth A. Winkelstein
Painful spinal disorders are common problems in society, affecting an estimated 50 million Americans. The societal costs (including litigation, work lost, treatment, and disability) for such disorders of the spine are staggering. For example, the cost of low back pain alone has been estimated at US$40–50 billion annually.1,2 Chronic neck pain has a similarly high cost of nearly US$30 billion in health-related expenses.3 Until a better understanding of the pathomechanisms of pain and the injuries which produce them are defined, the effective prevention and treatment of these disorders and their symptoms will remain elusive. Further, distinguishing those physiologic mechanisms which lead to persistent pain from those which differentially produce only transient symptoms is also important in understanding and managing these syndromes. It is the intent of this chapter to highlight traditional and emerging theories of pain detection and transmission in the context of spine-related syndromes. A brief discussion of the neurophysiology of pain highlights concepts of local responses, pain transduction, signal transmission, and processing and is integrated with more recent hypotheses of the central nervous system’s (CNS) neuroimmunologic involvement in persistent pain. This chapter focuses on the sensory system, presenting the general anatomy of the spinal cord, nerve roots, and nerves. There are many physiologic mechanisms by which pain is detected and through which they can elicit nociception and ultimately the perception of pain. Mechanisms of pain detection are presented with specific points related to transmission of pain signals. In persistent pain, CNS changes can produce hypersensitivity or central sensitization. In addition to the electrophysiologic changes leading to central sensitization, the spinal cord and brain mount a series of neuroimmune responses which may further contribute to sensitization and persistent pain symptoms. Findings related to neuroimmunity are briefly reviewed here to form a basis for discussing more recent views of mechanisms of persistent pain. Physiologic mechanisms, together with neurochemical responses, are addressed and discussed in the context of findings from animal models of persistent pain in which behavioral hypersensitivity is produced. In particular, studies examining mechanical injuries to different anatomical structures of the spine and which lead to persistent pain symptoms are used here to provide a comparative discussion of pain detection and transmission and perception, in the context of factors for consideration in the spine. As such, findings with radiculopathy models of nerve root compression are presented and compared for discussion of potential differences in mechanisms of transient and persistent sensitivity (pain). In addition, findings from the cervical radiculopathy model are directly compared to those behavioral responses for a facet-mediated distraction pain model in the cervical spine. These behavioral studies provide a platform for exploring similarities and differences in pain responses for different types of tissue injuries. Measures of injury responses are presented for these
models, including behavioral sensitivity, local structural changes, and cellular and molecular changes in the CNS, as they provide insight into understanding pain mechanisms. It is important to define, at the outset, relevant distinctions in terminology. ‘Pain’ is a complex perception that is influenced by prior experience and by the context within which the noxious stimulus occurs. Likewise, ‘nociception’ is the physiologic response to tissue damage or prior tissue damage. Similarly, for discussion in this chapter, ‘hyperalgesia’ is defined as enhanced pain to a noxious stimulus.4 Strictly speaking, this is a leftward shift of the stimulus–response function relating pain to intensity. The corresponding pain threshold is lowered and there is enhanced response to a given stimulus. Hyperalgesia is mediated by nociceptor sensitization, where ‘sensitization’ describes a corresponding shift in the neural response curve for stimulation. Sensitization is characterized by a decrease in threshold, an increased response to suprathreshold stimulus, and spontaneous neural activity. For this chapter, many of the examples are drawn from painful injuries related to the cervical or lumbar spine. These include both low back and neck pain from radiculopathy and facet-mediated injury. While it is recognized that these examples are by no means allinclusive of pain related to the spine, they do provide an ideal context for discussing many of the broader mechanisms presented here.
RELEVANT NEURAL ANATOMY Before presenting and discussing pain mechanisms, it is first necessary to describe the relevant anatomical structures, biological connections, and relationships of neural sensory and processing components. These are reviewed only briefly here to provide appropriate context; a more detailed presentation can be found in texts specifically focused in neural science and pain.4,5 The primary afferents, which relay pain signals from injured or stimulated tissues, terminate in the dorsal horn of the spinal cord. At each level in the spinal cord, the dorsal nerve roots carry sensory information from the periphery into the spinal cord. Dorsal roots contain sensory neurons, whose cell bodies make up the enlarged dorsal root ganglion (DRG) (Fig. 4.1). In contrast, the ventral root contains the axons of neurons whose cell bodies are within the ventral horn of the spinal cord and transmits efferent signals. At each spinal level, the dorsal and ventral nerve roots come together, outside of the spinal column and distal to the DRG, and combine to form the nerve which communicates with the peripheral nervous system. The spinal nerves further branch into smaller nerves in the periphery and innervate bones, ligaments, joints, discs, muscles, organs, and many other tissue types. Structurally, three protective layers surround the spinal cord, which are themselves extensions of the cranial meninges: the dura mater 29
Part 1: General Principles
Fig. 4.1 Axial section of dorsal and ventral C7 nerve root stained with osmium tetroxide. Small- and large-diameter fibers are apparent in the dorsal root (bottom), as well as cell bodies of the dorsal root ganglion. Scale bar is 100 μm.
(outermost), the arachnoid mater, and the pia mater (innermost layer closest to the spinal cord). Within the spinal column, the lumbar dorsal and ventral nerve roots extend below the spinal cord and this neural tissue, collectively called cauda equina, fills the sacral spinal column. The spinal cord is anatomically composed of two regions (Fig. 4.2). These are distinguished by their appearance, function, and
Dorsal root (primary afferents)
Tract of Lissauer
Dorsal column
I II X
Gray matter Dorsal horn
Lateral column
TRANSDUCTION
Ventrolateral column
Ventral root
Central canal
White matter
Fig. 4.2 Schematic illustration of the spinal nerve roots, spinal cord, and its regions of gray and white matter. Also indicated are columns of the neuronal tracts in the white matter. Those regions of the gray matter (laminae) of particular relevance to pain sensation and transmission are indicated. 30
cell populations. The gray matter, which has a darker appearance, contains the cell bodies of spinal neurons and makes up the central region of the spinal cord. It is surrounded by the white matter which contains the axons of the spinal neurons. The columnar tracts of the spinal cord are regionally specialized according to information they carry (see Fig. 4.2). The lateral column contains motor neurons; the dorsal column carries information related to mechanoreception; and the ventrolateral column houses neurons which communicate information regarding pain, temperature, and motor signals. In general, the sensory system ascending pathway comprises the dorsal portion of the spinal cord, while the descending pathway of the motor control system comprises the ventral aspect of the cord. Afferents of the dorsal nerve root enter the spinal cord dorsolaterally and branch in the white matter, with collaterals which terminate in the gray matter. Nerve fibers mediating pain pass through the tract of Lissauer and have branches which terminate in the most superficial regions of the dorsal horn, laminae I and II. Neurons in these laminae synapse on secondary neurons in laminae IV–VI of the dorsal horn and these secondary neurons cross the midline before ascending to the brain contralaterally in the anterolateral region of the cord. Lamina X, which is located in the gray matter region closest to the central canal, also receives sensory inputs related to pain. The neurons of the substantia gelatinosa receive information from Aδ and C fibers; Aβ afferents terminate in the deeper laminae. After injury, it is believed that Aβ afferents sprout from the deeper lamina into the dorsal horn where they make synaptic contacts with neurons.6,7 Nociceptive information is transmitted from the spinal cord to supraspinal sites, primarily in the pons, medulla and thalamus. The anterolateral ascending system has three tracts: spinothalamic, spinoreticular, and spinomesencephalic. The spinothalamic is the most prominent of the tracts. Briefly, the spinothalamic and spinoreticular tracts mediate noxious sensations, with axons terminating on neurons in the reticular formation of the medulla and pons. From there, signals are relayed to the thalamus, and then, neurons project to the somatosensory cortex. Each regional level of the spinal cord receives sensory information from specific regions of the body, known as dermatomes. Typically, nerves from approximately two spinal levels innervate any given region of the skin’s surface. These surfaces have been divided into discrete regions, providing a dermatomal map relating each region of the skin to a corresponding spinal level.8 Clinically, dermatomal maps are used to identify the origin of painful symptoms. However, nerve endings which innervate internal organs can also produce cutaneous sensation. This ‘referred pain’ sensation is experienced at sites other than its source and is due to the fact that nearly all spinal neurons that innervate internal organs also are associated with cutaneous sensation.
Nociceptive afferents are specific for sensing different noxious stimuli: thermal, mechanical, and chemical stimuli. Some nociceptors are polymodal and sense all types of stimuli. Broadly, sensory nerve fibers range in diameter from 5:1) male predominance and is often associated with intervertebral osteochondrosis, suggesting it is acquired. Venous hypertension induced in the coronal venous plexus induces progressive myelopathy (spinal cord edema, ischemia, and eventual infarction) known as the Foix-Alajouanine syndrome. Clinically, these patients typically present with an insidious, slowly progressive myelopathy that results in severe disability if not treated by endovascular or surgical obliteration. Neurological deterioration is usually not reversible, so an expedient diagnosis is essential. This diagnosis can be challenging since the clinical presentation can mimic other spine disorders such as degenerative disc disease and the imaging findings can be subtle. On MRI, the spinal cord can be normal in size or enlarged. Intramedullary high signal intensity on T2-weighted images is typically but not invariably visible (Fig. 6.48A). Peripheral T2-weighted hypointensity in the spinal cord can be seen and may increase the specificity for the diagnosis of venous hypertension.150 Prominent vessels along the dorsal aspect of the spinal cord are usually but not always visible (Fig. 6.48A, B). These vessels and the spinal cord can enhance (Fig. 6.48B). All patients with an otherwise unexplained progressive myelopathy and any suggestive MRI findings should undergo a comprehensive spinal angiogram that includes all intercostal and lumbar segmental arteries, and the subclavian, vertebral, thyrocervical, costocervical, median sacral, and internal iliac arteries.
A
B
Intramedullary spinal cord arteriovenous malformations (type II arteriovenous malformations) are supplied by branches of the anterior and posterior spinal arteries.149 There is an intraparenchymal nidus (compact or diffuse) drained by the spinal veins. The angioarchitecture is similar to brain arteriovenous malformations. Intranidal or feeding artery aneurysms may be present. These lesions usually present acutely secondary to intraparenchymal hemorrhage. Compression-induced myelopathy and progressive myelopathy due to vascular steal also occur. Diagnosis on MRI is usually straightforward. Prominent, tortuous feeding and draining vessels and a vascular nidus that contain flow voids and enhancement are visible. Conventional angiography is usually necessary for complete characterization. Extradural-intradural arteriovenous malformations (juvenile, metameric, type III arteriovenous malformations) are rare lesions that do not respect tissue boundaries and typically involve the spinal cord, vertebral body, and extraspinal structures.149 They usually become symptomatic during childhood or adolescence and require a multidisciplinary approach to treatment, and have a poor prognosis. Extensive involvement of the spinal cord, spine, and surrounding structures is typically seen on MRI. The spinal cord arteriovenous fistula (type IV arteriovenous malformation) is an intradural ventral arteriovenous fistula located on the anterior pial surface comprised of a direct arteriovenous connection involving the anterior spinal artery and an enlarged venous network.149 Clinical presentations include progressive myelopathy and acute subarachnoid hemorrhage. MRI demonstrates prominent pial vessels with flow voids without a parenchymal nidus.
Fig. 6.48 Spinal dural fistula. Sagittal T2-weighted (A) and contrast-enhanced T1-weighted (B) thoracic spine MRI images demonstrate multiple serpiginous tubular T2 flow voids with enhancement dorsal to the spinal cord consistent with pathologically enlarged perimedullary veins (arrows), and thoracic spinal cord T2-hyerintensity and enhancement caused by venous hypertension and interstitial edema (arrowheads). 85
Part 1: General Principles
SUMMARY MRI is the preeminent imaging modality for evaluation of spinal disorders; however, there remain important roles for plain films, CT, and myelography with postmyelography CT. Standardized nomenclature promises to improve communications between the physicians interpreting imaging examinations and those caring for the patients. Correlation of the imaging findings with the clinical presentation is essential.
References
25. Grenier N, Greselle JF, Douws C, et al. MR imaging of foraminal and extraforaminal lumbar disk herniations. J Computer Assist Tomogr 1990; 14(2):243–249. 26. Masaryk TJ, Ross JS, Modic MT, et al. High-resolution MR imaging of sequestered lumbar intervertebral disks. Am J Roentgenol1988; 150(5):1155–1162. 27. Silverman CS, Lenchik L, Shimkin PM, et al. The value of MR in differentiating subligamentous from supraligamentous lumbar disk herniations [see comment]. Am J Neuroradiol 1995; 16(3):571–579. 28. Oppenheim JS, Rothman AS, Sachdev VP. Thoracic herniated discs: review of the literature and 12 cases. Mount Sinai J Med 1993; 60(4):321–326.
1. Jarvik JG. Imaging of adults with low back pain in the primary care setting. Neuroimag Clin N America 2003; 13(2):293–305.
29. Russell EJ. Cervical disk disease. Radiology 1990; 177(2):313–325.
2. Herzog RJ, Guyer RD, Graham-Smith A, et al. Magnetic resonance imaging. Use in patients with low back or radicular pain. Spine 1995; 20(16):1834–1838.
30. Dubuisson A, Lenelle J, Stevenaert A. Soft cervical disc herniation: a retrospective study of 100 cases. Acta Neurochirurgica 1993; 125(1–4):115–119.
3. Mink JH, Deutsch AL, Goldstein TB, et al. Spinal imaging and intervention: 1998. Phys Med Rehabil Clin N Am 1998; 9(2):343–380.
31. Benoist M. The natural history of lumbar disc herniation and radiculopathy. Joint, Bone, Spine: Revue du Rhumatisme 2002; 69(2):155–160.
4. Kaiser JA, Holland BA. Imaging of the cervical spine. Spine 1998; 23(24): 2701–2712.
32. Kobayashi N, Asamoto S, Doi H, et al. Spontaneous regression of herniated cervical disc. Spine J 2003; 3(2):171–173.
5. Jarvik JG, Hollingworth W, Martin B, et al. Rapid magnetic resonance imaging vs radiographs for patients with low back pain: a randomized controlled trial.[see comment]. JAMA 2003; 289(21):2810–2818.
33. Dorwart RH, Vogler JB 3rd, Helms CA. Spinal stenosis. Radiologic Clin N Am 1983; 21(2):301–325.
6. Fritz RC, Kaiser JA, White AH, et al. Magnetic resonance imaging of a thoracic intraspinal synovial cyst. Spine 1994; 19(4):487–490. 7. Crim JR, Moore K, Brodke D. Clearance of the cervical spine in multitrauma patients: the role of advanced imaging. Sem Ultrasound CT MR 2001; 22(4): 283–305. 8. Shellock F. Reference manual for magnetic resonance safety, implants & devices. Los Angeles: Biomedical Research Publishing Group; 2004. 9. Ebraheim NA, Savolaine ER, Stitgen SH, et al. Magnetic resonance imaging after pedicular screw fixation of the spine. Clin Orthopaed Related Res 1992; 279: 133–137. 10. Demaerel P, Sunaert S, Wilms G. Sequences and techniques in spinal MR imaging. Jbr-Btr: Organe de la Societe Royale Belge de Radiologie. 2003; 86(4):221–222.
34. Schonstrom N, Willen J. Imaging lumbar spinal stenosis. Radiol Clin N Am 2001; 39(1):31–53. 35. Botwin KP, Gruber RD. Lumbar spinal stenosis: anatomy and pathogenesis. Phys Med Rehabi Clin N Am 2003; 14(1):1–15. 36. Hiwatashi A, Danielson B, Moritani T, et al. Axial loading during MR imaging can influence treatment decision for symptomatic spinal stenosis [see comment]. Am J Neuroradiol 2004; 25(2):170–174. 37. Jenis LG, An HS, Gordin R. Foraminal stenosis of the lumbar spine: a review of 65 surgical cases. Am J Orthoped (Chatham, NJ). 2001; 30(3):205–211. 38. Weishaupt D, Schmid MR, Zanetti M, et al. Positional MR imaging of the lumbar spine: does it demonstrate nerve root compromise not visible at conventional MR imaging? Radiology 2000; 215(1):247–253.
11. Goldberg AL, Soo MS, Deeb ZL, et al. Degenerative disease of the lumbar spine. Role of CT-myelography in the MR era. Clin Imaging 1991; 15(1):47–55.
39. Reul J, Gievers B, Weis J, et al. Assessment of the narrow cervical spinal canal: a prospective comparison of MRI, myelography and CT-myelography. Neuroradiology 1995; 37(3):187–191.
12. Bartynski WS, Lin L. Lumbar root compression in the lateral recess: MR imaging, conventional myelography, and CT myelography comparison with surgical confirmation.[see comment]. Am J Neuroradiol 2003; 24(3):348–360.
40. Muhle C, Metzner J, Weinert D, et al. Classification system based on kinematic MR imaging in cervical spondylitic myelopathy [see comment]. Am J Neuroradiol 1998; 19(9):1763–1771.
13. Botwin KP, Skene G, Tourres-Ramos FM, et al. Role of weight-bearing flexion and extension myelography in evaluating the intervertebral disc. Am J Phys Med Rehabil 2001; 80(4):289–295.
41. Chen CJ, Lyu RK, Lee ST, et al. Intramedullary high signal intensity on T2-weighted MR images in cervical spondylotic myelopathy: prediction of prognosis with type of intensity. Radiology 2001; 221(3):789–794.
14. Gray H. Anatomy of the human body. 20th edn. Philadelphia: Lea and Febiger; 2000.
42. Becciolini V, Flandroy P, Collignon J, et al. Synovial cyst of the lumbar spine. JbrBtr: Organe de la Societe Royale Belge de Radiologie 2000; 83(1):9.
15. Beers GJ, Carter AP, McNary WF. Vertical foramina in the lumbosacral region: CT appearance. Am J Roentgenol 1984; 143(5):1027–1029. 16. Kostelic JK, Haughton VM, Sether LA. Lumbar spinal nerves in the neural foramen: MR appearance. Radiology 1991; 178(3):837–839. 17. Ricci C, Cova M, Kang YS, et al. Normal age-related patterns of cellular and fatty bone marrow distribution in the axial skeleton: MR imaging study.[see comment]. Radiology 1990; 177(1):83–88. 18. Schellinger D, Manz HJ, Vidic B, et al. Disk fragment migration.[see comment]. Radiology 1990; 175(3):831–836. 19. Fardon DF, Milette PC, Combined Task Forces of the North American Spine Society ASoSR, et al. Nomenclature and classification of lumbar disc pathology. Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001; 26(5):E93–E113. 20. Brant-Zawadzki MN, Jensen MC, Obuchowski N, et al. Interobserver and intraobserver variability in interpretation of lumbar disc abnormalities. A comparison of two nomenclatures. Spine 1995; 20(11):1257–1263; discussion 1264.
86
24. Hammer A, Knight I, Agarwal A. Localized venous plexi in the spine simulating prolapse of an intervertebral disc: a report of six cases. Spine 2003; 28(1): E5–E12.
43. Jackson DE Jr, Atlas SW, Mani JR, et al. Intraspinal synovial cysts: MR imaging. Radiology 1989; 170(2):527–530. 44. Apostolaki E, Davies AM, Evans N, et al. MR imaging of lumbar facet joint synovial cysts. Eur Radiol 2000; 10(4):615–623. 45. Graham E, Lenke LG, Hannallah D, et al. Myelopathy induced by a thoracic intraspinal synovial cyst: case report and review of the literature. Spine 2001; 26(17): E392–E394. 46. Stoodley MA, Jones NR, Scott G. Cervical and thoracic juxtafacet cysts causing neurologic deficits. Spine 2000; 25(8):970–973. 47. Gadgil AA, Eisenstein SM, Darby A, et al. Bilateral symptomatic synovial cysts of the lumbar spine caused by calcium pyrophosphate deposition disease: a case report. Spine 2002; 27(19):E428–E431. 48. Borenstein DG, O’Mara JW Jr, Boden SD, et al. The value of magnetic resonance imaging of the lumbar spine to predict low back pain in asymptomatic subjects: a seven-year follow-up study. J Bone Joint Surg [Am] 2001; 83-A(9):1306–1311.
21. Saifuddin A, Braithwaite I, White J, et al. The value of lumbar spine magnetic resonance imaging in the demonstration of annular tears. Spine 1998; 23(4):453–457.
49. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg [Am] 1990; 72(3):403–408.
22. Modic MT, Steinberg PM, Ross JS, et al. Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology 1988; 166(1 Pt 1):193–199.
50. Boden SD, McCowin PR, Davis DO, et al. Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects. A prospective investigation [see comment]. J Bone Joint Surg [Am] 1990; 72(8):1178–1184.
23. Ketonen L, Gyldensted C. Lumbar disc disease evaluated by myelography and postmyelography spinal computed tomography. Neuroradiology 1986; 28(2): 144–149.
51. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography. I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984; 9(6):549–551.
Section 3: General Diagnostic Technique 52. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain [see comment]. N Engl J Med 1994; 331(2):69–73. 53. Greenberg JO, Schnell RG. Magnetic resonance imaging of the lumbar spine in asymptomatic adults. Cooperative study – American Society of Neuroimaging. J Neuroimag 1991; 1(1):2–7. 54. Borenstein DG, O’Mara JW Jr, Boden SD, et al. The value of magnetic resonance imaging of the lumbar spine to predict low back pain in asymptomatic subjects : a seven-year follow-up study. J Bone Joint Surg [Am] 2001; 83-A(9):1306–1311. 55. Slipman CW SC, Patel RK, Issac Z, et al. Etiologies of failed back surgery syndrome. Pain Med 2002; 3(3):200–214. 56. Waguespack A, Slosar P, Reynolds J. Etiology of long-term failures of lumbar spine surgery. Pain Med 2002; 3(1):18–22.
79. Cotten A, Boutry N, Cortet B, et al. Percutaneous vertebroplasty: state of the art. Radiographics 1998; 18(2):311–320; discussion 320–323. 80. Fitt GJ, Stevens JM. Postoperative arachnoiditis diagnosed by high resolution fast spin-echo MRI of the lumbar spine. Neuroradiology 1995; 37(2):139–145. 81. Ribeiro C, Reis FC. Aracnoidite adesiva lombar. Acta Medica Portuguesa 1998; 11(1):59–65. 82. Koenigsberg RA, Klahr J, Zito JL, et al. Magnetic resonance imaging of cauda equina syndrome in ankylosing spondylitis: a case report. J Neuroimag 1995; 5(1):46–48. 83. Modic MT, Feiglin DH, Piraino DW, et al. Vertebral osteomyelitis: assessment using MR. Radiology 1985; 157(1):157–166. 84. Dagirmanjian A, Schils J, McHenry M, et al. MR imaging of vertebral osteomyelitis revisited [see comment]. Am J Roentgenol 1996; 167(6):1539–1543.
57. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, et al. Causes of failure of surgery on the lumbar spine. Clin Orthopaed Related Res 1981; 157:191–199.
85. Smith AS, Weinstein MA, Mizushima A, et al. MR imaging characteristics of tuberculous spondylitis vs vertebral osteomyelitis. Am J Roentgenol 1989; 153(2):399– 405.
58. Burton CV. Causes of failure of surgery on the lumbar spine: ten-year follow-up. Mount Sinai J Med 1991; 58(2):183–187.
86. Muffoletto AJ, Ketonen LM, Mader JT, et al. Hematogenous pyogenic facet joint infection. Spine 2001; 26(14):1570–1576.
59. Ross JS. MR imaging of the postoperative lumbar spine. Mag Res Imaging Clin N Am 1999; 7(3):513–524.
87. Ergan M, Macro M, Benhamou CL, et al. Septic arthritis of lumbar facet joints. A review of six cases [see comment]. Revue du Rhumatisme (English Edition) 1997; 64(6):386–395.
60. Babar S, Saifuddin A. MRI of the post-discectomy lumbar spine. Clin Radiol 2002; 57(11):969–981. 61. Awwad EE, Smith KR Jr. MRI of marked dural sac compression by surgicel in the immediately postoperative period after uncomplicated lumbar laminectomy. J Comput Assist Tomogr 1999; 23(6):969–975. 62. Ross JS, Masaryk TJ, Modic MT, et al. Lumbar spine: postoperative assessment with surface-coil MR imaging. Radiology 1987; 164(3):851–860. 63. Bundschuh CV, Modic MT, Ross JS, et al. Epidural fibrosis and recurrent disk herniation in the lumbar spine: MR imaging assessment. Am J Roentgenol 1988; 150(4):923–932.
88. Wolfe BK, O’Keeffe D, Mitchell DM, et al. Rheumatoid arthritis of the cervical spine: early and progressive radiographic features. Radiology 1987; 165(1): 145–148. 89. Czerny C, Grampp S, Henk CB, et al. Rheumatoid arthritis of the craniocervical region: assessment and characterization of inflammatory soft tissue proliferations with unenhanced and contrast-enhanced CT. Eur Radiol 2000; 10(9): 1416–1422. 90. Stiskal MA, Neuhold A, Szolar DH, et al. Rheumatoid arthritis of the craniocervical region by MR imaging: detection and characterization. Am J Roentgenol 1995; 165(3):585–592.
64. Ross JS, Masaryk TJ, Schrader M, et al. MR imaging of the postoperative lumbar spine: assessment with gadopentetate dimeglumine. Am J Roentgenol 1990; 155(4):867–872.
91. Fox MW, Onofrio BM, Kilgore JE. Neurological complications of ankylosing spondylitis. J Neurosurg 1993; 78(6):871–878.
65. Tien RD, Olson EM, Zee CS. Diseases of the lumbar spine: findings on fat-suppression MR imaging. Am J Roentgenol 1992; 159(1):95–99.
92. Vinson EN, Major NM. MR imaging of ankylosing spondylitis. Sem Musculoskel Radiol 2003; 7(2):103–113.
66. Mullin WJ, Heithoff KB, Gilbert TJ Jr, et al. Magnetic resonance evaluation of recurrent disc herniation: is gadolinium necessary? Spine 2000; 25(12):1493–1499.
93. Cheng WC, Chang CN, Lui TN, et al. Surgical treatment for ossification of the posterior longitudinal ligament of the cervical spine. Surg Neurol 1994; 41(2): 90–97.
67. Jinkins JR, Osborn AG, Garrett D Jr, et al. Spinal nerve enhancement with GdDTPA: MR correlation with the postoperative lumbosacral spine. Am J Neuroradiol 1993; 14(2):383–394. 68. Lane JI, Koeller KK, Atkinson JL. Enhanced lumbar nerve roots in the spine without prior surgery: radiculitis or radicular veins? Am J Neuroradiol 1994; 15(7):1317–1325. 69. Kanis JA, Melton LJ 3rd, Christiansen C, et al. The diagnosis of osteoporosis [see comment]. J Bone Mineral Res 1994; 9(8):1137–1141. 70. Melton LJ 3rd. Epidemiology of spinal osteoporosis. Spine 1997; 22(24 Suppl): 2S–11S.
94. Jinkins JR, Matthes JC, Sener RN, et al. Spondylolysis, spondylolisthesis, and associated nerve root entrapment in the lumbosacral spine: MR evaluation. Am J Roentgenol 1992; 159(4):799–803. 95. Johnson DW, Farnum GN, Latchaw RE, et al. MR imaging of the pars interarticularis. Am J Roentgenol 1989; 152(2):327–332. 96. McGregor AH, Anderton L, Gedroyc WM, et al. The use of interventional open MRI to assess the kinematics of the lumbar spine in patients with spondylolisthesis. Spine 2002; 27(14):1582–1586.
71. Riggs BL, Melton LJ 3rd. The worldwide problem of osteoporosis: insights afforded by epidemiology. Bone 1995; 17(5 Suppl):505S–511S.
97. Bourgouin PM, Lesage J, Fontaine S, et al. A pattern approach to the differential diagnosis of intramedullary spinal cord lesions on MR imaging. Am J Roentgenol 1998; 170(6):1645–1649.
72. Mathis JM, Barr JD, Belkoff SM, et al. Percutaneous vertebroplasty: a developing standard of care for vertebral compression fractures. Am J Neuroradiol 2001; 22(2):373–381.
99. Kahan H, Sklar EM, Post MJ, et al. MR characteristics of histopathologic subtypes of spinal ependymoma. Am J Neuroradiol 1996; 17(1):143–150.
73. Uetani M, Hashmi R, Hayashi K. Malignant and benign compression fractures: differentiation and diagnostic pitfalls on MRI. Clinl Radiol 2004; 59(2): 124–131.
100. Furuya K, Sasaki T, Suzuki I, et al. Intramedullary angiographically occult vascular malformations of the spinal cord. Neurosurgery 1996; 39(6):1123–1130; discussion 1131–1132.
74. Moulopoulos LA, Yoshimitsu K, Johnston DA, et al. MR prediction of benign and malignant vertebral compression fractures. J Mag Res Imag 1996; 6(4): 667–674.
101. Gomori JM, Heching N, Siegal T. Leptomeningeal metastases: evaluation by gadolinium enhanced spinal magnetic resonance imaging. J Neuro-Oncology 1998; 36(1):55–60.
75. Maynard AS, Jensen ME, Schweickert PA, et al. Value of bone scan imaging in predicting pain relief from percutaneous vertebroplasty in osteoporotic vertebral fractures. Am J Neuroradiol 2000; 21(10):1807–1812.
102. Schmorl G JH. The human spine in health and disease. 2nd edn. New York: Grune and Stratton; 1971.
76. Do HM. Magnetic resonance imaging in the evaluation of patients for percutaneous vertebroplasty. Topics in Magnetic Resonance Imaging 2000; 11(4):235–244. 77. Jang JS, Kim DY, Lee SH. Efficacy of percutaneous vertebroplasty in the treatment of intravertebral pseudarthrosis associated with noninfected avascular necrosis of the vertebral body. Spine 2003; 28(14):1588–1592. 78. Lane JI, Maus TP, Wald JT, et al. Intravertebral clefts opacified during vertebroplasty: pathogenesis, technical implications, and prognostic significance [see comment]. Am J Neuroradiol 2002; 23(10):1642–1646.
98. Baleriaux DL. Spinal cord tumors. Eur Radiol 1999; 9(7):1252–1258.
103. Laredo JD, Reizine D, Bard M, et al. Vertebral hemangiomas: radiologic evaluation. Radiology 1986; 161(1):183–189. 104. Doppman JL, Oldfield EH, Heiss JD. Symptomatic vertebral hemangiomas: treatment by means of direct intralesional injection of ethanol. Radiology 2000; 214(2):341–348. 105. Inglis AE, Rubin RM, Lewis RJ, et al. Osteochondroma of the cervical spine. Case report. Clin Orthopaed Related Res 1977; 126:127–129. 106. Kenney PJ, Gilula LA, Murphy WA. The use of computed tomography to distinguish osteochondroma and chondrosarcoma. Radiology 1981; 139(1):129–137.
87
Part 1: General Principles 107. MacLellan DI, Wilson FC Jr. Osteoid osteoma of the spine. A review of the literature and report of six new cases. J Bone Joint Surg [Am] 1967; 49(1):111–121.
130. Thorpe JW, Kidd D, Moseley IF, et al. Spinal MRI in patients with suspected multiple sclerosis and negative brain MRI. Brain 1996; 119(Pt 3):709–714.
108. Gamba JL, Martinez S, Apple J, et al. Computed tomography of axial skeletal osteoid osteomas. Am J Roentgenol 1984; 142(4):769–772.
131. Thielen KR, Miller GM. Multiple sclerosis of the spinal cord: magnetic resonance appearance. J Comput Assist Tomogr 1996; 20(3):434–438.
109. Lucas DR, Unni KK, McLeod RA, et al. Osteoblastoma: clinicopathologic study of 306 cases. Hum Path 1994; 25(2):117–134.
132. Sze G, Kawamura Y, Negishi C, et al. Fast spin-echo MR imaging of the cervical spine: influence of echo train length and echo spacing on image contrast and quality. Am J Neuroradiol 1993; 14(5):1203–1213.
110. McLeod RA, Dahlin DC, Beabout JW. The spectrum of osteoblastoma. Am J Roentgenol 1976; 126(2):321–325. 111. Higinbotham NL, Phillips RF, Farr HW, et al. Chordoma. Thirty-five-year study at Memorial Hospital. Cancer 1967; 20(11):1841–1850.
133. Rocca MA, Mastronardo G, Horsfield MA, et al. Comparison of three MR sequences for the detection of cervical cord lesions in patients with multiple sclerosis [see comment]. Am J Neuroradiol 1999; 20(9):1710–1716.
112. Krol G, Sundaresan N, Deck M. Computed tomography of axial chordomas. J Comput Assist Tomogr 1983; 7(2):286–289.
134. Caldemeyer KS, Smith RR, Harris TM, et al. MRI in acute disseminated encephalomyelitis. Neuroradiology 1994; 36(3):216–220.
113. Sze G, Uichanco LS 3rd, Brant-Zawadzki MN, et al. Chordomas: MR imaging. Radiology 1988; 166(1 Pt 1):187–191.
135. Nesbit GM, Miller GM, Baker HL Jr, et al. Spinal cord sarcoidosis: a new finding at MR imaging with Gd-DTPA enhancement. Radiology 1989; 173(3):839–843.
114. Aisen AM, Martel W, Braunstein EM, et al. MRI and CT evaluation of primary bone and soft-tissue tumors. Am J Roentgenol 1986; 146(4):749–756.
136. Christoforidis GA, Spickler EM, Recio MV, et al. MR of CNS sarcoidosis: correlation of imaging features to clinical symptoms and response to treatment. Am J Neuroradiol 1999; 20(4):655–669.
115. Munk PL, Helms CA, Holt RG, et al. MR imaging of aneurysmal bone cysts. Am J Roentgenol 1989; 153(1):99–101. 116. Dahlin DC, Coventry MB. Osteogenic sarcoma. A study of six hundred cases. J Bone Joint Surg [Am] 1967; 49(1):101–110. 117. Zimmer WD, Berquist TH, McLeod RA, et al. Magnetic resonance imaging of osteosarcomas. Comparison with computed tomography. Clin Orthopaed Related Res 1986; 208:289–299. 118. Sundaram M, McGuire MH, Herbold DR. Magnetic resonance imaging of osteosarcoma. Skeletal Radiol 1987; 16(1):23–29. 119. Grubb MR, Currier BL, Pritchard DJ, et al. Primary Ewing’s sarcoma of the spine. Spine 1994; 19(3):309–313. 120. Pritchard DJ, Dahlin DC, Dauphine RT, et al. Ewing’s sarcoma. A clinicopathological and statistical analysis of patients surviving five years or longer. J Bone Joint Surg [Am] 1975; 57(1):10–16. 121. Frouge C, Vanel D, Coffre C, et al. The role of magnetic resonance imaging in the evaluation of Ewing sarcoma. A report of 27 cases. Skeletal Radiol 1988; 17(6):387–392. 122. Parker BR, Marglin S, Castellino RA. Skeletal manifestations of leukemia, Hodgkin disease, and non-Hodgkin lymphoma. Semin Roentgenol 1980; 15(4 Pt 2): 302–315. 123. Pear BL. Skeletal manifestations of the lymphomas and leukemias. Sem Roentgenol 1974; 9(3):229–240.
138. Campi A, Filippi M, Comi G, et al. Recurrent acute transverse myelopathy associated with anticardiolipin antibodies. Am J Neuroradiol 1998; 19(4):781–786. 139. Wang PY, Shen WC, Jan JS. MR imaging in radiation myelopathy. Am J Neuroradiol 1992; 13(4):1049–1055; discussion 1056–1058. 140. Schultheiss TE, Stephens LC, Maor MH. Analysis of the histopathology of radiation myelopathy. Int J Radiat Oncol Biol Phys 1988; 14(1):27–32. 141. Hsu CY, Shih TT, Huang KM, et al. Tophaceous gout of the spine: MR imaging features. Clin Radiol 2002; 57(10):919–925. 142. Evans A, Stoodley N, Halpin S. Magnetic resonance imaging of intraspinal cystic lesions: a pictorial review. Current Problems in Diagnostic Radiology 2002; 31(3):79–94. 143. Brooks BS, Duvall ER, el Gammal T, et al. Neuroimaging features of neurenteric cysts: analysis of nine cases and review of the literature. Am J Neuroradiol 1993; 14(3):735–746. 144. Abou-Fakhr FS, Kanaan SV, Youness FM, et al. Thoracic spinal intradural arachnoid cyst: report of two cases and review of literature. Eur Radiol 2002; 12(4):877– 882.
124. Daffner RH, Lupetin AR, Dash N, et al. MRI in the detection of malignant infiltration of bone marrow. Am J Roentgenol 1986; 146(2):353–358.
145. Rimmelin A, Clouet PL, Salatino S, et al. Imaging of thoracic and lumbar spinal extradural arachnoid cysts: report of two cases. Neuroradiology 1997; 39(3):203– 206.
125. Weaver GR, Sandler MP. Increased sensitivity of magnetic resonance imaging compared to radionuclide bone scintigraphy in the detection of lymphoma of the spine. Clin Nuclear Med 1987; 12(4):333–334.
146. Gupta S, Gupta RK, Gujral RB, et al. Signal intensity patterns in intraspinal dermoids and epidermoids on MR imaging. Clin Radiol 1993; 48(6):405–413.
126. Punt J, Pritchard J, Pincott JR, et al. Neuroblastoma: a review of 21 cases presenting with spinal cord compression. Cancer 1980; 45(12):3095–3101.
88
137. Morrissey SP, Miller DH, Kendall BE, et al. The significance of brain magnetic resonance imaging abnormalities at presentation with clinically isolated syndromes suggestive of multiple sclerosis. A 5-year follow-up study. Brain 1993; 116(Pt 1):135–146.
147. Voyadzis JM, Bhargava P, Henderson FC. Tarlov cysts: a study of 10 cases with review of the literature [see comment]. J Neurosurg 2001; 95(1 Suppl):25–32.
127. Siegel MJ, Jamroz GA, Glazer HS, et al. MR imaging of intraspinal extension of neuroblastoma. JComput Assist Tomogr 1986; 10(4):593–595.
148. Watters MR, Stears JC, Osborn AG, et al. Transdural spinal cord herniation: imaging and clinical spectra [see comment]. Am J Neuroradiol 1998; 19(7):1337– 1344.
128. Honig LS, Sheremata WA. Magnetic resonance imaging of spinal cord lesions in multiple sclerosis. J Neurol Neurosurg Psychiatr 1989; 52(4):459–466.
149. Spetzler RF, Detwiler PW, Riina HA, et al. Modified classification of spinal cord vascular lesions [see comment]. J Neurosurg 2002; 96(2 Suppl):145–156.
129. Tartaglino LM, Friedman DP, Flanders AE, et al. Multiple sclerosis in the spinal cord: MR appearance and correlation with clinical parameters. Radiology 1995; 195(3):725–732.
150. Hurst RW, Grossman RI. Peripheral spinal cord hypointensity on T2-weighted MR images: a reliable imaging sign of venous hypertensive myelopathy [see comment]. Am J Neuroradiol 2000; 21(4):781–786.
PART 1
GENERAL PRINCIPLES
Section 3
General Diagnostic Technique
CHAPTER
Nuclear Medicine Imaging With an Emphasis on Spinal Infections
7
Christophe Van de Wiele
INTRODUCTION Nuclear medicine imaging assesses pathophysiologic processes such as regional perfusion, permeability, accumulation of white blood cells, bone turnover, etc. These processes precede morphological changes as assessed by radiologic imaging. As such, it accounts for the high sensitivity of nuclear medicine procedures, but also for the low specificity in differential diagnosis of different diseases with similar pathophysiologic characteristics. As an established infectionimaging modality, nuclear medicine plays a vital healthcare role in the diagnosis and subsequent effective treatment of infection of the spine. Various radiopharmaceuticals have been shown to significantly aid diagnosis of infection of the spine: single photon emitting agents for single photon emission computerized tomography (SPECT), bone scanning agents, 111In-oxine-, 99mTc-hexamethylpropyleneamine oxime-, and 99mTc-stannous fluoride colloid-labeled leukocytes, 99mTcFanolesmab and 67Ga-citrate; and more recently 18fluorodeoxyglucose (FDG) for positron emission tomography (PET). This chapter describes and evaluates available data on FDG PET for assessment of infection of the spine as opposed to SPECT and radiologic examinations. First, technical aspects of PET and SPECT are described followed by a brief overview of routinely available radiopharmaceuticals of relevance for imaging infection of the spine. Subsequently, results obtained in clinical studies are described.
PET AND SPECT The gamma camera or SPECT camera is a camera that is able to detect scintillations (flashes of light) produced when gamma rays, resulting from radioactive decay of single photon emitting radioisotopes, interact with a sodium iodide crystal at the front of the camera. The scintillations are detected by photomultiplier tubes, and while the areas of crystal seen by tubes overlap, the location of each scintillation can be computed from the relative response in each tube.1 The energy of each scintillation is also measured from the response of the tubes, and the electrical signal to the imaging computer consists of the location and photon energy. In front of the crystal resides a collimator which is made of lead and usually manufactured with multiple elongated holes (parallel-hole collimator). The holes allow only gamma rays that are traveling perpendicularly to the crystal face to enter. The gamma photons absorbed by the crystal therefore form an image of the distribution of the radiopharmaceutical distribution in front of the camera. By rotating the camera around the patient and acquiring images at different angles, tomographic images, or SPECT images, can be generated through the use of specific reconstruction algorithms.2 As with SPECT, PET relies on computerized reconstruction procedures to produce tomographic images, but by means of indirectly detecting positron emission.3 Positrons, when emitted by radioac-
tive nuclei, will combine with an electron from the surroundings and annihilate it. Upon annihilation, both the positron and the electron are then converted to electromagnetic radiation in the form of two high-energy photons which are emitted 180 degrees away from each other. It is this annihilation radiation that can be detected externally and is used to measure both the quantity and the location of the positron emitter. Simultaneous detection of two of these photons by detectors on opposite sides of an object places the site of the annihilation on or about a line connecting the centers of the two opposing detectors. At this point, mapping the distribution of annihilations by computer is conducted. If the annihilation originates outside the volume between the two detectors, only one of the photons can be detected, and since the detection of a single photon does not satisfy the coincidence condition, the event is rejected. Since radioisotopes suitable for PET have a short half-life (e.g. 110 min for 18F), an on-site cyclotron is needed for production of such isotopes.4 Special radiosynthesis facilities are required, restricting the availability of noncommercially available PET radiopharmaceuticals to specialized centers. In contrast to PET, the synthesis of SPECT radiopharmaceuticals is much less expensive. As the half-lifes of the isotopes used in SPECT are longer than those of isotopes used in PET (hours versus minutes), longer acquisition times are possible in SPECT. On the other hand, the resolution of a conventional PET camera is twice as good as that of a conventional gamma camera and PET allows for more accurate quantification when compared to SPECT.
RADIOPHARMACEUTICALS AND METHODOLOGY Tc-MDP/HDP
99m
Bone scintigraphy makes use of 99mTc-labeled organic analogues of pyrophoshate which are characterized by P-C-P bonds and predominantly absorb at kinks and dislocation sites on the surface of hydroxyapatite crystals. The most commonly used diphosphonate agents are 99mTc hydroxyethylene diphosphonate (99mTc HDP) and 99mTc methylene diphosphonate (99mTc MDP). The major physiologic determinants of bone uptake of these phosphate agents are the rate of bone turnover and blood flow, and the bone surface area involved.5 When performed for osteomyelitis, the study is usually done in three or four phases. Three-phase bone imaging consists of a dynamic imaging sequence, the flow or perfusion phase, followed immediately by static images of the region of interest, which is the blood-pool or soft-tissue phase. The third, or bone phase, consists of planar static images of the area of interest, acquired 2–4 h later. SPECT is performed when deemed necessary by the nuclear medicine physician. The usual injected dose for adults is 740–925 MBq (20–25 mCi) of 99mTc-MDP. The nor89
Part 1: General Principles
mal distribution of this tracer, by 3–4 h after injection, includes the skeleton, genitourinary tract, and soft tissues.6
Ga
67 67
Ga-citrate has been used for localizing infection for more than three decades. 67Ga, which is cyclotron produced, emits 4 principal rays suitable for imaging: 93, 184, 296, and 388 keV. Several factors govern uptake of this tracer in inflammation and infection. When injected intravenously, 67Ga binds primarily to transferrin a β-globulin responsible for transporting iron. Increased blood flow and increased vascular membrane permeability associated with inflammation/infection result in increased delivery and accumulation of transferrin-bound 67 Ga at inflammatory foci. At the site of infection or inflammation, 67 Ga can then bind to lactoferrin, which is present in high concentrations in inflammatory foci, attach to leukocytes, or may be directly taken up by bacteria. Siderophores, low molecular weight chelates produced by bacteria, have a high affinity for 67Ga. The siderophore– 67 Ga complex is presumably transported into the bacterium, where it remains until phagocytosed by macrophages.7 Imaging is usually performed 18–72 h after injection of 185–370 MBq of 67Ga-citrate. The normal biodistribution of 67Ga, which can be variable, includes bone, bone marrow, liver, genitourinary and gastrointestinal tracts, and soft tissues.7
IgG1 (Granuloscint; CISBio International) that binds to non-specific cross-reactive antigen-95 present on neutrophils. Studies generally become positive by 6 h after injection; delayed imaging at 24 h may increase lesion detection.11 Another agent that has been investigated is a murine monoclonal antibody fragment of the IgG1 class that binds to normal cross-reactive antigen-90 present on leukocytes (LeukoScan; Immunomedics). Sensitivity and specificity of this agent range from 76% to 100% and from 67% to 100%, respectively.12 18
F FDG
18
Fluorodeoxyglucose is a fluorinated glucose analogue that, like glucose, passes through the cell membrane. Following subsequent phosphorylation by glucose-6-hexokinase it is trapped within the cell.13–15 Although FDG PET is reported to be a sensitive and specific technique in oncological imaging, it is well known that inflammatory and infectious lesions can cause false-positive results.16 Various types of inflammatory cells such as macrophages, lymphocytes, and neutrophil granulocytes as well as fibroblasts have been shown to avidly take up FDG, especially under conditions of activation. It even appears that on autoradiography, the FDG distribution in certain tumors is highest in the reactive inflammatory tissue, i.e. the activated macrophages and leukocytes surrounding the neoplastic cells.7,8
INFECTION OF THE SPINE Radiolabeled leukocytes Neutrophils concentrate in large numbers, up to 10% of the total number of neutrophils per day, at sites of infection. Their accumulation is stimulated by the presence of lactoferrin, local neutrophil secretions, and chemotactic peptides. Several techniques for in vitro radiolabeling of isolated leukocytes have been reported; the most commonly used procedures make use of the lipophilic compounds 111Inoxyquinoline (oxine) and 99mTc hexamethyl propyleneamine oxine (HMPAO).8 The lipophilic oxine binds bi- and trivalent ions such as 111In. Following diffusion of 111In-oxine across the cell membrane, 111 In is released from oxine, which leaves the cell and binds intracellularly. HMPAO forms a small neutral lipophilic complex with 99mTc that readily crosses the cell membrane and changes into a secondary hydrophilic complex that is trapped in cells. The radiolabeling procedure takes about 2–3 h. The usual dose of 111In-labeled leukocytes is 10–18.5 MBq (300–500 μCi); the usual dose of 99mTc-HMPAOlabeled leukocytes is 185–370 MBq (5–10 mCi). A total white count of at least 2000/mm3 is needed to obtain satisfactory images. Usually, the majority of leukocytes labeled are neutrophils, and hence the procedure is most useful for identifying neutrophil-mediated inflammatory processes, such as bacterial infections. The procedure is less useful for those illnesses in which the predominant cellular response is other than neutrophilic, such as tuberculosis.9 At 24 h after injection, the usual imaging time for 111In-labeled leukocytes, the normal distribution of activity is limited to the liver, spleen, and bone marrow. The normal biodistribution of 99mTc-HMPAO-labeled leukocytes is more variable. In addition to the reticuloendothelial system, activity is also normally present in the genitourinary tract, large bowel (within 4 h after injection), blood pool, and occasionally the gallbladder.10 The interval between injection of 99mTc-HMPAO-labeled leukocytes and imaging varies with the indication; in general, imaging is usually performed within a few hours after injection. 99m
Tc-labelled antibodies
Considerable effort has been devoted to developing in vivo methods of labeling leukocytes using peptides and antigranulocyte antibodies/ antibody fragments. One method makes use of a murine monoclonal 90
Vertebral infection represents 2–4% of all cases of osteomyelitis and its incidence is increasing.17 In order to prevent clinically significant consequences which include neural compromise and late spinal deformities, early diagnosis and prompt treatment are essential. Causative pyogenic microorganisms in decreasing order of frequency are Staphylococcus aureus, Streptococcus and Pneumococcus and Gram-negative bacteria.18 Tuberculous spondylitis is an important form of nonpyogenic granulomatous infection. The routes of spinal infection include hematogenous spread, postoperative infections, direct implantation during spinal punctures, and spread from a contiguous focus.
Acute osteomyelitis and spondylodiscitis The combination of physical examination and biochemical alterations in combination with three-phase bone scanning, and especially MRI, have a high sensitivity (>90%) for the detection of acute osteomyelitis and spondylodiscitis.19–21 Accordingly, in the absence of complicating factors, the added value of scintigraphic imaging techniques will be limited. Nevertheless, FDG PET especially may have a role in doubtful cases, albeit rarely. For instance, it may play a role in differentiating spondylodiscitis from erosive degenerative disc disease, a condition occasionally displaying a false-positive MRI and bone scan findings.20,22–24 When confronted with a negative PET scan in this clinical situation, infection can be excluded.
Chronic osteomyelitis Patients with chronic osteomyelitis may present with a variety of symptoms, including localized bone and joint pain, erythema, swelling, fevers, night sweats, etc. Laboratory tests, such as leukocyte count, estimated sedimentation rate, and C-reactive protein can be helpful in diagnosis but lack sensitivity and specificity in low-grade infections.25–28 C-reactive protein is also useful for gauging response to therapy. Many imaging modalities have been proposed for the noninvasive evaluation of chronic osteomyelitis.29 Radiographs are helpful in the diagnosis and staging of the patient. However, changes are
Section 3: General Diagnostic Technique
often subtle. Conventional radionuclide scans can also be useful in the diagnosis but do not aid in preoperative planning of resection. Combined three-phase bone scintigraphy and leukocyte scan has a good clinical accuracy (79–100%) when considering the peripheral skeleton;19,30–35 however, its accuracy decreases (1) in low-grade chronic infections(lower sensitivity);25,27 (2) in the presence of periskeletal soft tissue infection due to the limited resolution of conventional nuclear imaging (lower sensitivity and specificity); (3) in the central skeleton due to the presence of normal bone marrow and the possibility of so-called ‘cold lesions’ (lower sensitivity and specificity);24,31–35 and (4) after trauma or surgery due to the presence of ectopic hematopoietic bone marrow (lower specificity). To avoid false-positive studies due to ectopic bone marrow, the combination of leukocyte scanning with bone marrow scanning (99mtechnetium sulfur colloid) has been proposed.36 Congruency between leukocyte and bone marrow scanning indicates the presence of bone marrow, while the presence of a positive leukocyte scan and negative marrow scan suggests the presence of infection. Using this technique, diagnostic accuracy of up to 96% has been reported. In the vertebral column, a combination of bone and gallium scan has been proposed to improve both sensitivity and specificity.37 However, the need for two or even three (bone scan/leukocyte scan/bone marrow scan or bone scan/gallium scan) techniques is not practical, adds to the cost and patient radiation dose, and is time consuming. Computed tomography is used to identify a sequestered infection and for preoperative resection planning. Similarly, MRI is useful for surgical planning because it delineates intraosseous and extraosseous involvement. CT and MRI are, however, of limited value in the presence of metallic implants as well as for discriminating between edema and active infection after surgery.21,29,30 Overall, in spite of the available armamentarium of imaging modalities, clinicians are often confronted with an indeterminate diagnosis and the clinical strategy adopted is often limited to a ‘wait and see’ policy or empirical antibiotic treatment.25,38,39 Accordingly, novel imaging modalities with a very high accuracy for identification of sites of chronic osteomyelitis are of major interest. Several authors have addressed the value of FDG PET for this purpose. Guhlman et al. studied 51 patients suspected of having chronic osteomyelitis in the peripheral (n=36) or central (n=15) skeleton prospectively with static FDG PET imaging and combined 99mTc-antigranulocyte Ab/99m Tc-methylene diphosphonate bone scanning within 5 days.40 Obtained images were evaluated in a blinded and independent manner by visual interpretation, which was graded on a five-point scale of two observers’ confident diagnosis of osteomyelitis. Receiver operating characteristic (ROC) curve analysis was performed for both imaging modalities. The final diagnosis was established by means of bacteriologic culture of surgical specimens and histopathologic analysis (n=31) or by biopsy and clinical follow-up over 2 years (n=20). Of 51 patients, 28 had osteomyelitis and 23 did not. According to the unanimous evaluation of both readers, FDG PET correctly identified 27 of the 28 positives and 22 of the 23 negatives (IS identified 15 of 28 positives and 17 of 23 negatives, respectively). On the basis of ROC analysis, the overall accuracy of FDG PET and immunoscintigraphy in the detection of chronic osteomyelitis were 96%/96% and 82%/88%, respectively. Kälicke et al. evaluated the clinical usefulness of fluorine-18 fluorodeoxyglucose positron emission tomography (FDG PET) in acute and chronic osteomyelitis and inflammatory spondylitis.41 The study population comprised 21 patients suspected of having acute or chronic osteomyelitis or inflammatory spondylitis. Fifteen of these patients subsequently underwent surgery. FDG PET results were correlated with histopathological findings. The remaining six patients, who underwent conservative therapy, were excluded from any further
evaluation due to the lack of histopathological data. The histopathological findings revealed osteomyelitis or inflammatory spondylitis in all 15 patients: seven patients had acute osteomyelitis and eight patients had chronic osteomyelitis or inflammatory spondylitis. FDG PET yielded 15 true-positive results. However, the absence of negative findings in this series may raise questions concerning selection criteria. De Winter et al. reported on 60 patients suffering from a variety of suspected chronic orthopedic infections.42 In this prospective study, the presence or absence of infection was determined by surgical exploration in 15 patients and long-term clinical follow-up in 28 patients. As opposed to the study by Guhlmann et al., patients with recent surgery were not excluded. Considering only those patients with suspected chronic osteomyelitis, FDG PET was correct in 40 of 43 patients. There were three false-positive findings, 17 true-negative findings, and no false-negative findings. This resulted in a sensitivity of 100%, a specificity of 85%, and an accuracy of 93%. Two of three false-positive findings occurred in patients who had been operated on recently (6 weeks and 4 months, respectively). Zhuang et al. studied the accuracy of FDG PET for the diagnosis of chronic osteomyelitis.43 Twenty-two patients with possible osteomyelitis (5 in the tibia, 5 in the spine, 4 in the proximal femur, 4 in the pelvis, 2 in the maxilla, and 2 in the feet) that underwent FDG PET imaging and in whom operative or clinical follow-up data were available were included for analysis. The final diagnosis was made by surgical exploration or clinical follow-up during a 1-year period. FDG PET correctly diagnosed the presence or absence of chronic osteomyelitis in 20 of 22 patients but produced two false-positive results, respectively two cases of recent osteotomies, resulting in a sensitivity of 100%, a specificity of 87.5%, and an accuracy of 90.9%. It is, however, unclear from their report in how many patients histopathologic or microbiologic studies were available. Chako et al. retrospectively analyzed the accuracy of FDG PET for diagnosing infection in a large population of patients and in a variety of clinical circumstances, including suspicion of chronic osteomyelitis in 56 patients.44 Final diagnosis was made on the basis of surgical pathology and clinical follow-up for a minimum of 6 months. Among the patients suspected of having chronic osteomyelitis, the accuracy was 91.2%.
CONCLUSION Although limited, available data on FDG PET for imaging of the spine are promising, displaying a higher accuracy for diagnosing osteomyelitis when compared to other imaging modalities for this purpose, including conventional nuclear medicine examinations. For instance, in the study by Guhlman et al., comparing the combination of bone scan and leukocyte scan with FDG PET, the latter proved significantly more accurate for the diagnosis of osteomyelitis in the central skeleton. The fact that FDG PET is not disturbed by the presence of metallic implants and is able to differentiate between scar tissue and active inflammation constitutes a major advantage when compared to CT and MRI. As opposed to radiolabeled leukocytes or radiolabeled antibodies, FDG is likely to penetrate easier and faster in lesions than cellular tracers or antibodies.45 Aside from the potential for higher sensitivity, taking into account available data, a negative PET scan virtually rules out osteomyelitis.42,44 Initially, it was thought that the specificity of FDG PET for detection of infection of the spine may be limited by the fact that this tracer also accumulates in benign lesions and tumors. More recent papers, however, focusing on fractures, hemangioma, Paget’s disease, and endplate abnormalities of and in the spine, tend to contradict this hypothesis. Following traumatic fracture or surgical intervention, 91
Part 1: General Principles
bone scintigraphy reveals a positive result for an extended period of time, up to 2 years post-fracture, posing a challenge when evaluating patients for superimposed infection or for possible malignancy. Similarly, acute fracture or recent surgical intervention of the bone may cause increased FDG accumulation. However, available results suggest that FDG uptake patterns following fracture differ amongst various bones. In a series of 17 patients by Schmitz et al., MRI demonstrated a vertebral compression fracture generating from osteoporosis in 13 cases.46 In 12 of these 13 cases, PET scans were categorized as true negative. Comparable results were obtained by Zhuang et al. in a retrospective study assessing the pattern and time course of abnormal FDG uptake following traumatic or surgical fracture.47 Out of 10 patients with a documented fracture of the spine (interval between confirmation of the fracture and time of PET scanning, 24 days and 45 months), none displayed increased FDG uptake. Importantly, in other bone structures, if positive, uptake proved normal by a maximum of 3 months after fracture or surgical intervention of the bone. Accordingly, based on currently available data, there should be normal FDG uptake at spine fractures either initially or by a maximum of 3 months post-fracture. Bhargava et al. reported on a case of vertebral Paget’s disease showing normal FDG uptake and intense osteoblastic activity on the bone scan.48 Bybel et al. performed FDG PET to stage a nasopharyngeal carcinoma and found hypometabolic regions in multiple thoracic vertebrae.49 These corresponded to multiple hemangiomas as evidenced by MRI. These findings are in sharp contrast to those reported by Hatayama et al. in 16 patients with histopathologically documented hemangiomas of the extremities.50 In these authors’ experience, all 16 lesions examined by PET displayed FDG accumulation with standardized uptake values ranging from 0.7 to 1.67. Stumpe et al. performed prospectively FDG PET in 30 consecutive patients with substantial endplate abnormalities found during MR imaging of the lumbar spine.51 The sensitivity and specificity for differentiation of degenerative from infectious endplate abnormalities were 50% and 96% for MRI versus 100% and 100% for FDG PET. Finally, in most patients, a thorough medical history makes the presence of tumor unlikely, and sterile inflammations such as chronic polyarthritis, vasculitis, and tumors often appear at sites or show distribution patterns that are suggestive of these diseases. To conclude, based on available data, FDG PET has potential to become the imaging gold standard for detection of infection in the spine.
References 1. Eberl S Zimmerman RE. Nuclear medicine imaging instrumentation. In: Muray IPC, Ell PJ, eds. Nuclear medicine in clinical diagnosis and treatment. Edinburgh: Churchill Livingstone; 1998:1559–1569. 2. Bailey DL, Parker JA. Single photon emission computed tomography. In: Muray IPC, Ell PJ, eds. Nuclear medicine in clinical diagnosis and treatment. Edinburgh: Churchill Livingstone; 1998:1589–1601.
92
9. Palestro CJ, Torres MA. Radionuclide imaging of non-osseous infection. Q J Nucl Med 1999; 43:46–60. 10. Roddie ME, Peters AM, Danpure HJ. Inflammation: imaging with Tc-99m HMPAOlabeled leukocytes. Radiology 1988; 166:767–772. 11. Love C, Palestro CJ.99mTc-fanolesomab. I. Drugs 2003; 6:1079–1085. 12. Skehan SJ, White JF, Evans JW, et al. Mechanism of accumulation of 99mTc-sulesomab in inflammation. J Nucl Med 2003; 44:11–18. 13. Ak I, Stokkel MPM, Pauwels EKJ. Positron-emission tomography with 18F-fluorodeoxyglucose. Part 2. The clinical value in detecting and staging primary tumours. J Cancer Res Clin Oncol 2000; 126:560–574. 14. Bar-Shalom R, Valdivia AY, Blaufox MD. PET imaging in oncology. Sem Nucl Med 2000; 30:150–185 15. Coleman RE. Clinical PET in oncology. Clin Positron Imag 1998; 1:15–30. 16. Bakheet SM, Powe J. Benign causes of 18-FDG uptake on whole body imaging. Sem Nucl Med 1998; 28:352–358. 17. Jauregui LE, Senour CL. In: Jauregui LE, ed. Diagnosis and management of bone infections. New York: Marcel Dekker; 1995:37–108. 18. Beronius M, Bergman B, Andersson R. Vertebral osteomyelitis in Goteborg, Sweden: a retrospective study of patients during 1990–95. Scand J Infect Dis 2001; 33:527–532. 19. Palestro CJ, Torres MA. Radionuclide imaging in orthopaedic infections. Sem Nucl Med 1997; 27:33433–33435. 20. Kaiser JA, Holland BA. Imaging of the cervical spine. Spine 1998; 23:2701–2712. 21. Erdman WA, Tamburro F, Jayson HT, et al. Osteomyelitis: characteristics and pitfalls of diagnosis with MR imaging. Radiology 1991; 180:533–539. 22. Stabler A, Baur A, Kruger A, et al. Differential diagnosis of erosive osteochondrosis and bacterial spondylitis: magnetic resonance tomography. ROFO. Fortschritte auf dem Gebiet der Rontgenstrahlen und der neuen bildgebenden Verfahren 1998; 168:421–428. 23. Champsaur P, Parlier-Cuau C, Juhan V, et al. Differential diagnosis in infective spondylodiscitis and erosive degenerative disk disease. J Radiologie 2000; 81:516–522. 24. Even-Sapir E, Martin RH. Degenerative disc disease: a cause for diagnostic dilemma on In-111 WBC studies in suspected osteomyelitis. Clin Nucl Med 1994; 19:388– 392. 25. Zimmerli W. Role of antibiotics in the treatment of infected joint prosthesis. Orthopade 1995; 24:308–313. 26. Perry M. Erythrocyte sedimentation rate and C reactive protein in the assessment of suspected bone infection: are they reliable indices? JRCSE 1996; 41:116–118. 27. Sanzen L, Sundberg M. Periprosthetic low-grade hip infections. Erythrocyte sedimentation rate and C-reactive protein in 23 cases. Acta Orthopaedica Scandinavica 1997; 68:461–465. 28. Shih LY, Wu JJ, Yang DJ. Erythrocyte sedimentation rate and C-reactive protein values in patients with total hip arthroplasty. Clin Orthopaedi 1987; 225: 238–246. 29. Crim JT, Seeger LL. Imaging evaluation of osteomyelitis. Crit Rev Diagnostic Imaging 1994; 35:201–256. 30. Seabold JE, Nepola JV. Imaging techniques for the evaluation of postoperative orthopedic infections. Q J Nucl Med 1999; 43:21–28. 31. Becker W. The contribution of nuclear medicine to the patient with infection. Eur J Nucl Med 1995; 22:1195–1211. 32. Datz FL. Indium-111-labeled leukocytes for the detection of infection: current status. Sem Nucl Med 1994; 24:92–109.
3. Meikle SR, Dahlbom M. Positron emission tomography. In: Muray IPC, Ell PJ, eds. Nuclear medicine in clinical diagnosis and treatment. Edinburgh: Churchill Livingstone; 1998:1603–1616.
33. Kaim A, Maurer T, Ochsner P, et al. Chronic complicated osteomyelitis of the appendicular skeleton diagnosed with technetium-99 m labelled monoclonal antigranulocyte antibody-immunoscintigraphy. Eur J Nucl Med 1997; 24:732–778.
4. Boyd RE, Silvester DJ Radioisotope production. In: Muray IPC, Ell PJ, eds. Nuclear medicine in clinical diagnosis and treatment. Edinburgh: Churchill Livingstone; 1998:1617–1624.
34. Krznaric E, De Roo MD, Verbruggen A, et al. Chronic osteomyelitis: diagnosis with technetium-99m-D, L-hexamethylpropylene amine oxime labeled leukocytes. Eur J Nucl Med 1996; 23:792–797.
5. Genant HK, Bautovich GJ, Singh M, et al. Bone-seeking radionuclides: an in vivo study of factors affecting skeletal uptake. Radiology 1974; 113:373–382.
35. Peters AM. The use of nuclear medicine in infections. Brit J Radiol 1998; 71:252– 261.
6. McAfee JG, Reba RC, Majd M. The musculoskeletal system. In: Wagner HN Jr, Szabo Z, Buchanan JW, eds. Principles of nuclear medicine. 2nd edn. Philadelphia: WB Saunders; 1995:986–1012.
36. Palestro CJ, Kim CK, Swyer AJ, et al. Radionuclide diagnosis of vertebral osteomyelitis: indium-111-leukocyte and technetium-99m-methylene diphosphonate bone scintigraphy. J Nucl Med 1991; 32:1861–1865.
7. Palestro CJ. The current role of gallium imaging in infection. Semin Nucl Med 1994; 24:128–141.
37. Palestro CJ. The current role of gallium imaging in infection. Sem Nucl Med 1994; 24:128–141.
8. Karesh SM, Henkin RE. Preparation of 111In leukocytes after hemolytic removal of erythrocytes. Int J Rad Appl Instrum B 1987; 14:79–80.
38. Segreti J, Nelson JA, Trenholme GM. Prolonged suppressive antibiotic therapy for infected orthopaedic prostheses. Clin Infect Dis 1998; 27:711–713.
Section 3: General Diagnostic Technique 39. Spangehl MJ, Younger ASE, Masri BA, et al. Diagnosis of infection following total hip arthroplasty. Am J Bone Joint Surg 1998; 79A:1578–1588.
45. Chianelli M, Mather SJ, Martin-Comin J, et al. Radiopharmaceuticals for the study of inflammatory processes: a review. Nucl Med Commun 1997; 18:437–455.
40. Guhlmann A, Brecht-Krauss D, Suger G, et al. Fluorine-18-FDG PET and technetium-99m antigranulocyte antibody scintigraphy in chronic osteomyelitis. J Nucl Med 1998; 39:2145–2152.
46. Schmitz A, Risse JH, Textor J, et al. FDG-PET findings of vertebral compression fractures in osteoporosis: preliminary results. Osteoporos Int 2002; 13:755–761.
41. Kälicke T, Schmitz A, Risse JH, et al. Fluorine-18 fluorodeoxyglucose PET in infectious bone diseases: results of histologically confirmed cases. Eur J Nucl Med 2000; 27:524–528. 42. De Winter F, Van de Wiele C, Vogelaers D, et al. F-18 Fluorodeoxyglucose positron emission tomography: a highly accurate imaging modality for the diagnosis of chronic musculoskeletal infections. Am J Bone Joint Surg 2001; 83A:651–660.
47. Zhuang H, Sam JW, Chacko TK, et al. Rapid normalization of osseous FDG uptake following traumatic or surgical fractures. Eur J Nucl Med Mol Imaging 2003; 30:1096–1103. 48. Bhargava P, Naydich M, Ghesani M. Normal F-18 FDG vertebral uptake in Paget’s disease on PET scanning. Clin Nucl Med 2005; 30:191–192. 49. Bybel B, Raja S. Vertebral hemangiomas on FDG PET scan. Clin Nucl Med 2003; 28:522–523.
43. Zhuang H, Duarte PS, Pourdehand M, et al. Exclusion of chronic osteomyelitis with F-18 fluorodeoxyglucose positron emission tomography. Clin Nucl Med 2000; 25:281–284.
50. Hatayama K, Watanabe H, Ahmed AR, et al. Evaluation of hemangioma by positron emission tomography: role in a multimodality approach. J Comput Assist Tomogr 2003; 27:70–77.
44. Chacko TK, Zhuang H, Stevenson K, et al. The importance of the location of fluorodeoxyglucose uptake in periprosthetic infection in painful hip prostheses. Nucl Med Commun 2002; 23: 851–855.
51. Stumpe KD, Zanetti M, Weishaupt D, et al. FDG positron emission tomography for differentiation of degenerative and infectious endplate abnormalities in the lumbar spine detected on MR imaging. Am J Roentgenol 2002; 179:1151–1157.
93
PART 1
GENERAL PRINCIPLES
Section 3
General Diagnostic Technique
CHAPTER
Electrodiagnostic Approach to Patients with Suspected Radiculopathy
8
Timothy R. Dillingham
INTRODUCTION Cervical and lumbosacral radiculopathies are conditions involving a pathological process affecting the spinal nerve root. Commonly, this is a herniated nucleus pulposus that anatomically compresses a nerve root within the spinal canal. Another common etiology for radiculopathy is spinal stenosis resulting from a combination of degenerative spondylosis, ligament hypertrophy, and spondylolisthesis. Inflammatory radiculitis is another pathophysiological process that can cause radicular pain and/or radiculopathy. It is important to remember, however, that other more ominous processes such as malignancy and infection can present with the same symptoms and signs of radiculopathy as the more common causes. This chapter deals with the clinical approach used in an electrodiagnostic laboratory to evaluate a person with neck pain, lumbar spine pain, or limb symptoms which are suggestive of radiculopathy. The indications for referring for testing as well as the limitations of testing are discussed to give a greater understanding of this important diagnostic procedure. This is not intended to be a basic chapter dealing with how to perform electrodiagnostic studies. Given the extensive differential diagnosis for limb and spine symptoms, it is important for electrodiagnosticians to develop a conceptual framework for evaluating these referrals with a standard focused history and physical examination and a tailored electrodiagnostic approach. Accurately identifying radiculopathy by electrodiagnosis whenever possible, provides valuable information that helps guide treatment and minimizes other invasive and expensive diagnostic and therapeutic procedures.
SPINE AND NERVE ROOT ANATOMY: DEVIATIONS FROM THE EXPECTED Spinal anatomy is discussed in detail in Chapters 46 and 80 by Russell Gilchrist and will not be emphasized here. From an electrodiagnostic perspective, however, there are several specific anatomical issues that merit further discussion. At all levels the dorsal root ganglion (DRG) lies in the intervertebral foramen. This anatomical arrangement has implications for clinical electrodiagnosis of radiculopathy, namely that sensory nerve action potentials (SNAPs) are preserved in most radiculopathies as the nerve root is affected proximal to the DRG. Regarding the cervical nerve roots and the brachial plexus, there are many anatomic variations. Perneczky1 described an anatomic study of 40 cadavers. In all cases, there were deviations from accepted cervical root and brachial plexus anatomy. Levin, Maggiano, and Wilbourn2 examined the pattern of abnormalities on electromyography (EMG) in 50 cases of surgically proven cervical root lesions. A range of needle EMG patterns was found with EMG demonstrating less specificity for the C6 root level, but more specificity and consistent patterns for
C8, C7, and C5 radiculopathies. In subjects with C6 radiculopathies, half the patients showed findings similar to those with C5 radiculopathies and the other half demonstrated C7 patterns. This surgical group was more severely affected than patients who do not require surgical interventions, and this pattern may not hold for less symptomatic patients. In the lumbar spinal region dorsal and ventral roots exit the spinal cord at about the T11–L1 boney level and travel in the lumbar canal as a group of nerve roots in the dural sac. This is termed the ‘horse’s tail’ or cauda equina. This poses challenges and limitations to the EMG examination. A destructive intramedullary (spinal cord) lesion at T11 can produce EMG findings in muscles innervated by any of the lumbosacral nerve roots and manifest the precise findings on needle EMG as those seen with a herniated nucleus pulposus at any of the lumbar disc levels. For this reason, the electromyographer cannot precisely determine the anatomic location of a lumbar intraspinal lesion producing distal muscle EMG findings in the lower limbs. The needle EMG examination can only identify the root or roots that are physiologically involved, but not the precise anatomic site of pathology in the lumbar spinal canal. This is an important limitation requiring correlation with imaging findings to determine which anatomic location is most likely the offending site. This can be difficult in elderly persons with foraminal stenosis as well as moderate central canal stenosis at more than one site. In a prospective study of 100 patients with lumbosacral radiculopathy who underwent lumbar laminectomy, EMG precisely identified the involved root level 84% of the time.3 Needle EMG failed to accurately identify the compressed root in 16%. However, at least half of the failures were attributable to anomalies of innervation. Another component to this study involved stimulating the nerve roots intraoperatively with simultaneous recording of muscle activity in the lower limb using surface electrodes. These investigators demonstrated variations in root innervation, such as the L5 root innervating the soleus and medial gastrocnemius, in 16% of a sample of 50 patients. Most subjects demonstrated dual innervation for most muscles.3 These findings underscore the limitations of precise localization for root lesions with EMG. The electrodiagnostician should maintain an appreciation of these anatomic variations to better convey the level of certainty with respect to diagnostic conclusions.
PHYSICAL EXAMINATION The electrodiagnostic examination is an extension of the standard clinical examination. The history and physical examination are vital initial steps in determining what conditions may be causing the presenting symptoms. Most radiculopathies present with symptoms in one limb. Multiple radiculopathies such as are seen in cervical spinal stenosis or lumbar stenosis may cause symptoms in more than one limb. A focused neuromuscular examination that assesses strength, 95
Part 1: General Principles
reflexes, and sensation in the affected limb and the contralateral limb is important, providing a framework for electrodiagnostic assessment. An algorithmic approach to utilizing physical examination and symptom information to tailor the electrodiagnostic evaluation is shown in Figure 8.1. In this approach, symptoms and physical examination signs create a conceptual framework for approaching these sometimes daunting problems. Admittedly, there are many exceptions to this approach with considerable overlap in medical disorders which might fall within multiple categories. Radiculopathies and entrapment neuropathies are examples of such conditions with a variety of clinical presentations and physical examination findings, such that they are included in both focal symptom categories with and without sensory loss. In the case of a person with lumbosacral radiculopathy, a positive straight leg raise test may be noted in the absence of motor, reflex, or sensory changes. Conditions such as myopathies and polyneuropathies better fit this algorithmic approach, given that symptoms and physical examination signs are more specific. Figure 8.1 also contains musculoskeletal disorders and denotes how they fall into this conceptual framework. The electrodiagnostician must be willing to modify the electrodiagnostic examination in response to nerve conduction and EMG findings and adjust the focus of the examination in light of new information. The implications of symptoms and signs on electrodiagnostic findings were investigated by Lauder and colleagues for suspected cervical and lumbosacral radiculopathies.4,5 Even though physical examination findings were better at predicting who would have a radiculopathy, many patients with normal examinations had abnor-
mal electrodiagnostic studies, indicating that clinicians should not curtail electrodiagnostic testing simply because the physical examination is normal. For lower limb symptoms, loss of a reflex or weakness dramatically increased the likelihood of having a radiculopathy by EMG. Losing the Achilles reflex, for instance, resulted in an odds ratio of 8.4 (p8 mV were considered positive. This study assessed EMG parameters and used quantitative EMG with a unique grading scale not used in clinical practice. Fibrillations were infrequent. This limits the generalizability of this otherwise strong study. Unless otherwise stated the EMG parameters used in sensitivity calculations were fibrillation potentials. b
99
Part 1: General Principles
and rhythm as well as discharge morphology when evaluating for fibrillations and positive waves in the lumbar paraspinal muscles. Electrodiagnosticians should take care not to overcall fibrillations in lumbosacral paraspinal muscles by mistaking irregularly firing endplate spikes for fibrillations. Paraspinal muscles may be abnormal in patients with spinal cancers31–33 or amyotrophic lateral sclerosis,34 and following spinal surgery35 or lumbar puncture.36 In fact, fibrillations can be found years after lumbar laminectomy.35 The absence of paraspinal muscle fibrillations in such patients is helpful, but finding fibrillations in someone after laminectomy is of uncertain relevance as these fibrillations may be residual from the previous muscle damage or relatively new denervation. Investigations over the last decade have provided insights into better quantification and examination of lumbosacral paraspinal muscles. The lumbar paraspinal muscle examination has been refined through investigations that used a grading scale for the findings.37–40 The ‘mini PM’ score provides a quantitative means of deriving the degree of paraspinal muscle denervation.40 It distinguishes normal findings from persons with radiculopathy. This novel and quantitative technique may prove useful to identify subtle radiculopathies or spinal stenosis with greater precision. Cervical and lumbar paraspinal muscles should only be examined for insertional activity and spontaneous activity while at rest. Recruitment findings and motor unit morphology for these muscles has not been established and consequently we do not know for sure what constitutes normal. Examiners should not overcall radiculopathies based upon ‘reduced recruitment’ or ‘increased polyphasicity’ in the paraspinal muscles. Paraspinal muscles either show spontaneous activity and therefore localize the lesion to the root level or they do not. There is considerable overlap in paraspinal muscles with single roots innervating fibers above and below their anatomic levels. For this reason, the level of radiculopathy cannot be delineated by paraspinal EMG alone, but rather is based upon the root level that best explains the distribution of muscles demonstrating fibrillations.
IDENTIFICATION AS A SEPARATE CONCEPT FROM SENSITIVITY Electrodiagnostic testing is uncomfortable and expensive. Because electrodiagnosis is a composite assessment composed of various tests, a fundamental question is; when has the point of diminishing returns been reached? Some radiculopathies cannot be confirmed by needle EMG, even though the signs and symptoms along with imaging results suggest that radiculopathy is present. A screening EMG study involves determining whether or not a radiculopathy, if present, can be confirmed by EMG. If the radiculopathy cannot be confirmed, then presumably no number of muscles can identify the radiculopathy. If it can be confirmed, then the screen should identify this possibility with a high probability. The process of identification can be conceptualized as a conditional probability: given that a radiculopathy can be confirmed by needle EMG, what is the minimum number of muscles which must be examined in order to confidently recognize or exclude this possibility? This is a fundamentally different concept from sensitivity. It involves understanding and defining the limitations of a composite test (group of muscles).
HOW MANY AND WHICH MUSCLES TO STUDY The concept of a screening EMG encompasses identifying the possibility of an electrodiagnostically confirmable radiculopathy. If one of the muscles in the screen is abnormal, the screen must be expanded to exclude other diagnoses, and to fully delineate the radiculopathy 100
level. Because of the screening nature of the EMG exam, electrodiagnosticians with experience should look for more subtle signs of denervation and, if present in the screening muscles, then expand the study to determine if these findings are limited to a single myotome or peripheral nerve distribution. If they are limited to a single muscle, the clinical significance is uncertain.
The cervical radiculopathy screen Dillingham et al.41 conducted a prospective multicenter study evaluating patients referred to participating electrodiagnostic laboratories with suspected cervical radiculopathy. A standard set of muscles were examined by needle EMG for all patients. Those with electrodiagnostically confirmed cervical radiculopathies, based upon EMG findings, were selected for analysis. The EMG findings in this prospective study also encompassed other neuropathic findings: (1) positive sharp waves, (2) fibrillation potentials, (3)complex repetitive discharges (CRD), (4) high-amplitude, long-duration motor unit action potentials, (5) increased polyphasic motor unit action potentials, or (6) reduced recruitment. There were 101 patients with electrodiagnostically confirmed cervical radiculopathies representing all cervical root levels. When paraspinal muscles were one of the screening muscles, five-muscle screens identified 90–98% of radiculopathies, six-muscle screens identified 94–99%, and seven-muscle screens identified 96–100% (Tables 8.2 and 8.3). When paraspinal muscles were not part of the screen, eight distal limb muscles recognized 92–95% of radiculopathies. Six-muscle screens, including paraspinal muscles, yielded consistently high identification rates, and studying additional muscles lead to only marginal increases in identification. Individual screens useful to the electromyographer are listed in Tables 8.2 and 8.3. In some instances a particular muscle cannot be studied due to wounds, skin grafts, dressings, or infections. In such cases the electromyographer can use an alternative screen with equally high identification. These findings were consistent with those derived from a large retrospective study.42
The lumbosacral radiculopathy screen A similar prospective multicenter study was conducted at five institutions by Dillingham et al.43 Patients referred to participating electrodiagnostic laboratories with suspected lumbosacral radiculopathy were recruited and a standard set of muscles examined by needle EMG. Patients with electrodiagnostically confirmed lumbosacral radiculopathies, based upon EMG findings, were selected for analysis. As described above for the prospective cervical study, neuropathic findings were analyzed along with spontaneous activity. There were 102 patients with lumbosacral radiculopathies representing all lumbosacral root levels. When paraspinal muscles were one of the screening muscles, four-muscle screens identified 88–97%, five-muscle screens identified 94–98%, and six-muscle screens 98–100% (Tables 8.4–8.6). When paraspinal muscles were not part of the screen, identification rates were lower for all screens and eight distal muscles were necessary to identify 90%. If only four muscles can be tested due to limited patient tolerance, as seen in Table 8.4, and if one of these muscles are the paraspinals, few electrodiagnostically confirmable radiculopathies will be missed. A large retrospective study noted consistent findings, concluding that five muscles identified most electrodiagnostically confirmable radiculopathies.44 Dillingham and Dasher45 re-analyzed data from a study published by Knutsson almost 40 years earlier.46 In this detailed study, 206 patients with sciatica underwent lumbar surgical exploration. All subjects underwent standard EMG by the author (Knutsson) with a standard set of 14 muscles using concentric needles. The examiner was blinded to other test results and physical examination findings. In addition to
Section 3: General Diagnostic Technique
Table 8.2: Five-muscle screen identifications of patients with cervical radiculopathies
Table 8.3: Six-muscle screen identifications of the patients with cervical radiculopathies
Muscle screen
Muscle Screen
Neuropathic
Spontaneous activity
Without paraspinals Deltoid, APB, FCU
92%
65%
85%
54%
84%
58%
91%
60%
80%
55%
Deltoid, triceps
89%
64%
Biceps, triceps, EDC
94%
64%
Deltoid, triceps, PT
99%
83%
96%
75%
94%
77%
98%
79%
APB, EDC, PSM 95%
73%
FDI, PSM
Biceps, triceps, EDC FDI, FCU, PSM
90%
73%
PSM, FCU Biceps, FCR, APB
87%
With paraspinals 98%
APB, PSM
Deltoid, EDC, FDI
Biceps, triceps, FCU
PT, APB, FCU
With paraspinals
Biceps, triceps, EDC
66%
EDC, FDI, FCR, PT
PT, APB, FCU Deltoid, triceps, PT
93%
EDC, FCR, FDI
EDC, FDI, FCR Biceps, triceps
Deltoid, APB, FCU Triceps, PT, FCR
EDC, FCR, FDI Deltoid, triceps
Spontaneous Activity
Without paraspinals
Triceps, PT Biceps, triceps
Neuropathic
Deltoid, EDC, FDI PSM, FCU, triceps
95%
77%
Biceps, FCR, APB
PT, PSM
PT, PSM, triceps
The screen detected the patient with cervical radiculopathy if any muscle in the screen was one of the muscles which were abnormal for that patient. Neuropathic findings for nonparaspinal muscles included positive waves, fibrillations, increased polyphasic potentials, neuropathic recruitment, increased insertional activity, CRDs, or large amplitude/long duration motor unit action potentials. For paraspinal muscles the neuropathic category included fibrillations, increased insertional activity, positive waves, or CRDs. Spontaneous activity referred only to fibrillations or positive sharp waves. APB, abductor pollicis brevis; FCU, flexor carpi ulnaris; FCR, flexor carpi radialis; PSM, cervical paraspinal muscles; FDI, first dorsal interosseous; PT, pronator teres, supra-supraspinatus, infra-infraspinatus; EDC, extensor digitorum communis. Adapted with permission, Dillingham et al.41
Muscle abbreviations, identification criteria, and definitions are described in Table 8.2.
the EMG and surgical information, myelogram and physical examination data were derived. In this contemporary re-analysis, screens of four muscles with one being the PSM yielded an identification rate of 100%, a 92% sensitivity with respect to the intraoperative anatomical nerve root compressions, and an 89% sensitivity with respect to the clinical inclusion criteria.45 This study, using data from four decades ago, confirmed that four-muscle screening examinations provide high identification. These findings are consistent with contemporary work showing that screens with relatively few muscles (six) are optimal. As described above, these research efforts were undertaken to refine and streamline the EMG examination. The strongest studies, contemporary prospective multicenter investigations, provide the best estimates for a sufficient number of muscles.41,43 In summary, for both cervical and lumbosacral radiculopathy screens the optimal number of muscles appears to be six muscles, including the paraspinal muscles and muscles that represent all root level innervations. When paraspinal muscles are not reliable, then eight nonparaspinal muscles must be examined. Another way to think of this: ‘To minimize harm, six in the leg and six in the arm’
LUMBAR SPINAL STENOSIS With the aging population in the United States and the increasing prevalence of lumbar spinal stenosis that occurs in the elderly, this condition takes on greater public health significance. In fact, an entire edition of the Physical Medicine and Rehabilitation Clinics of North America was recently dedicated to this complex topic.47 There are few studies involving spinal stenosis and electromyography. For lumbosacral spinal stenosis, Hall and colleagues48 showed that 92% of persons with imaging-confirmed stenosis had a positive EMG. They also underscored the fact that 46% of persons with a positive EMG study did not demonstrate paraspinal muscle abnormalities, only distal muscle findings. In 76%, the EMG showed bilateral myotomal involvement.48 These results suggest that in such patients, distal limb findings may be the most prominent and electromyographers should not expect fibrillations in lumbosacral paraspinal muscles. In the United States, diabetes is on the increase, with increasing prevalence and incidence.49 Diabetes often confounds accurate diagnosis of radiculopathy and spinal stenosis.50,51 Inaccurate recognition of sensory polyneuropathy, diabetic amyotrophy, or mononeuropathy can lead to unnecessary surgical interventions. In a recent prospective study by Adamova and colleagues,50 the value of electrodiagnostic testing was assessed. There were three groups; one group composed of 29 persons with imaging confirmed clinically mild lumbar spinal stenosis, 24 subjects with both diabetes and polyneuropathy, and 25 healthy age-matched volunteers served as control subjects. In this well-designed study, sural sensory amplitudes distinguished the diabetic polyneuropathy group (an amplitude of 4.2 microvolts or less was found in 47% of diabetic patients and only 17% of stenosis patients). The ulnar F-wave was prolonged in polyneuropathy patients and not lumbar stenosis 101
Part 1: General Principles
Table 8.4:
Four-muscle screen identifications of patients with lumbosacral radiculopathies
Screen
Neuropathic
Spontaneous Activity
Four muscles without paraspinals
Screen
Neuropathic
Spontaneous Activity
Six muscles without paraspinals
ATIB, PTIB, MGAS, RFEM
85%
75%
ATIB, PTIB, MGAS, RFEM, SHBF, LGAS
89%
78%
VMED, TFL, LGAS, PTIB
75%
58%
VMED, TFL, LGAS, PTIB, ADD, MGAS
83%
70%
VLAT, SHBF, LGAS, ADD
52%
35%
VLAT, SHBF, LGAS, ADD, TFL, PTIB
79%
62%
ADD, TFL, MGAS, PTIB
80%
67%
ADD, TFL, MGAS, PTIB, ATIB, LGAS
88%
79%
97%
90%
ATIB, PTIB, MGAS, PSM, VMED, TFL
99%
93%
Four muscles with paraspinals ATIB, PTIB, MGAS, PSM
Six muscles with paraspinals
VMED, LGAS, PTIB, PSM
91%
81%
VMED, LGAS, PTIB, PSM, SHBF, MGAS
99%
87%
VLAT, TFL, LGAS, PSM
88%
77%
VLAT, TFL, LGAS, PSM, ATIB, SHBF
98%
87%
ADD, MGAS, PTIB, PSM
94%
86%
ADD, MGAS, PTIB, PSM, VLAT, SHBF
99%
89%
VMED, ATIB, PTIB, PSM, SHBF, MGAS
100%
92%
99%
91%
The screen identified the patient if any muscle in the screen was abnormal for that patient. The muscle either demonstrated neuropathic findings or spontaneous activity. Neuropathic findings for nonparaspinal muscles included positive waves, fibrillations, increased polyphasic potentials, neuropathic recruitment, increased insertional activity, CRDs, or large amplitude long duration motor unit action potentials. Spontaneous activity referred only to fibrillations or positive sharp waves. For paraspinal muscles the neuropathic category included fibrillations, increased insertional activity, positive waves, or CRDs. PSM, lumbosacral paraspinal muscles; PTIB, posterior tibialis; ATIB, anterior tibialis; MGAS, medial gastrocnemius, LGAS, lateral gastrocnemius, TFL, tensor fascia lata, SHBF, short head biceps femoris; VMED, vastus medialis; VLAT, vastus lateralis; RFEM, rectus femoris; ADD, adductor longus. Adapted from Dillingham, et al.43, with permission.
patients and the radial SNAP was similarly reduced in the group with polyneuropathy.50 These findings underscore the value of performing sensory testing in the involved extremity as well as an upper limb to fully recognize diabetic polyneuropathy when pres-
Table 8.5: Five-muscle screen identifications of patients with lumbosacral radiculopathies Screen
Neuropathic
Spontaneous activity
ATIB, PTIB, MGAS, RFEM, SHBF
88%
77%
VMED, TFL, LGAS, PTIB, ADD
76%
59%
VLAT, SHBF, LGAS, ADD, TFL
68%
50%
ADD, TFL, MGAS, PTIB, ATIB
86%
78%
ATIB, PTIB, MGAS, PSM, VMED
98%
91%
VMED, LGAS, PTIB, PSM, SHBF
97%
84%
VLAT, TFL, LGAS, PSM, ATIB
97%
86%
ADD, MGAS, PTIB, PSM, VLAT
94%
86%
Five muscles without paraspinals
Five muscles with paraspinals
Abbreviations and definitions of muscle abnormalities are the same as in Table 8.4.
102
Table 8.6 Six-muscle screen identifications of patients with lumbosacral radiculopathies
VMED, TFL, LGAS, PSM, ATIB, PTIB ADD, MGAS, PTIB, PSM, ATIB, SHBF
Abbreviations and definitions of muscle abnormalities are the same as in Table 8.4.
ent and differentiate this condition from lumbar spinal stenosis or radiculopathy.
LIMITATIONS OF THE EMG SCREEN These cervical and lumbosacral muscle screens should not substitute for a clinical evaluation and differential diagnosis formulation by the electrodiagnostic consultant. Rather, information from investigations described above allows the electrodiagnostician to streamline the EMG evaluation and make better-informed clinical decisions regarding the probability of missing an electrodiagnostically confirmable radiculopathy when a given set of muscles are studied. Performing a focused history and physical examination is essential, and these screens should not supplant such clinical assessment or a more detailed electrodiagnostic study when circumstances dictate. If one of the six muscles studied in the screen is positive, there is the possibility of confirming electrodiagnostically that a radiculopathy is present. In this case, the examiner must study additional muscles to determine the radiculopathy level and to exclude a mononeuropathy. If the findings are found in only a single muscle, they remain inconclusive and of uncertain clinical relevance. If none of the six muscles are abnormal, the examiner can be confident of not missing the opportunity to confirm by EMG that a radiculopathy is present, and can curtail the painful needle examination. The patient may still have a radiculopathy, but other tests such as MRI will be necessary to confirm this clinical suspicion. This logic is illustrated in Figure 8.2. It is important to remember that the EMG screens for cervical and lumbosacral radiculopathies were validated in a group of patients with limb symptoms suggestive of radiculopathies. These screens will not provide sufficient screening power if a brachial plexopathy is present or if a focal mononeuropathy such as a suprascapular neuropathy is the cause of the patient’s symptoms. The electrodiagnostician should always perform EMG on weak muscles to increase the diagnostic yield. These screens do not sufficiently screen for myopathies or motor neuron disease. It is incumbent upon the electrodiagnostician to formulate a differential diagnosis and methodically evaluate for the likely diagnostic possibilities, further refining the examination as data are acquired.
Section 3: General Diagnostic Technique Suspected radiculopathy
Six muscles (with PSM)-lumbar screen Six muscles (with PSM)-cervical screen
If one muscle is positive, expand study
If all muscles negative, stop EMG exam in this limb
Determine if EMG reflects 1 radiculopathy (which level), 2 entrapment neuropathy, 3 generalized condition, or 4 findings that are of uncertain relevance.
The patient will not have an electrodiagnostically confirmable radiculopathy. They may 1 not have radiculopathy, or 2 have a radiculopathy but you will not confirm this with EMG. Other diagnostic tests must be utilized such as MRI or SNRB .
Fig. 8.2 Implications of a positive EMG screening evaluation.
SYMPTOM DURATION AND THE PROBABILITY OF FIBRILLATIONS In the past, a well-defined temporal course of events was thought to occur with radiculopathies despite the absence of studies supporting such a relationship. It was a commonly held notion that in acute lumbosacral radiculopathies, the paraspinal muscles denervated first, followed by distal muscles, and that reinnervation started with paraspinal muscles and then the distal muscles. This paradigm was recently addressed with a series of investigations.52–55 For both lumbosacral and cervical radiculopathies, symptom duration had no significant relationship to the probability of finding spontaneous activity in paraspinal or limb muscles. There is no evidence to support a relationship between the duration of a patient’s symptoms and the probability of finding fibrillations in paraspinal or limb muscles. This simplistic explanation, although widely quoted in the older literature, does not explain the complex pathophysiology of radiculopathies. Electrodiagnosticians should not invoke this relationship to explain the absence or presence of fibrillations in a particular muscle.
IMPLICATIONS OF AN ELECTRODIAGNOSTICALLY CONFIRMED RADICULOPATHY It is important that the electrodiagnostician not forget that EMG does not indicate the exact cause of the symptoms, only that motor axonal loss is taking place. A spine tumor, herniated disc, bony spinal stenosis, chemical radiculitis, or severe spondylolisthesis can all yield the same EMG findings. This underscores the need to image the spine with MRI to assess for significant structural causes of electrodiagnostically confirmed radiculopathy. A negative EMG test should not curtail obtaining an MRI if clinical suspicion for radiculopathy is high. Given the low sensitivities of needle EMG, it is not an optimal screening test, but rather a confirmatory test.
There are few studies that examine outcomes and the usefulness of electrodiagnosis in predicting treatment success, the exception being surgical outcomes for lumbar discectomy in patients with herniated nucleus pulposus. Tullberg et al.56 evaluated 20 patients with lumbosacral radicular syndromes who underwent unilevel surgery for disc herniations. They evaluated these patients before surgery and 1 year later with lower limb EMG, nerve conduction studies, F-waves, and SEPs. They showed that the electrodiagnostic findings did not correlate with the level defined by CT for 15 patients. However, those patients in whom electrodiagnostic testing preoperatively was normal were significantly more likely to have a poor surgical outcome (p150
See note 2
Skin 0.50 Sv (50 rems)
Eyes 0.15 Sv (15 rems)
Elbows to hands 0.50 Sv (50 rems)
1. Half-value layers (HLV) for intermediate selected voltages are to be obtained by linear interpolation. 2. Linear extrapolation is to be used. Reference: http://www.doh.gov.za/ department/radiation/licensing/ electronicproducts/protocols/new/general.pdf
Knees to feet 0.50 Sv (50 rems)
Table 21.4: Radiation dose limits Annual
50 mSv
5 rem
Cumulative
10 mSv
1 rem × age
Annual dose limits for tissues and organs Lens of the eye
150 mSv
15 rem
Skin, hands, and feet
500 mSv
50 rem
Total dose equivalent
5 mSv
0.5 rem
Monthly dose equivalent
0.5 mSv
0.05 rem
Total effective dose equivalent TEDE (whole body) 0.05 Sv (5 rems)
Fig. 21.3 The total annual allowable radiation exposure for various portions of the body.
Fetus
9
From Gruber et al. 2000 with permission of Hanley & Belfus.
interventionist is solely responsible. Therefore, any questions, right down to the issue of fluoroscope maintenance, must be asked sooner rather than later. Radiation exposure to the patient is also a very important consideration and most of the issues discussed which limit exposure to the medical personnel also limit exposure to the patient. The major factors impacting radiation dose are field size, subject density (body part, etc,), c-arm position, proximity of the body part to the X-ray source, shielding and time of exposure, and clinical efficiency.
Basic safety procedures of dose management for radiology staff Distance: Increasing the distance between the source of radiation and the object being radiated is the most effective means of reducing exposure to a given source of ionizing radiation. The physician's exposure is 1/1000th the patient's exposure at a distance of 1 meter from the X-ray tube. As a result of this observation and logic, it is
strongly suggested that the technician and physician remain as far away from the fluoroscopic table as practical during fluoroscopic procedures. This is due to the fact that radiation follows the inverse square law. As X-ray beams travel through space they diverge. Therefore, radiation intensity decreases as the inverse square of the distance from the source of radiation (I2/I1 = d12/d22).2 This can also be thought of in terms of radiation density. At a distance of 1 standard unit from the point source of radiation, the radiation density will be 1/12 or 1, meaning that unit is the reference and all radiation is equal in that sphere. Any initial unit can be taken as one.2 At a distance of 2 units, one sees the effects of the inverse square law where the distance is great enough to have allowed the radiation beams to diverge, decreasing radiation density at the target distance so the density drops to 1/22 or 1/4. At a distance of 3 units, the effect grows ever greater at 1/32 or 1/9, followed by 1/16 and 1/25, etc. The physician's exposure is 1/1000th the patient's exposure at a distance of 1 meter from the X-ray tube (Fig. 21.4). Strictly speaking, this postulate is for a point source of radiation and may not be precisely applicable to the clinical use of radiation in the context discussed in this chapter; however, the general principle may be applied effectively. Additionally, good technique dictates that the X-ray source be kept as far from the patient as possible. By default, this will place the image intensifier as close to the patient as is reasonable, allowing 233
Part 2: Interventional Spine Techniques Sphere area 4πr2 Source strength
Intensity at surface of sphere S 4πr2 = I
S
I 9 I 4
I
r 2r The energy twice as far from the source is spread over four times the area, hence one-fourth the intensity.
3r
Fig. 21.4 Radiation deteriorates at the inverse square of the distance from the source.
room to work between the skin surface and the image intensifier (Figs 21.5, 21.6). Control: Who will control the on/off function of the fluoroscope, the proceduralist or the technician? This may seem to be a trivial question, yet it can make a large difference in exposure. Operating the fluoroscope via foot pedal allows the proceduralist to be sure the beam will not be activated inadvertently while one's hand is in the path of the beam, and allows for the foot pedal to be placed a safe distance away from the cathode. This requires the operator to take one step away from the fluoroscope before activating the beam whenever practical. For many, this choice is simply a matter of style. Nonetheless, whether one works consistently in the same procedure suite, or move consistently, the decision as to who will operate the fluoroscope should be crystal clear before anyone presses any buttons. If practical during the procedure, the physician should step away from the patient before acquiring each image and also use extension tubing during contrast injection to maximize the physician's distance from the beam.16 This once again argues for the logic of having the interventionist use the foot pedal for activation of the beam. Placing the foot pedal 1 meter away from the table thereby requires the interventionist to take one step away from the table before activating the beam. This may seem cumbersome, but the reduction in radiation dose over time can be enormous. It should be clear that distance between the source of radiation and the object being radiated is the most effective means of reducing exposure to a given source of ionizing radiation. As a result of this
X-ray tube positioning
ESER (mGy/min): 22 DAP rate (Gy-cm2/min): 4.8 Scatter rate (mGy/hr): 6.3
18
18
4.8
4.3
6.1
5.2
Fig. 21.5 The energy scatter rate is least with the energy source furthest from the patient and the image intensifier distance controlled. 234
observation and logic, it is strongly suggested that the technician and physician remain as far away from the examining table as practical during fluoroscopic procedures. If practical during the procedure, the physician should step away from the patient before acquiring each image and also use extension tubing during contrast injection to maximize the physician's distance from the beam.17 Shielding has a major impact on radiation dose. The radiation intensity of an X-ray beam decreases exponentially as the beam passes through a material. The relevant equation is (I=I0e−ux). In this equation, I = the ‘initial’ and I0 = ‘resultant’ radiation intensity’ respectively; whereas u is the attenuation coefficient of the material and x is the thickness of the attenuating material. In keeping with these postulates, the principles of time, dose, and shielding must be considered when evaluating safety. Given the above information, it becomes clear that each factor must be considered in very different ways in limiting radiation exposure in clinical practice. Shielding produces the most utilitarian results in the reduction of staff dose, as there are times when the proceduralist simply must function in close proximity, even directly in cinefluoroscopy. In these circumstances there simply is no substitute for the best modern flexible lead gloves, lead glasses, lightweight lead aprons, and lead-lined thyroid shields available. Appropriate shielding is mandatory for the safe use of ionizing radiation for medical imaging.17 Other methods of shielding include beam collimation, protective drapes, and panels. Protective apparel such as aprons should be lined with 0.5 mm thick lead or greater to reduce 90% of the radiation exposure of the physician or other medical personnel. Half-a-millimeter thick lead reduces 90% of the radiation exposure at 80 kVp while 0.58 mm thick lead reduces 90% of the radiation exposure at 120 kVp.18 Leadlined glasses and thyroid shields likewise reduce 90% of the exposure to the eyes and thyroid, respectively. Lead-lined gloves reduce radiation exposure to the hands; however, they are no substitute for strict observation of appropriate fluoroscopic hygiene.18 Gloves should be considered as an effective means of reducing scatter radiation only. If the interventionist places his or her gloved hands in the fluoroscopic field, he or she will note that initially their phalanges are barely visible; however, as exposure time increases, the phalanges become progressively more visible. This is because the automatic adjustment features of the fluoroscopy unit automatically increase the intensity of radiation, thus penetrating the gloves with stronger radiation. Also note that for the interventionist to see their phalanges on the fluoroscopic monitor the radiation is penetrating both the dorsal and ventral surfaces of the glove and those radioactive particles that only penetrate the ventral surface of the glove and not the dorsal surface of the glove may cause additional damage to the phalanges as they reverberate in the interventionist's digits. The major factors in radiation dosimetry are collimation, time, distance, and shielding. Clinical planning and the use of contrast will also be discussed. Time: Radiation dose is directly proportional to time; thus, by doubling the radiation time the dose is doubled and by halving the radiation time the dose is halved.1 Many factors impact the ‘on time’ of a fluoroscopic procedure. Modern fluoroscopes provide a variety of technique-based systems that assist in the reduction of fluoro time per procedure. These include pulse mode, last image hold, and minimization of the use of magnification. Exposure time: As discussed in this chapter, exposure time should be kept to an absolute minimum. Methods of reducing exposure time include meticulous advanced planning of the procedure, judicious use of contrast enhancement, appropriate positioning of the patient, orientation of the fluoroscopic unit prior to beginning the procedure, utilization of the pulsed mode of fluoroscopy, appropriate training of
Section 1: Principles and Concepts Underpinning Spinal Injection Procedures
0.25
1.0
5
0.5
0.2
5
0.2
1.0
8.0 4.0
0.5
4.0
0.25
2.0
0.2
5
2.0
1.0
1.0
0.5
0.5
A
B
0.5
0.25
0.2
5
0.5
0.5
4.0
2.0 2.0
0.5
1.0
1.0
0.25
5
0.2
0.5 C
0.5
D
Fig. 21.6 Stray radiation fields measured in a cardiac catheterization suite for a 90° left anterior oblique projection, with the X-ray beam approximately 1 m above the floor. Scale bar is 0.5 m. Curves represent the kerma rates at 1.5 m above the floor (approximating eye level) (A) and 1.0 m above the floor (approximating waist level) (B). (From Balter 199815 with permission of Radiological Society of North America) Stray radiation fields measured in a cardiac catheterization suite for a 60° left anterior oblique projection, with the X-ray beam approximately 1 m above the floor. Scale bar is 0.5 m. Curves represent the kerma rates at 1.5 m above the floor (approximating eye level) (C) and 1.0 m above the floor (approximating waist level) (D). 235
Part 2: Interventional Spine Techniques
the interventionist and/or technician to only radiate the patient when the interventionist is looking at the monitor, using the last image hold functions, and saving images to review during the case to minimize retracing steps during the procedure with active fluoroscopy.
RADIATION DOSE MONITORING Radiation badges must be worn if it is at all likely that a person could receive 25% of the maximum permissible dose in the discharge of his or her duties.19 At minimum, a radiation badge should be worn on the trunk under the lead apron and under the thyroid shield.20 Other places where it may be important to wear a radiation badge is on the outside of the thyroid shield to measure the radiation exposure to the face and eyes, on the finger in the form of a ring badge if the interventionist may have his or her hands in the field, and on the posterior torso under the wrap-around lead jacket if the staff member may have his or her back turned to the field during fluoroscopy.
STAFF RADIATION MANAGEMENT DURING FLUOROSCOPY The radiation exposure to the interventionist is largely dependent on positioning of the radiation source. There is a tremendous increase in operator exposure when the X-ray tube is not positioned properly, or is not directly below the patient (Fig. 21.7). This increase occurs for two reasons: the overall intensity of the scattered radiation beam is approximately 1000 times greater at the radiation entrance site on the skin compared to the exit site, and there is less attenuating material (e.g. image intensifier) between the patient and the operator. As a rule of thumb, the maximum operator exposure at a given distance occurs when there is an unobstructed path between the operator and the location at which the X-ray beam enters the patient.19
STAFF RADIATION MANAGEMENT IN COMPUTED TOMOGRAPHY Radiation exposure to the interventionist during a procedure guided by computed tomography may be quite high unless appropriate precautions are taken. Absorbed doses range from 3–9 mGy for a procedure involving 10–20 images. However, if the interventionist
X-ray tube
A
B
X-ray tube
Fig. 21.7 The radiation exposure effects to the interventionist when improper radiation source positioning is used. 236
stands to the side of the gantry instead of directly in front of it, the radiation dose is greatly reduced. Collimation: Radiation field size effects radiation dose directly.1 Clearly, the larger the field to irradiate, the more radiation is required. For this reason, collimation is the first factor to consider in attempting to minimize radiation dose to the patient, the staff, and the interventionist. The only time the collimator should be wide open is when the interventionist is performing the initial scout films for localization of anatomic structures. Once the interventionist has become oriented to the anatomy, the following images should be collimated as tightly as possible to minimize dosing.1 C-arm position: C-arm positioning effects radiation scatter in two major modes. For the vast majority of projections the X-ray source should be under the table. Placing the X-ray source above the table dramatically increases scatter (see Fig. 21.5). Scatter is likewise increased ipsilateral to the tube by oblique views (see Fig. 21.5). Good technique demands that the X-ray source be placed as far from the patient as possible while concomitantly placing the image intensifier as close to the patient as possible in order to minimize scatter and even out the distribution of incident X-rays. When it is absolutely necessary to work on an oblique view or a cross-table lateral, the operator and other staff must be places on the side of the table away from the X-ray source, and follow the same directions as above for proximity of the tube and intensifier. Turning the room around like this can be a cumbersome process, yet it is critical in managing staff dosing. Technique factors: Collimation reduces exposure simply by reducing beam size, as well as by reduction of beam source area minimizing scatter. Magnification control allows the field size to be adjusted. The smaller the field size, the more magnified the image appears on the television monitor. The entrance dose rate increases if the image is magnified. The most appropriate rule is that the smallest magnification mode consistent with the type of procedure being performed should be used with tight collimation. Using a minimal magnification setting is preferred from a risk management standpoint because it allows for a lower mA setting to be employed and decreased scatter. Pulsed mode fluoroscopy ensures an adequate exposure with minimal ‘on time’ of the beam. When using pulsed fluoroscopy in the 7.5 pulses-per-second mode, radiation exposure can be reduced by as much as 75% of that from conventional fluoroscopy.21 Contrast enhancement: In the process of the pursuit of a minimal dose of radiation during interventional procedures in which fluoroscopy is utilized, always consider the use of a contrast agent in advance. The contrast, being radiodense, will produce a focal increase in cathode output. However, in skilled hands, judicious placement of contrast can dramatically shorten procedure time by outlining anatomic structures that would otherwise be obscure. Likewise, injudicious placement of contrast will obscure the operating field, resulting in the nearly insurmountable obstacle of dense clouding. In the hands of the novice interventionist this generally leads to the ongoing process of additional volumes of contrast media being placed in non-helpful locations, serving only to further obscure the field and increase the radiodensity of the field. In this circumstance there is the double jeopardy of a field obscured by contrast causing the interventionist to have great difficulty visualizing anatomic structures, causing a lengthening of the time of radiation exposure. Still worse, the high density of the dye will cause the automatic output of the fluoroscope to increase via automatic increases in kVp and mA. This significantly increases radiation exposure per unit time. If the target is obscured by contrast injection, the interventionist should abort the procedure, attempt to ‘wash it out’ with normal saline, or approach the target via a different trajectory.
Section 1: Principles and Concepts Underpinning Spinal Injection Procedures
In order to minimize the occurrence of the above situation, remember to ‘plan the procedure, and proceed along the plan,’ acknowledging that even the best-laid plan in medicine must be open to modification in the face of evolving circumstance. Few things can be more clinically dangerous than a poorly planned procedure. Contrast dye: In this modern era of medicine there is little debate that nonionic contrast is the medium of choice for interventional pain procedures for a wide variety of reasons. Ionic contrast has the potential to produce significant complications. Specifically when inadvertently introduced into the intrathecal space, ionic contrast has the significant possibility of producing a stereotypical syndrome of ascending myoclonic spasms, resulting in rhabdomyolysis and possibly death.22–24 For this reason nonionic contrast, such as iohexol or iopamidol, has become the medium of choice when there is any risk of penetrating the thecal sac. These agents are relatively safe for intrathecal injection and are in fact routinely used for myelography.25–27
PATIENT PROTECTION DURING RADIATION EXPOSURE Patient skin doses are 8–10 times higher during interventional procedures than during angiography, which are about 10 times higher than from conventional diagnostic procedures utilizing fluoroscopy or computed tomography. Skin entrance doses have been reported in the range of 6–18 Gy for certain interventional procedures.9,28 On the basis of reports of a small number of severely injured patients, in 1994 the FDA issued a warning to all users of fluoroscopy equipment to be alert for doses that may lead to severe skin damage. Acute doses in excess of 2 Gy may lead to erythema and localized, transient alopecia; 6 Gy may cause permanent alopecia; 10 Gy may lead to dry desquamation, dermal atrophy, and telangiectasia; and 15 Gy or more may lead to moist desquamation and necrosis. Injury to other organs may also be possible at these higher dose levels.28,29 Reducing radiation doses to the patient also generally reduces doses to the medical personnel. Methods of limiting radiation exposure include: making certain that the fluoroscopy unit is functioning properly through routine maintenance, limiting fluoroscopic exposure time, reducing field of exposure through collimation, keeping the X-ray source under the table by avoiding cross-table lateral visualization when possible, utilizing pulsed fluoroscopic visualization when possible, and bringing the image intensifier down close to the patient are all methods of reducing radiation exposure to the patient and medical personnel. The latter method causes the automatic brightness system of the X-ray generator to drop the radiation output. Regulatory authority for radiation safety: X-ray use is not completely regulated at the federal level. There is not a single regulatory body that oversees the use of X-rays in medicine. Regulations concerning equipment are devised by the Center for Devices and Fluoroscopic Health within the US Food and Drug Administration (FDA);8 the Occupational Safety and Health Administration (OSHA) places limits on the radiation doses of employees in the workplace, and individual state departments of services place additional regulations on users of X-ray equipment. Most states patterned their regulations after the recommendations of the National Council on Radiation Protection and Measurements (NCRP). This body has developed an extensive set of regulatory guidelines that have become de facto standards for the safe and proper use of ionizing radiation. Other sources give further details of the general philosophy of radiation protection, as well as specific recommendations for particular situations. The International Commission on Radiation Protection (ICRP) and the International Commission on Radiological Units and Measurements (ICRU) publish recommendations for radiation protection.11–14,19,30–32
The Occupational Safety and Health Administration (OSHA) allow only one-third the maximum quarterly dose to the eyes permitted by other regulatory organizations. Doses should always be kept ‘as low as reasonably achievable’ (ALARA). These quarterly allowances set I and Io as the initial and transmitted radiation intensity, respectively; K is the attenuation coefficient of the material (which depends on the atomic number and density of the material and on the energy of the photons); and x is the thickness of the attenuating material. Small amounts of attenuating (shielding) material can greatly reduce the intensity of an X-ray beam. For example, more than 90% reduction of a diagnostic X-ray beam is obtained by using material equivalent to 0.5 mm of lead (the nominal equivalent of a typical lead apron). Lead aprons should always be worn by anyone in a fluoroscopy suite. Because fluoroscopy is used extensively during some interventional procedures, the continual observation of these fundamental principles is of far greater importance than in other areas of diagnostic fluoroscopy.
Fluoroscopic systems – basic set-up This is a selected listing of basic factors essential for the set-up of a fluoro suite. Derived from the State of Tennessee Deptartment of Environment and Conservation.24 For a full list of regulations see applicable state or national regulations. 1. A dead-man switch must control X-ray production. A dead man switch is a device (switch) constructed so that a circuit closing contact can only be maintained by continuous pressure on the switch by the operator. Therefore, when the machine is turned on by any means, whether by the push button at the control panel, or by the foot pedal, this switch must be held in for the machine to remain ‘on.’ 2. The ‘on-time’ of the fluoroscopic tube must be controlled by a timing device, and must end or alarm when the exposure exceeds 5 minutes. An audible signal must alert the user to the completion of the preset on time. This signal will remain on until the timing device is reset. 3. The X-ray tube used for fluoroscopy must not produce X-rays unless a barrier is in position to intercept the entire cross-section of the useful beam. The fluoroscopic imaging assembly must be provided with shielding sufficient that the scatter radiation from the useful beam is minimized. 4. Protective barriers of at least 0.25 mm lead equivalency must be used to attenuate scatter radiation above the tabletop (e.g. drapes, bucky-slot covers). This shielding does not replace the lead garments worn by personnel. Scattered radiation under the table must be attenuated by at least 0.25 mm lead equivalency shielding. Additionally, most c-arm fluoroscopes have a warning beeper or a light that activate when the beam is ON, some have both. NEVER inactivate any warning devices, and keep one's foot OFF the foot pedal whenever possible. Planning: No single issue is more significant in the reduction of flouro time than advanced planning. Prior to entering the procedure room review all materials, particularly all radiologic films in detail. With the understanding that even the best laid plans must be subject to modification in the face of the unexpected, plan your procedure in detail, based on the unique clinical situation involved with each individual patient. This simple process will produce a striking decrease in your fluoro time. Contrast media can be an invaluable boon in localizing anatomic structures for the interventionist. However, when used injudiciously or haphazardly contrast will obscure the operating field making it nearly impossible to visualize the target structure, while increasing the radiodensity of the operating field, thereby causing a compensatory increase in the radiation output of the fluoroscope. 237
Part 2: Interventional Spine Techniques
When thinking in terms of the reduction of radiation time exposure remember, ‘Plan your procedure, and proceed along your plan.’
Considerations for pregnant workers – regulations Consistent with the Supreme Court decision in the case of UAW vs. Johnson Controls, a woman has the right to choose whether or not to declare her pregnancy, including the right to revoke her declaration. It is the woman's right to choose the declaration of pregnancy regardless of any evidence pregnancy. The key issue is the pregnant worker's right to privacy. Until such time as the pregnant worker makes it known that she is pregnant, i.e. officially declares her pregnancy in writing including the estimated date of conception, no specific rules apply to the conceptus. After declaration of the pregnancy the following rules apply. (1) The licensee shall ensure that the dose equivalent to the embryo/ fetus during the entire pregnancy, due to the occupational exposure of a declared pregnant woman, does not exceed 0.5 rem (5 mSv). (For recordkeeping requirements, see Section 20.2106.) (2) The licensee shall make efforts to avoid substantial variation above a uniform monthly exposure rate to a declared pregnant woman so as to satisfy the limit in paragraph (a) of this section. (3) The dose equivalent to the embryo/fetus is the sum of: (A) The deep-dose equivalent to the declared pregnant woman; and (B) The dose equivalent to the embryo/fetus resulting from radionuclides in the embryo/fetus and radionuclides in the declared pregnant woman. (4) If the dose equivalent to the embryo/fetus is found to have exceeded 0.5 rem (5 mSv), or is within 0.05 rem (0.5 mSv) of this dose, by the time the woman declares the pregnancy to the licensee, the licensee shall be deemed to be in compliance with paragraph (a) of this section if the additional dose equivalent to the embryo/fetus does not exceed 0.05 rem (0.5 mSv) during the remainder of the pregnancy. [56 FR 23396, May 21, 1991, as amended at 63 FR 39482, July 23, 1998] Maternity aprons are available and are constructed with a double thickness of lead in the sensible area. The declared pregnant worker should be aware that the back of the apron still leaves her unprotected.
CONCLUSION In conclusion, radiation exposure is critical to the well-being of both healthcare staff and patients. The physics and biological impact of radiation as well as methods of reducing exposure to radiation during interventional procedures have been discussed. Radiation safety should be a mutual goal for all healthcare workers, not only for their own health, but also for the health of their patients. The reader is encouraged to pursue further investigation utilizing the references cited.
References
6. Parry RA, Glaze SA, Archer R. The AAPM/rsna physics tutorial for residents typical patient radiation doses in diagnostic radiology. Radiographics 1999; 19:1289–1302. 7. Wycoff HO The international system of units. Radiology 1978; 128:833–835. 8. Raj PP, Lou L, Erdine S, et al. Equipment used for radiographic imaging. In: Raj PP, Lou L, Erdine S, et al., eds. Radiographic imaging for regional anesthesia and pain management. New York: Churchill Livingstone; 2003:5–8. 9. Gruber RD, Botwin KP, Shah CP. Radiation safety for the physician. In: Lennard T, ed. Pain procedures in clinical practice. Philadelphia: Hanley & Belfus; 2000:31. 10. Brateman L. The AAPM/RSNA physics tutorial for residents radiation safety considerations for diagnostic radiology personnel. Radiographics Volume 19. Number 4 11. Broadman LM, Navalgund YA, Hawkinberry DW. Radiation risk management during fluoroscopy for interventional pain medicine physicians. Current pain and headache reports. 2004; 8:49–55. 12. Performance standards for ionizing radiation emitting products. 21 CFR part 1020.30(k): leakage radiation from the diagnostic source assembly. 1998; April 1; 562. 13. National Council on Radiation Protection and Measurements: Medical X-ray, Electron Beam, and Gamma Ray Protection for Energies Tip to 50 Mev. NCRP Report No. 102. Washington, DC; 1989. 14. International Commission on Radiological Protection (ICRP): Radiation Protection. ICRP Publication No. 26. Oxford, Pergamon Press; 1977. 15. Balter S. Stray radiation in the cardiac catheterization laboratory. In: Nickoloff EL, Strauss KJ, eds. Categorical course in diagnostic radiology physics: cardiac catheterization imaging. Oak Brook, Ill: Radiological Society of North America; 1998:223–230. 16. Marshall NW, Faulkner K. The dependence of the scattered radiation dose to personnel on technique factors in diagnostic radiology. Med Phys 1996; 23:1271–1276. 17. Payne JT, Shope TB. Proceedings of the ACR/FDA Workshop on Fluoroscopy: Strategies for Improvement in Performance. In: Payne JT, Shope TB, eds. Radiation Safety and Control. American College of Radiology. 1993. 18. Boone JM, Levin DC. Radiation exposure to angiographers under different fluoroscopic imaging conditions. Radiology 1991; 180:861–865. 19. National Council on Radiation Protection and Measurements: Limitation of Exposure to Ionizing Radiation. NCRP Report No. 116. Washington, DC; 1993. 20. Code of Federal Regulations, Title 29, Part 16, Chapter 17, Section 1910.96. Washington, DC, US Government Printing Office; 1971. 21. Hernandez RJ, Goodsitt MM. Reduction of radiation dose in pediatric patients using pulsed fluoroscopy. Am J Roentgenol 1996; 167:1247–1253. 22. Killeffer JA, Kaufman HH. Inadvertent intraoperative myelography with Hypaque: case report and discussion. Surg Neurol 1997; 48(1):70–73. PMID: 9199689 23. Sahjpaul RL, Lee D, Munoz DG. Fatal reaction from inadvertent intrathecal entry of ionic contrast medium during a nephrogram. Acta Neuropathol (Berl) 1997; 93(1):101–103. PMID: 9006664 24. Rosati G, Leto di Priolo S, Tirone P. Serious or fatal complications after inadvertent administration of ionic water-soluble contrast media in myelography. Eur J Radiol 1992; 15(2):95–100. PMID: 1425760 25. Latchaw RE, Hirsch WL Jr, Horton JA, et al. Iohexol vs. metrizamide: study of efficacy and morbidity in cervical myelography. Am J Neuroradiol 1985; 6(6):931–933. PMID: 3934932 26. Haughton VM. Intrathecal toxicity of iohexol vs. metrizamide. Survey and current state. Invest Radiol 1985; 20(1 Suppl):S14–S17. PMID: 3918951 27. Wang YS, Jiang YH, Hou ZY. Intrathecal injection of Iohexol for routine myelography and CT myelography in 1,000 cases. Chin Med J (Engl) 1990; 103(6):497–502. PMID: 2209203 28. Houda W, Peters KR. Radiation-induced temporary epilation after a neuroradiologically guided embolization procedure. Radiology 1994; 193:642–644. 29. Wagner LK, Eifel PJ, Geise RA. Potential biological effects following high X-ray dose interventional procedures. J Vasc Intervent Radiol 1994; 5:71–84.
1. Schueler BA. The AAPM/RSNA physics tutorial for residents general overview of fluoroscopic imaging. Radiographics 2000; 20:1115–1126.
30. Code of Federal Regulations, Title 21, Parts 1000–1050. US Government 1985. Revision of the Radiation Control for Health and Safety Act of 1968.
2. Carlton RR, Adler AM. Principles of radiographic imaging. Stamford: Delmar; 2001:111–114.
31. National Council of Radiation Protection and Measurements: Recommendations on Limits for Exposure to Ionizing Radiation. NCRP Report No. 91. Washington, DC; 1987.
3. Wang J, Blackburn, TJ. The AAPM/RSNA physics tutorial for residents x-ray image intensifiers for fluoroscopy. Radiographics 2000; 20:1471–1477. 4. Statkiewicz MA, Ritenour ER. Radiation protection for student radiographers. St. Louis: Mosby; 1983.
238
5. Gruber RD, Botwin KP, Shah CP. Radiation safety for the physician. In: Lennard T, ed. Pain procedures in clinical practice. Philadelphia: Hanley & Belfus; 2000:25,26.
32. National Council on Radiation Protection and Measurements: Structural Shielding Design and Evaluation for Medical Use of Xrays and Gamma Rays of Energies up to 10 Mev. NCRP Publication No. 49. Washington, DC; 1976.
PART 2
INTERVENTIONAL SPINE TECHNIQUES
Section 1
Principles and Concepts Underpinning Spinal Injection Procedures
CHAPTER
Sedation for Percutaneous Procedures
22
Mohammad Uddin and Salahadin Abdi
INTRODUCTION ‘Sedation and analgesia’ describe a state in which patients can tolerate unpleasant procedures while maintaining cardiac and respiratory function and still maintain the ability to respond purposefully to both verbal commands and tactile stimulation. The Task Force on sedation and analgesia decided that the term ‘sedation and analgesia’ (sedation/analgesia) more accurately defines this therapeutic goal than does the commonly used but imprecise term ‘conscious sedation.’ This level of sedation does not include a level in which the only intact reflex is withdrawal from a painful stimulus.1 Although sedation has been described as ‘light sleep’2 and textbooks note that ‘the terms sleep, hypnosis, and unconsciousness are used interchangeably in anesthesia literature to refer to the state of drug-induced sleep,’3 pharmacological sedation is not the same as physiological sleep. During interventional procedures the goal is to provide enough sedation to keep the patient comfortable, relaxed, and communicative. Even though this preferred light sedation is relatively safe, rescue medications and equipment to support respiration and circulation should be readily available.
LEVELS OF SEDATION See Table 22.1. Minimal sedation (anxiolysis) is a drug-induced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular functions are unaffected. Moderate sedation/analgesia (i.e. ‘conscious sedation’) is a druginduced depression of consciousness during which patients respond
purposefully* to verbal commands, either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained. Deep sedation/analgesia is a drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully* following repeated verbal or painful stimulation. The ability to independently maintain ventilatory function may be impaired, necessitating assisted airway support. Cardiovascular function is usually maintained. General anesthesia is a drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients often require assistance in maintaining a patent airway, and positive-pressure ventilation may be required because of depressed respiration or drug-induced neuromuscular depression. Cardiovascular function may be impaired. Because sedation is a continuum, it is not always possible to predict how an individual patient will respond. Hence, practitioners intending to produce a given level of sedation should be able to rescue patients whose level of sedation becomes deeper than initially intended. Individuals administering moderate sedation/analgesia (i.e. ‘conscious sedation’) should be able to rescue patients who enter a state of deep sedation/analgesia, while those administering deep sedation/analgesia should be able to rescue patients who enter a state of general anesthesia. Deep sedation and general anesthesia are not usually recommended for most of pain management procedures, as an awake, cooperative patient is needed to prevent complications related to nerve injury, allergic reactions, or medication toxicity (Table 22.2).
Table 22.1: Definition of General Anesthesia and Levels of Sedation/Analgesia1 Minimal Sedation (Anxiolysis)
Moderate Sedation/Analgesia (Conscious Sedation)
Deep Sedation/ Analgesia
General Anesthesia
Responsiveness
Normal response to verbal stimulation
Purposeful response to verbal or tactile stimulation
Purposefula response following repeated or painful stimulation
Unarousable even with painful stimulus
Airway
Unaffected
No intervention required
Intervention may be required
Intervention often required
Spontaneous ventilation
Unaffected
Adequate
May be inadequate
Frequently inadequate
Cardiovascular function
Unaffected
Usually maintained
Usually maintained
May be impaired
a Monitored Anesthesia Care does not describe the continuum of depth of sedation; rather it describes ‘a specific anesthesia service in which an anesthesiologist has been requested to participate in the care of a patient undergoing a diagnostic or therapeutic procedure.’
239
Part 2: Interventional Spine Techniques
Table 22.2: Ramsay Level of Sedation Scale2 Clinical Score
Level of Sedation Achieved
6
Asleep, no response
5
Asleep, sluggish response to light glabellar tap or loud auditory stimulus
4
Asleep, but with brisk response to light glabellar tap or loud auditory stimulus
3
Table 22.4: Summary of American Society of Anesthesiologists Preprocedure Fasting Guidelines for Healthy Patients Who Are Undergoing Elective Procedures Ingested Material
Minimum Fasting Period
Clear liquids
2h
Nonhuman milk
6h
Sleepy, but responds to commands
Light meal
6h
2
Patient cooperative, oriented and tranquil
1
Patient anxious, agitated or restless
The fasting periods noted in Table 22.4 apply to all ages. Examples of clear liquids include water, fruit juices without pulp, carbonated beverages, clear tea, and black coffee. Since nonhuman milk is similar to solids in gastric emptying time, the amount ingested must be considered when determining an appropriate fasting period. A light meal typically consists of toast and clear liquids. Meals that include fried or fatty foods or meat may prolong gastric emptying time. Both the amount and types of foods ingested must be considered when determining an appropriate fasting period.
GENERAL PREPARATION The risks, benefits, and alternatives of sedation should be explained to the patient in lay terms. The main goals in administering sedatives and analgesic medications are to facilitate the completion of a potentially difficult procedure and to provide a safe and comfortable environment for the patient. The most feared risk of sedation is respiratory depression, which can result in catastrophic consequences if not recognized and treated promptly. The patient may also decline sedation, at which point alternatives can be considered including local anesthesia, relaxation techniques and, for pediatric patients, general anesthesia. After thorough explanation is provided and all questions are answered, informed consent is obtained before any sedation is administered.
Preprocedural assessment All patients who are scheduled to receive sedation should be thoroughly evaluated prior to the procedure. Relevant issues that should be addressed include past medical history, past surgical history to include any anesthetic complications, drug allergies, and current medications to include anticoagulants, smoking, alcohol use and recreational drug history, and NPO status. The risk stratification classification of the American Society of Anesthesiologists (ASA) provides an excellent preprocedure assessment tool for this purpose (Table 22.3). Table 22.4 provides a summary of the American Society of Anesthesiologists preprocedure fasting guidelines. The recommendations apply to healthy patients who are undergoing elective procedures. They are not intended for women in labor. Following the guidelines does not guarantee complete gastric emptying has occurred.
bronchospasm, and laryngospasm requiring tracheal intubation and ventilatory support. Intubation may be especially difficult in patients with atypical airway anatomy. Airway abnormalities may also increase the likelihood of airway obstruction following the administration of sedatives and analgesics. Warning signs of a difficult airway are listed in Table 22.5. Recommendations for frequency of monitoring and documentation during sedation/analgesia are listed in Table 22.6.
Table 22.5: Warning Signs of a Difficult Airway Previous problems with sedation Stridor, snoring, or sleep apnea Advanced rheumatoid arthritis Chromosomal abnormality (e.g. trisomy 21) Significant obesity (especially involving the neck and facial structures) Short neck and limited neck extension Decreased hyoid-mental distance (2 y and >10 kg
i.v.: 0.05 μg/kg increments Max: 2 μg/kg
Onset: 1–3 min Duration: 30 min to over an hour
Rapid IV infusion can cause maseter and chest wall rigidity Assess for respiratory depression and bradycardia May cause pruritus and urinary retention Assess for hypotension, especially if hypovolemic Assess for nausea & vomiting
All doses should be titrated to effect. Decrease doses to 25% when used in conjunction with benzodiazepines.
Table 22.10: Sedatives Drug
Pediatric Dosing
Adult Dosing
Onset/Duration
Comments
Diazepam
i.v.: 0.05–0.25 mg/kg Max 10 mg p.o.: 0.1–0.25 mg/kg
i.v.: 1–5 mg titrate p.o.: 1–5 mg titrate i.m.: 1–5 mg titrate Max 20 mg healthy Max 5 mg for elderly and debilitated
Onset: 0.5–2 min Duration: 2–8 h
Respiratory depression synergistic with narcotics… reduce dose by 1/3 Irritates veins…can cause phlebitis, thrombosis, swelling, local inflammation…use large veins Precipitates when mixed Contraindicated in acute narrow glaucoma
i.v.: 0.02–0.08 mg/kg Max 0.15 mg/kg i.m.: 0.02–0.1 mg/kg Max 2.5–5 mg p.o.: 0.25–0.75 mg/kg Max 20 mg p.r.: 0.5–0.75 mg/kg
i.v.: 0.5–1 mg until desired effect is achieved. i.m.: 0.02-0.1 mg/kg Max 1–7.5 mg p.o.: 0.5–0.8 mg/kg Max 50 mg
Onset: 3–5 min Duration: max. 5 min declined 30–40 min Gross recovery 6 h
Synergistic action with narcotics Retrograde and antegrade amnesia Reduce dose in elderly, debilitated and patients With compromised renal function May result in patient agitation and myoclonic activity Does not irritate veins Dilution to 1 mg/ml is suggested for accurate dosing
reversal agent is available, the authors recommend that these drugs should only be used by an anesthesia team.
Complications The main complication of the sedation is oversedation. Since oversedation can cause respiratory and cardiovascular depression, the person responsible for monitoring the patient must be capable of rescuing the patient. Other side effects include irritation of the injection site, cognitive impairment and, rarely, allergic reactions.
POSTOPERATIVE CARE It is important for the recovery room personnel to monitor vital signs and neurological condition of the patient. The duration in recovery 242
room is determined by the both the condition of the patient and institution protocols. When necessary, a wheelchair can be used fortransporting patients until full motor strength and recovery from the sedation is achieved. Then patients should be discharged from the recovery room with an escort.
Recovery and discharge criteria following sedation and analgesia1 Patient care facilities administering sedation/analgesia must each develop recovery and discharge criteria based on the type of patients seen and the type of procedures performed. Some of the basic principles are detailed below.
Section 1: Principles and Concepts Underpinning Spinal Injection Procedures
Table 22.11: Reversal Agents Drug
Pediatric Dosing
Adult Dosing
Onset/Duration
Comments
Naloxone
i.v.: 0.5–1 μg/kg titrate Max 1 mg i.v.: 0.1 mg/kg in respiratory arrest Max 2 mg
i.v.: 0.1–0.2 mg slow and titrate to response
Onset: 1–2 min Duration: 30 min when given i.v.
‘Reverses’ narcotics only Rapid administration can produce nausea, sweating, hypertension and dysrhythmias. May cause pulmonary edema, MI and seizures Contraindicated in drug abusers or chronic pain patients who regularly take narcotics Reversal effect may not outlast narcotic effect … consider giving an i.m. dose
Nalmefene (Revex)
i.v.: 10 μg/kg May repeat at 2 and 5 min Max 1 mg
i.v.: 0.25 ug/kg May repeat at 2 and 5 min Max: 1 μg/kg
Duration: half life is 9 times longer than Narcan
‘Reverses’ narcotics only
Flumazenil
i.v.: 10 μg/kg slow Max 0.2 mg/kg or 2 mg i.m./s.c.: 0.005– 0.001 mg/kg Max 1 mg
i.v.: 0.2 mg slow Onset: 1–2 min May repeat peak in 10 min q60 sec Duration: 30–60 min Max 1 mg Max/hr: 3 mg i.m./s.c.: 0.1–0.2 mg Max 1 mg
General principles 1. Medical supervision of recovery and discharge following moderate or deep sedation is the responsibility of the operating practitioner or a licensed physician. 2. The recovery area should be equipped with or have direct access to appropriate monitoring and resuscitation equipment. 3. Patients receiving moderate or deep sedation should be monitored until appropriate discharge criteria are satisfied. The duration and frequency of monitoring should be individualized depending upon the level of sedation achieved, the overall condition of the patient, and the nature of the intervention for which sedation/ analgesia was administered. Oxygenation should be monitored until patients are no longer at risk for respiratory depression. 4. Level of consciousness, vital signs and oxygenation (when indicated) should be recorded at regular intervals. 5. A nurse or other individual trained to monitor patients and recognize complications should be in attendance until discharge criteria are fulfilled. 6. An individual capable of managing complications (e.g., establishing a patent airway and providing positive-pressure ventilation) should be immediately available until discharge criteria are fulfilled.
Guidelines for discharge 1. Patients should be alert and oriented; infants and patients whose mental status was initially abnormal should have returned to their baseline. Practitioners and parents must be aware that pediatric patients are at risk for airway obstruction should the head fall forward while the child is secured in a car seat. 2. Vital signs should be stable and within acceptable limits. 3. Use of scoring systems may assist in documentation of fitness for discharge. 4. Sufficient time (up to 2 hours) should have elapsed following the last administration of reversal agents (naloxone, flumazenil) to ensure that patients do not deteriorate after reversal effects have worn off.
‘Reverses’ benzodiazepines, not narcotics May cause seizures, cardiac arrhythmias and death Causes anxiety, dizziness, sweating and emotional liability Reversal effect may not outlast sedative … monitor for one hour after reversal. Resedation may occur requiring additional doses. Question administration to patients who take benzodiazepines regularly…may cause seizures in these patients.
5. Outpatients should be discharged in the presence of a responsible adult who will accompany them home and be able to report any postprocedure complications. 6. Outpatients and their escorts should be provided with written instructions regarding postprocedure diet, medications, and activities, and a phone number to be called in case of emergency.
Continuing quality improvement indicators8 If any of the following occur and are caused by the sedatives and/ or analgesics administered, and not the preexisting and underlying disease or its treatment, a review of the chart must be performed and appropriate action taken immediately. 1. Oxygen saturation 90% and a drop of 5% from baseline for longer than 1 min. 2. Use of opioid or benzodiazepine reversal agents. 3. A decrease in blood pressure or heart rate requiring pharmacologic intervention or rapid fluid administration. 4. Failure to respond to physical stimulation. 5. Assisted ventilation and/or unanticipated endotracheal intubation. 6. Unplanned admission. 7. Cardiac or respiratory arrest.
SUMMARY The choice of sedating drugs is based on patient health, type of procedure, and the level of cooperation needed. Each of the sedative agents has advantages and disadvantages. There are no perfect agents. Physicians administering sedation should follow national and institutional guidelines throughout the sedation period. Sedated patient require vigilant monitoring by trained professionals during the entire period of sedation. Monitoring is required during the procedure, during transport, and during recovery. Finally, using strict discharge criteria and warning the patient about possible delayed side effects will further decrease sedation-related complications. 243
Part 2: Interventional Spine Techniques
References 1. Gross JB, Bailey PL, Caplan RA, et al. Practice guidelines for Sedation and Analgesia by Non-Anesthesiologist. A report developed by the Task Force on Sedation and Analgesia by Non-Anesthesiologists. Anesthesiology 1996; 84:459–71. 2. Lydic R, Baghdoyan HA, eds. Handbook of behavioral state control: cellular and molecular mechanisms. Boca Raton, FL: CRC Press; 1999. 3. Lydic R, Biebuyck JF. Sleep neurobiology; relevance for mechanistic studies of anesthesia. Br J Anesth. 1994; 72:506–508.
244
4. Warner MA, Robert A. Caplan RA, Burton S, Epstein BS, et al. Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures. A report by the American Society of Anesthesiologists. Developed by the Task Force on Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration.
PART 2
INTERVENTIONAL SPINE TECHNIQUES
Section 2
Interventional Spine Techniques
CHAPTER
Spinal Injections
23
Christopher W. Huston, Curtis W. Slipman, Michael B. Furman, Syed Hasan and Richard Derby
INTRODUCTION A variety of spinal injections are currently utilized in the diagnosis and treatment of axial and radicular pain. The various diagnostic and therapeutic injections include epidural injections, selective nerve root/ spinal nerve injections, zygapophyseal intra-articular joint injections, synovial cyst aspiration, medial branch and dorsal ramus nerve blocks, atlanto-occipital joint injection, lateral atlantoaxial joint injection, sacroiliac joint injection, and sacrococcygeal disc injection. The epidural space can be entered by different anatomic approaches: epidural injections are further divided into transforaminal, interlaminar, and caudal. Though there are subtle differences, terminology for the transforaminal approach differs depending on whether it is used for therapeutic or diagnostic purposes. The term ‘selective nerve root block’ is often used synonymously with selective nerve root injection. This procedure has been used for both diagnostic and therapeutic purposes. Selective nerve root injections may be performed both diagnostically and therapeutically. At the Penn Spine Center we differentiate a transforaminal injection from selective nerve root injection by the explicit purpose of the procedure. Transforaminal injections are meant to address axial pain, presumably arising from a lumbar disc. This necessitates that the needle is placed in a location that assures spread of the therapeutic agent ventrally. In contrast, a therapeutic selective nerve root injection requires more posterior needle placement so that the nerve root, dorsal root ganglia (DRG), and some of the epidural space are bathed with the therapeutic solution. Finally, a diagnostic selective nerve block is one that only anesthetizes the existing (target) nerve root. It should be pointed out that the term selective nerve root injection has been challenged. Some interventionalists would classify the injection as a selective spinal nerve injection. While the spinal nerve is targeted, for diagnostic purposes the DRG needs to be anesthetized. Many spinal disorders such as foraminal stenosis or disc herniation involve the DRG. Blocking only the spinal nerve distal to the DRG could result in a false-negative injection. The injection incorporates the spinal nerve, ventral ramus, and dorsal root ganglion. Zygapophyseal intra-articular injections may be performed for diagnostic or therapeutic purposes. Frequently, medial branch blocks are performed instead of intraarticular zygapophyseal joint injections to diagnose pain emanating from the zygapophyseal joints. Each of these spinal injections may be performed in the cervical, thoracic, and lumbosacral spine. The thought process underpinning the use of these injections for specific diagnosis is discussed in other chapters. It should be emphasized that a general principle invoked is that injections are performed for specific diagnoses and that proper testing is performed prior to an injection procedure. This insures that the minimum number of invasive procedures is performed. This chapter focuses on technique and not rationale. Contraindications to the performance of spinal injections include systemic infection, local infection at the injection site, bleeding dyscrasia, and anticoagulation. A detailed analysis of the variety
of complications that can result from each of the described spinal injections is covered in Chapter 20 by Botwin. Spinal injections are performed under fluoroscopic guidance to improve accuracy, efficacy, and safety. The interventionalist must be cognizant to limit radiation exposure to the patient, staff, and interventionalist to a minimum. The reader is directed to the radiation safety chapter by Windsor. Local anesthesia is recommended prior to performing the spinal injection procedures discussed in this chapter. Unless there are known ‘caine’ allergies, local anesthesia is done with 1% Xylocaine injecting through a 25-gauge needle creating a skin wheal. The skin wheal can be quite small as it needs to only be greater than the diameter of the needle. Larger skin wheals provide more flexibility for selection of needle placement. The disadvantage of a larger skin wheal is that the skin wheal can be painful to the patient. The acidity of Xylocaine injection can cause a painful burning sensation. Because of this, the Xylocaine can be mixed with sodium bicarbonate to neutralize the acidity and make the injection more comfortable. A 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate is used. The decision to use 1% Xylocaine or the Xylocaine–bicarbonate mixture is under the discretion of the interventionalist. For very experienced spine interventionalists local anesthesia may not be required. Some patients may prefer moderate sedation to better tolerate the procedure. This includes those patients who are anxious, needle-phobic, have lower pain thresholds or are at increased risk of a vasovagal reaction. Additionally, some patients in severe pain may have difficulty getting into the proper position on the fluoroscopy table and may benefit from moderate sedation. In particular, those with severe radicular pain, particularly in the presence of a foraminal disc protrusion or foraminal stenosis may experience severe pain with injection of medication around the involved spinal nerve. However, the level of moderate sedation should be limited. The patient still needs to be awake to appropriately respond to painful stimuli, and should have the ability to communicate with the interventionalist. If nerve is contacted, the patient requires the ability to verbalize that extremity pain is perceived to avoid nerve injury. If the patient is too sedated, the nerve or spinal cord could be penetrated with the patient and interventionalist unaware, resulting in neurologic injury. It is preferable to avoid moderate sedation for diagnostic injections, but this is not always feasible. The intravenous anxiolytic or opiate medication may influence the results, increasing the risk of a false-positive diagnostic injection. One way to mitigate that scenario is to ask the patient to complete the pain drawing and VAS scale after sedation is provided.
NEEDLE TECHNIQUES The standard spinal needle has an angled opening of the needle referred to as the bevel. The hub of the needle has a ‘notch.’ The notch and bevel are on the same side in a standard spinal needle. As a needle is advanced through tissue it tends to move towards the 245
Part 2: Interventional Spine Techniques
sharper side and away from the bevel and notch. The interventionalist, however, does not see the needle tip and bevel, which are already in the patient’s soft tissues. Instead, one typically sees the part of the needle protruding from the skin, the hub portion and notch. Therefore, the interventionalist must be cognizant of the orientation of the notch as the needle is advanced, since the needle tip will tend to move 180 degrees away from the notched side as it is advanced. Novice interventionalists ignore this tendency and often end up trying to fight the needle’s trajectory, while advanced interventionalists learn to use this ‘bevel control’ to their advantage and, instead, drive the needle. Bevel control can be even more accentuated by placing a 10–20 degree bend on the needle tip away from the notched and bevel side as close to the needle tip as possible. We recommend using a sterile gauze when placing the bend to prevent inadvertent contamination of the needle tip. Another technique to enhance control of the needle is to use a concave arc on the needle for even more precision and steerability. The arc is created by holding the needle between the thumb and index fingers while using one of the other digits closer to the skin surface to create the concavity on the same side the needle is being directed toward (Fig. 23.1). This concavity tends to further slide the needle into position. The combination co of bevel control and a concave arc directing the needle are effectively like having ‘power steering’ to direct the needle tip wherever it is needed. However, like power steering, the needle will be much more sensitive and less forgiving if these techniques are not understood. Thinner needles (i.e. 25 or 27 gauge) are much more responsive to these techniques than the thicker (18 gauge) needles which tend to respond more to ‘brute force.’ Twenty-two-gauge needles tend to be intermediate in response to these techniques and brute force.
FLUOROSCOPIC VIEWS All physicians practicing fluoroscopically guided procedures understand that at least two views are needed to confirm needle tip position. Biplanar imaging, such as anteroposterior (AP) and lateral, are typically utilized. Additionally, other views may be utilized to increase precision, safety, and efficiency in interventional spine care. Therefore, throughout this section, we will describe additional terminology regarding fluoroscopic imaging for each spinal procedure: Trajectory
Fig. 23.1 Bent needle technique of medication delivery. Same technique for bending needle may be utilized to advance needle without syringe attached. 246
view, Safety view, and the two final-position views. These views are obtained by appropriately positioning the fluoroscope and/or patient. Each procedure is done by using a trajectory view for original needle entry, the Safety View during needle advancement to avoid relevant structure, and two final views to confirm needle position prior to contrast and subsequent medication injection. Trajectory view (aka hubogram, needle view) is the initial one which visualizes the path or route the needle will travel to get to the ultimate target. The image is obtained on the fluoroscope, and this determines the initial skin entry position. When utilizing an unencumbered trajectory view during needle advancement, the target can be efficiently approached without encountering obstructions. As well, radiation and procedure time can be minimized by making sure the needle is positioned parallel to the fluoroscopic beam prior to taking additional fluoroscopic pictures. This is accomplished by advancing the needle along the trajectory established by the fluoroscope’s image intensifier relative to the patient. As the needle is advanced down the fluoroscope’s beam a ‘dot’ rather than a ‘line’ is noted on the image (Fig. 23.2). As the needle tip is advanced close to the desired target, biplanar imaging is utilized. However, to safely advance the needle and avoid penetrating ‘dangerous’ structures, we recommend using the ‘Safety (aka danger)’ view during needle advancement. The ‘Safety’ view is used to ensure that the needle does go where it is supposed to and, more importantly, does not go where it should not be. Careful interventionalists are cognizant of the structures to avoid such as thecal sac, spinal cord, major vessels, lung, and kidney. The safety view is that which best visualizes where these structures are known to lie. Unfortunately, fluoroscopy does not enable visualization of the soft tissue structures to be avoided. However, understanding the correlation of fluoroscopic with three-dimensional anatomy enables safe advancement of the needle using identifiable landmarks. Once the needle tip is believed to be at the desired target, we recommend confirming location with biplanar imaging, or two views prior to confirming with contrast injection. For the experienced interventionalist, biplanar imaging at this stage may not be required. Subsequent to this confirmation, contrast is injected. Once the ideal position and contrast flow is confirmed, the injectate is administered. When advancing spinal needles, the needle should be advanced parallel to the X-ray beam towards the target using the trajectory view. The needle tip and hub of the needle will be superimposed, resembling a target when viewed on the monitor (see Fig. 23.2). When advancing
Fig. 23.2 Spinal needle parallel to X-ray beam resembles a target with hub of needle the outer target and needle shaft the bull’s eye.
Section 2: Interventional Spine Techniques
the needle, the hand holding the needle should be braced against the patient. This keeps the needle from advancing with inadvertent patient movement. In the cervical spine or with other delicate procedures, a two-handed technique is often utilized. The ulnar palm of the hand is placed against the patient with thumb and index finger on the sides of the hub to maintain correct orientation of the needle. Such positioning guards against advancing the needle too deep, especially if the patient moves. The second hand advances the needle in small increments in the desired direction (Fig. 23.3). The needle is advanced under intermittent fluoroscopic guidance, checking the direction and advancement of the needle. A metal surgical sponge stick can be used in some injections under continuous fluoroscopic guidance. This is an advanced technique and not recommended in the cervical spine or for novice interventionalists. Total fluoroscopy time with continuous fluoroscopy should not exceed that for the same procedure utilizing intermittent fluoroscopy. If it does, the interventionalist should do the procedure with intermittent fluoroscopy. Additionally, the interventionalist must be careful not to expose his/her hand to the X-ray beam. When viewing the monitor, the interventionalist’s hand should not be present on the images. Partitions on the c-arm can be adjusted to cone down the view and decrease radiation exposure to both the patient and interventionalist. Extension tubing between the needle and syringe limits radiation exposure to the interventionalist’s hands. As well, the using of tubing prevents inadvertent movement of the needle tip during the exchange of syringes and while any agent is being injected. As of 2003, the standard of care for injections that involve the epidural space and/or nerve root dictates that extension tubing be utilized.1 Usually, when performing spinal injection procedures, the needle is advanced to abut upon bone or periosteum next to the target for injection. While some advocate that ‘bone is the interventionalist’s friend,’ others argue that teaching a novice to advance until contact with periosteum may lead to false security while advancing the needle too far. Most of the techniques utilize an approach that traverses skin, subcutaneous tissue, muscle, and then bone. The various approaches try to provide the safest path to the desired target. Bone is often utilized to gauge needle depth and avoid dangerous advancement into deeper structures such as subarachnoid space, spinal cord, spinal nerve, vertebral artery, and/or peritoneum. Once periosteum is reached, the needle is usually carefully redirected only a few millimeters in the desired
location utilizing biplanar imaging. A thorough understanding of three-dimensional anatomy and the associated structures is required. The needle is advanced in the ‘Safety’ view which demonstrates structures that must be avoided. Non-ionic contrast is utilized to confirm proper spinal needle placement. Contrast may also demonstrate inadvertent intravascular placement, thereby minimizing potential complications due to vascular injection of medications and will increase the probability of an effective injection. The non-ionic contrast agents typically utilized for spinal procedures are Omnipaque or Isovue, both approved for intrathecal usage. When injecting contrast or medication, it is important not to move the needle tip. As previously mentioned, extension tubing is frequently used for this purpose and is required for epidural space and or nerve root injections. With longer spinal needles in the thoracic and lumbar spine, the needle may be bent while injecting. This keeps the force of depressing the plunger from inadvertently advancing the needle (Fig. 23.4). Of course, since extension tubing is used this potential problem should not be an issue. It should be understood that for intra-articular injection, the therapeutic agent must be injected by connecting the syringe to the hub or the joint space will be rapidly and unnecessarily filled with extra contrast (the contrast that filled the extension tubing). Real-time imaging must be employed regardless of whether extension tubing is used or not. When real-time imaging is used to confirm accurate placement, it inherently means the needle has come to a stop. Then contrast is injected. Simultaneous advancement of the needle and contrast injecting while using continuous fluoroscopy is not appropriate. Unless real-time imaging is performed, vascular uptake may be missed. This means that relying on static fluoroscopy performed after the injection of contrast is insufficient. Aspiration looking for vascular flash-back has a sensitivity of only 46% in the cervical spine2 and 45% in the lumbosacral spine.3 In caudal injections, negative vascular flash-back occurred in only 9.2% of venously placed injections.4 For transforaminal lumbosacral epidural injections, the overall rate of vascular placement was 11.2%.3 At the level of S1, the rate was as high as 21% and in the lumbar level 8.1%. Not only do misplaced needle tips result in suboptimal treatment, but inadvertent intravascular injections can lead to serious complications to include cardiovascular collapse requiring resuscitation,1 spinal cord infarction and cerebral vascular thrombosis.19,20 For these reasons, we reiterate our recommendation that real-time injection of a non-iodinated contrast agent such
Fig. 23.3 Two-handed technique. The lower hand controls needle orientation and prevents uncontrolled needle advancement. The hand on top gently advances the needle.
Fig. 23.4 Bent needle technique to inject non-ionic contrast. The hand is kept out of the X-ray beam. The needle is bent to avoid advancement of needle by depressing the plunger. 247
Part 2: Interventional Spine Techniques
as Isovue or Omnipaque (and in rare cases gadolinium) be utilized. Some advocate using digital subtraction to even further confirm a nonvascular injection.
DIAGNOSTIC PROCEDURES When correct needle placement is confirmed by the injection of contrast, medication can then be instilled. Injections may be of two types: diagnostic or therapeutic. With diagnostic injections, local anesthetics without preservatives are used. The agents most frequently used are 1–2% Xylocaine and 0.25–0.5% bupivacaine. A double-block paradigm has been described to reduce false-positive injections.5–7 With the comparative block paradigm, anesthetics of two different half-lifes are utilized. Typically, Xylocaine or bupivacaine is used. The patient is blinded to the medication utilized. Another method to reduce false positives is the use of placebo–control blocks. For that type of double-block paradigm local anesthetic is injected on one occasion and normal saline during another. Ideally, the patient and the interventionalist are blinded to the agent used. With either a comparative or placebo–control injection, the patient is instructed post injection to perform maneuvers that would typically aggravate pain. At The Penn Spine Center we usually require at least an 80% decrement in pain from pre- to post-injection for the diagnostic injection to be considered positive. Others use 50% as the target decrement. Following the injection, the patient is instructed to keep a prospective pain dairy. Since we have found that many patients forget their pain diaries on follow-up, we recommend recording pain response every 15 minutes for 2 hours post procedure, keeping the patient for at least 1 hour and copying their pain diary before they leave. After the first 2 hours, the patient records on an hourly basis the maximum percentage of relief and severity of pain on visual numeric scale until pain returns to less than 50% relief. The patient then returns on a separate day for repeat injection with the other anesthetic. Prior to injection, the patient’s pain dairy is reviewed and the duration of relief and maximum percentage of relief is recorded. If the patient once again has at least 80% relief with the other anesthetic, the patient is instructed in keeping a pain dairy. At follow-up, the patient’s pain dairy is reviewed. The appropriate response is longer relief with bupivacaine over Xylocaine. If this occurs, the patient passes the double-block paradigm and pain is attributed to the structure injected. The patient is then a candidate for various therapeutic interventions related to the structure, as clinically indicated. If the patient has longer relief with the shorter-acting agent or less than the targeted percentage of relief for the procedure to be deemed positive with the second injection, the initial injection was a false positive. In that case, the patient is not a candidate for therapeutic intervention. Most studies utilizing the double-block paradigm have not used a strict criteria regarding the degree of pain relief to be determined a positive block. Studies of the zygapophyseal joint utilized definite relief as positive for the initial injection and 50% relief with the second injection.5,7 Use of 80% relief with the second injection probably increases the specificity by eliminating patients with 50–79% relief. However, sensitivity is lowered and potential positive responders are lost.
THERAPEUTIC PROCEDURES Corticosteroids For therapeutic injections, a mixture of local anesthetic and corticosteroid or just corticosteroid is used. The corticosteroids most frequently used are betamethasone, dexamethasone, triamcinolone, and methylprednisolone. In the discussion of the specific injections, the preferred agents and dosages of the authors is presented. These recommendations are guidelines and interventionalists may have other reasonable preferences. 248
Additional recommendations We recommend that procedures are done in a fluoroscopy suite with personnel trained in advanced cardiac life support nearby. As a minimum, continuous monitoring of blood pressure heart rate should be done every 1–5 minutes. If moderate sedation is administered, oxygen saturation, pulse, blood pressure, and level of sedation should be monitored.8–10 In those with hypertension or cardiac pathology, continuous electrocardiogram monitoring should be included.8 Airway and ventilator support should be available in case of respiratory depression. After the procedure, the patient should be taken to recovery and monitored for at least 20–30 minutes for any adverse reaction. Prior to discharge, patients should be alert and able to ambulate independently. We recommend a pain assessment be done prior to discharge. A driver should be present to take the patient home.
Considerations for specific procedures Anatomic considerations in epidural injections The epidural space is a triangular space extending from the foramen magnum to the sacral hiatus. The inner border of the epidural space is the thecal sac with the outer meningeal layer of the thecal sac, the dura mater. The dura extends from the foramen magnum to the level of S2. The outer border of the epidural space is the bony spinal canal with its covering periosteum. The anterior border is the posterior longitudinal ligament. The posterior border is composed of the lamina and ligamentum flavum. The lateral border is the pedicle and intervertebral foramina. The epidural space contains loose areolar tissue, a venous plexus, spinal nerve roots, radicular arteries, superficial and deep cervical arteries, arachnoid granules, and lymphatics. A cryomicrotome study of the epidural space found the epidural space to be widest at the midlumbar level with progressive narrowing at more cephalad levels.11 Above C7–T1 no posterior epidural space was evident.11 The width of the epidural space is 1–1.5 mm at C5, 2.5–3 mm at T6, and 5–6 mm at L2.12 In the cervical and thoracic region, the ligamentum flavum in about half of specimens did not fuse in the midline.11 In the cervical spine, the interspinous ligament was absent.11 Absence of the interspinous ligament and midline fusion of the ligamentum flavum have clinical significance when utilizing the loss of resistance technique with a midline interlaminar epidural injection. The lack of resistance from these ligaments could lead to inadvertent entry into the epidural space or dura unbeknownst to the interventionalist. In the lumbar and lower thoracic region exists the dorsomedian dural fold (plica mediana dorsalis).13 The dorsomedian dural fold divides the epidural space into three compartments: ventral and two dorsolateral compartments. The dorsomedian fold also affects the width of the space dorsally, which may be as little as 2 mm or less.13 The presence of the dorsomedian fold can affect epidural injections. The smaller width may predispose to dural puncture with a midline interlaminar approach.13 Additionally, the separate compartments can lead to incomplete flow of medication. Within the thecal sac the spinal cord is present until approximately L2. Rootlets arise from the cord to form the ventral and dorsal nerve roots and pass inferiorly. These roots exit the thecal sac with the dura forming the root sleeve. The dura ends at the proximal margin of the DRG. The dorsal and ventral roots then coalesce to form the spinal nerve as it exits the neural foramen. The dura extends as the epineurium of the spinal nerve. Fibrous tissue of the anterior and posterior epidural space extends as the epiradicular sheath. The epiradicular sheath encloses the dorsal root ganglion and spinal nerve. The epiradicular sheath is the target for a diagnostic selective spinal nerve root injection as it exits the foramen. The foramen is formed superiorly and inferiorly by the pedicle of the superior and inferior vertebrae, respectively. The superior articular process of the zygapophyseal joint forms
Section 2: Interventional Spine Techniques
the posterior wall. The inferior vertebral endplate and disc form the anterior wall. The foramen consists of entrance, mid, and exit zones. The mid-zone of the foramen contains the DRG, ventral root, sinuvertebral nerve, and vascular interconnections. Approaching the exit zone, the ventral root and DRG coalesce to form the spinal nerve. In general, the relation of the DRG to the pedicle is immediately inferior in 90%, medial 2%, and inferolateral in 8%.14 However, in the lumbar spine the location of the DRG may vary dependent upon the level of the lumbar spine.15 Hamanaishi and Tanaka,15 studying the location of 442 DRGs in 104 MRI scans reported: (1) extraforaminal location in 100% at L2, 48% L3, 27% L4, and 12% L5; (2) intraforaminal location in 52% L3, 72% L4, and 75% L5; and (3) intraspinal location 13% L5 and 65% S1. In the cervical spine, the spinal nerve exits in the inferior aspect of the foramen with vascular structures in the superior aspect of the foramen. The spinal nerve is posterior to the vertebral artery.16 In the lumbar spine, the spinal nerve and vessels are in the superior aspect of the foramen. The spinal nerve upon exiting the foramen travels inferior, lateral, and anterior. The spinal cord receives blood supply to the posterior third via the two posterior spinal arteries. The posterior spinal arteries arise from the posterior inferior cerebellar arteries. The posterior spinal arteries consist of plexiform channels and run along the line of attachment of the dorsal roots of the spinal nerves.17 The arteries also receive supply from the posterior radicular arteries. The anterior spinal artery arises from the vertebral artery and is only sufficient for the upper cervical region.17 The vertebral artery arises from the subclavian and enters the costotransverse foramen at C6 and exits at C1 and crosses posteriorly behind the arch of C1 before entering the skull through the foramen magnum. Branches from the vertebral artery descend and form a single artery, the anterior spinal artery. The anterior spinal artery receives added supply at different intervals throughout the spine. The anterior spinal artery is divided into cervical, thoracic, and lumbar segments.18 Spinal arteries arising from the vertebral, subclavian, intercostals, aortic, and iliac arteries enter through the intervertebral foramen and divide into the anterior and posterior radicular arteries.17 The majority of the radicular arteries supply primarily the nerve root. A variable number of anterior radicular arteries help supply the anterior spinal artery. These feeder arteries are larger arteries and have been termed radiculomedullary arteries.19 These arteries may ascend and descend within the thecal sac to supply the anterior spinal artery. A variable number of these feeder arteries are present in the cervical region but at least one or two are typically present, usually entering at the level of C5–6.20 Below T8 the major supply of the anterior spinal artery is through the artery of Adamkiewicz.19 Interruption of this artery can result in cord infarction of the anterior two-thirds, the anterior spinal artery syndrome. The artery of Adamkiewicz arises as a branch from the aorta and enters from the left side at T9–L2 in 85% but can enter as low as S1.21,22 A right-sided radiculomedullary artery in the lumbar region can contribute to the anterior spinal artery. Injury to a radiculomedullary artery compromises circulation to the cord with the risk of ischemia or infarction. Drainage of blood from the cord occurs through the anterior and posterior spinal veins. These veins drain into radicular veins which in turn drain into the epidural venous plexus. The plexus exits the intervertebral foramen and enters into the external venous plexus. Blood then drains into the vertebral, intercostals and lumbar veins.17
Clinical considerations regarding pathoanatomy The typical therapeutic goal of placing glucocorticoids into the epidural space and/or around a nerve root is to treat the nerve(s) affected by the herniated disc(s) or stenotic levels. Since we are advocating treating specific levels using these precision techniques, a clear understanding of ‘which nerve’ to treat is paramount to improving
clinical outcomes. In the cervical level (above C8), a central or far lateral disc will involve the more inferiorly numbered level. For example a central or far lateral C5–6 herniation will involve the C6 (more inferior) nerve. Likewise, a stenotic C5–6 foramen will involve the more inferiorly numbered nerve (C6). To access the nerve, one directs treatment between the same numbered levels, in this example, between C5 and C6. In the thoracic and lumbar levels, however, this can be more challenging for the novice injectionist. Central herniations involve the more inferiorly numbered nerve and far lateral herniations involve the more superiorly numbered nerve. For example, a central L4–5 herniation will involve the L5 (more inferiorly numbered) nerve and a far lateral L4–5 disc herniation will involve the L4 (more superiorly numbered) nerve. A stenotic L4–5 foramen will involve the more superiorly numbered L4 nerve since the pathology is also far lateral. Choosing injection levels is ‘easier’ for the stenotic foramen and far lateral herniations since the involved nerve and injected level is the same as the pathologic level. For example, for a far lateral or stenotic L4–5 level, the L4 nerve is involved and the treatment is directed at the L4–5 level to treat the L4 nerve. Central herniations, however, are far more frequent than far lateral herniations. Choosing the level to inject for these central herniations can be a bit more challenging. For example, an L4–5 central herniation involves the L5 nerve. To treat the L5 nerve, one needs to place the needle between the L5 and S1 levels. In contrast, novices often incorrectly surmise that to treat an L4–5 central herniation, they should access the ‘L4–5 foramen’ which would instead place the needle, incorrectly, at the L4 level. With the above in mind, it is more prudent to think about the nerve that needs to be treated (i.e. L5) rather than the disc to be treated (i.e. L4–5).
TYPES OF EPIDURAL INJECTIONS Injections into the epidural space are of three general types: caudal, interlaminar, and transforaminal. Although interlaminar and caudal injections may be performed with or without fluoroscopic guidance (we advocate the former as routine), transforaminal injections require fluoroscopic guidance. Interlaminar or caudal epidural injections done without fluoroscopic guidance are also termed blind epidural injections. Techniques of hanging drop and loss of resistance are utilized to identify entry into the epidural space. The accuracy of blind epidurals has been tested. The loss of resistance technique in the cervical spine for blinded interlaminar injections has a miss rate of 53%.23 In the lumbar spine the miss rate ranges from 17% to 30%.24,25 Caudal epidural injections have a miss rate of 25–52%.4,25 However, if the sacral cornu are easily palpated and there is no palpation of subcutaneous air, loss of resistance blinded injection with an experienced interventionalist may be successfully performed in 91.3%.26 If the landmarks are not easily the palpated, the success rate in the same study was 54.5%. Landmarks were readily palpable in only 59.3% of subjects.27 Under fluoroscopic guidance, El-Khoury27 had a failure rate of 2.5% for caudal injections. Of two failures, one was secondary to dural puncture and the other was from inability to place the needle in a subject who had suffered a sacral fracture. Anatomic variance of the sacral hiatus in 15% may prevent successful caudal injection.28 Variations included a hiatus of less than 8 mm in length, severe partial agenesis, complete agenesis, absent hiatus, bony septum in canal, and angulation of the sacrum.29 The rate of misplacement of blind epidural injections is unacceptable, especially considering the routine availability of fluoroscopy. For additional safety, digital subtraction should be considered, if available, when performing transforaminal injections with precarious vascular anatomy such as in the cervical spine or high lumbar locations (L1–3, artery of Adamkiewicz watershed zone). Other safety measures include using a local anesthetic test dose and 249
Part 2: Interventional Spine Techniques
routine remixing of the glucocorticoid if it is of the type that tends to accrete. Transforaminal injections have theoretic advantages over interlaminar injections. Interlaminar injections place medication in the posterior epidural space. Stojonavic et al.23 demonstrated that cervical interlaminar injections contrast entered the ventral epidural space in only 28% and remained unilateral in 51% of injections. In the thoracic spine, contrast entered the ventral epidural space in only 24% injections.29 Kraemer et al.30 demonstrated medication flowed dorsally with interlaminar epidural injections. In a randomized, controlled trial, perineural injection was found to be superior to interlaminar epidural injection in radiculitis from herniated lumbar disc,30 supporting the benefits of target-specific injection. With therapeutic selective nerve injections, medication is delivered directly to the targeted spinal nerve, dorsal root ganglion, and nerve root. This is particularly important where resistance to fluid flow occurs such as in spinal stenosis, foraminal disc protrusions, and epidural fibrosis. In cases of axial pain felt to be discogenic in origin, transforaminal injections place the medication ventrally in the epidural space adjacent to the posterior anulus, posterior longitudinal ligament, and sinuvertebral nerve. Diagnostic selective spinal nerve root injections target the spinal nerve, nerve root, and DRG only. A small aliquot of local anesthetic is injected to anesthetize the spinal nerve to determine if pain is emanating from the specific spinal nerve and nerve root. Diagnostic selective spinal nerve root injections are indicated when the etiology of pain radiating into an extremity is in question. A pre- and postinjection pain drawing and visual analogue scale is obtained. Post procedure, the patient should perform activities which usually provoke the pain. If the patient has an 80% decrement in pain, the diagnostic injection is considered positive.31
General techniques Non-ionic contrast is utilized to confirm proper needle placement. Contrast should outline the epidural space and/or the spinal nerve depending on the type of injection performed. The contrast will display either a negative or positive outline of the epidural space or the nerve (Fig. 23.5). Injection into the epiradicular sheath usually is of low resistance and not painful. However, the injections may be painful when there is severe nerve irritation and/or compression, such as with a foraminal disc herniation. In these situations, inject
A
medication slowly, approximately 1 second per 0.25 cc per second, to minimize pain. Also, slower injection may reduce the incidence of postinjection headache. If pain develops during the injection, stop injecting until the discomfort dissipates. Then resume injecting, but slowly to avoid pain. If significant resistance is encountered, do not force the medication. Recheck the needle placement with real-time fluoroscopy to insure proper placement and that the needle tip has not been advanced intraneurally. With intraneural needle placement and injection of contrast, the patient typically experiences severe radicular pain. When severe radicular pain is described by the patient the injection should be stopped immediately. The contrast will usually demonstrate a sharp line within the substance of the nerve. The needle should be withdrawn back into the epiradicular sheath and rechecked with real-time fluoroscopy. The other contrast pattern that is important to recognize is a subarachnoid pattern. This pattern will give a myelographic outline. If this occurs, the procedure is abandoned as subarachnoid instillation of medication can be catastrophic. There is the risk of respiratory depression, hypotension, syncope, and arachnoiditis.32–36 Transforaminal injections can be performed by CT scan with advantages of less radiation to the interventionalist along with visualization of nerve and soft tissue structures.37 However, CT has disadvantages of greater expense, being less rapid to perform, and there being no ability to perform real-time injection of contrast.37 The latter is a major disadvantage as inadvertent radiculomedullary injection can result in paralysis.19,20 Fluoroscopic guidance with real-time injection of contrast is recommended.
Caudal epidural injection The caudal epidural space extends between the sacral hiatus and the caudal end of dura which terminates anywhere between S1 and S3, but usually at the inferior border of S2 segment. The contents of the canal include sacral nerves, fatty tissue, and sacral venous plexus, the latter usually terminating at S4 segment but may continue inferiorly in some patients. The canal size is variable, with documented volumes from 15 to 60 ml. Variations in sacral anatomy have been mentioned by several authors. These variations include, but are not limited to absence of sacral hiatus (prevalence in general population is reported to be about 8%), location of the sacral hiatus, curvature and location of sacral foramina, bifid sacrum and sacral canal stenosis secondary to previous sacral fracture. The radiologi-
B
Fig. 23.5 Epiradicular sheath injection with (A) negative outline of spinal nerve and (B) positive outline of spinal nerve. 250
Section 2: Interventional Spine Techniques
cal landmark of the sacral canal is a translucent layer posterior to the sacral segments in lateral views with the sacral hiatus visible as a translucent opening at the base of the caudal canal. After consenting, the patient is placed prone on the fluoroscopic table with a pillow under the abdomen and legs abducted. For the right-handed interventionalist, it is usually recommended to stand on the left side of the patient. In nonobese patients, the sacral cornua can actually be palpated, which provide landmark to locate the hiatus. The skin of the region is then prepped with povidone-iodine and draped with a fenestrated sterile drape. A 3 inch, 22-gauge needle is usually selected for the procedure. The entry point of the skin is approximately 2 cm distal to the sacral hiatus. The needle is advanced at about 45 degrees until it reaches the sacrococcygeal ligament. The needle is then slightly withdrawn, and the hub made to lie parallel to the skin surface, before advancing the needle through the sacral hiatus into the sacral canal. The needle is advanced to the interval between the sacral foramina of S2 and S3. Any further advancement of the needle could result in advertent dural puncture. The position of the needle is verified on lateral fluoroscopic views to avoid the incorrect placement because of anatomical variations. The use of contrast material is highly recommended to confirm the absence of venous run off, as the needle might be in the sacral venous plexus without actually causing a flash back. The most common contrast spread pattern is a ‘Christmas tree’ shape. Typically, 1.0–3.0 mL of contrast material will demonstrate appropriate position. After aspiration for blood and CSF is negative and venous run-off ruled out by contrast fluoroscopy, 2–3 mL of methylprednisolone along with 10 mL of lidocaine is instilled. This provides enough volume for the injectate to reach the level of L3 vertebral body.
Interlaminar epidural injection Cervical With progressive cephalad narrowing of the epidural space, the width at C5 has been shown to be 1–1.5 mm12 with no evident posterior epidural space above C7–T1. It has also been shown11 that in 50% of the specimens ligamentum flavum did not fuse in the midline, and the interspinous ligament was absent. With these anatomic considerations, the most common injection site for cervical interlaminar injection is the C7–T1 or C6–7 interspace. Because of the relatively small size of the cervical epidural space, a catheter technique is recommended, particularly in an elderly population. Feeding a catheter from the upper thoracic, preferably T1–2, epidural space to the desired segmental level in the cervical spine significantly reduces the chance of cervical cord damage. The recommended positions for the cervical interlaminar injections include sitting, lateral, and prone. The sitting position is easiest for the patient and enhances operator’s ability to flex the cervical spine and identify the midline. However, its use is limited practically in patients prone to vasovagal syncope and those who are unable to assume a sitting position because of underlying vertebral compression fractures. In these situations, a lateral position is recommended, particularly when tunneled epidural catheters or implantable devices are considered. This position may, however, pose technical difficulty because of spine rotation. The most commonly used position is the prone position. One must, however, ensure flexion of the cervical spine to widen the epidural space. After optimal position and skin prep with povidone-iodine, the appropriate landmarks are identified. A midline approach is selected. The midline of the desirable interspace is identified by palpating the spinous processes above and below the space, with a lateral rocking motion of these processes. Usually 3 inch or 1½ inch, 22-gauge needle is selected, and advanced in the midline. Cervical epidural injections have been performed blind
without fluoroscopic guidance. However, anatomic studies have found high rates of discontinuity in the ligamentum flavum in the cervical region and a smaller epidural space than lumbar levels. This variability can potentially result in higher rate of dural puncture and unsuspected spinal cord injections during blinded injections. Fluoroscopy and contrast administration are, therefore, highly recommended to obviate these complications. If a blind technique is used, the epidural space is identified by the loss of resistance technique without ballottement. The hanging drop method is not used because of the associated 2.0% failure rate, compared with less than 0.5% failure rate for the loss of resistance technique. After satisfactory needle position is confirmed and gentle aspiration negative for both blood and the CSF, medications are injected. Because of the relatively small size of the cervical epidural space, a catheter technique is recommended, particularly in an elderly population. Feeding a catheter from the upper thoracic, preferably T1–2, epidural space to the desired segmental level in the cervical spine significantly reduces the chance of cervical cord damage.
Thoracic The thoracic vertebral column has a kyphotic apex at T6 with the inclination different at each level: T1–4 and T9–12 incline very little while T5–8 inclines downward significantly. With steep inclination of the spinous processes at T5–8, often covering the entire interlaminar space below, a paraspinous, paramedian approach is recommended at this level in contrast to upper thoracic level where a median approach is possible. The thoracic ligamentum flavum is thinner than in the lumbar area. Thus, when inserting the needle within the epidural space, resistance will not be encountered. It is recommended to advance the needle during inspiration to allow for the maximum pressure gradient between the epidural space and outside of the body. When considering the paraspinous approach for lower thoracic spine, the entry point of the needle is next to the caudal edge of the superior spinous process of the required interspinous space. The needle is advanced with an upward angulation of 55 degrees to the long axis of spine and inward angulation of 10–15 degrees. The choice of needles is between Crawford and Tuohy needles, with the bevel of former oriented cephalad and that of the latter directed caudally. Similar to cervical epidural injection, a catheter technique may be used.
Lumbar The lumbar interlaminar epidural injection is performed at the interspace most closely located to the level of suspected source of pain, with the needle placed just below the target level. The sitting and lateral positions are recommended, with the latter favoring the spread of injectate to the dependent side. Either the midline or paraspinous approach can be used in the lumbar spine. As with the cervical and thoracic spine, fluoroscopy and real-time injection of contrast is essential. With the midline position, the entry point is closer to the superior spinous process of the required space with an upward angulation of 10 degrees. When using the paraspinous approach, the entry point is close to the cauded edge of the inferior spinous process with 45 degrees angulation to the long axis of spine below.
Transforaminal epidural injection Cervical Anterior, lateral, posterior and oblique approaches have been utilized for cervical transforaminal epidural injections. The anterior approach has been described by many practitioners.16,38–40 The main disadvantage 251
Part 2: Interventional Spine Techniques
of this technique is the vertebral artery is at risk of puncture since it is located anterior to the spinal nerve. When placing the needle into the foramen, the posterior wall of the foramen is targeted to avoid vertebral artery puncture.37 Also, the interventionalist has to use their fingers to push the trachea and esophagus to one side and the carotid artery to the other. These structures are also at risk for puncture. With a left-sided approach, the thoracic duct could also be inadvertently punctured. These problems led Vallee et al.41 to propose a sitting, lateral approach. With the lateral technique, the patient is placed in a sitting position to help lower the shoulder.41 The lateral approach targeted the superior articular process to gauge depth and to avoid the more anteriorly located vertebral artery. The c-arm is then aligned obliquely to advance the needle medially and ventrally into the foramen under fluoroscopy. Position is then checked in the anterior plane. The main disadvantage of placing the patient in a sitting position would be in the event a vasovagal reaction or in a patient requiring moderate sedation. A posterior approach has been described.16 The patient is placed in the lateral decubitus position. The needle is entered 5–7 cm from midline and directed at 45–60 degree angle until it touches the transverse process.16 The needle is then advanced to touch the nerve root extraforaminally. An oblique approach with the patient lying supine has the advantages of the lateral technique without its disadvantages. With this technique the needle can be placed into any portion of the foramen instead of being relegated to an extraforaminal location. The oblique approach also keeps the spinal nerve posterior to the vertebral artery, decreasing the risk of puncture compared to an anterior approach. The oblique approach is the recommended technique. Patient and fluoroscopy positioning are critical to allow the procedure to be done safely and easily. The patient is placed in a supine or supineoblique position. A towel or blanket is placed under the head to place the spine parallel to the fluoroscopy table. A common mistake is to allow the patient to shrug the shoulder (Fig. 23.6A). The shoulder
A
C
252
should be depressed to keep it from interfering with viewing the spine under fluoroscopy (Fig. 23.6B). The patient or c-arm is then rotated to place the foramen perpendicular to the radiographic imager. In this position, the superior articular process is well visualized (Fig. 23.6C). Avoid placing the spine too obliquely, which can rotate the vertebral artery into the area of injection (Fig. 23.7). Remember, the vertebral artery runs through the costotransverse foramen from C1 to C6. Once positioned, the patient is prepped and draped in a sterile manner. A skin wheal is raised with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, though some interventionalists do not perform this step. The bicarbonate is used to neutralize the acidic Xylocaine and diminish the burning sensation the patient may feel with the skin wheal. A 22or 25-gauge 1.5–2.5 inch spinal needle is then inserted perpendicular to the midportion of the superior articular process and advanced until bone is reached. As touching periosteum is painful, one must only gently touch bone. As described above, it is not necessary to contact periosteum. During needle insertion, the ulnar aspect of the hand that is holding the needle should be against the patient. If the patient moves, the hand against the patient keeps the needle from inadvertently being advanced. By utilizing bone to gauge depth, dural puncture and spinal cord puncture can be averted. As well, biplanar imaging and utilizing a ‘safety’ view will also assist in avoiding inadvertent injection into undesired structures. Additionally, by targeting the superior articular process in the oblique position, the vertebral artery, which is anterior, is kept away from the needle. For a therapeutic injection, the needle is directed only slightly caudal and ventral a couple of millimeters into the foramen. Transforaminal injections are completed by passing the needle tip to the anterior half of the foramen. This is accomplished with minimal pain when the needle tip is advanced along a line that bisects the cephalad and caudal portions of the foramen. In this fashion, the existing root is typically missed and unnecessary pain is avoided. A diagnostic selective nerve root injection requires the needle
B
D
Fig. 23.6 Cervical spine patient positioning. (A) Incorrect patient positioning with shoulder shrugged. (B) Correct patient positioning with shoulder depressed. Fluoroscopy images with shoulder shrugged (C) and depressed (D).
Section 2: Interventional Spine Techniques
be directed caudally and slightly ventral to touch the spinal nerve just as it exits or where it resides outside of the foramen. Care must be taken not to pierce the spinal nerve and every effort is made to minimize the production of radicular pain during needle placement. If radicular pain is experienced, the needle should be slightly withdrawn. Position is then checked in the oblique and AP planes. In the oblique plane, the needle should just be slightly anterior to the superior articular process but still in the posterior aspect of the foramen. In the AP plane the needle should not be beyond the six o’clock position of the pedicle or there may be risk of dural puncture (Fig. 23.8). The stylus is then removed. A syringe filled with contrast agent is connected to tubing and flushed with contrast. The tubing is then connected to the spinal needle. Under real-time fluoroscopy, contrast is injected to confirm needle placement (Fig. 23.9). Contrast flow should clearly be along the targeted spinal nerve and if desired into the epidural space (medial to the ipsilateral lateral mass) (Fig. 23.10). One must carefully watch for any vascular pattern. If available, digital subtraction is used to confirm a nonvascular injection. If a vascular pattern is noted, the needle needs to be repositioned in the foramen. If there is an arterial pattern, we recommend aborting the injection at that level. When repositioning the needle away from a venous injection, the needle is withdrawn out of the foramen. The tubing is removed and the stylus replaced into the spinal needle. The needle is then repositioned on the
Fig. 23.7 Cervical spine transforaminal injection: too oblique with vertebral artery rotated near path of injection.
A
B
C
D
Fig. 23.8 (A) Oblique position with neuroforamen perpendicular to imager and spinal needle within inferior–posterior foramen. (B) AP view of spinal needle at six o’clock position. (C) Contrast outline spinal nerve in oblique orientation. (D) AP view with negative outline of cervical spinal nerve.
253
Part 2: Interventional Spine Techniques
there is no adverse reaction. At 90 seconds post-injection, the patient must be queried regarding experiencing periorbital numbness, a metallic taste, auditory changes, agitation, and difficulty breathing and observed for seizure activity. If no complaints are articulated that would suggest intravascular or subarachnoid placement of the local anesthetic, a quick motor screen must be conducted. The patient is asked to move the fingers and toes. If no paresis is observed, a glucocorticoid with or without local anesthetic may then be injected. We typically utilize 1–2.0 cc of dexamethasone Soluspan and 0.25 cc of 1% Xylocaine. Some interventionalists are now injecting the therapeutic agent under continuous fluoroscopy to ensure there is no intravascular flow. It is believed that this will help prevent radiculomedullary injection with risk of anterior spinal artery syndrome or vertebral artery injection with subsequent cerebral or spinal cord ischemic event. This latter step is unnecessary provided the other safety measures described have been properly performed. For a diagnostic selective spinal nerve root injection, the needle bevel is rotated inferiorly and 0.5 cc of contrast injected. Contrast should outline the spinal nerve root and DRG but should not extend beyond this (Fig. 23.11). Then 0.5 cc of 1% Xylocaine is instilled. Again, continuous fluoroscopy with injection is recommended.
Additional safety concerns in cervical transforaminal epidural steroid injections Fig. 23.9 Tubing connection to spinal needle for contrast instillation. Tubing allows continuous fluoroscopic imaging with injection: recommended method.
There have been many recent reports regarding serious adverse outcomes directly related to cervical transforaminal ESIs. Although they are not published, the authors are aware of at least 10 litigation cases involving post-procedural infarction of structures supplied by either the cervical, cerebellar, or cerebral vasculature. These procedures have resulted in long-term cognitive or physical dysfunction and
Fig. 23.10 Cervical transforaminal injection. Contrast outlines spinal nerve and demonstrates epidural flow.
superior articular process. The needle is then advanced in a different angle, typically more caudally as radicular vein and artery are in the cranial aspect of the foramen. The position is once again checked in the oblique and AP planes. With correct placement, the tubing with contrast is then reattached and contrast injected to check placement. Contrast should outline the spinal nerve and demonstrate epidural flow without evidence of subarachnoid flow. It is absolutely necessary to use a test dose of about 0.8–1.0 cc of 1–2% lidocaine to confirm that 254
Fig. 23.11 Diagnostic cervical selective nerve root injection. Contrast outlines spinal nerve with no epidural flow.
Section 2: Interventional Spine Techniques
even death. The current consensus theory for the etiology of these catastrophic events is that particulate from the steroid suspension is injected into the cervical arterial vasculature, resulting in subsequent infarction. In an effort to lower the risk:benefit ratio, we reiterate our recommendations. We need to clarify, however, that these recommendations have not been proven to decrease the procedural risk but are based on informal consensus discussions. Nevertheless, the following steps, exclusive of the use of digital subtraction, represent the minimum standard that must be followed to be safe: 1. Confirm that the patient’s clinical scenario warrants the procedure and that conservative treatments have been attempted. Verify that the patient is on no medications which can increase bleeding (i.e. aspirin, Coumadin, nonselective NSAIDs, Plavix, etc.). 2. Informed consent should include the potential for nerve damage, paralysis, stroke, and/or death. 3. Fluoroscopic and patient oblique positioning should demonstrate the best possible view of the foramen to be injected. The needle tip needs to clearly be in the posterior aspect of the foramen in oblique view and not beyond the six o’clock position of the lateral mass in AP view. Document these two pre-contrast pictures. 4. Prior to injecting contrast, drip a small amount of the contrast into the needle hub. This will decrease the chance of injecting air. 5. Use a small extension tube during all injections. As described above, always have physical contact with the patient while handling the extension tube or needle. This will minimize the chance of unintended needle movement during the injection. 6. Real-time fluoroscopy should demonstrate that there is no arterial flow. Digital subtraction should be utilized, if available, to enhance sensitivity. Arterial flow will be either horizontal or cephalad. Document biplanar contrast flow images as well as one from digital subtraction, if available. Should an arterial injection be observed, abort the procedure at that level. Flow should clearly be along the targeted spinal nerve and, if desired, into the epidural space (medial to the ipsilateral lateral mass). 7. Once satisfactory placement is obtained, utilize a test dose of 1% lidocaine without epinephrine (0.5–1 cc). Ninety seconds postinjection, confirm there are no neurologic sequelae or other adverse events before injecting the final steroid or steroid/anesthetic. 8. Use a steroid solution which minimizes particulate size in the suspension. 9. Should an adverse event occur, insure you have access to appropriate imaging (i.e. CT/MRI) and neurosurgical consultation.
keeping the needle posterior to avoid a pneumothorax. The position of the needle should be checked frequently in the AP and lateral planes to ensure the needle is neither too ventral nor dorsal. In the AP plane the needle is advanced just short of the six o’clock position of the pedicle. Position is then checked in the lateral plane to ensure the needle is in the foramen. Contrast is then injected to confirm needle placement and should outline the spinal nerve around the pedicle and demonstrate no vascular or subarachnoid pattern (Fig. 23.12). In the case of a diagnostic injection, there should be no contrast flow to adjacent levels or epidural spread. To help avoid epidural spread, the bevel of the spinal needle should be directed inferiorly. With a therapeutic injection, 2.0 cc of Celestone Soluspan and 1.0 cc of 1% Xylocaine may be instilled. Of course, the therapeutic agent is only injected once the a test dose of local anesthetic is injected through extension tubing. Each of the steps previously enumerated for the cervical region regarding assessing for neurologic sequelae must be followed. With a diagnostic injection, 0.5–1.0 cc of 1% or 2% Xylocaine is instilled, dependent upon the amount of contrast injected that did not result in extension beyond the nerve root.
Lumbar In 1971, MacNab42 discussed the use of selective spinal nerve root injections to identify radicular pain that allowed for successful surgical explorations in the setting of a negative imaging work-up. Various causes were found to include foraminal stenosis, subarticular stenosis, foraminal disc herniation, lateral disc herniation, and pedicular kinking. The method of nerve root injection was a posterolateral approach. The patient was placed in a lateral position. The needle was directed under fluoroscopic guidance until nerve pain was experienced. The illustration in the study demonstrated a cranial to caudal and posterolateral approach which abuts the spinal nerve extraforaminally. Several authors have utilized a similar approach in the prone or lateral position.41–47 In each study, the spinal nerve was targeted extraforaminally, with the needle striking the nerve perpendicularly, resulting in radicular pain. A spinal needle was inserted 4–10 cm lateral to the spinous process and directed to the inferior edge of the transverse process. Once touched, the needle was redirected caudally and medially until the patient experienced lacinating radicular pain. Contrast was
Thoracic The patient is placed in the prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile fashion. The level to be injected is located by counting the ribs to the appropriate level. One must be cognizant of whether a cervical rib exists to ensure proper level identification. A metal pointer is utilized to mark the proper level. The c-arm is then rotated obliquely and the pedicle, rib, and transverse process are identified. A metal pointer is used to place a skin wheal with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, although not all interventionalists perform this step. A 22or 25-gauge 3.5 inch needle is then grasped by the sponge stick and advanced under continuous fluoroscopy to touch the inferior edge of the costotransverse joint. During advancement, the hand grasping the sponge stick should have the fingertips braced against the patient. This helps prevent any inadvertent needle advancement if the patient moves. Alternatively, the needle may be advanced by hand under intermittent fluoroscopy to the inferior edge of the costotransverse joint. Then under intermittent fluoroscopy the needle is advanced toward the inferior aspect of the pedicle along the margin of the ribs,
Fig. 23.12 Thoracic transforaminal injection. Contrast outlines spinal nerve and demonstrates transforaminal epidural flow. 255
Part 2: Interventional Spine Techniques
Fig. 23.13 Lumbar transforaminal injection. Advancement of needle under continuous fluoroscopy utilizing sponge stick.
then injected and outlined the spinal nerve with both proximal and distal flow. This approach has the risk for neural injury. The needle is perpendicular to the nerve and not parallel, increasing the chance for intraneural injection. When attempting to anesthetize higher roots, one would be concerned about injuring renal structures. Castro and van Akkerveeken48 described a posterolateral approach in which the needle is directed just inferior to the pedicle to the midline of the pedicle, the six o’clock position.48,49 Van Akkerveeken49 also notes referral of pain into the extremity is not reliable for nerve root pain as periosteum, joint capsule, and anulus may result in referred pain. Van Akkerveeken49 utilized 0.2–0.5 mL of 0.5% Marcaine for diagnostic selective spinal nerve root injections. The specificity was 90% and sensitivity of 100%. North et al.50 concluded diagnostic selective nerve root injections were non-specific. However, North utilized 3 cc of bupivacaine.50 This large volume would not be selective and would result in adjacent levels being anesthetized along with the sinuvertebral nerve. The study emphasized the importance of utilizing a small aliquot of anesthetic (0.2–1.0 mL) to target the spinal nerve and dorsal root ganglion only. We currently utilize a technique similar to van Akkerveeken.49 The advantage of this technique is to place the needle in the epiradicular sheath more parallel to the nerve than perpendicular to avoid intraneural injection. We do not attempt to induce radicular pain. The following technique can be utilized for both transforaminal epidural injection and diagnostic selective spinal nerve injections with slight modifications. The patient is placed in a prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile manner. The level to be injected is established by locating the lowest lumbar segment. For those with a transitional segment, such as a lumbarized S1 or sacralized L5, the level should be adjusted accordingly. The c-arm is rotated obliquely to create the trajectory view visualizing the pedicle and superior articular process. The pedicle will appear oblong. The superior articular process will point up at the pedicle. The target is just inferior to the pedicle and just lateral to the point of the superior articular process. A metal pointer is then utilized to locate the skin wheal of a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, though not all interventionalists perform this step. Care must be taken to avoid too lateral an approach which could result in peritoneal or renal puncture. Typically, 12 cm from 256
the midline is the furthest recommended lateral distance for needle insertion. A 22- or 25-gauge, 3.5 inch spinal needle is grasped with the sponge stick and under continuous fluoroscopy is then advanced just anterior to the uppermost aspect of superior articular process and just inferior to the pedicle (Fig. 23.14). Once the needle finds purchase in adjacent paraspinal muscle, the c-arm is rotated to the AP position. With intermittent fluoroscopy and utilizing the two-hands technique, the needle is advanced just inferior to the pedicle and to the six o’clock position. The needle should be in the safe triangle formed by the pedicle, the outer line of the foramen, and the spinal nerve.51 Position is then checked in the lateral plane to ensure the needle is within the foramen. One milliliter of contrast agent is then injected though extension tubing and under continuous fluoroscopy. The spinal nerve should be outlined without any demonstration of a vascular pattern or subarachnoid flow. With a therapeutic injection contrast should flow around the spinal nerve, the DRG, and into the epidural space (Fig. 23.15). When a transforaminal injection is done, flow should be demonstrated ventrally such that it encompasses the most ventral aspect of the epidural space. A diagnostic injection should not demonstrate contrast spread beyond the dorsal root ganglion. To minimize excess spread during a diagnostic injection, the bevel of the spinal needle should be rotated inferiorly. With a therapeutic injection for radicular pain, a mixture of 1.0–2.0 cc of Celestone Soluspan mixed with 1.0–2.0 cc of 1% Xylocaine may be injected. Transforaminal injections typically involve 3 cc of Celestone and 5 cc of 1% Xylocaine. With a diagnostic injection, 0.5–1.0 cc of 2% Xylocaine may be utilized. In the past, CT-guided transforaminal technique utilizing CT was believed to be superior to utilizing c-arm fluoroscopy.52 However, there was no statistical significance in the outcomes between the two techniques. Additionally, while contrast was utilized to confirm placement with the CT method, no contrast was utilized with the c-arm method. As previously discussed, real-time contrast is required not only to exclude intravascular placement but also to ensure the correct structures are infused with the injected agents.
Fig. 23.14 Lumbar transforaminal injection. (A) Proper needle position at the six o’clock position. (B) Contrast outline spinal nerve with contrast around medial aspect of pedicle.
Section 2: Interventional Spine Techniques
Fig. 23.15 Sacral transforaminal injection: Sponge stick superior and lateral to S1 pedicle is point for raising skin wheal.
Fig. 23.16 Sacral transforaminal injection: Needle at one o’clock position adjacent to foramen to gauge depth.
Sacral The sacral foramen posteriorly is directed lateral to medial. Early techniques utilized a 10–15 degree prone oblique approach with reproduction of radicular pain.44,45 We utilize a similar approach, but avoid spearing the nerve. The patient is placed in a prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile manner. The sacral foramen is located under fluoroscopic guidance and a metal pointer is placed on the patient’s back superior and lateral to the foramen (Fig 23.16). The c-arm may be obliqued slightly to allow better visualization of the sacral foramen. At the marked point, a skin wheal is raised with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, although not all interventionalists complete this step. A 22- or 25-gauge, 3.5 inch needle is grasped by a sponge stick and under continuous fluoroscopy is advanced to abut upon the periosteum adjacent to the sacral foramen at the eleven o’clock or one o’clock position for left and right sides, respectively (Fig. 23.17). The needle is advanced in a cranial to caudal direction and lateral to medial direction to conform to the direction of the sacral foramen. Once periosteum is reached, redirect the needle 2–3 mm medially and inferiorly by hand into the foramen. Often, a slight loss of resistance will be felt upon entering the foramen. Onehalf to 1 mL of contrast agent is injected. For a S1 transforaminal injection, contrast should outline the S1 nerve and flow around the S1 pedicle (Fig. 23.18). Position is checked in the AP and lateral planes. There should be no vascular or subarachnoid pattern. With a diagnostic spinal nerve injection, there should be no epidural spread to adjacent levels. Once proper placement is confirmed, medication can then be instilled. For therapeutic injection, a mixture of 2.0 cc of Celestone Soluspan and 2.0 cc of 1% Xylocaine is used. For a diagnostic injection, 1.0 cc of 2% Xylocaine may be used.
Special situations A patient’s anatomy may prevent a straight-line approach to the intervertebral foramen. The L5–S1 foramen may be blocked by the iliac crest
Fig. 23.17 S1 transforaminal injection. Contrast around S1 nerve spinal nerve and flows medial to S1 pedicle demonstrating proper placement.
or a broad L5 transverse process. In skilled hands, a single-needle technique utilizing the bevel to curve the needle around bony structures can be used (Fig. 23.19). The needle will tend to curve away from the bevel. Another approach is to start the needle more ventrally than usual toward the iliac crest, then bounce the needle off the crest, directing the needle medially towards the foramen. One should note this technique can be painful when the needle touches the iliac crest, so be gentle with this technique or instill local anesthetic at the target site of the iliac crest. These latter two techniques are advanced and great care needs to be taken to avoid placing the needle too ventrally with possible peritoneal or vascular penetration of the common iliac vessels. Another method is a two-needle technique. An 18–20-gauge, 3.5 inch needle can be directed toward the inferior aspect of the transverse process of L5. Once bone is touched to gauge depth, the needle is directed inferiorly and ventrally 257
Part 2: Interventional Spine Techniques
Fig. 23.18 L5 transforminal injection entry blocked by iliac crest. Use of curved, single-needle technique to direct needle past iliac crest and around superior articular process to enter foramen.
underneath the transverse process. The bevel is rotated towards the foramen with the needle tip dorsal and lateral to the foramen. A 22–25gauge, 6 inch needle is then curved. Hold the needle at the hub with one hand. With the opposite hand, fold sterile gauze around the needle with the index finger and thumb grasping the needle. Then slide the gauze down the needle and curve the needle away from the bevel (Fig. 23.20).
A
The amount of curve is based upon a three-dimensional visualization of the path the curved needle will need to travel to reach the foramen. Insert the pre-curved needle through the 3.5 inch, 20-gauge needle and direct it toward the foramen. This may require frequent checks in both the AP and lateral planes to avoid too ventral placement with subsequent viscus perforation. As the curved needle extends beyond the shorter needle, the shorter needle may be withdrawn slightly. This allows more of the curve to develop without having to advance the needle too ventrally. Once the needle reaches the foramen, check proper placement in the AP and lateral planes. One-half to 1 mL of contrast is then infused to ensure proper placement and is checked in two planes under fluoroscopy. Contrast should outline the L5 nerve and spread around the medial aspect of the L5 pedicle. There should be no vascular or subarachnoid pattern. Once proper placement is confirmed medication can be instilled. Patients who have undergone a posterolateral fusion may present similar problems. A single technique with curving the needle around the fusion can be done in some cases. Otherwise, a two-needle technique is utilized. The method is similar as that described above except for placement of the 20-gauge, 3.5 inch needle. With a posterolateral fusion the transverse process cannot be directly targeted. The c-arm is slightly obliqued and the 3.5 inch, 20-gauge needle is directed to the fusion mass just inferior to the transverse process. The needle should abut the fusion mass on the lateral edge. The needle is then directed ventrally just beyond the fusion. The needle bevel is rotated toward the foramen. The pre-curved 25-gauge, 6 inch needle is then inserted. With frequent checks in AP and lateral planes, the needle is directed towards the foramen. Once reached, confirmation is obtained with instillation of contrast and checking in two planes. Contrast should outline the spinal nerve and flow around the medial aspect of the pedicle. The pedicle may not be directly visualized secondary to pedicle screws, but since the screw is in the pedicle, one may visualize contrast around the medial aspect of the screw (Fig. 23.21). Sometimes the posterolateral approach may be unsuccessful. If a posterolateral fusion is present with concomitant laminectomy, a medial approach may be tried. A 22- or 25-gauge, 3.5 inch needle in the AP plane is inserted 1 cm medial to the pedicle at the inferior edge.51 The needle is advanced to the five o’clock or seven o’clock position for left and right sides, respectively. The needle is advanced until bone is reached.51 This method is similar to the technique for perineural injection described by Kraemer and co-investigators.30 In their technique, a medial to lateral approach with the needle parallel to the plane of the lamina, is utilized. The needle is advanced until bone is reached.30 Both techniques risks spearing the nerve root, intravascular
B
Fig. 23.19 Technique for bending needle. (A) Holding needle with gauze and curving needle away from bevel. (B) Curved needle. 258
Section 2: Interventional Spine Techniques
Fig. 23.20 Lumbar transforaminal injection in patient’s instrumented posterolateral fusion. Note bend in needle near foramen. A bent needle technique was utilized to go around the fusion.
penetration (epidural plexus is lateral, and radicular vessels accompany the nerve roots), and dural puncture. To obviate spearing of the nerve, the needle can be directed to the superior articular process to gauge depth. With laminectomy, a medial facetectomy may be done, but the lateral facet (superior articular process) is still present. Once the needle touches the superior articular process the needle may be advanced slowly a few millimeters ventrally. Non-ionic contrast can then be injected to confirm placement. If a soft tissue pattern occurs, the needle may be slightly advanced and contrast agent re-injected. Once a spinal nerve
A
B
pattern with flow around the pedicle occurs, injection of medication can then be done. If during advancement the patient experiences radicular pain, the needle should be slightly withdrawn. Contrast can then be injected to confirm proper placement. If a dural puncture occurs, the procedure is discontinued. Transitional segments can pose technical challenges. First, the correct level needs to be identified. This should have been determined as part of the presurgical evaluation process. An MRI with scout view or AP view plain films of the cervical, thoracic, and lumbosacral spine is utilized. The vertebrae are counted from C2 caudally to determine if the transitional segment is a sacralized L5 or lumbarized S1 segment. In partial sacralization of L5, a PA or slightly obliqued view of the foramen is obtained.51 A 22-gauge, 3.5 inch spinal needle is inserted obliquely until there is gentle contact with the medial edge of the iliac crest. Two-tenths to 1.0 cc of 1% Xylocaine can be infused to anesthetize the periosteum of the iliac crest. The needle is then deflected off the crest medially and ventrally to the foramen.53 Alternatively, the spinal needle may not need deflection off the iliac crest and can be curved by utilizing the bevel of the needle. When the needle is near the depth of the iliac crest, the needle is curved medially and ventrally toward to the foramen. The foramen is typically larger with the transitional segment.53 As the needle is advanced, a loss of resistance occurs before reaching the pedicle as it enters this potentially larger space.53 Care must be taken to gently advance the needle, as the L5 nerve root is a risk of being contacted. The patient should be instructed to inform the interventionalist of any lower extremity pain. If this occurs the needle may need to be readjusted more cranially. The needle is then slowly advanced to the six o’clock position of the L5 pedicle. However, if a diagnostic injection is being performed, this extraforaminal location may be acceptable. One cubic centimeter of contrast may then be injected. If the contrast outlines the L5 spinal nerve and extends to the dorsal root ganglion, 1.0 cc of 2% Xylocaine may then be infused. For therapeutic selective nerve injection, combined nerve root, DRG, and epidural flow is desirable. For a transforaminal injection, placement of the medication should be along the ventral epidural space. In the presence of partial lumbarization of S1, a skin wheal is raised with 1% Xylocaine just lateral and parallel to the foramen rather than superior and lateral to the foramen.53 A 22–25-gauge, 3.5 inch spinal needle is then advanced to abut upon periosteum adjacent to the lateral aspect of the foramen to gauge depth. The needle is then redirected medially into the foramen. Contrast is then infused. Contrast should outline the S1 nerve root. In the presence of a lateral disc herniation, the involved spinal nerve and DRG is targeted. The goal is to place medication between the lateral disc herniation and the epiradicular sheath of the spinal nerve and not the nerve root.54 The spinal nerve is targeted more infe-
C
Fig. 23.21 Lateral C1–2 joint injection. (A) Lateral view with arthrogram. (B) AP view. (C) Slightly oblique view to visualize joint better. 259
Part 2: Interventional Spine Techniques
rior and at the five o’clock or seven o’clock position of the pedicle for right and left sides, respectively. On lateral view, the needle will be more ventral and inferior. With injection of contrast, distal spread should be along the ventral ramus at the level of the disc and proximally around the spinal nerve and DRG.
CERVICAL SYNOVIAL JOINTS Anatomy The C1 vertebra consists of an anterior and posterior arch that are connected by paired lateral masses. The lateral masses are concave and articulate with the occipital condyles superiorly. The atlantooccipital joint is a synovial joint with an average joint space of 1 mm on CT scan.54 The vertebral artery exits the costotransverse foramen and passes posteriorly around the lateral masses. The vertebral arteries then run along a smooth groove in the posterior arch before piercing the atlanto-occipital membrane. The C1 spinal nerve gives off the dorsal and ventral rami as it crosses inferior to the third part of the vertebral artery and just superior to the posterior arch of C1.55 The atlanto-occipital joint receives innervation from the C1 ventral ramus and not the dorsal ramus.56 The C1 dorsal ramus and vertebral artery are adjacent to the medial, posterior aspect of the atlanto-occipital joint. The superior and lateral aspect of the atlanto-occipital joint is farthest away from the vertebral artery.57 The inferior articular process of C1 articulates with the superior articular process of C2. The C1 inferior articular process is concave and points medially. The C2 superior articular process is convex and slopes laterally. The lateral C1–2 joint is also known as the lateral atlantoaxial joint and is a synovial joint. The median atlantoaxial joint is the synovial joint between the median-located facet of the anterior arch of C1 and the dens. The anterior or posterior joint gap for the lateral atlantoaxial joint is 3.5 mm but the main part of the joint is 1 mm wide.55 The lateral atlantoaxial joint is innervated by the C2 ventral ramus and not the dorsal ramus.56 The C2 spinal nerve exits the dura medial to the lateral atlantoaxial joint. The dura covers the medial half of the joint. The C2 spinal nerve quickly divides into ventral and dorsal rami. The C2 ganglion lies across the posterior medial half of the joint. The ventral ramus travels laterally across the lateral mass and vertebral artery to join the cervical plexus. The dorsal ramus passes inferior and posterior to the joint. The spinal cord is medial to the joint. Dreyfuss evaluated the location of the internal carotid artery to the atlanto-dental space.58 Fifty lateral internal carotid artery angiograms were reviewed with variation in the anteroposterior position.58 In the majority, the ICA was anterior to the atlanto-dental interval. Occasionally, arterial loops or curves in the ICA juxtaposed the artery to the lateral anterior atlantoaxial joint and posterior to the atlanto-dental interval. There were no cases with the ICA at the mid or posterior part of the atlantoaxial joint.58 Dreyfuss also reports the occipital artery frequently passes anterior to the midlateral lateral atlantoaxial joint space and rarely the external carotid artery anterior to the joint.58 Posterior to the lateral atlantoaxial joint are the C2 ganglion, anterior posterior ramus, dural sac, venous plexus, and posterior musculature, subcutaneous tissue, and skin. As the dorsal rami of C1 and C2 do not supply the atlanto-occipital or atlantoaxial joints, blockade of these nerves is not discussed. Additionally, the proximity of the vertebral artery to the C1 dorsal ramus makes this unsuitable for blockade.56
Technique Atlanto-occipital joint The technique as described by Dreyfuss et al. is utilized.57 The patient is placed in a lateral decubitus position. The head is rotated 30 degrees down to the table and the neck flexed. The mastoid pro260
cess and occipital prominens are palpated. An indelible skin marking pen is used to mark the location of these two structures. Between these two structures one then palpates a cleft. The skin is once again marked. The neck is prepped and draped in the usual sterile fashion. A metal pointer is placed over the cleft. The head is then rotated up or down from the table and the neck flexed and extended until the cleft overlies the most superior, lateral, and posterior aspect of the atlantooccipital joint.57 The occipital brim must also be superior to this target location. In some cases, the occipital brim may overlie the target location. Moving the neck into flexion and extension should be tried to avoid this. If unavoidable, the skin wheal is located slightly below the target location and occiput. At the target position – superior, lateral, and posterior aspect of the joint – the vertebral artery is furthest away from the joint.57 A skin wheal is raised with 1% Xylocaine. A 22–25gauge, 3.5 inch spinal needle is guided toward the target point under intermittent fluoroscopic guidance with the needle parallel to the Xray beam. The needle is advanced until bone is reached or there is 3–5 cm of needle advancement.57 The c-arm is then rotated to provide an AP open-mouth view. The needle should be just lateral and inferior to the superior-lateral aspect of the joint. If the needle is too far medial or lateral the needle will need to be withdrawn somewhat and redirected to the target position by alternating frequently between AP and oblique views. If the needle is placed too medial and inferior, there is risk of vertebral artery or dural puncture.57 Further advancement could result in cord puncture. If the needle is advanced too lateral and anterior there is risk of penetrating the internal jugular vein and vagus nerve.57 Once the needle abuts bone at the target location, the needle is walked off the joint edge into the most superior-lateral joint space. After negative aspiration, tubing containing contrast agent is attached to the needle. Position of the needle is rechecked to ensure the needle was not moved when attaching the tubing. Then 0.2 cc of contrast is injected and should demonstrate an arthrographic pattern with no vascular or soft tissue flow. If soft tissue or vascular flow occurs, stop injecting contrast immediately. Remove the tubing and replace the needle stylus. The needle is withdrawn back to the edge of the joint/ target location. The needle is then walked off the joint edge into the joint. After negative aspiration, the tubing is reconnected and contrast is once again instilled. Once an arthrogram is obtained without vascular flow or soft tissue pattern, medication is instilled. For diagnostic injection, 0.5 cc of 1% Xylocaine or 0.5% bupivacaine is instilled. For therapeutic injections, 0.8 cc of Dexamethasone or Celestone Soluspan mixed with 0.2 cc of 1% Xylocaine is infused. Injection is done until resistance is reached or 1.0 cc is instilled. The joint volume is 1–1.2 mL.59
Lateral atlantoaxial synovial joint The patient is placed in the prone position on the fluoroscopy table. A pillow is placed under the chest and a cushion under the forehead. The height of the pillow and cushion can be adjusted to place the spine in neutral and allow the patient to breathe comfortably. In the AP view, bilateral C1–2 joints should be visualized. The joints should appear symmetric bilaterally to ensure the joint is in the AP position with no rotation. The c-arm is rotated in a cranial or caudal direction to optimally visualize edges of both the inferior articular process of C1 and the superior articular process of C2. Sometimes the mandible, teeth, or dental work may obscure visualization of the joint. Movement of the c-arm, the patient’s head in flexion or extension, or opening the mouth may help improve joint visualization. Once the joint is well visualized in the AP position, a metal pointer is placed over the target area – the juncture between the middle and lateral third of the C1 inferior articular process. A skin wheal is raised with 1% Xylocaine overlying the target. A 22–25-gauge, 3.5 inch spinal needle is advanced under intermittent fluoroscopy parallel to the X-ray beam. The needle needs to be kept at the juncture of the middle
Section 2: Interventional Spine Techniques
and lateral third of the joint. If the needle is directed to the medial half of the joint, dural puncture can occur. If the needle is lateral to the joint, vertebral artery puncture can occur. If the superior articular process of C2 is targeted, there is a risk of C2 ganglion penetration. The needle is slowly advanced until the needle abuts bone of the inferior articular process of C1. The needle is then withdrawn a couple of millimeters and redirected inferiorly a couple of millimeters into the joint. Needle position is then checked in the lateral plane. The c-arm is then rotated back to the AP position. Tubing filled with contrast is connected to the spinal needle and 0.2 cc are injected. Contrast should demonstrate an arthrographic pattern (Fig. 23.22). For diagnostic injections, 0.5 cc of 1% Xylocaine or 0.5% bupivacaine is then infused. The double-block paradigm should be followed. For therapeutic injections, 0.8 cc of Celestone Soluspan or dexamethasone mixed with 0.2 cc of 1% Xylocaine are infused. Injection is done until resistance is reached or 1.0 cc of the mixture is infused.
ZYGAPOPHYSEAL JOINT INJECTIONS The zygapophyseal joints are a potential source of axial pain. The joints have been shown to contain nociceptive fibers and mediators.60–62 The prevalence of pain due to the zygapophyseal joints is unknown. Schwarzer et al.63 performed both discography and zygapophyseal joint injections in suffers with chronic low back pain and found pain emanating from these joints in 14%.63 In a second study of 176 sufferers with chronic low back pain, Schwarzer et al.64,65 reported 15% with Z-joint pain based upon diagnostic Z-joint injections utilizing a doubleblock method. In the cervical spine, skilled physical examiners have demonstrated some ability to diagnose Z-joint pain utilizing manual techniques.66 However, in the lumbar spine both history and physical examination have not been reliable in diagnosing Z-joint pain.64,65,67 Radiographic studies also have been unreliable in diagnosing Z-joint pain as abnormalities on imaging studies have been demonstrated in asymptomatic subjects. The current standard for diagnosing Z-joint pain is by diagnostic intra-articular Z-joint injections or medial branch blocks. A double-block paradigm has been recommended to avoid falsepositive diagnostic injection.5,7 The false-positive rate for single diagnostic intra-articular Z-joint injection or medial branch block in the lumbar spine is 38% with a positive predictive value of 31%.7 In the cervical spine the false-positive rate was 27% for single blocks.5 In these studies
the patient had to have definite relief with Xylocaine but 50% relief with bupivacaine. Reproduction of pain with injection is not diagnostic.68 The double-block paradigm was described earlier and should be followed. The correct response is to have longer relief with bupivacaine compared to Xylocaine. If the patient has longer relief with Xylocaine over bupivacaine, the test is a false-positive. False-negative medial branch blocks occurred in 11% of subjects with experimentally induced lumbar Z-joint pain.69 One explanation has been venous uptake of medication with medial branch blockade.69 Additionally, the stricter criteria of 80% relief we propose may increase the false-negative rate. In the presence of Z-joint pain a therapeutic intra-articular injection with corticosteroid may be performed. However, some consider this treatment controversial. At the Penn Spine Center, we routinely offer intra-articular steroid injection prior to considering more aggressive treatments. Of course, the injection is combined with physical therapy that does not stress the joint and, lastly, the patient is expressly prohibited from performing activities that will stress the joint. In the absence of a steroid effect, or if the treatment fails, radiofrequency ablation of the medial branches supplying the involved Z-joint is a viable alternative.
Anatomy The zygapophyseal joints are paired joints in the posterior spinal column and form part of the three-joint complex of the spine. The intervertebral disc is the third joint. The zygapophyseal joints are diathrodial joints with hyaline cartilage, a fibrous joint capsule, synovial membrane, and joint space. The joint capsule blends with the ligamentum flavum at the medial and superior aspects.70
Cervical The cervical pillar is made up of the superior and inferior articular processes of the zygapophyseal joints. From C3 to C7, the superior articular processes are directed upward and backward and the inferior articular processes downward and forward.71 The joints are angled approximately 45 degrees from the coronal plane. The joints are angled 30–50 degrees from the transverse plane.72 The C2–3 Z-joint is oriented more vertical and medial.73 In the cervical spine from C4 to C8, the posterior primary ramus crosses the root of the transverse process. As it crosses the transverse process it divides into the medial and lateral branches. The medial branch curves around the waist of the articular pillar and is covered by tendinous slips from the semispinalis capitis.56 These tendinous slips are equivalent to the mamilloaccessory ligament seen in the lumbar region.56 Articular branches from each of the C4–8 medial branches will innervate the Z-joint above and below.56 At C3, the dorsal ramus divides into a superficial and deep medial branch. The superficial medial branch is the third occipital nerve and innervates the C2–3 Z-joint. The deep medial branch supplies the C3–4 Z-joint and follows the same path around the waist of the articular pillar as more inferiorly located cervical medial branches.
Thoracic
Fig. 23.22 Cervical Z-joint injection. Needle in joint with arthrogram.
The thoracic Z-joints run from C7–T1 to T12–L1. The first thoracic segment more closely resembles the cervical spine and T11–12 resembles the lumbar spine.71 The thoracic articular processes are in the coronal plane with the superior articular process anterior. The joints are rotated from the coronal plane with the lateral aspect anterior and medial aspect of the joint posterior. Quantitative analysis of the thoracic Z-joint shows the approximate rotation from the sagittal to be 16 degrees.72 The rotation from the transverse plane at T6 is approximately 74 degrees.72 Rossi and Pernak74 report the thoracic dorsal ramus courses differently than in the cervical and lumbar spine. The thoracic dorsal ramus crosses the inferior instead of the superior aspect of the 261
Part 2: Interventional Spine Techniques
transverse process.74 The initial course of the dorsal ramus is through an osseoligamentous tunnel. The tunnel is formed by the transverse process superiorly, neck of the rib inferiorly, superior costotransverse ligament laterally, and the Z-joint capsule medially.74 The nerve then courses laterally through the space formed by the anterior and posterior lamella of the superior costotransverse ligament.73,75 After exiting this space, the dorsal ramus divides into medial and lateral branches. The medial branch crosses the transverse process and underneath and medial to the multifidus and semispinalis muscles. The medial branch courses through another osseofibrous tunnel along the posteromedial border of the costotransverse joint.74 The medial branch supplies the joint above and below along with the mutlifidus and semispinalis.73 A cutaneous branch is seen with T1–7 medial branches.74
Lumbar In the adult lumbar spine, the joint is oriented between the coronal and sagittal planes with variable curvature of the articular surface.76,77 In the fetus and infant, the joints are oriented in the coronal plane plane.78 During early childhood, the joint becomes curved and biplanar.78 The posterior aspect of the joint becomes more sagittally oriented. In adults, there is considerable individual variation and segmental variation. The joint is most often either hemicylindrical or boomerang-shape – biplanar.78 The larger concave superior articular process is juxtaposed against the convex smaller inferior articular process.78 The lumbar Z-joints are rotated from approximately 50 degrees at L1 to 28 degrees at L5 from the sagittal plan.72 In the transverse plane the lumbar Z-joints are close to 90 degrees.72 Anteromedially and superiorly, the joint capsule blends with the ligamentum flavum.70,78 Laterally, the intertranverse ligament has two layers that are just dorsal and lateral to the ligamentum flavum.79 The ventral layer extends lateral to the intervertebral foramen and ventrally along the vertebral body to the anterior longitudinal ligament.79 Posteriorly, the fibrous capsule is reinforced by a fascicle from the multifidus muscle that runs from the spinous process to the mammillary process.78,79 The multifidus muscle covers the joint posteriorly and has attachments to the superior articular process but not the inferior articular process.79 The fibrous capsule posteriorly is contiguous with the cartilage of the superior articular process. The fibrous capsule blends with fibrocartilage which then transitions to hyaline cartilage.78 The superior and inferior recesses of the joint capsule have loose capsular fibers that are incomplete where the neurovascular bundle enters the joint.78 The inferior recess is larger than the superior recess.70 Large synovially lined adipose tissue fill the joint recesses and project into the joint space as synovial folds or villi.70,78 The folds can be fibrous and compressed between the articular surface as meniscoid inclusions.78 The role of these menisci in pain generation is unclear.80 The superior articular process has a bony process on the dorsolateral aspect called the mammillary process.81 On the dorsal surface of the transverse process is an accessory process.81 The mammilloaccessory ligament runs from the mammillary process to the accessory process.70,81 The band can become ossified and forms a tunnel.70,81 The medial branch of the posterior primary ramus passes through the tunnel. The proximal branch hugs bone, running through the groove formed by the junction of the superior articular process and the transverse process. At this level the medial branch innervates the Z-joint and continues as the descending branch, passing medially and inferiorly to the superior-medial joint capsule below.70,81–83 An ascending branch arises just anterior to the intertransverse fascia and ascends to the posterior aspect of the joint above.70,81 This holds for the medial branches of L1 to L4. For L5, the dorsal ramus travels around the superior articular process of S1 and the sacral ala with the medial branch arising opposite the inferolateral corner of the base of the L5–S1 Z-joint.84 262
Injection technique Intra-articular Cervical A posterior approach has been described.78 The patient is placed in a prone position on the fluoroscopy table with a pillow under the chest, placing the neck in slight flexion. The needle is advanced from an inferior and lateral approach at 45 degrees towards the cervical pillar. Frequent rotation between PA and lateral must be done to avoid inadvertent medial or lateral placement. Directing the needle too medial result in interlaminar penetration with dural or cord puncture. Directing the needle too lateral and ventral could result in vascular penetration. The lateral approach to the cervical Z-joints is simpler to perform, passes through less soft tissue, and is less apt to puncture cord or vertebral artery. In the lateral approach, the patient is placed in the lateral decubitus position to allow visualization of the Z-joints. A towel is placed under the head to place the spine parallel to the fluoroscopy table. Make sure the head is not too high to avoid neck lateral bending with resultant joint space closure. Additionally, avoid shrugging of the shoulders, as the glenohumeral joint will obscure fluoroscopic Z-joint visualization. The neck is prepped and draped in the usual sterile manner. In the lateral view, one counts from the level of the odontoid process to determine the correct level. Once this is established, one has to determine the correct side. In the lateral view, the Z-joints from the right and left side overlap. Before proceeding, the interventionalist must determine which joint is closest to the surface. Failure to determine this can result in catastrophic consequences. Mistakenly targeting the contralateral joint could lead to spinal cord puncture as the needle is passed through the spine to get to the opposite side. To determine which joint is closest, the patient or the gantry angle of the X-ray beam often will have to be rotated forward and backwards on the fluoroscopy table. As the patient is rolled anteriorly, the proximal joint will move anteriorly. As the patient is rolled posteriorly, the proximal joint will roll posteriorly. Once the correct level and side are established, a metal pointer is placed over the midportion of the inferior articular process of the superior vertebra. A skin wheal is raised with a 10:1 mixture of 1% Xylocaine and 8.4% bicarbonate, though some interventionalists skip this step. A 22–25-gauge, 1.5–2.5 inch spinal needle is inserted parallel to the X-ray beam. Under intermittent fluoroscopy, the needle is advanced to abut upon the midportion of the inferior articular process. With the lateral approach, the needle passes through skin, subcutaneous tissues, and muscle before reaching bone. Touching bone keeps the needle from advancing into the spinal canal. Care must be taken not to advance anterior to the joints as this could result in vertebral artery puncture. This is done by keeping the needle advancing straight down, parallel to the X-ray beam. Once bone is touched, the needle is withdrawn slightly and redirected 1–2 mm caudally into the joint. One may feel the needle walk off the inferior articular process into the joint. Often, there is loss of resistance at the tip of the needle with a sensation of the needle being hugged on the sides by the joint wall. Care must be taken not to advance the needle more than a few millimeters to avoid placing the needle through the joint with subsequent dural puncture or injury to joint cartilage. Once the needle is in the joint, 0.2 cc of non-ionic contrast agent (Isovue or Omnipaque) is injected. An arthrogram confirms proper placement (see Fig. 23.22). If a soft tissue pattern occurs, do not inject additional contrast agent to avoid obscuring the joint line. The needle can be viewed in the lateral and oblique planes to determine whether the needle needs just slight adjustment or a return to the starting position on the inferior articular process. If a return to the starting position is required, the needle may be redirected to a different part of the joint when osteophytic ridging is precluding entrance into the joint. Typically,
Section 2: Interventional Spine Techniques
one redirects to the posterior half of the joint as this is safer. The anterior aspect of the joint is closer to the vertebral artery and spinal nerve. The needle is once again walked 1–2 mm into the joint. Nonionic contrast agent, 0.2 cc, is instilled. Once an arthrogram pattern is obtained, injection of medication can be done. Yet another option is to approach the joint with an anterolateral approach with the patient in the supine position. In a diagnostic injection, the double-block paradigm as described earlier is followed. The patient is blinded to the medication utilized. When comparative blocks are performed, the patient receives either 1% Xylocaine or 0.5% bupivacaine. A volume of 0.5–0.7 cc is utilized. Care must be taken to avoid total volumes of contrast and anesthetic agent greater than 1.0 cc which can lead to capsular rupture and subsequent leakage.85 If the patient has 80% relief, the patient should also perform maneuvers that typically aggravate the pain. If the patient continues with 80% relief, the diagnostic injection is positive. If the patient passes the double-block paradigm, the Z-joint is diagnosed as the source of pain. A therapeutic Z-joint injection may be performed. A therapeutic injection is done with a mixture of 0.2 cc of 1% Xylocaine and 0.8 cc of either Celestone Soluspan or dexamethasone. Therapeutic injections may be repeated at 2-week intervals, with no more than 3–4 in a 6–12-month period. However, therapeutic injections are controversial. Since this chapter is limited to the discussion of techniques, the reader is redirected to the appropriate chapter regarding indications and contraindications.
Thoracic The patient is placed in the prone position on the fluoroscopy table. The back is prepped and draped in the usual sterile manner. To locate the proper level, one should count from C1. The technique as described by Dreyfuss is utilized.86 It is important that the level being targeted is in an AP position; the left and right pedicles should appear symmetric and the spinous process should be directly midline. A skin wheal is raised with 1% Xylocaine overlying the pedicle inferior to the targeted pedicle. For example, if the T5–6 Z-joint is targeted, the skin wheal is raised over the pedicle of T7. A 22- or 25-gauge, 3.5 inch needle is then inserted at 30–45 degrees from the skin surface. The needle is advanced along this plane, targeting the middle to inferior half of the inferior pedicle in the midline of the pedicle. In a T5–6 Z-joint, this would be the pedicle of T6. The spinal needle is kept in the midline of the targeted pedicle. The midline is a line drawn from the twelve o’clock and six o’clock position of the pedicle. By staying in midline, the spinal needle passes through muscle and will then strike bone. If one deviates too medially, there is a risk of dural and spinal cord puncture. If the needle deviates too laterally, there is a risk of puncture of the lung pleura and spinal nerve. Once bone is touched, the c-arm is rotated to the lateral view. The needle should be adjacent or just inferior to the inferior aspect of the targeted Z-joint. If the needle is too cephalad and dorsal to the joint, the needle will need to be withdrawn and positioned inferiorly. If the needle is inferior to the joint, the c-arm is rotated back to the AP position. The AP position is safer for needle advancement, as the line between the twelve and six o’clock positions on the pedicle can be visually maintained. In the AP position, one can rotate the bevel of the needle to face ventrally. This facilitates the needle gliding along bone from the pedicle onto the superior articular process and wedging into the inferior aspect of the Z-joint. The needle can also be directed slightly medially to pierce the dorsomedial capsule.86,87 Fortin and Mckee recommend a gentle bend of approximately 15 degrees of the distal one-half inch of the needle with the bevel directed away from the bend.87 The bend allows the needle to conform to the slope of the joint. The apex of the bend can be utilized as a fulcrum to redirect the needle.87 Correct positioning of the needle should be confirmed on lateral view with the needle in the inferior aspect of the joint.
Non-ionic contrast, 0.2 cc, is then injected. Contrast on the AP view will form a circle filling the inferior and superior capsular recesses. In the lateral view there should be linear arthrogram (Fig. 23.23). Two separate studies have reported on the volume of the thoracic Z-joint. The first suggested the volume of the joint to be less than 0.8 cc.87 The second study reported thoracic Z-joint volumes of 0.4–0.6 cc.88 Dreyfuss et al.88 noted epidural spread occurred in 2/40 joints injected in 9 subjects. To avoid capsular rupture and reduce the risk of epidural spread, the volume injected is only 0.5 cc.86 In a diagnostic injection, 0.5 cc of 1% or 2% Xylocaine or 0.5% bupivacaine is injected. If a diagnostic block is positive, the patient is a candidate for a therapeutic injection, though some prefer comparative blocks to be positive prior to injection of steroid intra-articularly. When radiofrequency ablation is considered, a double-block paradigm should be followed; either comparative or placebo controlled. For a therapeutic intra-articular injection, 0.5–1.0 cc of a 1:1 mixture of anesthetic and steroid is infused. Injection is completed until resistance is reached or 1.0 cc total volume is instilled.
Lumbar Mooney and Robertson first described in the English literature the technique of fluoroscopic intra-articular Z-joint injection.83 The patient is placed on the fluoroscopy table in a prone position. A pillow may be placed under the abdomen to flatten the spine and open up the joint, though many practitioners do not do this. If performing injections unilaterally, the patient can alternatively be placed in the prone–oblique position. The back is prepped and draped in the usual sterile fashion. The lumbar Z-joint are often curved and obliquely oriented.89 The c-arm is rotated into the oblique position to allow visualization of the Z-joints, approximately 45 degrees for the L4–5, L5–S1
A
B Fig. 23.23 Thoracic Z-joint injection. (A) AP view. (B) Lateral view. 263
Part 2: Interventional Spine Techniques
Z-joints and 30 degrees for upper lumbar Z-joints.90 Because of the curved appearance, over-rotating the c-arm will result in visualization of the anterior joint space. If a needle is directed to the anterior joint space, the needle will strike the dorsal side of the inferior articular process and not enter the joint.70 The c-arm should be rotated until the posterior wall is just visualized (Fig. 23.24).70,91 A skin wheal is raised with 1% Xylocaine just medial to the joint line of the inferior articular process. With the superior articular process curved around the inferior articular process, entry from lateral to medial will result in the needle tilted away from the joint space and will not allow entrance into the joint. A 22- or 25-gauge, 3.5–5 inch spinal needle is then advanced under fluoroscopic guidance to abut upon the inferior articular process at the inferior aspect of the joint (Fig. 23.25). The needle is then advanced laterally to pierce the inferior subcapsular recess. Alternatively, the superior subcapsular recess can be targeted (Fig. 23.26). The disadvantages of targeting the superior capsular recess are the recess is smaller92 and the spinal nerve is adjacent to the superior aspect of the joint. With the needle situated in the inferior or superior recess, 0.2 cc of non-ionic contrast is infused. Contrast may demonstrate filling in the superior recess, inferior recess, diverticula of the
A
B Fig. 23.26 Lumbar Z-joint-superior approach. (A) Needle in superior capsular recess with image rotated more obliquely demonstrating contrast in superior and inferior capsule. (B) Needle on edge of inferior articular process with contrast in superior and inferior capsular recess.
Fig. 23.24 Lumbar Z-joint oblique view. C-arm rotated until posterior wall just visible.
Fig. 23.25 Lumbar Z-joint: inferior approach. Needle within inferior aspect of joint with contrast in inferior capsular recess, superior capsule, and classic arthrogram. 264
recess,92 linear arthrogram, S-shaped configuration, or any combination of the above. Capsular leakage with epidural spread may also be noted.66,68,75,90,91,93 Small volumes of contrast should be utilized to avoid filling the joint and prohibiting further injection of anesthetic or steroid medication.88,94 Additionally, larger volumes can result in capsular rupture. Destouet et al.77 noted rupture of the superior or inferior recess when injection contrast volumes were 0.5–1.5 cc. Dory92 also noted frequent rupture, most frequently at the inferior recess and medially into the epidural space. Dory injected contrast volumes of 1–3 mL.92 Raymond and Dumas reported no extravasation with total volumes of contrast and anesthetic less than 1.0 cc.95 With confirmation of placement, a diagnostic injection can be done with instillation of 0.5 cc of 2% Xylocaine or 0.5% bupivacaine.7,96 Even with these lower volumes, capsular leakage may occur.68 Injection is completed until resistance is reached – to avoid capsular rupture – or 0.5 cc is infused. Capsular leakage is particularly undesirable in diagnostic injections. Leakage into the epidural space could hypothetically result in anesthetizing the sinuvertebral nerve. A false-positive injection could then occur in the presence of discogenic low back pain. Also, to reduce false-positive diagnostic injection, the double-block paradigm should be utilized. If the patient had the appropriate response with the double-block paradigm, a diagnosis of pain emanating from the zygapophyseal joints can be made. In that scenario the patient may be a candidate for radiofrequency ablation. Some authors would perform an intra-articular Z-joint steroid injection before considering radiofrequency ablation. However, this is controversial. With a therapeutic Z-joint injection, the technique is exactly the same. Instead of just anesthetic agent, 0.5–1.0 cc of a 1:1 mixture of 1% Xylocaine and Celestone Soluspan or Kenalog is instilled. Injection is completed until resistance is reached or a total volume of 1.0 cc is infused. Intra-articular injections are considered more effective than periarticular injections.97
Section 2: Interventional Spine Techniques
Medial branch blocks These are simpler to perform than intra-articular injections. The disadvantages of medial branch blocks are two needle punctures need to be performed and the injections are diagnostic only and carry no therapeutic benefit.
Cervical To anesthetize a cervical zygapophyseal joint from C3 to C7 two medial branches need to be blocked. For example, for the C3–4 joint, the C3 and C4 medial branch is blocked. Two approaches can be used to block the medial branch, a posterior or a lateral approach. In the posterior approach the patient is placed in a prone position on the fluoroscopy table. A pillow is placed under the chest and a cushion under the forehead to place the cervical spine in a neutral position and allow the patient to breathe comfortably. The level to be injected is localized by counting caudally from C1 or C2. The level of interest should be checked to ensure it is in a pure AP view. The waist of the cervical pillar targeted as the medial branch is consistently located here.98 A skin wheal is raised with 1% Xylocaine just lateral to the waist of the cervical pillar. A 22–25-gauge, 2.5–3.5 inch spinal needle is advanced under intermittent fluoroscopy in a slight lateral to medial angle to abut upon the posterior aspect of the cervical pillar waist. Touching bone on the posterior cervical pillar guards against advancing the needle too ventrally. If the needle is recklessly advanced ventrally there is the possibility of spinal nerve, internal jugular vein, and carotid artery puncture. Care must be taken not to advance too medially and superiorly as a dural puncture can occur. Once bone is touched on the posterior cervical pillar, the needle is slightly withdrawn and redirected laterally to abut bone of the lateral waist of the cervical pillar. Needle position is checked in
A
C
the AP and lateral view. Two-tenths of a cubic centimeter of contrast is infused to confirm needle placement and should demonstrate a soft tissue pattern with no vascular flow. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is then infused. The advantage of the posterior approach is that bilateral procedures are easily performed without having to reposition the patient. The lateral approach is preferred over the posterior approach as the lateral approach is simpler to perform. Additionally, since the needle passes through less soft tissue, there is less patient discomfort compared to a posterior approach. To perform a bilateral procedure, the patient would have to move from one lateral decubitus position to the other and be re-prepped and draped. However, this is only a minor inconvenience. When using the lateral approach, the patient is placed in a lateral decubitus position on the fluoroscopy table.99 The head is placed on a cushion or towel roll to position the spine in a neutral position. The neck is prepped and draped in the usual sterile fashion. The level to be injected is determined by counting from the odontoid process. A skin wheal is raised with 1% Xylocaine overlying the centroid of the cervical pillar. For example, with a C4 medial branch block, the centroid position of the C4 cervical pillar is targeted (Fig. 23.27A). A 22–25-gauge, 1.5–2.5 inch spinal needle is advanced parallel to the X-ray beam to abut upon the cervical pillar in the centroid position. In the lateral position, the spinal needle passes through skin, subcutaneous tissue, muscles, and then abuts bone. Non-ionic contrast, 0.2 cc, is injected to confirm needle placement. Contrast should demonstrate a soft tissue pattern with no vascular flow. Barnsley and Bogduk99 studied contrast patterns. Contrast was most dense over the centroid target site and covered at least 5 mm along the medial branch. Contrast did not flow anteriorly to the ventral ramus or spinal nerve. Contrast tended to flow posterosuperiorly along the semispinalis capitus muscle and occasionally superior to the multifidus (Fig. 23.27B,C).99
B
D
Fig. 23.27 Cervical medial branch block: lateral approach. (A) Needle in centroid position. (B) Lateral view of contrast with typical soft tissue pattern. (C) Needle in waist of pillar with contrast in typical soft tissue pattern. (D) Oblique view: no contrast into the foramen or epidural space. 265
Part 2: Interventional Spine Techniques
After contrast demonstrates proper placement, 0.5 cc of 1 or 2% Xylocaine or 0.5% bupivacaine is then slowly injected (over 30 seconds). Attention should then be addressed to the adjacent medial branch. To block a cervical zygapophyseal joint from C3 to C7, the two adjacent medial branches need to be blocked. For example, to block the C3–4 Z-joint the C3 and C4 medial branches need to be blocked. To block the C2–3 joint, the third occipital nerve is targeted.99,100 A technique with the patient in the prone position has been described.98,100 In this technique, under PA fluoroscopic guidance the lower half of the C2–3 joint is targeted. Once the posterior aspect of the joint is touched by the needle, the needle is redirected laterally along the lower half of the C2–3 joint, touching bone. The nerve is blocked in three locations: midpoint of the convexity, lower end, and midway between the other two.100 A lateral approach is simpler to perform. The third occipital nerve is blocked in three locations. Injections of 0.5 cc of local anesthetic are performed along a vertical line that bisects the superior articular process of C3 at a point just superior to the inferior subchondral plate of C2, just inferior to the superior subchondral plate of C3, and a point midway between the two points.5 The block is done with the patient in the lateral position on the fluoroscopy table. A towel roll is placed under the head to position the spine in neutral. The C2–3 joint is located. The c-arm may need cranio-caudal tilt and rotation of the patient anteriorly or posteriorly to find the joint space. A skin wheal is raised with 1% Xylocaine overlying the midpoint of the C3 pillar in the lateral view. Along the axis of this point in a cranial and caudal line injections are performed in three positions. A 22–25-gauge, 1.5–2.5 inch spinal needle is advanced parallel to the X-ray beam to abut upon the inferior subchondral plate of C2. Two-tenths of a cubic centimeter of contrast is injected to confirm needle placement. Contrast should demonstrate a soft tissue pattern with no vascular flow. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is slowly injected. The needle is then slightly withdrawn and redirected caudally to abut upon the superior subchondral plate of C3. Two-tenths of a cubic centimeter of contrast is infused and should demonstrate a soft tissue pattern with no vascular flow. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is then slowly injected. The needle is then slightly withdrawn and redirected cranially at a point midway between the two previous injections. The needle should abut bone. Two-tenths of a cubic centimeter of contrast is then infused to ensure proper placement as previously. Half a cubic centimeter of 1 or 2% Xylocaine or 0.5% bupivacaine is then infused slowly. The needle is withdrawn and a bandage placed. Anesthesia of the third occipital nerve, indicating adequate block, can be tested by checking for numbness in the suboccipital region just lateral to midline.5,98 After diagnostic block, the patient is assessed for pain relief. The patient should perform activities that typically would increase pain. If the patient has 80% relief, the injection is considered positive. As previously mentioned, most practitioners perform a double-block paradigm prior to completing a therapeutic injection or radiofrequency ablation. At the Penn Spine Center, our preference is to use history and examination skills to increase the prevalence of the disorder in the population of patients that may undergo a therapeutic intra-articualr injection. When those skills are employed, a single diagnostic block is sufficient for us to perform an intra-articular glucocorticoid injection. If the patient fails to improve, we use a placebo-controlled paradigm to determine whether radiofrequency ablation is warranted. This conceptual framework is used for cervical, thoracic, and lumbar Z-joint injections and will not be repeated in the following subsections.
Thoracic The technique of thoracic medial branch block is utilized as described by Stolker et al.101 The patient is placed in a prone position on the fluoroscopy table. The c-arm is rotated 20–30 degrees to visualize the juncture of the superior articular process and the transverse process. 266
The rib of same level passes anterior to the juncture of the transverse process and SAP. To block a zygapophyseal joint, the adjacent two medial branches must be blocked. For example, to block the T7–8 Z-joint, the medial branch of T6 and T7 must be blocked. A skin wheal is raised with 1% Xylocaine superior and slightly lateral to the target. A 22–25-gauge, 3.5 inch spinal needle is advanced caudally and slightly inferiorly, targeting the juncture of the SAP and transverse process. Once bone is struck, the needle is checked in the AP plane and lateral planes. Two-tenths of a cubic centimeter of contrast is then instilled and should demonstrate a soft tissue pattern with no vascular flow. Two-tenths to 0.5 cc of 2% Xylocaine is slowly infused. The authors of this technique acknowledge that the course of the medial branch in the thoracic spine has not been adequately studied. They hypothesize the medial branch will follow a similar course in the thoracic spine as it does in the cervical and lumbar spine.101 However, Rossi and Pernak74 state the course of the medial branch passes inferiorly, not superiorly, across the transverse process.
Lumbar To block a lumbar Z-joint the two adjacent medial branches need to be blocked. For example, to block the L4–5 Z-joint, the L3 and L4 medial branches need to be blocked. For L5–S1 Z-joint, the L4 medial branch and L5 dorsal ramus is blocked. The L5 dorsal ramus runs in the groove at the juncture of the SAP of S1 and the sacral ala. Additionally, the L5–S1 Z-joint receives supply from a small branch of the S1 dorsal ramus, though this branch is not considered important to anesthetize the joint.90 The patient is placed in a prone position on the fluoroscopy table. The c-arm is rotated to allow visualization of the juncture between the SAP and transverse process. A skin wheal is raised with 1% Xylocaine superior and lateral to the target point. A 22–25-gauge, 3.5 inch spinal needle is utilized. For larger patients, a 22-gauge, 5 inch spinal needle or two-needle technique is used. Under intermittent fluoroscopic guidance, the spinal needle is advanced until it abuts upon the juncture of the base of the SAP and transverse process (Fig. 23.28A). Avoid placing the needle near the superior border of the transverse process and higher up on the SAP, as this increases the chance for medication to flow around the spinal nerve, foramen, or epidural space.84 The needle bevel should be directed inferiorly and medially to prevent spread to the spinal nerve, foramen, or epidural space.84 Even with excellent technique, there is a 15% incidence of contrast spread extending to the spinal nerve, foramen, or epidural space.84 However, the amount of anesthetic agent that would reach the spinal nerve or enter the epidural space is postulated to be unlikely to be sufficient to anesthetize the spinal nerve or nerve root.84 Confirmation is established by injection of 0.2 cc of contrast, which demonstrates a soft tissue pattern with no vascular flow (Fig. 23.28B,C). Venous uptake of contrast has been demonstrated in medial branch blocks and can result in a false-negative study.69,84 If venous uptake occurs, the needle should be repositioned. Non-ionic contrast infusion should demonstrate no venous uptake. There should be no contrast flow into the foramen, spinal nerve, or epidural space. With proper placement, 0.5 cc of 0.5% bupivacaine or 2% Xylocaine is slowly infused. Speed of infusion has been demonstrated to not affect aberrant flow to the foramen, spinal nerve, and epidural space.84 However, slower infusion tends to be more comfortable for the patient. Attention is then addressed to the next level. The same technique is utilized. After blocking the medial branches supplying a zygapophyseal joint, the patient is assessed 15–20 minutes postprocedure. If the patient has 80% pain relief from pre- to post-block, the patient is asked to perform activities that would typically aggravate symptoms. If the patient continues with 80% relief, the initial injection is considered positive. The patient is asked to keep a pain dairy as previously discussed. The patient then
Section 2: Interventional Spine Techniques
A
C
B
Fig. 23.28 Lumbar medial branch block. (A) Needle at juncture of transverse process and superior articular process on oblique view. (B) AP view of needle placement. (C) Typical soft tissue pattern with instillation of contrast.
returns for a repeat diagnostic injection following the double-block paradigm. Figure 23.29 demonstrates an L5 dorsal ramus injection.
used to treat the radicular pain that can ensue when a cyst is present. This is not treatment for axial pain of Z-joint etiology.
Special situations
Lumbar spondylolysis
Synovial cyst To aspirate a synovial cyst, the same technique as used for Z-joint injections is performed. However, a larger-gauge needle is recommended to facilitate aspiration of the cyst. A 20-gauge spinal needle is usually adequate to aspirate the cyst but still allow advancement into the Z-joint. After contrast confirms placement within the Z-joint, aspiration of the cyst is attempted. A 10 cc syringe is attached to the spinal needle and the plunger pulled back to aspirate fluid. Slightly advancing or withdrawing and rotating the needle may facilitate aspiration, as the needle can abut against bone, cartilage, or joint capsule, inhibiting aspiration. Be careful not to advance the needle through the joint with resultant dural puncture. The fluid aspirated should be consistent with joint fluid – straw colored, clear, and viscous. After aspiration is complete, 0.5 cc of a 1:1 mixture of local anesthetic and steroid is infused. If this technique fails to provide symptom relief, one should consider expanding the cyst beyond its capacity so that it ‘ruptures.’ If this technique is pursued, the patient should be informed that there may be a temporary increase in pain as the cyst expands. This will typically irritate and/or compress the adjacent root until the cyst ruptures. In over 50 cases using this technique no permanent nerve pain has resulted. The success rate remains to be reported, but preliminary observations suggest it is in excess of 60%. Finally, it must be emphasized that either aspiration or cyst rupture is
A
B
In the presence of a pars fracture, injection into the adjacent Z-joint can result in spread of medication into the pars fracture.91,92 Maldague et al.91 demonstrated communication between the Z-joint and pars fracture in 11 subjects. In 9 subjects, contrast extended through a channel from the pars to the adjacent Z-joint. In the presence of bilateral spondylolysis, a channel may communicate with bilateral Z-joints.91 Additionally, channels can occur between a pars fracture and the Z-joint above.91 When injecting a Z-joint adjacent to a pars fracture, one must be cognizant that medication may communicate with the pars fracture. If this occurs, a false-positive diagnostic Z-joint injection may occur. The pars fracture can be a source of low back pain as the pars fractures do contain nociceptive fibers and neuromediators.102,103 However, the exact innervation of pars fractures is unknown. Whether the adjacent medial branch supplies the pars fracture is not known. In the presence of a pars fracture, medial branch blockade may not be specific to pain emanating from the Z-joint. The pars fracture has been injected diagnostically to select patients for surgical treatment.104–106 When performing a pars fracture injection, the patient is placed in a prone position on the fluoroscopy table. The back is prepped and draped in the usual sterile fashion. The carm is rotated to visualize the pars fracture through the neck of the ‘Scottie dog.’ A skin wheal is raised with 1% Xylocaine overlying the superior edge of the fracture. A 22–25-gauge, 3.5 inch spinal needle
Fig. 23.29 L5 dorsal ramus block. (A) Needle at juncture of sacral ala and superior articular process of S1. (B) Contrast demonstrates typical soft tissue pattern on AP view. 267
Part 2: Interventional Spine Techniques
is advanced under intermittent fluoroscopy to abut upon bone at the superior edge of the pars fracture. The needle should be advanced parallel to the X-ray beam. If the needle is too lateral and inferior, the spinal nerve can be contacted. If the needle is too medial and superior, dural puncture can occur. Once bone is touched, the needle is then redirected and advanced 1–2 mm into the fracture. Care must be taken not to advance the needle too deep as dural puncture can occur. One-tenth to 0.2 cc of contrast is then infused and should demonstrate filling within the fracture. Two-tenths to 0.5 cc of 2% Xylocaine is then slowly infused. The patient is taken to the recovery room. After 15–20 minutes the patient is assessed for the degree of pain relief as denoted by the change in the postprocedure VAS rating. In presence of a pars fracture, the interventionalist must be cognizant that diagnostic injections into either the adjacent Z-joint or pars fracture may be at risk for a false-positive result. This may be minimized by limiting injections to small aliquots or mixing the local anesthetic with contrast agent. For example, 0.5 cc of Omnipaque 300 and 0.5 cc of 4% Xylocaine could be mixed to yield a 2% strength Xylocaine injectate. If the anesthetic–contrast mixture begins to leak outside of the intended structure, the injection is stopped. As previously mentioned, the rational use of medial branch blocks to differentiate pain emanating from the Z-joint or pars fracture remains unproven. However, if patients obtained relief and passed the double-block paradigm, they may be candidates for radiofrequency ablation to alleviate back pain. However, if the patient is being selected for surgical treatment of the pars defect such as modified Scott wiring technique,104 medial branch block results would not be helpful. In patients who may undergo surgery for a painful spondylolysis, both intra-articular Z-joint injection and pars fracture diagnostic injections should be done. The patient is blinded to the structure to be blocked and the anesthetic utilized. In random order and on separate days, the adjacent Z-joint and pars fracture should be injected. In the initial step of this evaluation process, the same local anesthetic mixture should be utilized. If the patient has negative Z-joint injections but a positive pars fracture diagnostic injection, the patient then undergoes the double-block paradigm targeting the pars fracture. If the patient has the appropriate response, then the patient may undergo a therapeutic injection or be a candidate for surgical treatment. For a therapeutic injection, 0.5 cc of 1:1 mixture of steroid and local anesthetic is utilized.
SACROILIAC JOINT
Injection technique A modification of the technique described by Hendrix et al. is utilized.123 The patient is placed in a prone position on the fluoroscopy table and the back is prepped and draped in the usual sterile fashion. With the auricular shape of the sacroiliac joint, both the anterior and posterior joint will be seen on fluoroscopy. The c-arm is rotated until a lucent zone is seen at the caudal aspect of the joint (Fig. 23.30). This is the target for injection. A skin wheal is raised with 1% Xylocaine overlying the sacral bony edge adjacent to the lucent zone. A 22–25-gauge, 3.5 inch spinal needle is advanced under fluoroscopic guidance to abut upon the periosteal edge of the sacrum to gauge depth. The needle is then redirected laterally into the caudal aspect of the joint. Two-tenths of a cubic centimeter of contrast is then infused. Contrast should demonstrate an arthrographic pattern with or without filling in the inferior recess (Figs 23.31, 23.32). Diverticula or extravasation through rents in the sacroiliac joint cap-
Fig. 23.30 Sacroiliac joint. Target for injection is the lucent zone at caudal aspect of joint.
Anatomy The sacroiliac joint is an auricular-shaped diarthrodial joint with joint capsule, synovial fluid, hyaline cartilage on the sacral side, and fibrocartilage on the iliac side.107 The fibers of the joint capsule blend with supporting ligaments both anteriorly and posteriorly.108 With aging, ankylosis of the joint begins to occur in 27–50% over the age of 50.108–111 An accessory sacroiliac joint may be present in 13–35.8% of individuals.112,113 The accessory sacroiliac joint when present is at the level of the S2 foramen at the lateral sacral tuberosity and medial to the posterior superior iliac spine.112,113 The innervation of the sacroiliac joint has not been completely delineated. The sacroiliac joint is innervated by the posterior rami of the lumbosacral roots.114 The anterior joint receives innervation from L3–S2 and the superior gluteal nerve.115 The posterior joint innervation has been reported from S1–2115 and L4–S3.116 The S1 level may be the major contributor to the joint.117 Possible autonomic contribution contributes to the complexity of innervation of the sacroiliac joint.118,119 The lumbosacral trunk is just anterior to the joint in the lower third.120,121 The L4 and L5 nerve roots are 1 cm medial to the sacroiliac joint at the level of the pelvic brim.122 The L4 and L5 nerve root are 23 and 26 mm medial to sacroiliac joint and 4.0 cm above the pelvic brim.122 268
Fig. 23.31 Sacroiliac joint injection. Needle in lucent zone with contrast demonstrating arthrogram.
Section 2: Interventional Spine Techniques
the joint capsule. This is one of the reasons for limiting the volume to 2.0 cc.124 Another alternative would be to mix anesthetic and contrast together and inject under continuous fluoroscopy.127 If leakage began to occur, the injection is stopped (Fig. 23.33). A false-negative injection may occur if anesthetic agent does not reach the painful portion of the joint. This may occur if loculations in the joint exist.128 Faulty needle placement could also result in a false-negative or false-positive injection. The radiation exposure to the patient has been evaluated with the Hendrix technique. Skin exposure was 1200–3000 mR/minute. Gonad exposure was 40–60 mR/minute and 10–15 mR/minute for females and males, respectively. In comparison, an AP scout film results in 150–200 mR and 20–30 mR for females and males, respectively. Skin exposure was 500–650 mR.123 Maugars et al.129 reported fluoroscopy time of less than 1 minute to do bilateral sacroiliac joint injections with the Hendrix technique.
SACROCOCCYGEAL AND COCCYGEAL DISC Anatomy A
The distal apex of the sacrum articulates with the first coccygeal segment at the sacrococcygeal disc.71 A synovial joint instead of disc at the sacrococcygeal junction has been reported.128 The first coccygeal segment has small transverse processes and cornu, which articulates with the sacral cornu.71 The coccyx usually consists of four segments that terminates just above the anus.71 The coccyx may have only three or up to five segments.71 The first and second segment often move upon each other and have an intercoccygeal disc. The other coccygeal segments tend to be fused.130
Injection technique
B
Dynamic sitting and standing films helps in determining which level to target first.131,132 The most mobile segment should be targeted first.131,132 If there is no hypermobility detected, the sacrococcygeal disc should be targeted first and the more caudal unfused coccygeal segments next. Reviewing the lateral sacrococcygeal view also helps in planning needle direction and placement. If there is little angulation at the sacrococcygeal junction, little craniocaudal rotation will be needed. If, however, there is significant angulation or displacement of the segment to be injected, the angle and point of entry can be determined. A modification of the technique as described by Maigne et al.
Fig. 23.32 Sacroiliac joint injection: arthrograms. (A) Contrast seen in both anterior joint, posterior joint and inferior recess. (B) Arthrogram with contrast in superior aspect of joint.
sule may be demonstrated.124 Care must be taken not to advance the needle too ventrally through the inferior joint or capsular recess as the lumbosacral plexus is just anterior to the joint.120,121 With confirmation of placement, 1.0–2.0 cc of 2% Xylocaine is infused for a diagnostic injection.124,125 For therapeutic injection, 2.0 cc of steroid mixed with 1.0 cc of local anesthetic is injected. For both, injection is continued until resistance is reached or the full volume of injectate has been infused. For diagnostic injection, pain relief and not pain provocation is considered diagnostic of sacroiliac joint pain.124,126 The patient should do maneuvers that typically aggravate the pain. An 80% decrement in pain is considered positive. The false-positive rate for single sacroiliac joint injections has been estimated at 47%.6 To help minimize a placebo effect, the double-block paradigm may be utilized. Other potential causes of a false-positive injection would be anesthetizing other structures through extravasation of anesthetic through rents in
Fig. 23.33 S1 joint injection under live fluoroscopy with combined anesthetic agent and contrast. When leakage occurred, inferior joint lateral to arthrogram, the injection was stopped. 269
Part 2: Interventional Spine Techniques
is used.131 The patient is place in a prone position of the fluoroscopy table. Sterile gauze is folded and place in the cephalad portion of the gluteal cleft. This serves two purposes. The first is to separate the buttock to allow easier access to the sacrococcygeal or intercoccygeal disc. The second is to allow absorption of the cleansing solution to avoid excess dripping into the perineum. After gauze placement, the sacrococcygeal region is prepped and draped in the usual sterile fashion. For sacrococcygeal disc injection, the c-arm is rotated in a cranial or caudal direction to provide optimal visualization of the sacrococcygeal joint. A skin wheal is raised with 1% Xylocaine overlying the sacral edge of the joint. A 22–25-gauge, 2.5 inch spinal needle is advanced parallel to the X-ray beam under intermittent fluoroscopy to abut upon the edge of the sacral aspect of the joint. During advancement, it is important to keep the needle from veering off to either side of the joint to avoid inadvertent puncture of the rectum (Fig. 23.34). Once bone is touched, the needle is slightly withdrawn and redirected caudally into the sacrococcygeal disc. The c-arm is then rotated to the lateral position. The needle should be seen within the disc but not extending through the disc with risk of perforating the rectum. One-tenth to 2.0 cc of contrast is then injected to confirm needle placement. With a diagnostic injection, 0.1–0.3 cc 2% Xylocaine in then injected. Diagnostic injection is considered positive with 80% decrement in pain with sitting or concordant reproduction of pain with injection of contrast.131 With a therapeutic injection, 0.2–0.5 cc of a 1:1 mixture of local anesthetic and steroid is injected. For intercoccygeal disc injection, the same technique as with sacrococcygeal disc injection is utilized. Frequently, with the angulation at the coccygeal level, the c-arm is caudally rotated to view the edges of the joint. A skin wheal is raised with 1% Xylocaine overlying the inferior edge of the more superior coccygeal segment. A 22–25-gauge, 2.5 inch spinal needle is then advanced to abut upon the inferior edge of the superior coccygeal segment (Fig . 23.35A). The needle is then redirected slightly into the disc. Position is checked in the lateral plane to ensure the needle is within the disc and not through the disc (Fig. 23.35B). One-tenth to 0.2 cc of contrast is then infused to confirm needle placement within the disc (Fig. 23.36). One-tenth to 0.5 cc of 2% Xylocaine is infused for diagnostic injection. For a therapeutic
A Fig. 23.35 Needle in intercoccygeal disc. (A) View (B) Lateral view. 270
Fig. 23.34 Lateral view of sacrum and coccyx demonstrates close proximity of rectum and bowel.
B
Section 2: Interventional Spine Techniques
A
B
Fig. 23.36 Contrast in intercoccygeal disc. (A) AP view.
injection, a 1:1 mixture of local anesthetic and steroid is infused. The sacrococcygeal and intercoccygeal discs hold very little volume. Frequently, there is resistance to injection because of the low volume. Typically, only 0.1 cc of contrast and 0.2–0.3 cc of medication can be infused. A 3 cc volume syringe is utilized. Because of the resistance encountered with injection, great care needs to be taken that the needle is not advanced while injecting. When injecting, the needle is flexed and held by the opposite hand by the hub. Also, one needs to be confident that the needle is within the disc before injecting. If there is any doubt, injection should not be performed.
References
12. Bridenbaugh PO, Greene NM. Spinal (subarachnoid) neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd edn. Philadelphia: Lippincott; 1988:213–251. 13. Husemeyer RP, White DC. Topography of the lumbar epidural space. A study in cadavers using injected polyester resin. Anaesthesia 1980; 35:7–11. 14. Cohen MS, Wall EJ, Olmarker K, Rydevik B. et al. Anatomy of the spinal nerve root in the lumbar and lower thoracic spine. In: Herkowitz HN, Garfin SR, Balderston RA, et al., eds. Rothman-Simeone. The spine. 4th edn. Philadelphia: WB Saunders; 1999:83–88. 15. Hamanishi C, Tanaka S. Dorsal root ganglia in the lumbosacral region observed from the axial views of MRI. Spine 1993; 18:1753–1756. 16. Kikuchi S, MacNab I, Moreau P. Localisation of the level of symptomatic cervical disc degeneration. J Bone Joint Surg [Br] 1981; 63:272–277. 17. Barr ML. Blood supply of the central nervous system. In: Barr ML, ed. The human nervous system. 3rd edn. Philadelphia: Harper Row; 1979:293–303.
1. Baker R, Dreyfuss P, Mercer S, et al. Cervical transforaminal injection of corticosteroids into radicular artery: a possible mechanism of injury. Pain 2003; 103: 211–215.
18. Adriani J, Naragi M. Paraplegia associated with epidural anesthesia. South Med J 1986; 79:1350–1355.
2. Furman MB, Giovanniello MT, O’Brien EM. Incidence of intravascular penetration in transforaminal cervical epidural steroid injections. Spine 2003; 28:21–25.
19. Houten JK, Errico TJ. Paraplegia after lumbosacral nerve root block: report of three cases. Spine J 2002; 2:70–75.
3. Furman MB, O’Brien EM, Zgleszewski TM. Incidence of intravascular penetration in transforaminal lumbosacral epidural steroid injections. Spine 2000; 25:2628–2632.
20. Brouwers PJAM, Kottink EJBL, Simon MAM, et al. A cervical anterior spinal artery syndrome after diagnostic blockade of the right C6-nerve root. Pain 2001; 91:397–399.
4. Renfrew DL, Moore TE, Kathol MH, et al. Correct placement of epidural steroid injections: fluoroscopic guidance and contrast administration. Am J Neuroradiol 1991; 12:1003–1007. 5. Barnsley L, Lord S, Wallis B, et al. False-positive rates of cervical zygapophyseal joint blocks. Clin J Pain 1993; 9:124–130.
21. Conners J, Wojack J. Interventional neuroradiology: strategies and practical techniques. Philadelphia: WB Saunders; 1999. 22. Tventen L. Spinal cord vascularity. Acta Radiol 1976; 17:1–16. 23. Stojanovic MP, Vu T, Caneris O, et al. The role of fluoroscopy in cervical epidural steroid injections. An analysis of contrast dispersal patterns. Spine 2002; 27:509–514.
6. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892.
24. Mehta M, Salmon N. Extradural block: confirmation of the injection site by x-ray monitoring. Anaesthesia 1985; 40:1009–1012.
7. Schwarzer AC, Aprill CN, Derby R, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophyseal joints. Pain 1994; 58:195–200.
25. White AH, Derby R, Wynne G. Epidural injections for the diagnosis and treatment of low-back pain. Spine 1980; 5:78–86.
8. Practice guidelines for sedation and analgesia by non-anesthesiologists: a report by the American Society of Anesthesiologists task force on sedation and analgesia by non-anesthesiologists. Anesthesiology 1996; 84:459–471.
26. Stitz MY, Sommer HM. Accuracy of blind versus fluoroscopically guided caudal epidural injection. Spine 1999; 24:1371–1376.
9. Bahn EL, Holt KR. Procedural sedation and analgesia: a review and new concepts. Emerg Med Clin N Am 2005; 23:503–517. 10. Martin ML, Lennox PH. Sedation and analgesia in the interventional radiology department. J Vasc Interv Radiol 2003; 14:1119–1128. 11. Hogan QH. Epidural anatomy examined by cryomicrotome section. Reg Anesth 1996; 21:395–406.
27. El-Khoury GY, Ehara S, Weinstein JN, et al. Epidural steroid injection: a procedure ideally performed under fluoroscopic control. Radiology 1988; 168:554–557. 28. Black MG. Anatomic reasons for caudal anesthesia failure. Anesth Analg 1949; 28:33–39. 29. Tomczak R, Seeling W, Rieber A, et al. Epidurography: comparison with CT, spiral CT and MR epidurography Rofo. Fortschritte auf dem Gebiete der Rontgenstrahlen und der Neuen Bildgebenden Verfahren. 1996; 165:123–129.
271
Part 2: Interventional Spine Techniques 30. Kraemer J, Ludwig J, Bickert U, et al. Lumbar epidural perineural injections: a new technique. Eur Spine J 1997; 6:357–361.
60. Giles KG, Taylor JR. Innervations of lumbar zygapophyseal joint synovial folds. Acta Orthop Scand 1987; 58:43–46.
31. Huston CW, Slipman CW. Diagnostic selective nerve root blocks: indications and usefulness. Phys Med Rehabil Clin N Am 2002; 13:545–565.
61. Ashton IK, Ashton BA, Gibson SJ, et al. Morphological basis for back pain: the demonstration of nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum. J Orthop Res 1992; 10:72–78.
32. Jurmand SH. Corticotherapie peridurale des lombalgies et des sciatiques f ’origine discale. EPU Rhum 1972; 24:5061–5070. 33. Brown FW. Management of diskogenic pain using epidural and intrathecal steroids. Clin Orthop 1977; 129:72–78. 34. Bernat JL. Intraspinal steroid therapy. Neurology 1981; 31:168–171.
63. Schwarzer AC, Derby R, Aprill CN, et al. The relative contributions of the disc and zygapophyseal joint in chronic low back pain. Spine 1994; 19:801–806.
35. Nelson DA. Dangers from methylprednisolone acetate therapy by intraspinal injection. Arch Neurol 1988; 45:804–806.
64. Schwarzer AC, Derby R, Aprill CN, et al. Pain from the lumbar zygapophyseal joints: a test of two models. J Spinal Disorders 1994; 7:331–336.
36. Cicala RS, Turner R, Moran E, et al. Methylprednisolone acetate does not cause inflammatory changes in the epidural space. Anesthesiology 1990; 72:556–558.
65. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137.
37. Wagner AL, Murtagh FR. Selective nerve root blocks. Tech Vasc Interv Radiol 2002; 5:194–200. 38. Katz J,ed. Atlas of regional anesthesia. Norwalk, CT: Appleton-Century-Crofts; 1985:124. 39. Chen Y, Derby R, Kim B-J, et al. Current concepts invited review. epidural steroid injections: past, present and future. Spineline 2003; 9:1–19. 40. Morvan G, Mompoint D, Bard M, et al. Direct intra-foraminal injection of corticosteroids in the treatment of cervico-brachial pain. In: Bard M, Laredo JD, eds. Interventional radiology in bone and joint. New York: Springer Verlag; 1988:253–257. 41. Vallee JN, Feydy A, Carlier RY, et al. Chronic cervical radiculopathy: lateralapproach periradicular corticosteroid injection. Radiology 2001; 218:886–892. 42. MacNab I. Negative disc exploration. An analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg [Am] 1971 53:891–903. 43. Haueisen DC, Smith BS, Myers SR, et al. The diagnostic accuracy of spinal nerve injection studies: their role in the evaluation of recurrent sciatica. Clin Orthop Rel Res 1985; 198:179–183.
66. Jull G, Bogduk N, Marsland A. The accuracy of manual diagnosis for cervical zygapophyseal joint pain syndromes. Med J Aust 1988; 148:233–236. 67. Jackson RP, Jacobs RR, Montesano PX. Facet joint injection in low-back pain. A prospective statistical study. Spine 1988; 13:966–971. 68. Schwarzer AC, Derby R, Aprill CN, et al. The value of the provocation response in lumbar zygapophyseal joint injections. Clin J Pain 1994; 10:309–313. 69. Kaplan M, Dreyfuss P, Halbrook B, et al. The ability of lumbar medial branch blocks to anesthetize the zygapophyseal joint. A physiologic challenge. Spine 1998; 23:1847–1852. 70. Jeffries B. Facet steroid injections. spine: state of the art review 1988; 2:409–417. 71. Gardner E, Gray DJ. Vertebral column. In: Garnder E, Gray DJ, O’Rahilly R, eds, Anatomy. A regional study of human structure, 4th edn. Philadelphia: WB Saunders; 1975:509–524. 72. Panjabi MM, Oxland T, Takata K, et al. Articular facets of the human spine. Quantitative three-dimensional anatomy. Spine 1993; 18:1298–1310.
44. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13:79–83.
73. Dreyfuss P, Lagattuta FP, Kaplansky B, et al. Zygapophyseal joint injection techniques in the spinal axis. In: Lennard TA, ed., Physiatric procedures in clinical practice. Philadelphia: Hanley Belfus; 1995:206–226.
45. Herron LD. Selective nerve root block in patient selection for lumbar surgery: surgical results. J Spinal Disord 1989; 2:75–79.
74. Rossi U, Pernak J. Low back pain: the facet syndrome. Adv Pain Res Ther 1990; 13:231–244.
46. Krempen JF, Smith BS. Nerve root injection: a method for evaluating the etiology of sciatica. J Bone Joint Surg [Am] 1974; 56:1435–1444.
75. Bogduk N, Valencia F. Innervation and pain patterns of the thoracic spine. In: Grant R, ed. Physcial therapy of the cervical and thoracic spine. Edinburgh: Churchill Livingstone; 1988:27–37.
47. Tajima T, Furukawa K, Kuramochi E. Selective lumbosacral radiculography and block. Spine 1989; 5:68–77. 48. Castro WHM, van Akkerveeken PF. Der diagnostische wert der selektiven lumbalen nervenwurzelblockade. Z Orthop 1991; 129:374–379. 49. Van Akkerveeken PF. The diagnostic value of nerve root sheath infiltration. Acta Orthop Scand 1993: 251(suppl):61–63. 50. North RB, Kidd DH, Zahurak M, et al. Specificity of diagnostic nerve blocks: a prospective, randomized study of sciatica due to lumbosacral spine disease. Pain 1996; 65:77–85. 51. Derby R, Bogduk N, Kine G. Review article: precision percutaneous blocking procedures for localizing spinal pain. Part 2. The lumbar neuroaxial compartment. Pain Digest 1993; 3:175–188.
76. Carrera GF, Williams AL. Current concepts in evaluation of the lumbar facet joints. CRC Critical Reviews in Diagnostic Imaging 1984; 21:85–104. 77. Destouet JM, Gilula LA, Murphy WA, et al. Lumbar facet joint injection: indication, technique, clinical correlation, and preliminary results. Radiology 1982; 145:321–325. 78. Taylor JR, Twomey LT. Age changes in lumbar zygapophyseal joints. Observations of structure and function. Spine 1986; 11:739–745. 79. Pedersen HE, Blunck CFJ, Gardner E. The anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves (sinu-vertebral nerves). J Bone Joint Surg [Am] 1956; 38:377–391. 80. Lewin T, Moffett B, Viidik A. The morphology of the lumbar synovial intervertebral joints. Acta Morphol Neerl Scand 1962; 4:299–319.
52. Lutze M, Stendel R, Vesper J, et al. Periradicular therapy in lumbar radicular syndromes: methodology and results. Acta Neurochir (Wien) 1997; 139: 719–724.
81. Bogduk N, Engel R. The menisci of the lumbar zygapophyseal joints. A review of their anatomy and clinical significance. Spine 1984; 9:454–560.
53. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies. Phys Med Rehabil Clin N Am 2002; 13:697–711.
82. Lippitt AB. The facet joint and its role in spine pain. Management with facet joint injections. Spine 1984; 9:746–750.
54. Weiner BK, Fraser RD. Foraminal injection for lateral lumbar disc herniation. J Bone Joint Surg [Br] 1997; 79:804–807.
83. Mooney V, Robertson J. The facet syndrome. Clin Orthop Rel Res 1976; 115: 149–156.
55. Daniels DL, Williams VM. Computed tomography of the articulation and ligaments of the occipito-atlantoaxial region. Radiology 1983; 146:709–716.
84. Dreyfuss P, Schwarzer AC, Lau P, et al. Specificity of lumbar medial branch and L5 dorsal ramus blocks. A computed tomography study. Spine 1997; 22:895–902.
56. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine 1982; 7: 319–330.
85. Hove B, Gyldensted C. Cervical analgesic facet joint arthrography. Neuroradiology 1990; 32:456–459.
57. Dreyfuss P, Rogers J, Dreyer S, et al. Atlanto-occipital joint pain. A report of three cases and description of an intra-articular joint block technique. Reg Anesth 1994; 19:344–351.
86. Dreyfuss P, Tibiletti C, Dreyer S, et al. Thoracic zygapophyseal joint pain: A review and description of an intra-articular block technique. Pain Digest 1994; 4:46–54.
58. Dreyfuss P. Atlanto-occipital and lateral atlanto-axial joint injections. In: Lennard TA, ed., Physiatric procedures in clinical practice. Philadelphia: Hanley Belfus; 1995:227–237. 59. Dreyfuss P, Michaelsen M, Fletcher D. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine 1994; 19:1125–1131.
272
62. Beaman DN, Graziano GP, Glover RA, et al. Substance P innervation of lumbar spine facet joints. Spine 1993; 18:1044–1049.
87. Fortin JD, Mckee MJ. Thoracic facet blocks: bent needle technique. Pain Physician 2003; 6:513–516. 88. Dreyfuss P, Tibiletti C, Dreyer S. Thoracic zygapophyseal joint pain patterns. A study in normal volunteers. Spine 1994; 19:807–811. 89. Carrera GF. Lumbar facet joint injection in low back pain and sciatica. Description of technique. Radiology 1980; 137;661–664.
Section 2: Interventional Spine Techniques 90. Derby R, Bogduk N, Schwarzer A. Precision percutaneous blocking procedures for localizing spinal pain. Part 1: the posterior lumbar compartment. Pain Dig 1993; 3:89–100. 91. Maldague B, Mathurin P, Malghem J. Facet joint arthrography in lumbar spondylolysis. Radiology 1981; 140:29–36. 92. Dory MA. Arthrography of the lumbar facet joints. Radiology 1981; 140:23–27. 93. Moran R, O’Connell D, Walsh MG. The diagnostic value of facet joint injections. Spine 1988; 13:1407–1410.
113. Ehara S, El-Khoury GY, Bergman RA. The accessory sacroiliac joint: a common anatomic variant. Am J Radiol 1988; 150:857–859. 114. Steindler A, Luck JV. Differential diagnosis of pain low in the back. Allocation of the source of pain by the procaine hydrochloride method. JAMA 1938; 110:106–113. 115. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological and clinical studies. Acta Orthop Scand 1957; 27(Suppl):1–127.
94. Carrera GF. Lumbar facet joint injection in low back pain and sciatica. Preliminary results. Radiology 1980; 137:665–667.
116. Bernard TN Jr, Cassidy JD. The sacroiliac joint syndrome. Pathophysiology, diagnosis, and management. In: Frymoyer JW, Ducker TB, Hadler NM, et al., eds. The adult spine: principles and practice. New York: Raven Press; 1991:2107–2130.
95. Raymond J, Dumas JM. Intraarticular facet block: diagnostic test or therapeutic procedure. Radiology 1984; 151:333–336.
117. Greenman PE. Clinical aspects of sacroiliac function in walking. J Man Med 1990; 5:25–130.
96. Fairbanks JCT, Park WM, McCall IW, et al. Apophyseal injection of local anesthetic as a diagnostic aid in primary low-back pain syndromes. Spine 1981; 6:598–605.
118. Norman GF, May A. Sacroiliac conditions simulating intervertebral disk syndrome. West J Surg Obstet Gynecol 1956; 64:641–642.
97. Lynch MC, Taylor JF. Facet joint injection for low back pain. A clinical study. J Bone Joint Surg [Br] 1986; 68:138–141. 98. Bogduk N, Marsland A. The cervical zygapophyseal joints as a source of neck pain. Spine 1988; 13:610–617. 99. Barnsley L, Bogduk N. Medial branch blocks are specific for the diagnosis of cervical zygapophyseal joint pain. Reg Anesth 1993; 18:343–350. 100. Bogduk N, Marsland A. On the concept of third occipital headache. J Neurol Neurosurg Psychiatry 1986; 49:775–780.
119. Pitkin HC, Pheasant HC. Sacroarthrogenetic telalgia. 1: a study of referred pain. J Bone Joint Surg [Am] 1988; 70:31–40. 120. Hershey CD. The sacro-iliac joint and pain of sciatic radiation. JAMA 1943; 122:983–986. 121. Albee FH. A study of the anatomy and the clinical importance of the sacroiliac joint. J Am Med Assoc 1909; LIII:1273–1276. 122. Ebraheim NA, Padanilam TG, Waldrop JT, et al. Anatomic consideration in the anterior approach to the sacro-iliac joint. Spine 1994; 19:721–725.
101. Stolker RJ, Vervest ACM, Groen GJ. Percutaneous facet denervation in chronic thoracic spinal pain. Acta Neurochir (Wien) 1993; 122:82–90.
123. Hendrix RW, Lin PJP, Kane WJ. Brief note. Simplified aspiration or injection technique for the sacro-iliac joint. J Bone Joint Surg [Am] 1982; 64:1249– 1252.
102. Eisenstein SM, Ashton IK, Roberts S, et al. Innervation of the spondylolysis ‘ligament.’ Spine 1994; 19:912–916.
124. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.
103. Schneiderman GA, McLain RF, Hambly MR, et al. The pars defect as a pain source. A histologic study. Spine 1995; 20:1761–1764.
125. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrograpy technique. Part I: asymptomatic volunteers. Spine 1994; 19:1475–1482.
104. Hambly MF, Wiltse LL. A modification of the Scott wiring technique. Spine 1994; 19:354–356. 105. Bradford DS, Iza J. Repair of the defect in spondylolysis or minimal degrees of spondylolisthesis by segmental wire fixation and bone grafting. Spine 1985; 10:673–679. 106. Suh PB, Esses SI, Kostuik JP. Repair of pars interarticularis defect. The prognostic value of pars infiltration. Spine 1991; 16(Suppl):445–448. 107. Bowen V, Cassidy JD. Macroscopic and microscopic anatomy of the sacroiliac joint from embryonic life until the eighth decade. Spine 1981; 6:620–628. 108. Sashin D. A critical analysis of the anatomy and the pathologic changes of the sacro-iliac joints. J Bone Joint Surg [Am] 1930; 12:891–910. 109. MacDonald GR, Hunt TE. Sacro-iliac joints. Observations on the gross and histological changes in the various age groups. Canad MAJ 1952; 66:157–163. 110. Walker JM. Age-related differences in the human sacroiliac joint: a histological study; implications for therapy. J Orthop 1986; 7:325–334. 111. Stewart TD. Pathologic changes in aging sacroiliac joints. A study of dissectingroom skeletons. Clin Orthop Rel Res 1984; 183:188–196. 112. Trotter M. Accessory sacro-iliac articulations. Am J Phys Anthrop 1937; 22: 247–261.
126. Derby R. Point of view. Spine 1994; 19:1489. 127. Slipman CW, Huston CW. Diagnostic sacroiliac joint injections. In: Manchikanti L, Slipman C, Fellows B, eds. Interventional pain management. Low back pain. Diagnosis and treatment. Paducah, Kentucky: ASIPP Publishing; 2002:269–274. 128. Miskew DB, Block RA, Witt PF. Aspiration of infected sacro-iliac joints. J Bone Joint Surg [Am] 1979; 61:1071–1072. 129. Maugars Y, Mathis C, Vilon P, et al. Corticosteroid injection of the sacroiliac joint in patient with seronegative spondyloarthropathy. Arthritis Rheum 1992; 35:564–568. 130. Fogel GR, Cunningham PY, Esses SI. Coccygodynia: evaluation and management. J Am Acad Orthop Surg 2004; 12:49–54. 131. Maigne JY, Guedj S, Straus C. Idiopathic coccygodynia. Lateral roentgenograms in the sitting position and coccygeal discography. Spine 1994; 19:930–934. 132. Maigne JY, Tamalet B. Standardized radiologic protocol for the study of common coccygodynia and characteristics of the lesions observed in the sitting position. Clinical elements differentiating luxation, hypermobility, and normal mobility. Spine 1996; 21:2588–2593.
273
PART 2
INTERVENTIONAL SPINE TECHNIQUES
Section 2
Interventional Spine Techniques
CHAPTER
Technique of Radiofrequency Denervation
24
Sara Haspeslagh and Maarten Van Kleef
INTRODUCTION History The use of electrical current to create lesions for the treatment of pain began in 1931, when Kirschner introduced it for the treatment of trigeminal neuralgia.1 In 1965, Mullan used direct current to perform percutaneous lateral cordotomy for unilateral malignant pain.2 Later that year, Rosomoff modified this technique and used radiofrequency (RF) current for this treatment.3 An RF current was found to produce more predictable, circumscribing lesions. Several years later, Sweet and Wepsic described their technique for the use of RF lesions of the Gasserian ganglion in the treatment of trigeminal neuralgia.4 In spinal pain, the use of RF current was reported in a series of cases by Shealy (1975).5 He described RF lesioning of the medial branch to treat lumbar facet joint pain. Subsequently, more options for the use of RF lesioning in various spinal pain syndromes were introduced into clinical practice.6–8 The introduction of a small-diameter (22-gauge) temperature monitoring electrode system by Sluijter and Mehta in 19819 increased the safety of the current method used.10 Since then, RF procedures have been widely adopted by many pain practitioners. In addition there have been many new technical developments, such as the improvement of the quality of C-arm image intensifiers. All these developments have contributed to a widespread use of RF lesioning. Recently, a modification of the traditional RF method was introduced by Sluijter et al.11 They used the same output setting of the lesion generator that was used for making heat lesions as in RF lesioning, but they interrupted this output to allow generated heat to be washed out by thermal conductivity and circulation. This technique is called ‘pulsed radiofrequency’ (PRF) and is claimed to be nondestructive. Until now, there are no reports of any sensory or motor loss following this procedure. However, it is too soon to categorically recommend this technique because the mechanism of action is still unknown. Until several double-blind, randomized, controlled trials are conducted this new approach should not be routinely employed.
Physics Radiofrequency current An RF current is applied by an RF lesion generator through an electrode, which is insulated except for the most distal part. This exposed region is the active portion of the electrode. The RF current flows from the electrode tip to the dispersive ground plate, which is placed on the arm or leg of the patient and leads the current back to the RF lesion generator. RF current flows through tissue and results in an electric field. This electric field places an electric force on the ions within tissue electrolytes, causing them to oscillate at a high rate (i.e.
300 000 times per second).12 Tissue heating is created by frictional dissipation of the ionic current within the fluid medium, which heats the electrode.
Lesion size The size of the lesion not only depends on the diameter of electrode and the length of the uninsulated electrode tip, but also depends on tip temperature. This was confirmed in animal studies by Cosman et al. in 1984.13 Bogduk et al. studied not only the size of the lesions, but also the shape of the lesion.14 They performed experimental lesions in egg white and fresh meat. They found that RF lesions do not extend distal to the tip of the electrode, but extend radially around the active electrode tip in a spheroidal shape. Based on these observations, Bogduk suggested that the best placement of the electrode tip was parallel to the target structure. Other research methods involving computerized or mathematical modeling of similar experiments have been used. For example, Moringlane et al. studied experimental RF coagulation with a computer-based on-line monitoring of temperature and power.15 Vinas et al. also studied lesion size in vivo using fresh eggs and in vitro using the subcortical white matter of rabbits.16 Both investigators obtained results that were similar to those reported by Bogduk et al. Once equilibrium temperature is reached (after 20–40 seconds), the size of the lesion does not increase. However, some variables such as circulation effect and the tissue heat conductivity may also produce a variation in lesion size, but are unpredictable.13 Consequently, the lesion size may therefore be variable at different locations within the body.
Radiofrequency lesion generator The modern RF lesion generating system has different functions, including a pulsed RF mode. There is continuous on-line impedance measurement to confirm continuity of the electrical circuit and to detect any short circuits. One of the key components of the system is nerve stimulator function. It is used to confirm the proper position of electrode tip (it indicates the electrode-to-nerve distance) and to permit minor adjustments. To ensure the proximity of the active tip to the sensory fibers, stimulation is performed at 50 Hz. The 2 Hz stimulation is carried out to detect extraspinal muscle contractions that occur when the needle is placed too close to a nerve root motor fiber. Voltage, current, and wattage during an RF procedure are also monitored. Finally, a generator monitors temperature using a thermocouple. This is an important lesion parameter, but the temperature is only measured at the tip of the electrode and not in the more peripheral zones of the lesion area. The usefulness of tip temperature to monitor the lesion size is minimized because the lesion size is dependent on local blood circulation. There is a rapid drop in temperature over the first few millimeters from the electrode tip.13,17
275
Part 2: Interventional Spine Techniques
Effect of radiofrequency current on nerve tissue The effect of RF lesions on nerve tissue is controversial. Letcher and Goldring, in 1968, investigated the effect of RF current and heat on the nerve action potential of the saphenous nerve in cats.18 Delta and C-fibers were blocked before the alpha-beta group by both RF current and heat. Uematsu,19 and subsequently Smith et al.,20 reported quite disparate results. Smith et al. created RF lesions of different temperatures by placing an electrode into the lumbar intervertebral foramina of dogs.20 Indiscriminate damage of both small and large fibers by RF current was observed. Uematsu conducted a histological analysis of feline sciatic nerves that sustained RF thermocoagulation.19 These studies have been criticized because large,14-gauge electrodes were used; in addition, they were placed close to the dorsal root ganglion during open surgery. However, these methods are not comparable to the technique which is commonly used in clinical practice today, since 22-gauge needles where not available at that time.21 In response to this critique, de Louw et al., in 2001, tried to investigate morphological effects of RF lesions as they develop in normal clinical situations.21 A percutaneous RF lesion adjacent to the dorsal root ganglion (DRG) of goats was created with a 22-gauge electrode at a tip temperature of 67°C. Immunocytochemical changes indicative of proliferation and regeneration was observed 2 weeks after the RF lesion was created. These alterations occurred outside the DRG, without interfering with the function of large myelinated fibers.
Effect of pulsed radiofrequency current on nerve tissue Recently, the importance of heat as the definitive mechanism of action RF lesioning has been questioned.11 In 1998, Sluijter et al. investigated isothermic RF lesioning also termed pulsed RF (PRF) treatment.11 Ostensibly, PRF generates its therapeutic effects independent of thermal factors. The pulses are given at a rate of 2 Hz and last 20 msec. The rest period is 480 msec, and this allows the generated heat to be washed out by thermal conductivity and circulation. The mechanism by which pulsed RF treatment effects symptom relief remains unknown. In 2002, Higuchi et al. undertook a study to elucidate this mechanism. They attempted to identify spinal cord neuron activation following the exposure of the dorsal ganglion of rats to PRF currents.22 A significant increase in the number of cFosimmunoreactive neurons in the superficial laminae of the dorsal horn was observed. This finding indicates that PRF current activates painprocessing neurons in the dorsal horn and that this effect is not mediated by tissue heating. This technique is considered to be a safer method of treatment because until now the observations showed no signs of neurodestruction and thus neurological side effects.11,23 Cahana et al., in 2003, compared the acute effects of pulsed versus continuous RF energy on impulse propagation and synaptic transmission in hippocampal slice cultures and on cell survival in cortical cultures of rats.24 In both systems, they found an induction of distance-dependent tissue destruction under the stimulating needle (namely, an inhibition of evoked synaptic activity), but this was more pronounced in the continuous RF group. Thus, they concluded that the acute effects of PRF are more reversible and less destructive in nature than the acute effects of classic continuous RF mode. Nevertheless, the safety, efficacy, and the mechanism of action of pulsed RF current remains unresolved at the present time. Clinical trials still are needed to prove its potential efficacy. 276
RADIOFREQUENCY DENERVATION IN THE CERVICAL REGION Cervical percutaneous radiofrequency denervation of the facet joints Relevant anatomy The cervical zygapophyseal joints are innervated in the same way as the lumbar zygapophyseal joints (Fig. 24.1). The cervical segmental nerves divide into the primary anterior ramus and the primary posterior ramus on exiting the neuroforamen. Immediately, the posterior branch divides into a lateral and a medial branch in the cervical intertransverse space. The medial branches of C4 to C8 run dorsally and medially through the ‘waist’ of their respective articular pillars. They innervate the facet joints at the level of the exiting segmental nerve and at the level below. Because of this multilevel innervation of the facet joints, usually the medial branch procedure is performed at several levels. Furthermore, the medial branches give deep branches to multifidus muscles and superficial branches to semispinal cervical muscles. The anatomy of the innervation of the C2–3 facet joint is distinct from the lower cervical joints. It receives innervation by branches of the greater occipital nerve, which is the continuation of the posterior primary ramus of the C2 segmental nerve. The C3 posterior primary ramus of the segmental nerve gives a medial branch that innervates the C2–3 facet joint, but also gives a branch that forms the third occipital nerve that runs cranially to innervate the skin of the lower part of the occipital region. There is no facet joint between the C1 and the C2 vertebrae.
Procedure Sedation is not employed because of the need for continuous communication between practitioner and patient. Several approaches to
Fig. 24.1 Anatomy of cervical facet joints and their innervation. The medial branches of the posterior primary rami of the segmental nerves C3, C4, and C5 are indicated by red lines, the vertebral artery by the blue line
Section 2: Interventional Spine Techniques
reach the medial branch of the dorsal ramus at the upper and middle cervical area can be used. The most commonly used approach by these authors is the posterolateral approach.25 For this technique, the patient is positioned supine on the operating table, which is tolerated well. The occiput is placed on a headrest and the cervical spine is slightly extended. The C-arm is positioned in a moderately oblique (±30°) location to secure a safe distance between the electrode tip and the exiting segmental nerve. In this position the gantry angle is parallel to the axis of the intervertebral foramen that is upward and slightly caudal. In this position the segmental nerves exit in a plane approximately perpendicular to the monitor screen. The degree of obliquity should be such that the projection of the pedicles is seen a little anterior to 50% of the vertebral body (Fig. 24.2). In the frontal plane, there should be a small angle of the C-arm with the transverse plane. This provides clear visibility of the intervertebral discs and the neuroforamina. In this projection, the medial branch runs over the base of the superior articular process, which is easily viewed. Entry points are marked on the skin, somewhat posterior and caudal to the target points as seen on the monitor, i.e. dorsal from the posterior border of the facet column and slightly caudal. Care should be taken to ensure that the entry point is not too anterior in the neck to avoid important vascular structures such as the carotid artery. The first needle (preferably the most cranial) is inserted in a horizontal plane and in a slightly cranial direction not deeper than 2 cm, so that the needle point is in line with the target point. Then the needle is carefully advanced anteriorly and cranially until bone contact is made with the facet column at the target point (see Fig. 24.2). During the first step of the procedure, several things can go wrong. The needle tip may be projecting over or anterior to the target point without any bone contact. Should the needle then be introduced further and more anteriorly to an imaginary line connecting the posterior aspects of the neural foramina it could make contact with the segmental nerve or even with the vertebral artery. To avoid this, each advancement of the needle should be checked and, if necessary, should be redirected more posteriorly. As the needle is advanced it becomes increasingly difficult to reposition the needle tip to an accurate location. If the needle tip is projecting posterior to the bone of the facet column and is advanced further, there is the possibility that it will pass between the laminae and make contact with the spinal cord. This can occur if the entry point of the needle is too far posterior in the neck. To avoid this, an anteroposterior (AP) check should be made to confirm an ideal starting point. The position of the C-arm in the AP direction should confirm the position of the needle tip adjacent to the concavity (‘waist’) of the articular pillars of the cervical spine at the corresponding level (Fig. 24.3). Once the first needle is in the proper position, the other
Fig. 24.2 Oblique fluoroscopic view of cervical facet joints with three needles aiming for the medial branches of the C3–4, C4–5, and C5–6 facet joints. The red line indicates the position of the pedicles projection a little anterior to 50% of the vertebral body. The green dots indicate the target points.
Fig. 24.3 Antero-posterior fluoroscopic view of the needles aiming for the medial branches of the cervical facet joints C3–4, C4–5, and C5–6. The target points are indicated with green dots. Notice that the needle aiming for the C3–4 medial branch has to be redirected more cranially.
needles are introduced in the same way as described above. The authors prefer to take advantage of the first needle serving as an indicator for the direction and depth for subsequent needles, which accounts for their recommendation of placing all needles before applying RF rather than lesioning a single medial branch and then placing the next needle. The technique is identical for the facet joints from C3–4 until C6–7. The direction of the needle at the C2 level is different. It should be oriented toward the small branches that innervate the C2–3 facet joint and not toward the medial branch, which is the greater occipital nerve. For the RF treatment of this facet joint, the needle should be placed at the arch of C2 at the level of the upper border of foramen C3. When optimal anatomical localization of the needles transpires, an electrical stimulation is performed to confirm correct needle position, i.e. parallel to the medial branch. This can be accomplished by identifying the stimulation thresholds. First, an electrical stimulation rate of 50 Hz should be given and should elicit a response (tingling sensation) in the neck at less than 0.5 volts. Next, a stimulation at 2 Hz is performed to confirm accurate needle position. Contractions of the paraspinal muscles will be noticed. Muscle contractions in the arm indicate needle placement too close to the exciting nerve root. In that case the needle should be repositioned more posteriorly. Once proper positioning of the needle is confirmed, the medial branch of the dorsal ramus is anesthetized with 1–2 mL local anesthetic solution (lidocaine 1–2%). An 80°C radiofrequency thermal lesion is made for 60 seconds at each level. To date, there have been no reported complications from cervical facet joint denervation when the procedure is methodically performed.26 Some postoperative burning pain is described in >30% of patients.27 It disappears spontaneously after 1–3 weeks. One should always bear in mind that there is risk of puncture of the vertebral artery when the needle is positioned anterior to the foramen in the posterolateral approach. A second approach, which is more popular in the United States, is the posterior approach of the facet joint. This was first introduced by Lord et al. in 1995.28 In this technique, the patient is positioned prone on the operating table, with the head flexed (about 5–10°) and with the face resting on a padded ring. This is a ‘tunnel vision’ technique, in which the target points are the posterior aspects of the waists of the articular pillars at the levels to be blocked and are the same as the entry points. The needle is introduced from posterior of the neck to make contact with each of the two nerves supplying the painful joints. When bone contact is made, the C-arm is turned to give a lateral view in which the needle tip should be seen in the posterior aspect of the waist of the articular pillar. A deviation toward the midline should be avoided because of risk of penetration 277
Part 2: Interventional Spine Techniques
into the epidural and subarachnoid space. Subsequently, the needle is incrementally advanced until the tip is projecting at the center of the pedicle. Then, a slightly lateral deviation should be made so that the needle tip is in the most lateral aspect of the articular pillar in the posteroanterior view. When this position is confirmed, stimulation is performed as described above to determine the 50 Hz and 2 Hz thresholds. If these are acceptable, local anesthetic is injected and an RF lesion (80°C for 60 sec) is made. At each location two lesions are made: the second one after a rotation of the RF needle over 90° from its first position.
Equipment Different radiofrequency lesioning probes can be used. A SMK-C5 (Sluijter-Mehta Kit, 22-gauge, 50 mm) cannula with a 4 mm active tip or, alternatively, an RCN-6 (24-gauge, 60 mm) needle is used. The advantage of an SMK needle is its ability to measure temperature, but there is the risk of displacement of the needle while inserting the RF probe. The RCN-6 electrode has a connecting tube that allows injection of local anesthetics before lesioning, minimizing potential displacement of the needle once it is positioned. There is no temperature measurement while using the RCN-6 electrode, but this is not thought to be a critical issue, although recently Buijs et al. reported that lesion size is more predictable while measuring the temperature.29 A 10 cm, 22-gauge SMK-electrode with a 4 mm tip is used for the posterior approach. With an SMK probe, an 80°C radiofrequency thermal lesion is made for 60 seconds at each level. With a RCN-6 needle, 20 volts over 60 seconds is applied to the electrode, which should heat the electrode tip to the correct temperature. An alternative is to use a 5 cm or 10 cm curved Racz-Finch radiofrequency thermocoagulation (RFTC) needle (blunt or sharp) with a 10 mm active tip. Individual practitioners have specific beliefs regarding possible advantages of curved needles in comparison to straight needle and of a blunt needle in comparison to a sharp needle, but no definitive answers regarding these issues are available.
Postprocedure care The patient is allowed to go home immediately after the procedure. A feeling of dizziness and vertigo is frequently described, especially after the higher median branch blocks. RF of the third occipital nerve secondarily can partially block the upper cervical proprioceptive afferents and can result in transient ataxia and unsteadiness.30,31 When this situation can possibly occur, patient should be advised not to drive a car or handle other dangerous machinery for the initial 24 hours following the procedure. Some patients report a transient exacerbation of their pain, which they described as burning in nature. It occurs as a result of neuritis caused by the proximity of the RF needle to a large nerve root. This side effect is a self-limiting process and resolves in 2–6 weeks. The patient can take oral analgesics (WHO step 1 or 2) during this period.
Case study A 62-year-old male attended the pain clinic. He complained of an almost continuous pain localized in the cervical area (right > left) in the shoulder not beyond the acromion. Neurological examination showed no abnormalities. X-ray and MRI scan showed severe degenerative change in the midcervical area. On physical examination there was a reduced range of motion on rotation of the head. During palpation there was severe pain elicited on pressure over the facet joints. Test blocks of the facet area were not performed.
278
The authors performed a radiofrequency lesion of the primary dorsal rami of the segmental nerves C3–6 on right and left side. There were no complications after the procedure. Eight weeks after the procedure there was 60% pain relief. Six months after the procedure, the patient still has satisfactory pain relief.
Cervical radiofrequency lesioning of the dorsal root ganglion Relevant anatomy The segmental nerves of C3 to C8 exit through the lower parts of the neuroforamina on the transverse processes just below the level of the facet joints. They pass obliquely forward and downwards and posterior to the vertebral arteries and veins in grooves formed by the anterior and posterior tubercles of the corresponding transverse processes. In these grooves, they lie on the medial parts. Just anterior and inferior to them lie the small ventral roots. The first cervical nerve passes between the posterior arch of C1 and the vertebral artery. The dorsal ramus of the first spinal nerve becomes the suboccipital nerve and supplies the suboccipital muscles. This first cervical nerve has almost exclusively motor fibers and only seldom any significant sensory component. Thus, there is usually no need to block this nerve. The second cervical nerve passes transversely behind the C1–2 joint, and the large dorsal ramus forms the greater occipital nerve, which innervates the posterior scalp.
Procedure Again, this technique is performed without any sedation because of the need of cooperation of the patient. The radiofrequency lesioning of the dorsal root ganglion (RF-DRG) is only performed after a positive diagnostic segmental nerve block (usually several diagnostic blocks are performed). For this procedure, the patient is lying supine on the operating table with a slight extension of the neck. Firstly, the C-arm should be positioned obliquely so that the first three contralateral pedicles are projecting just posteriorly to the anterior line of the vertebral bodies. Secondly, the intervertebral discs should be clearly visible. To do so, the C-arm is orientated in the frontal plane. One should adapt C-arm positioning to have an optimal view of the intervertebral foramen of the level one wants to treat. The axis of the intervertebral foramen points 25–35° anteriorly and 10° caudally. The inclination of the C-arm in the frontal plane should be such that there is no double contour in the caudal aspect of the foramen. Then the target point is identified: it is posterior in the neuroforamen between the caudal and the middle third. This dorsal position is chosen in order to avoid possible damage to the motor fibers of the segmental nerve and to the vertebral artery, which runs anterior to the ventral part of the foramen. The entry point is marked on the skin and is the same as the target point. This technique is a ‘tunnel vision’ technique what means that the entry of the needle is in the direction of the Xrays.32 The needle is than projected on the screen like a dot and the field of vision can theoretically be narrowed down to a tunnel-like diameter (Fig. 24.4). After injection of local anesthetic (lidocaine 1%) into the skin with a 22-gauge subcutaneous needle, a 22-gauge spinal needle or, preferably, a needle with a connecting tube is inserted into the superficial layers of the skin, in the direction of the X-rays so that the electrode is projected on the screen as a dot. Subsequently, the needle is advanced carefully and every step is checked with fluoroscopy. There is the possibility of inadvertent puncture of the segmental nerve. That is why an early check in the anteroposterior (AP) view is done. In this view, the endpoint is the point where the tip of the needle is projecting 1–2 mm lateral to the lateral border of the facet column. Thereafter, only 0.2–0.5 mL of water-soluble dye (Iohexol
Section 2: Interventional Spine Techniques
Fig. 24.6 Lateral fluoroscopic view of the block of the C2 segmental nerve. The target point is the same as the entry point (tunnel vision technique), namely approximately 3 mm posterior to the tip of the dome-shaped space between the laminae of the C1 and C2 vertebrae.
Fig. 24.4 Oblique fluoroscopic view of blocking the C6 segmental nerve. Notice the needle in tunnel vision (projecting as a dot) posterior in the C6 foramen between caudal and middle third of this foramen.
240 mg/mL; Omnipaque® 240) is injected to confirm the proper position of the needle tip close to the segmental nerve and to exclude an accidental intradural or intravascular position of the electrode. When this is confirmed, 0.5 mL of local anesthetic (lidocaine 1–2%) is injected. Alternatively, to perform a radiofrequency lesion, the cannula is advanced until the tip projects into the middle of the facet column (Fig. 24.5). Then the stylet is removed and 0.2–0.5 mL of dye is injected to confirm proximity to the targeted nerve root. The RF probe is now inserted through the cannula. After checking the impedance, electrical stimulation is started at a rate of 50 Hz. The patient should feel a tingling sensation. If the stimulation threshold is felt under 0.4 volts, the needle is withdrawn until the threshold is between >0.4 and 50 psi above opening in a disc with a grade 3 annular tear or 80–100 psi in a normal-appearing nucleogram, or a total of 3.5 mL of contrast medium has been injected.
Imaging The appearance of the normal nucleus following the injection of contrast medium is unmistakable: the contrast medium assumes a lobular pattern or a bilobed ‘hamburger’ pattern (Fig. 25.6A). A variety of patterns may occur in abnormal discs.9 Contrast medium may extend into radial fissures of various lengths but remain contained within the disc (Fig. 25.6B), or it may escape into the epidural spaces through a torn anulus (Fig. 25.6A).
In some cases (Fig. 25.6C), the contrast medium may escape through a defect in the vertebral endplate.3 However, none of these patterns alone is indicative of whether the disc is painful; that can be ascertained only by the patient’s subjective response to disc injection. Immediately after discography, CT–discography may be performed to define fissures extending to the outer third of the anulus and extending circumferentially within the anulus fibrosus. Radial annular tears can be found by discography, but only the postdiscogram CT axial view clearly shows the location and size of fissures within the anulus fibrosus.3 Sachs et al.10 developed the Dallas discogram scale, in which annular disruption is graded on a 4-point scale. Grade 0 describes contrast medium contained wholly within a regular nucleus pulposus. Grades 1 to 3 describe the extension of contrast medium along radial fissures into the inner third, middle third, and outer third of the anulus fibrosus, respectively. Aprill and Bogduk11 proposed a modified Dallas description scale which includes grade 4, distinguished from grade 3 by the spread of contrast medium circumferentially within the substance of the anulus fibrosus and subtending a >30° arc at the disc center.
Interpretation The most important information obtained from discography is whether the patient’s pain is reproduced. There is no alternative or superior means of determining if a disc is the source of a patient’s pain. Conceptually, discography is an extension of clinical examination, tantamount to palpating for tenderness. It is only the inaccessibility of a disc to palpation that requires the use of needles. In this regard, it is critical that the criteria for a painful disc be rigorously satisfied. Internal control observations are mandatory: a disc cannot be deemed the source of a patient’s pain if stimulating other discs or other structures in the same region reproduce similar pain. Assessing patient response to discography requires measuring the pain reproduced by injection. Pain may be characterized by three components: intensity, location, and character. If the location and character of pain provoked during discography are similar to or the same as the patient’s clinical symptoms, the criteria for concordant pain are satisfied. The intensity of pain is measured by the patient (e.g., by using a numerical rating scale) and by observed pain behaviors. The intensity of provoked pain, however, is dependent on stimulus intensity. In simple terms, the harder one pushes on the syringe the more likely the disc is to hurt. By measuring intradiscal pressures, stimulus intensity can be quantified and standardized, permitting more reliable comparisons among patients and discographers. While injection pressures may be manually estimated, use of a controlled inflation syringe with digital pressure readout is more precise.
LT L4/5
A
B
C
Fig. 25.6 The appearance of the nucleus following the injection of contrast media. (A) The contrast medium assumes either a lobular pattern or a bilobed (‘hamburger’) pattern (black arrowhead) as a normal nucleogram. Contrast medium escaped into the epidural space through a radial fissure at L5–S1 level (white arrow). (B) Contrast medium extended into radial fissures (arrow) but remain contained within the disc. (C) The contrast medium escaped through a defect in the vertebral end plate (white arrowheads). 294
Section 2: Interventional Spine Techniques
Adding pressure monitoring to provocative discography improves interobserver reliability and, as a result, reproducibility. A positive discogram requires an abnormal disc, pain response =6/10 (numeric rating scale; NRS), pressure level =50 psi, pain described by the participant as ‘familiar,’ and at least one negative control disc. One must, however, be aware that transient pain is often provoked when fissures are suddenly opened. In most cases, such pain should not be used as evidence of a true-positive response unless pain >6/10 is sustained for more than 30 seconds. Most experienced discographers will perform a confirmatory re-pressurization once a suspected positive response is provoked. If re-pressurization does not again provoke significant concordant pain at 50 psi or less above opening pressure, then the initial response will remain indeterminate. These criteria for positive response were reconfirmed in a study performed in 13 normal asymptomatic volunteers.11a,11b When the operational criteria for discography were set to pressure =50 psi and evoked pain intensity >4, the expected false-positive rate was 50 psi, the response cannot be considered clinically significant, since it is difficult to distinguish from the effect of mechanically stimulating a normal or subclinically symptomatic disc.13 Excessive stimulation involving pressures >50 psi above opening pressure and uncontrolled, high injection speeds increase false-positive responses.
TECHNIQUE OF CERVICAL DISCOGRAPHY Patient position The patient is placed on the fluoroscopy table in a supine position. Extension of the neck may help improve disc access, and can be achieved by elevating the upper trunk and placing a cushion or a triangular sponge under the shoulders. The head is gently lowered and rested on a small supporting sponge, and the chin is extended. Rotating the head to the left may help move the trachea and esophagus toward the left. While the side to be punctured in lumbar discography is that opposite the patient’s dominant pain, a right-sided approach is used for cervical discography because the esophagus lies to the left in the lower neck. The skin of the right anterior and anterolateral neck is prepped from the mandible to the supraclavicular region. Sterile drapes are applied with their margins overlapping the sternocleidomastoid muscles.
Disc puncture Midline approach The disc level to be studied is identified by fluoroscopy. Most discographers use the AP view and count both upwards from the C7–T1 level and downwards from the C2–3 level. Counting down from the C2–3 level using the lateral fluoroscopic view is more accurate. The lateral views of lower cervical segments are usually attenuated by the
Midline approach Lateral approach
scm
ij
T
t
t
ic e
lc
scm ic
ij
lc D sc
Trapezius R
L
Fig. 25.7 Needle trajectories for midline and lateral approaches. In the midline approach, the needle will pass through the platysma muscle, between carotid sheath and airway, longus colli muscle and intervertebral disc. In the lateral approach, the needle will pass through the lateral neck muscles, posterior to internal jugular vein, 1–2 mm anterior to uncinate process.
overlying shoulders. To optimally visualize these segments, longitudinal, downward traction of the bilateral upper limb is often necessary. Once the levels are identified, the fluoroscopy tube is rotated in a cephalad–caudal direction to bring the endplates parallel to the beam. Pressure is applied with the index finger to the space between the trachea and the medial border of the sternocleidomastoid. Firm but gentle pressure will displace the great vessels laterally and the laryngeal structures and trachea medially. Below C4, the right common carotid artery and the internal carotid artery above C4 artery are palpated. The fingers are insinuated until they encounter the anterior surface of the vertebral column. The patient is monitored closely for vasovagal signs, which may be caused by compression of the catrotid artery during manual displacement with needle entry.14 The spinal needle or metal instrument can be used as a guide for needle insertion. The instrument is placed on the skin parallel to the disc space using fluoroscopic guidance and a marker pen is used to draw the lines on the skin over the intervertebral disc spaces. The needle entry point should be medial to the medial border of the sternocleidomastoid, and not through that muscle. The declination of the sternocleidomastoid ensures that at C3–4 the puncture point lies more laterally and will avoid the pharynx, whereas at C7–T1 it will be more medial and avoid the apex of the lung. One should use the shortest needle possible to reach the center of the target disc. Longer needles are more difficult to hold and direct and easier to inadvertently pass through the disc. A 23- or 25-gauge, 2.5-inch spinal needle is typically used for the procedure. With the point of the needle just medial to or under the index finger, both the needle and index finger can be moved in unison. The trachea is pushed medially by the fingernail of the index finger, and when the needle overlies the disc at a 20–40° angle, the needle is introduced through the skin directed toward the anterior lateral aspect of the disc (Fig. 25.7). In some patients, the discs can be directly palpated and the finger moved almost perpendicular to the disc center. Patients with short, thick necks or a large, immobile larynx are a challenge. On contact with the anulus, the patient may experience transient pain. The needle is advanced into the substance of the disc under direct AP fluoroscopic visualization. All movements of the needle should be slow and deliberate. One must be very careful not to pass the needle through the disc and into the epidural space or spinal cord. Use of a short needle may be helpful. Novice discographers may want to touch the anterior 295
Part 2: Interventional Spine Techniques
Fig. 25.9 For the midline approach, the fingernail of the left index finger applies firm pressure to push the great vessels laterally and the trachea medially. The medial border of the sternocleidomastoid is a relative skin surface marker.
Fig. 25.8 Needle insertion point. The target insertion point is 1–2 mm medial to the anterior margin of the uncinate process using an oblique view (UP, uncinate process).
disc body just above or below the disc margin to help judge the depth of penetration. Once the needle is passed several millimeters into the disc, the lateral view is used to guide further advancement.
Lateral approach Although in the medial approach the needle traverses the same tissue plane used by surgeons to gain access to the cervical intervertebral disc during open and percutaneous surgical procedures, many nonsurgeon interventionists have been trained to use a more lateral approach. In this approach, the disc level is identified by fluoroscopy, and the AP view is adjusted until the vertebral endplates of the target level show parallel lines on the fluoroscopic image. The fluoroscopic beam is then axially rotated until the anterior margin of the uncinate process is moved approximately one-quarter of the distance between the anterior and posterior lateral vertebral margins. In this view, the target insertion point is 1–2 mm medial to the anterior margin of the uncinate process (Fig. 25.8). The skin entry point will be over the lateral neck muscles and posterior to the great vessels or trachea (Fig. 25.9). Pressure displacement of the great vessels is difficult and usually not done. However, this anatomic region is highly vascular and one should carefully observe patients for signs of hematoma during and after the procedure. A 25-gauge, 2.5-inch spinal
A
296
B
needle is directed toward the anterior aspect of the uncinate process and should enter the disc 1–2 mm anterior to the process, then slowly advanced to the center of the disc. One should use a needle no longer than is required to reach the center of the target disc. Before injection of contrast, the needle position within the disc is confirmed with both AP and lateral fluoroscopic images (Fig. 25.10). At C7–T1 the medial approach is preferred to avoid puncturing the apex of the lung.
Provocation and interpretation The utility of discography for solving puzzling presentations of atypical pain resulting from cervical lesions has been demonstrated. In such cases, MRI did not disclose the pain-producing lesion.14,15 Normal cervical discs accept fairly small volumes (0.25–0.5 mL) and intradiscal injection of normal discs is not painful.15,16 Schellhas et al.15 studied the accuracy of discography and MRI in the identification of source(s) of cervical discogenic pain. The results showed that discographically normal discs were never painful, significant cervical disc anulus tears often escape MRI detection, and that MRI cannot reliably identify the sources of cervical discogenic pain.15 Pain questioning and fluoroscopic imaging are performed as in lumbar discography. However, pressure-controlled injections are usually
Fig. 25.10 The needle placement. AP (A) and lateral (B) views demonstrating the needle tip (arrowhead) in the center of discs.
Section 2: Interventional Spine Techniques
not used. If the tip of the needle has been correctly placed in the center of the disc, a 1 mL or 3 mL syringe containing contrast media is attached. Manual syringe pressure is increased slowly until the intrinsic disc pressure is exceeded. Volumes as small as 0.2 mL may cause visible separation of the vertebrae, which should be monitored by fluoroscopy. Concordancy and pain intensity are recorded at 0.2 mL increments. Use of an NRS can help the patient quantify the intensity of pain experienced relative to the intensity of pain during the injection of adjacent discs. In healthy adults, the intervertebral discs of the cervical spine have a structure similar to that of the lumbar discs, consisting of an anulus fibrosus and nucleus pulposus. However, it has been observed that in the first and second decades of life before complete ossification occurs, lateral tears occur in the anulus fibrosus. Tears are most probably induced by motion of the cervical spine in the bipedal posture.17 In childhood, the uncovertebral joints begin to undergo an ongoing transformation.18 Tears in the lateral part of the disc tend to enlarge toward the medial aspect of the intervertebral disc. The development of such tears, uncinate fissures, through both sides may result in a complete transverse splitting of the disc. Such a process may be observed in the second and third decades of life in the lower cervical spine when the intervertebral disc is split in the middle into equal halves.17 These uncinate fissures are a normal finding, and rarely will one see a ‘normal’ nucleogram. A normal cervical disc offers firm resistance, and accepts less than 0.5 mL of solution with little discomfort at the time of distention. In most patients there will be transient pain when the uncinate fissures fill with contrast (Fig. 25.11). Pain provocation should be ignored unless persistent, concordant, and significant pain can be reproduced by repeated gentle manual pressurizations. Approximately 1 mL of injected contrast medium is usually enough to opacify the nucleus and fill lateral or posterior annular fissures. A positive response requires provocation of significant (>6/10) concordant pain during a confirmatory repeat injection of another 0.1– 0.2 mL of contrast medium. One should also consider retesting adjacent levels to compare pain intensities and concordance of pain. It is not uncommon to provoke concordant pain at multiple levels. In addition, one often will cause separation of the endplates during pressurization, and this movement may cause pain secondary to a symptomatic z-joint. A convincing, positive response to disc stimulation is one in which the patient reports exact or similar reproduction of pain on stimulation of a given disc, stressing one or two adjacent discs is painless or evokes pain totally foreign to the patient’s previous experience. Any other pattern of response is not held to be reliably indicative that the
A
B
Fig. 25.11 Cervical nucleogram. (A) Postinjection AP view. All needles were placed in the center of the discs. Contrast medium extended into uncinate recesses. Extension of contrast media to uncinate recesses are common after adolescence with maturation of cervical disc. (B) Postinjection lateral view.
stimulated disc is the source of the patient’s pain. It is common for a patient to have two symptomatic discs, but under those circumstances, one should still identify an adjacent disc that is asymptomatic. Without an asymptomatic ‘control’ disc, there is no evidence that the patient can discriminate between a symptomatic and asymptomatic discs, and there is no evidence that what is reported as disc pain is not simply the pain of needles felt in the back or the neck. Patients may also simply comply with the operator’s expectation that there should be pain. Although the authors agree in principle, in the common occasion when more than four discs provoke concordant pain, performing additional levels (usually the C2–3 or C7–T1) may be inappropriate. In addition to provocative testing, analgesic discography may be a useful technique for the evaluation of chronic cervical pain.14 Patients whose clinical pain pattern is reproduced or provoked during the injection of contrast media may benefit from analgesic discography. Once a painful disc has been identified in the course of discography, and once all discographic radiographs have been taken, 0.5 mL of bupivacaine can be injected into the disc to test pain relief. The patient’s accustomed pain should be relieved by this action. The duration of relief should be monitored and recorded by the patient. Relief of accustomed pain for a period consistent with the expected duration of action of the local anesthetic agent used constitutes strong evidence that the disc in question is the pain source. In practice, however, pain relief following multiple-level provocation discography is difficult to assess. Analgesic discography is probably best evaluated at a separate session, and only the one disc in question should be injected with local anesthetic. Finally, there are some patients who cannot tolerate the procedure. In these cases, little or no useful information may be obtained except that either the patient has a low pain tolerance or the operator performing the procedure is inept.
TECHNIQUE OF THORACIC DISCOGRAPHY Patient position The patient lies in a prone position on the fluoroscopy table. A wide area of the skin of the upper back is prepped and draped from the midline to the lateral wall of the chest on the side selected for puncture. As a rule, the side to be punctured is that opposite the patient’s dominant pain.
Disc puncture The current standard technique of thoracic discography was described by Shellhas et al.19 in 1994. Prior to the procedure, a fluoroscopic examination of the thoracic spine is performed to confirm segmentation and determine the safest and most accessible route to each disc. After the discographer selects the target disc on AP view, the fluoroscope is rotated in a cephalad–caudal direction to align the endplates. The fluoroscopic beam is then rotated ipsilaterally until the corner of the intervertebral disc space is visualized between the superior articular process and the costovertebral joint. Typically, this degree of ipsilateral rotation will superimpose the tip of the spinous process on the edge of the contralateral vertebral body. In this view, the insertion point is just lateral to the interpedicular line (Fig. 25.12) and approximately 3 cm lateral to the spinous process. Prior to needle placement, the skin and subcutaneous and deep muscular tissues along the trajectory of each needle are infiltrated with local anesthetic. Most discographers prefer a single-needle technique using either a 23- or 25-gauge, 3.5-inch needle. A slight bend placed on the end of the needle will facilitate changing directions by needle rotation. The trajectory of the needle is roughly parallel and behind the rib as it passes anterior to attach to the spine at the costovertebral joints. One aims at a round to square section of the posterior lateral disc that can be seen through a 1–3 mm opening between the superior articular process and the rib (Fig. 25.13). The needle should be advanced in short 297
Part 2: Interventional Spine Techniques
following end points is reached: the subject experiences pain greater than 6/10 or 7/10, intradiscal pressure reaches a firm end point, or a total of 2.5 mL of contrast medium has been injected.
Imaging
Fig. 25.12 Target point for needle insertion at thoracic spine (oblique view) (SAP, superior articular process; P, pedicle; CVJ, costovertebral joint; EP, endplate).
increments and the direction changed as necessary by needle rotation. If one stays behind the rib there is no chance of penetrating the lung. Although passage of the needle behind the rib is usually uneventful, passage of the needle between the rib and superior articular process may be difficult. The needle often contacts either the superior articular process or the body of the rib, and it is often difficult to tell which structure obstructs needle advancement. The bend on the needle can be rotated one way or the other and readvanced to assist a needle direction change and allow passage through the small aperture. Once the needle has passed anterior to the superior articular process using a lateral fluoroscopic view, the needle bend is turned posteriorly to facilitate advancing the needle in a more posterior direction (Fig. 25.13).
Provocation and interpretation Provocation Once the tip of needle has been properly placed in the center of the nucleus pulposus, nonionic contrast medium mixed with antibiotic is slowly injected into each disc in 0.2–0.5-mL increments under direct fluoroscopic observation. If firm resistance to injection is encountered before the nucleus opacifies, the needle may be embedded in the anulus or in the cartilage of a vertebral endplate. At 0.2–0.3 mL increments, pain response including behavior, NRS pain intensity, and concordance should be evaluated. At any incremental injection volume, one should record the presence of morphologic abnormalities such as grade 1–3 annular tears or endplate defects. Injection is continued until one of the
A
298
B
The appearance of the normal thoracic nucleus following contrast medium injection varies, but is usually either a diffuse, elongated homogeneous pattern or a lobulated pattern. Contrast medium may extend into one or many radial fissures in various locations and may remain contained within the disc, or escape into the epidural spaces through an outer annular tear. Vertebral endplate defects may allow contrast medium to flow into the vertebra or the vertebral veins. Following discography, computerized tomography (CT–discography) is often performed to define the exact location and size of annular fissures and protrusions.
Interpretation The most important information obtained from discography is whether the patient’s pain is reproduced. Assessing the patient’s response to discography requires evaluating pain evoked by injection. Pain may be characterized by three components: intensity, location, and character. Pain intensity is reported by the patient as an NRS score and observed pain behaviors are used. If the location and character of pain provoked during discography is similar to or the same as the patient’s clinical symptoms, the criteria for concordant pain are satisfied. a positive discogram requires an abnormal disc, pain response =6/10 (NRS), pain described by the participant as ‘familiar,’ and at least one negative control disc.
POSTPROCEDURAL CARE Patients are carefully examined for vital signs and any evidence of subcutaneous bleeding or hematoma immediately after discogram, and again 30 minutes later. After the second postprocedure check, patients are advised of any possible side effects to watch for during the next several days and are allowed to leave the department on the same day. The patient should be warned to expect postprocedure discomfort, including difficulty swallowing after cervical discography and lingering back pain after lumbar discography. One should also inform the patient that there will probably be a flare-up in usual symptoms that lasts 2–7 days, but infrequently can last for an indefinite period of time. The patient should be instructed to call if he or she experiences fever, chills, or severe (or delayed) onset of pain. Patients are contacted by telephone 48–96 hours after discography to screen for any possible complications or side effects.
Fig. 25.13 The needle placement. AP (A) and oblique (B) views demonstrating the needle tip (arrowhead) in the center of discs.
Section 2: Interventional Spine Techniques
POTENTIAL RISKS AND COMPLICATIONS Lumbar discography The main complications of lumbar discography include infection (e.g. discitis) and neural injury.20 Discitis following lumbar discography has been more frequently documented and studied than cervical discitis. Causative organisms have been identified as Staphylococcus aureus, S. epidermis, and E. coli,21,22 suggesting inoculation with surface organisms or misadventure through bowel perforation. To prevent discitis, prophylaxis with antibiotics before and after the procedure may be used; however, this practice remains controversial. To avoid infection, stringent attention to aseptic technique is critical. Some authors consider discitis a rare complication of lumber discography,23–25 whereas others have found overall rates of 2.3% per patient and 1.3% per disc7 or 0.1% per patient and 0.05% per disc.22 Discitis incidence is higher for single, large-gauge needles and much lower for doubleneedle techniques.26 The authors have avoided discitis in all but one case in over 2000 lumbar discograms over a 10-year period. Animal studies have shown that intradiscal8 and intravenous7 antibiotics prevent discitis. The recommended regimen is 1 mg of cefazolin per mL of contrast medium injected into the disc at the time of discography.8 However, many discographers use 3–6 mg cefazolin (or equivalent antibiotic) per mL of contrast. Even with prophylactic antibiotics, epidural abscess after discography have been reported.27,28 Striking a ventral ramus is a potential hazard, but may be avoided by careful attention to correct technique. Any needle should be prevented from straying beyond its required and intended course. Fortunately, in a conscious patient, contact with the ventral ramus will be indicated by severe, sharp lancinating pain, which is an indication to withdraw and redirect the needle. Penetration of the intervertebral foramen or the lumber nerve roots should never be a problem, for the needle should never be permitted to stray behind the midpoint of the target disc. Other complications include spinal cord or nerve root injury, cord compression or myelopathy, urticaria, retroperitoneal hemorrhage, nausea, convulsions, headache, and most commonly, increased pain.5 Disc herniation following discography is very rare,29 and there is little evidence that discography damages the disc.30 Freeman et al.31 recently reported no histological damage following needle insertion into sheep discs.
Cervical discography Major neural structures are not along the course of the needle to the target disc. However, one must be aware that it is possible to pass a needle through the disc and into the spinal cord. Unrecognized, the injection of contrast could traumatize the spinal cord. Using the shortest needle possible to reach the center of the disc, touching the anterior vertebral margin to confirm needle depth, and checking the lateral fluoroscopic view prior to injection will minimize this risk. During injection, the operator’s second hand should be used to brace the needle hub to prevent inadvertent overpenetration of the needle. Penetration of viscera such as the pharynx and esophagus is not a problem per se, but increases the risk of infection such as epidural abscess, retropharyngeal abscess, and discitis.22,32–34 Introduced organisms may be external, or from the pharynx or esophagus if penetrated. The reported incidence of cervical discitis is 0.1–0.5%.22,33 The most common presentation is severe exacerbation of axial pain, usually beginning 5–21 days following the procedure.22 Although the patient usually experiences chills, fever is an inconsistent finding. Administering preoperative intravenous antibiotics and adding antibiotics to the contrast solution will help minimize this risk. However,
significant increases in pain following cervical discography should be investigated with tests that include a minimum of sedimentation rate and C-reactive protein. Any elevation in the former should be investigated with a contrast-enhanced MRI scan. Passage of a 23- or 25-gauge needle though the carotid artery may occur in patients with heavy, short necks where displacement of the medial structures is difficult. Although this event may result in a hematoma, the swelling usually causes minor discomfort to the patient. Continued bleeding due to a genetic- or medication-related bleeding disorder could cause airway obstruction. Cervical discography is not an inherently unsafe procedure and can be performed with few complications when performed in sterile conditions by those well experienced with cervical disc injections.35
Thoracic discography The main complications of thoracic discography include pneumothorax, discitis, and neural injury. Pneumothorax can complicate cervical, thoracic, or lumbar discography, but usually occurs in the thoracic spine with traumatic pleural puncture during discography, paravertebral block,36 or needle biopsies.37 Since Shellhas et al.19 described, and experts quickly adopted, the technique of accessing the thoracic disc behind the rib, pneumothorax has been a rare event. A small traumatic pneumothorax after percutaneous needle procedures without other significant injuries can be treated conservatively and usually does not need chest tube insertion.38 The complications with infection or neural injury at thoracic spine should be similar to those of the lumbar spine. To prevent discitis at thoracic spine, stringent attention to aseptic technique is critical, and prophylaxis with antibiotics before and after the procedure may be used.
CLINICAL TRIALS: LITERATURE REVIEW Discography has been proposed as a potential solution to the diagnostic dilemma concerning which patients to treat surgically and at what segmental level. Lumbar discography for the diagnosis of abnormalities involving intervertebral discs has been used extensively as a diagnostic tool for evaluating low back pain (LBP) since the 1950s. Although new diagnostic imaging tools have been developed and are widely used, discography is still practiced. Discography remains particularly useful in problematic cases unresolved by MRI or myelography, and for patients for whom surgery is contemplated.6 In 1992, Osti and Fraser39 compared MRI with discography in disc disease and found that, using the current standard techniques, MRI failed to demonstrate some structural changes in the anulus that were visualized by discography. A similar result was obtained in a comparison of high-resolution CTs with discography.40 Several studies have demonstrated that MRI cannot reliably predict which discs are painful upon discography, at least not to the level of confidence required to rely solely on MRI for surgical decision making.41,42 A high intensity zone (HIZ) in the posterior anulus visualized by MRI has been proposed as a marker for painful discs.11,43 While highly specific, the sensitivity of this finding is only 26%, limiting the usefulness of the HIZ in selecting patients for surgery.44 While numerous papers have examined the usefulness of discography, some physicians still question its reliability.45,46 Critics point towards mismatches between morphological features and clinical complaints and false-positive rates. Discography, especially combined with CT scanning, is exquisitely sensitive for identifying morphologic disc abnormalities, and the frequency of discography-detected abnormal discs in the LBP population is quite high. For example, Grubb et al.29 found that in 78% of their patients with LBP, discography afforded positive findings for abnormality at one or more levels, 299
Part 2: Interventional Spine Techniques
whereas plain radiography and myelography demonstrated no such disease. Brodsky and Binder23 also found that discography revealed abnormalities in many patients with normal-appearing myelograms. The frequency of morphologic abnormalities revealed via discography in the back pain population is high, and increases with age,47,48 putatively due to painless degenerative changes.48 In addition, the location of an annular tear and the location of pain appear to be uncorrelated.49 Discrepancies between morphological appearance and pain provocation have also been described.50 Millete and Melanson51 reported retrospectively that concordant pain was evoked by injection in only 37% of patients with a morphological abnormality documented by discography. Antti-Poika et al.52 reported only a 52.8% concordant pain provocation rate in discs where discography showed abnormal morphological changes. There have been some reports that only anulus tears may be reliably associated with pain provocation, and that other degeneration patterns were not necessarily associated with a pain response. It is clear that abnormal morphological structures revealed by discography are considered too non-specific to be clinically useful, and that positive results should be limited to those eliciting concordant pain.46,53 Several series of asymptomatic patients have shown abnormal morphological findings using discography and CT–discography.53–55 Sachs et al.10 reported a 13% incidence of abnormal disc structure detected by postdiscography CT scanning without pain provocation in a large series of patients. Several authors have also discussed that severe back pain may be elicited by discography in patients without a prior history of such pain.45,54,55 Early work by Holt55 reported a 36% rate of positive discography in asymptomatic subjects, although this study contained methodological flaws. These findings were subsequently refuted by Walsh et al.,53 who demonstrated a 0% rate of positive discography in asymptomatic volunteers and established reproducible criteria for positive discography. Walsh studied 10 asymptomatic subjects and 7 patients with chronic LBP. Criteria for a positive result included 3/5 pain intensity (using a pain thermometer), similar distribution of pain, two types of pain behavior assessed by videotape review, and structural degeneration. Antti-Poika et al.52 reported in a prospective study of 279 injected discs in 100 patients that injection elicited concordant pain in >13% of patients with normal disc anatomy. Caragee et al.54 expanded on Walsh’s study of asymptomatic subjects by examining a cohort without LBP but with clinical characteristics closely matching those of patients with LBP. Results showed that, in individuals with normal psychometrics without chronic pain, the rate of false positives is very low if strict criteria are applied, and that false-positive rates increase with abnormal psychometrics and increased annular disruption. The authors have recently studied the reliability of discogram using precise criteria for positive discography (e.g. reproducible NRS pain over 6/10 with 50% reduction from baseline pain score) or side effects. During phase II of the study, each patient received a combination consisting of 50% of the final dosage of morphine combined with 50% of the final dosage of clonidine. The authors compared the proportion of those patients who had a positive response at any time during the assessment. Five of 15 patients responded positively to saline, 3 of 15 responded to the largest dosage of clonidine alone, 5 of 15 responded to the largest dosage of morphine alone, and 7 of 15 to the combination of one-half the largest dosage of clonidine plus one-half the largest dosage of morphine. These data suggest that morphine and clonidine is a worthwhile combination to achieve improvement in analgesia. In a prospective study, Uhle et al. reported on 10 patients with neuropathic pain syndromes who received clonidine at an average of 44 mcg/day in combination with morphine sulfate or buprenorphine.85 All patients had a 70–100% reduction in pain after the addition of clonidine to either morphine or buprenorphine. Four of eight patients with non-neuropathic pain syndrome also appeared to benefit from the addition of clonidine. The most frequent adverse effects noted in this study were hypotension, fatigue, dry mouth, and impaired bowel (N=10, 4, 3, 1 patients, respectively). Tizanidine is an alpha2 agonist used clinically as a muscle relaxant. It appears to have a potential role as an intrathecal analgesic drug. In a dog model, Kroin et al.86 reported that tizanidine and clonidine at dosages of 3.0–18.0 mg/day yielded equivalent analgesia using a thermal withdrawal test, but that clonidine, when compared to tizanidine, was associated with greater toxicity (hypotension, bradycardia, and bradyarrhythmias). A further toxicity study of 3–6 mg/day in dogs was performed and these authors found no significant side effects or 357
Part 2: Interventional Spine Techniques
differences in spinal cord histopathology between the 3 mg/day and 6 mg/day groups. Kawamata et al.87 studied the effects of clonidine and tizanidine on a rat model of neuropathic pain. Sprague-Dawley rats were chronically implanted with lumbar intrathecal catheters, and the sciatic nerve was loosely ligated. Twenty-one to 28 days after surgery, the rats received intrathecal clonidine (0.3, 1.0, and 3.0 μg) and tizanidine (1.0, 2.0, and 5.0 μg), and the antihyperalgesic effects of thermal and mechanical stimuli were examined. In addition, changes in blood pressure and heart rate, sedation level, and other side effects after intrathecal administration of drugs were studied. The authors found that the administration of 3.0 micrograms of intrathecal clonidine or 5 micrograms of tizanidine significantly reversed both thermal and mechanical hyperalgesia. The administration of 3.0 micrograms of intrathecal clonidine, but not 5.0 micrograms of tizanidine, significantly decreased mean blood pressure and heart rate and produced urinary voiding. A greater sedative effect was produced by the clonidine when compared to the tizanidine. The authors concluded that the antihyperalgesic dose of intrathecal clonidine and the antinociceptive doses produced several side effects. Intrathecal tizanidine at the dose that reversed hyperalgesia would be preferable for neuropathic pain management because of absence of hypotension and bradycardia and lower incidence of sedation. Ziconotide is an omega-conopeptide, a synthetic form of the cone snail peptide, varpi-conotoxin MVIIA. Ziconotide is a neuron-specific, N-type voltage-gated calcium channel blocking agent with an analgesic and neuroprotective effect.88 Spinally administered ziconotide blocks neurotransmitter release from primary nociceptive afferents to prevent pain signal propagation to the brain. It has an advantage over intrathecal morphine in that it is a non-opioid and tolerance does not developed after its prolonged use. Although it has been used extensively in humans, ziconotide is approved by the FDA for clinical intrathecal use. Ziconotide is indicated for both nociceptive and neuropathic type of pain. It has been shown to be effective not only for chronic pain but also for acute postoperative pain. Atanassoff et al.89 performed a randomized, double-blind pilot study in patients undergoing elective total abdominal hysterectomy, radical prostatectomy, or total hip replacement. After intrathecal injection of local anesthetic and before surgical incision, a continuous intrathecal infusion of either placebo or 1 of 2 doses of ziconotide (0.7 mcg/hour or 7 mcg/hour) was started and continued for 48–72 hours postoperatively. Thirty patients received the study drug and 26 of them were evaluable for efficacy. It was found that the mean daily patient-controlled analgesia (PCA) morphine equivalent consumption was less in patients receiving ziconotide than in placebo-treated patients. The visual analogue scale of pain intensity (VASPI) scores during the first 8 hours postoperatively were remarkably lower in ziconotide-treated than in placebo-treated patients. In 4 of 6 patients receiving the high dose of ziconotide (7 mcg/hour), adverse events such as dizziness, blurred vision, nystagmus, and sedation led to discontinuation of the study drug infusion. After ziconotide discontinuation, these symptoms resolved. In a double-blind, placebo-controlled, short-term trial of ziconotide in 257 patients with non-cancer pain by Presley et al.,90 31% of the ziconotide-treated patients reported significantly lower pain scores, compared to 6% of the placebo-treated patients. Moderate to complete pain relief was achieved in 43% of patients in the ziconotide arm versus 18% in the placebo arm. Patients who received ziconotide also decreased their systemic opioid intake and reported improved quality of life compared to patients who received placebo. Staats et al., in a double-blind, placebo-controlled, randomized trial,91 studied 111 patients (ages between 24 to 85 years) with cancer or AIDS pain with VASPI score of 50 mm or greater. Patients 358
were randomly assigned in a 2 to 1 ratio to receive ziconotide or placebo treatment. Intrathecal ziconotide was titrated over 5–6 days followed by a 5-day maintenance phase for responders and crossover of nonresponders to the opposite treatment group. Pain relief was moderate to complete in 53% of patients in the ziconotide group compared to 17.5% in the placebo group. Five of 111 (4.5%) patients receiving ziconotide achieved complete pain relief. In spite of being a promising analgesic, ziconotide, like all analgesics, is not free of side effects, and side effects increase with a rapid titration of the agent and decrease with reduction in dose.91 Adverse events associated with intrathecal ziconotide have included vestibular disorders such as nystagmus, abnormal gait, nausea/vomiting and dizziness, urinary retention, blurred vision, diplopia, memory impairment, and orthostatic hypotension.90–92 Apparently, these side effects do decrease over time. In the study by Penn and Paice93 involving the use of intrathecal ziconotide in three patients with both neuropathic and nociceptive pain mechanisms, in dosages between 0.2 mcg/hour and 5.3 mcg/hour, significant pain relief was achieved. Side effects seen included nausea, diarrhea, nystagmus, dysmetria, sedation, confusion, and hallucinations. With intrathecal ziconotide doses of 0.9 mcg/hour or greater, much more serious side effects occurred including disorientation, agitation, and in two of three patients, unresponsiveness, which only resolved at some point after intrathecal ziconotide was discontinued. Midazolam. Midazolam is a GABA-alpha receptor agonist. GABAergic neurons appears to have a modulatory effect on pain processing both at the spinal and supraspinal levels. At the supraspinal level, the GABAergic neurons appear to have a tonic inhibitory effect over the descending noradrenergic inhibitory neurons. In contrast to that, at the spinal level, GABAergic neurons have an antinociceptive effect. Intrathecal midazolam works on the spinal GABA receptors to potentiate this analgesic effect. Midazolam has been used as a sole drug for intrathecal therapy for the management of postoperative pain.94 In animal studies, it has been shown that the antinociceptive analgesic effect of intrathecal midazolam can be reversed by naloxone; more specifically, this analgesic effect of intrathecal midazolam was blocked by delta-selective antagonists in rats.95 Midazolam has been shown to have a synergistic analgesic effect when given with bupivacaine intrathecally, and in animals this synergistic analgesic effect was demonstrated, giving midazolam with clonidine and with NMDA and AMPA receptors antagonists in rats.96,97 Because of conflicting reports of different toxicities in differing animal models, the use of midazolam, although used emperically by some in humans, continues to be controversial. Toxicity has not been associated with the intrathecal infusion of midazolam in studies on rats,96 cats,98 pigs and sheep;99 however, there has been, in contrast to these studies in rats, cats, pigs and sheep, evidenced toxicity with the intrathecal infusion of midazolam in rabbits.100 For a detailed review of preclinical safety issues with midazolam see the excellent review by Yaksh and Allen.101 In a prospective study by Rainov et al., 26 patients received a combination of various intrathecal agents as follows: four patients received midazolam 0.4 mg/day plus morphine sulfate 0.5 mg/day, clonidine 0.03 mg/day, and bupivacaine 1.0 mg/day; four patients received morphine/bupivacaine/midazolam; and two patients received morphine/ midazolam.102 Overall, 19/26 patients (73%) achieved good to excellent pain relief, 6/26 patients (23%) achieved sufficient pain relief, and one patient reported poor pain relief. No information was provided regarding outcomes according to drug combination received on-study. Baclofen is a GABA-beta agonist that has been used to treat spasticity since 1984. Intrathecal baclofen is FDA approved for the
Section 2: Interventional Spine Techniques
treatment of spasticity caused by upper motor neuron disease; however, questions remain as to whether baclofen is an analgesic when given intrathecally. Baclofen is stable alone or in combinations with clonidine when placed into intrathecal pump systems.103
Other non-opioid agents used intrathecally Other agents shown to be effective for the relief of pain when given intrathecally include neostigmine,104,105 adenosine,106,107 and octreotide.108,109 Neostigmine is an acetylcholinesterase (Ach) inhibitor which increases the availability of acetylcholine at the neuromuscular and the dorsal horn level. Since muscarinic receptor2 agonists produce antinociception in rats,110 and because muscarinic receptors have been detected at the level of the substantia gelatinosa and to a lesser extent in laminae III and V of the dorsal gray matter of the spinal cord, it was felt that neostigmine would be an effective analgesic if given intraspinally in humans. Neostigmine does produce analgesia in humans; however, its use is associated with an extremely high incidence of nausea and vomiting.105 Endogenous adenosine may be involved in the mediation of the spinal antinociception induced by descending adrenergic fibers originating from the locus ceruleus. This antinociceptive effect is blocked by intrathecal aminophylline (an adenosine receptor antagonist).111 Kekesi et al.106 reported that adenosine has little antinociceptive efficacy during continuous intrathecal administration, but appears to potentiate the effect of endomorphin-1. Eisenach et al.107 compared intrathecal adenosine with intravenous adenosine for chronic neuropathic pain in seven patients with hyperalgesia and allodynia. In intrathecal group, spontaneous pain was not relieved; however, evoked dysesthesias such as allodynia and mechanical hyperalgesia were markedly reduced. Five of seven patients developed back pain after the induction of adenosine. Octreotide (Sandostatin), a synthetic octapeptide derivative of somatostatin, has been found to be beneficial in the treatment of chronic pain, although the mechanisms underlying its therapeutic effect are not completely understood. Somatostatin is distributed in the substantia gelatinosa. It has been shown to have analgesic effect without adverse effects if given intrathecally, but the high cost, more than US$20 000.00 per year, prevents its widespread use.113 In a recent double-blinded study, octreotide was found to exert primarily an antihyperalgesic rather than analgesic effect on visceral pain perception.112
SELECTION OF DRUGS FOR LONG-TERM INTRATHECAL INFUSION In year 2000, an expert panel of physicians was convened to review what was known about common practices of European and American physicians using intrathecal agents and to review what was known about the drugs that were being used by these physicians up to 1999. This Polyanalgesic Consensus Conference 2000 published their review of common and experimental intrathecal agents and proposed guidelines for the appropriate use of these agents.112 Most recently a second expert panel, the Polyanalgesic Consensus Conference 2003, convened to review newer information since 1999 and to modify the 2000 guidelines. The purposes of this expert consensus panel were to: review the medical literature since 1999 pertaining to intraspinal agents; update the algorithm for intraspinal drug selection; propose guidelines for optimizing drug concentration and dosing during therapy; develop consensus regarding the evidence required to support use of a drug for long-term intrathecal infusion; and clarify existing regulations and guidelines pertaining to the use of compounded drugs for intrathecal administration.113 Regarding guidelines for intrathecal therapy, the panel suggests six lines of approach (Fig. 31.7).
According to the recommendations of this expert panel, firstline therapy, a Line-1 approach, includes morphine, the only opioid approved by the FDA for long-term intrathecal administration, and hydromorphone, which is supported by an extensive medical literature28–34 and clinical experience. In order to avoid the risk of the development of catheter tip granuloma, the panel recommends an upper limit for drug dosage and concentration as shown in Table 31.2. If side effects come before efficacy, or if efficacy is not established at the highest recommended dose with either morphine or hydromorphone (as shown in Table 31.2), the panel recommends switching to the alternate drug on Line-1 or moving to Line-2 therapy. The latter approach, moving to Line-2 therapy, is appropriate if the pain is neuropathic in nature. Some of the experts on the panel endorsed the idea of omitting Line-1 completely and moving to Line-2 if the patient has severe neuropathic pain that had not responded to systemically administered opioids. Line-2 includes morphine or hydromorphone combined with either bupivacaine or clonidine. The hypotensive side effects associated with clonidine makes bupivacaine more favorable over clonidine. Some physicians prefer to resort directly to a Line-2 approach with patients with mixed or neuropathic pain. There are no solid data, however, to support this approach, nor are there data to support the usage of bupivacaine or clonidine for intrathecal monotherapy. If patients do not respond to the agents in Line-2, in any combination, or are intolerant to the side effects of the agents in Line-2, the panel recommends moving to the Line-3 approach of using 3drug combinations, the addition of both clonidine and bupivacaine to either morphine or hydromorphone. If the analgesic response to this 3-drug combination with morphine is inadequate, then the panel recommends moving to hydromorphone plus bupivacaine and clonidine before moving to Line-4 therapies. Line-4 therapies include the lipophilic opioids, fentanyl and sufentanil, the GABA-alpha agonist, midazolam, and the GABAbeta agonist, baclofen. The strategy here, basically, is to switch opioid treatment from morphine or hydromorphone to fentanyl or sufentanil. Baclofen is approved for a long-term infusion for spasticity. Data, however, do support its use as an analgesic agent for intrathecal therapy. Although the data for their safety and efficacy are limited, intrathecal fentanyl and sufentanil have been used in clinical practice.20,53 As stated before, the high lipophilicity of these agents minimizes their diffusion to rostral pain centers. Therefore, the supraspinal side effects induced by these agents are less than those induced by the more hydrophilic agents such as morphine or hydromorphone. In the United States, midazolam is not available commercially as a preservative-free compound for intrathecal therapy.101 There are few data and limited experience to suggest the intrathecal infusion of drugs in Line-5, which includes neostigmine, adenosine, and ketorolac, and Line-6, which includes ropivacaine, meperidine, gabapentin, buprenorphine, octreotide and others. Drugs in Line-5 have some degree of preclinical evaluation including toxicity evaluation; drugs in Line-6 have little or no preclinical investigation and minimal or no clinical experience to warrant suggestion of their use by the panel.
COMPOUNDING OF DRUGS FOR INTRATHECAL DELIVERY Because many physicians use off-labeled analgesic agents for intrathecal delivery, and because many of these agents are not manufactured in concentrations necessary for intrathecal use, many physicians rely on the compounding of these off-labeled analgesics 359
Part 2: Interventional Spine Techniques
Fig. 31.7 Amended guidelines of the Polyanalgesic Consensus Conference, 2003. (Used with permission of the authors.)
for their practices. The Polyanalgesic Consensus Conference 2003113 felt it necessary to guide this part of the physician’s practice [compounding] to assure that patients would not be hurt by poor practice. According to the American Society of Health System Pharmacists
Table 31.2: Recommended intrathecal dosages and concentrations Drug
Dosage (mg/day)
Concentration (mg/mL)
Morphine
15
30
Hydromorphone
10
30
Bupivacaine
30
38
Clonidine
1.0
2.0
Recommended intrathecal dosages and concentrations106 to prevent the formation of intrathecal tip granuloma. These recommendations represent general recommendations of the expert consensus panel and are dependent upon the specific patient and the clinical experience of the physician; thus, maximum dosage and/or concentration may vary from these.Re volorem num voloreet ut vullamc ortisim zzriliscilit prate
360
(ASHSP),114 compounding is defined as the process of mixing of ingredients to prepare a medication for patient’s use, including dilution, admixture, repackaging, reconstitution, and other manipulations of sterile products. Morphine sulfate is the only available, commercially packaged, preservative free, FDA approved opioid for intrathecal use, while baclofen is the only available, commercially packaged, preservative free, FDA approved spinal antispasmodic for intrathecal use and ziconotide is the only available, commercially packaged, preservative free non-opioid intrathecal analgesic that is FDA approved. Most other intrathecal agents, in concentrations that are needed for monotherapy or combination therapy, require compounded formulations from compounding pharmacies. The United States Pharmacopoeia (USP)115 and the ASHSP have issued standards for compounding sterile products. These standards also apply to the compounding of solutions for intrathecal drug delivery. According to these standards, all sterile compounded and preservative free preparations, administered via an intrathecal delivery system, are classified as, at least, level 2 (medium risk), and many are classified as level 3 (high risk) preparations.114,115 The Polyanalgesic Consensus Conference 2003 suggests a set of considerations that need to be respected when preparing com-
Section 2: Interventional Spine Techniques
pounded formulations for intraspinal delivery.113 The following is a list of does and don’ts when compounding intrathecal agents: 1. Avoid preservatives, antioxidants, and solubility enhancers, as they may be neurotoxic and/or may be incompatible with the delivery system. 2. Use products that are compatible with the delivery system. 3. Use a pH that is physiologically appropriate and is consistent with the drug solubility and delivery system, generally in the range of pH 4 to 8. 4. In order to avoid exposing spinal tissues to the drug for a prolonged period of time, use solutions that are ideally isotonic with normal CSF (approximately 300 mOsm/L), so that the drug in solution can distribute evenly and quickly in the CSF. 5. Prepare the solution in a manner that does not alter the solubility of the constituents within the solution. Solubility enhancers should be avoided as they may be neurotoxic or incompatible with the delivery system. 6. Verify the chemical and physical stability of the preparation under relevant conditions in accordance with the USP and ASHSP applications. 7. Verify the stability of the preparation in accordance with the USP and the ASHSP publications. 8. Ensure appropriate control of bacterial endotoxins (pyrogens). Bacterial endotoxins are safety concerns, even for products that are sterilized, because sterilization does not remove endotoxins.
THE SIDE EFFECTS OF INTRASPINAL ANALGESIC THERAPY Patients might or might not tolerate a drug well during its administration for the screening trial. However, during therapy, patients may develop intolerance or tolerance to the drug. Should side effects of intrathecal delivery (nausea and vomiting, urinary retention, generalized pruritus, constipation, oversedation, confusion, paranoia, hyperalgesia/myoclonus syndrome, Meniere’s-like symptoms, nystagmus, the development of tip granuloma, or herpes reactivation) develop during therapy, an attempt should be made to manage these problems pharmacologically, if possible, before switching to another spinal agent. Although respiratory depression is a known consequence of the use of intrathecal opioids in the opioid-naive patient, it is rarely seen in patients who are receiving intrathecal agents because most of these patients have had extensive systemic exposure to opioid use. As stated above, there is incomplete cross-tolerance of one opioid agonist to other opioid agonists. Therefore, patients who have side effects from one intrathecal agent may not have the same side effects with another drug at equivalent doses.
Gastrointestinal complications Constipation. The incidence of constipation from intrathecal delivery of opioids is less than when the opioids are given systemically.116 The management of intrathecal opioid induced constipation is the same as the management of systemic opioid induced constipation using stool softeners and gentle laxatives. If this approach does not resolve the problem, one should consider switching to another opioid or, if possible, lowering the dose of the opioids. Nausea and vomiting. Opioids are thought to induce nausea and vomiting by a direct action on the chemoreceptor trigger zone (CTZ), an area of the hindbrain, which is outside the blood–brain barrier. This is supported by evidence showing that ablation of the CTZ prevents the induction of vomiting by opioids.117 The mechanism of action of opioids in emesis is, however, complicated. Biphasic dose–response curves have been reported and, in certain circumstances, opioids can
have antiemetic actions.118 Vomiting as a side effect of intrathecal administration of opioids is infrequent; however, should it happen, antiemetic therapy usually will resolve the problem. If nausea and vomiting persist, the clinician should use an agent that has less spread to supraspinal centers when given intrathecally. Agents that have less spread to supraspinal centers are agents of greater lipophilicity, including methadone, fentanyl, and sufentanil. Urinary retention is an early common side effect of intrathecally administered opioids in males, especially elderly males, and is infrequent in females. Urinary retention is most common when therapy is first initiated, but fortunately resolves spontaneously with continued therapy. Bethanechol (Urecholine) is the agent of choice for urinary retention.116 It is indicated for the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. Dosage must be individualized, depending on the type and severity of the condition to be treated. The usual adult oral dose ranges from 10 to 50 mg three or four times a day. The effects of the drug appear in 30–90 minutes and persist for approximately 1 hour. If necessary, the effects of the drug can be abolished promptly with atropine. Should urinary retention persist, in spite of adequate pharmacologic therapy, decreasing the dose of intrathecal medication would be the next step, and if that does not work, perhaps changing agents from a hydrophilic agent to a lipophilic agent would be appropriate. Pruritus a fairly common side effect. The incidence of this opioid side effect is higher in opioid-naive patients than in those patients who are opioid tolerant. The use of antihistamines may ameliorate the problem; however, using opioid antagonists or partial antagonists, in combination with opioids in the pump, has been suggested as a possible solution.45
Central nervous system side effects Sedation, dizziness, and memory problems are not unusual and are related to the rostral spread of the opioids within the CSF. If these side effects develop and become a serious problem, using a more lipophilic opioid might ameliorate the problem. Although, in our practice, the use of modafenil and other psycho-stimulants have helped some of our patients to overcome the sedating side effect. Sexual and endocrine dysfunction. The prevalence of these side effects is quite high in patients who are receiving intrathecal opioid therapy. In a study of 73 patients, the majority had hypogonadotropic hypogonadism, 13% developed central hypocorticism, and 17% growth hormone deficiency. These abnormalities affected the sexual function in this group of patients.27 Leg and pedal edema. These side effects are not infrequent in patients receiving intrathecal opioid therapy. In a study by Aldrete and da Silva et al.,119 five out of 23 patients (21.7%) who received intrathecal opiates for longer than 24 months developed pedal or leg edema. However, the symptoms improved by the discontinuation or reduction of the dose; the most effective treatment was elevation of the legs and dose reduction. The use of diuretics with elastic stockings can be helpful in overcoming this side effect. In our experience, the incidence of peripheral edema is greater with the use of hydrophilic agents such as morphine or hydromorphone than with lipophilic agents such as fentanyl, sufentanil, and methadone. Consequently, if peripheral edema develops and does not respond to diuresis, we switch hydrophilic agents to lipophilic agents. Tolerance is a phenomenon in which exposure to a drug results in the diminution of effect, either desired or undesired, or the need for a higher dose to maintain the effect, desired or undesired. Tolerance can be considered an adaptation process which may be traced back to cellular and molecular levels. Receptor mechanisms of tolerance 361
Part 2: Interventional Spine Techniques
include downregulation and upregulation of numbers of receptors. Also, there is evidence that the higher the intrinsic activity of the opioids at only one receptor site, fewer receptors are needed in order to induce a potent analgesic effect; therefore, the incidence of tolerance is less. Drugs with high intrinsic activity include sufentanil and fentanyl.120 NMDA receptor activation through protein kinase, phospholipase C translocation, and activation of nitric oxide synthetase also contributes to the formation of tolerance.120,121 If titrating the dose up does not resolve the problem, changing into a new opioid or giving the patient a ‘holiday’ from opioid intrathecal therapy should be considered.
Although intrathecal therapy is helpful for patients with chronic intractable pain that fails to respond to other modalities of therapy, this treatment modality is not free of complications. Complications of intrathecal therapy may be divided into surgical complications, complications related to the drug delivery system, and iatrogenic complications.
Hematoma is a collection of blood in the surgical wound and seroma is a collection of the serum in a wound. A hematoma might develop secondary to the tissue trauma of surgery or the nonmeticulous attention to homeostasis. After surgery, and because the body abhors a vacuum, most newly created pump pockets do develop a fluid collection or seroma that may last for up to 1–2 months post implantation. These fluid collections are self-limiting and usually are of no clinical significance. Patient reassurance is usually the only treatment necessary. If fluid collection is excessive and bothersome to the patient, an abdominal binder usually will decrease the size of the seroma and promote healing. If infection is suspected (rubor, dolor, calor), an aspiration for Gram-stain, and culture-and-sensitivity should be performed. Restated, Gram-stains must show bacteria to differentiate from simple seroma. All seroma contain large amounts of white blood cells. If there is a proven bacterial contamination of the wound, the patient should be placed on intravenous antibiotics with antibiotic irrigation of the pocket itself.
Surgical complications
Infections
Bleeding. Bleeding may occur despite meticulous surgical incisions and dissection. In order to minimize this, the surgeons screen their patients appropriately for coagulopathies, especially in cancer patients undergoing chemotherapy who may have low platelet counts or in those patients taking excessive amounts of NSAIDs. Patients who are pharmacologically anticoagulated or those who have physiologic coagulopathies are not candidates for these procedures until anticoagulation is corrected and bleeding parameters return to normal. In spite of good surgical evaluative and technical skills, surgical bleeding is often unavoidable. A good rule for the implantation surgeon to follow is to close a wound only after carefully inspecting the wound area for active bleeding. Wound bleeding provides a good medium for the growth of bacteria, leading to postoperative infections. Since the technique for catheter implantation of drug delivery systems passes through the epidural space, bleeding may occur within the epidural space without the surgeon being aware of it. This bleeding, if significant, could lead to epidural hematoma, spinal cord compression, and a cauda equina syndrome leading to paralysis with bowel and bladder dysfunction. The surgeon should expect this complication if the patient complains of persistent back pain and tenderness, urinary incontinence, anal sphincter tone weakness and fecal incontinence. The diagnosis of epidural hematoma is confirmed with emergent MRI or CT with contrast of the spine. Epidural hematoma is a neurosurgical emergency which may require evacuation. To avoid postoperative bleeding, patients should be screened for coagulopathies. Cancer patients and some patients with comorbid disease such as bleeding dyscrasia or liver disease might be thrombocytopenic, and some patients with chronic pain might be on nonsteroidal antiinflammatory agents. Physicians must be aware of all of the possible causes of surgical and postsurgical bleeding and take steps to correct them appropriately. Patients with thrombocytopenia should receive platelet transfusion preoperatively and patients on NSAIDs must have their medications discontinued 72 hours before surgery and 12 days before surgery, if the patient is taking aspirin. Patients who are on warfarin should have their medication stopped, if appropriate, at least 4 days prior to the planned surgery. If not appropriate, the patient should be placed on an agent such as enoxaperin (Lovenox) for 4 days prior to surgery after discontinuing warfarin. The enoxaperin can be discontinued safely 12 hours before surgical time. The meticulous attention to hemostasis intraoperatively is also an important measure to prevent postoperative bleeding.
Appropriate preoperative antibiotics, and strict adherence to intraoperative external measures, help minimize the problem of postoperative infection. Since most postoperative infections are caused by the Gram-positive cocci, S. aureus and S. epidermidis, agents specific for these bacteria, such as the cephalosporins or vancomycin, should be used preoperatively. If a postoperative infection does occur and is superficial and not deep, systemic antibiotics should be used to prevent deepening of the infection to involve the pump pocket itself. If the infection does involve the implanted catheter or the pocket of the implanted pump, removal of the entire system is mandatory to prevent epidural abscess or meningitis. The development of epidural or intrathecal infections mandates the immediate removal of the system. In case of intrathecal infection, attention should be paid to meningeal irritation signs and consultation with an infectious disease consultant is recommended. Remember, not all fever spikes in the first 72 hours after implantation of an intrathecal catheter means meningitis. In our experience, a good percentage of patients with newly implanted intrathecal catheters do develop fever spikes within the first 72 hours after implantation. These noninfectious fevers, probably a foreign body reaction to the implanted catheter, may be associated with a slightly stiff neck due to the CSF leakage, and may be associated with headache. In these cases, CSF withdrawn from the side port of the pump will be negative for bacteria, but will be positive for a mild to moderate leukocytosis, a spinal response to the implanted foreign body. If the CSF culture is negative for bacteria, the physician should take a wait and see attitude before starting antibiotics unnecessarily.
Complications
362
Hematoma and seroma
CSF leakage Leakage of CSF around the catheter as it enters the dural sac is a frequent occurrence after intrathecal catheter placement. Fortunately, CSF leakage is a self-limiting occurrence. CSF leakage usually resolves within a week after catheter implantation. However, should the problem persist, resulting in either a postural headache or leakage of CSF from the skin suture site which might require an epidural blood patch as a treatment option of PDPH, care should be taken when this procedure is performed. This autologous blood patch is prefereably done one level below the entrance level of the catheter to avoid catheter damage and should be performed under fluoroscopy to prevent catheter damage. If CSF leakage persists with formation of a subcutane-
Section 2: Interventional Spine Techniques
ous CSF collection (hygroma), aspiration of the CSF collection must be avoided to prevent development of an infection. Aspiration does not cure the problem of the leak and fistula between the thecal sac and subcutaneous collection. Instead, applying an abdominal binder that increases pressure in the pocket might decrease CSF drainage and may help the fistula to close spontaneously. If that fails, surgical intervention might be indicated to close the fistula.
Spontaneous malpositioning of the pump Accumulation of fluid in the pump pocket such as CSF traveling from the thecal sac along the catheter to the pump pocket prevents healing of tissues, prevents capsule formation around the pump, and increases movement of the pump within the pocket. The pump, if you will, becomes a ‘floating pump.’ If a capsule does not form snuggly around the pump or if the pump is not suture-anchored to a strong tissue plane, the pump may flip over, which may lead to kinking, obstruction, or even separation of the catheter. Also, a pump flipped over in its pocket is impossible to fill. If one cannot rectify this problem by digital manipulation, a surgical revision of the pump pocket, decreasing the size of the pocket, is indicated.
Complications related to the intrathecal delivery system Complications related to the intrathecal delivery system are not unusual, but may be prevented. These complications include complications of the implanted pump or catheter system or both. Pump complications include battery failure or breakdown of the internal workings of the pump, if the pump is a programmable one. Nonprogrammable pumps, by virtue of their simplicity, usually do not break down. Catheter complications include system dislodgements, catheter kinks, breaks, shears, or obstruction. Catheter complications are heralded by a sudden loss of pain control or spasticity control, or sudden withdrawal symptoms. Examination of the catheter system under fluoroscopy and/or X-ray examination of entry site and tip site is warranted to diagnose this problem. If the system appears to be intact, a dye study of the system should be performed to discern any small breaks in the system. One must remember that there is dead space within the catheter system, containing drug, and these drugs may be of high concentrations. If one pushes a high-concentration drug within the dead space by injecting dye through the pump side port, untoward and unintended complications may arise due to inherent toxicities of the drug ‘pushed.’ To prevent this, one should aspirate all of the drug out of the dead space before injecting dye through the side port. If it is expected that one might not be able to aspirate from the side port at the time of the dye study, then all concentrations of drug in the pump should be diluted way in advance of the study to prevent toxic levels of the drug or drugs from being injected intrathecally. An alternative to this strategy for detection of breaks within the system, in programmable pumps, is to drain the pump of drug in advance of the study, and, after an appropriate time interval, inject the side port, or as Medtronic, Inc. (Minneapolis, Minnesota) recommends, filling the pump with an isotope, then programming the pump to deliver the isotope while observing the system by nuclear medicine scanning. Pump ‘breakdown’ is most usually heralded by a sudden loss of pain or spasticity control, sudden withdrawal syndrome, or an observed discrepancy between observed residual volume and expected residual volume at the time of refill. Pump breakdowns do occur and may be related to faulty manufacturing or damage by a nonapproved drug placed within the pump, which might damage the internal catheter system. Diagnosis of a faulty motor/rotor, within the pump, is made by real-time, fluoroscopic observation of motor/rotor performance.
The programmable pump is programmed to bolus inject over a relatively short period of time. The motor/rotor is observed under fluoroscopy to either move or not. If the rotor, after programming of a bolus, does not move, there is breakdown of the pump.
Iatrogenic complications Iatrogenic complications may be related to errors in formulating admixtures of drugs, refilling pumps with wrong medications, technical errors in refilling pumps, or errors in programming pumps. Infection, as it relates to poor sterile technique, is also an iatrogenic complication. Medications injected into the pocket surrounding the pump instead of into the pump requires immediate aspiration of the drug from the pocket and close observation for an appropriate period of time to rule out drug overdose from systemic uptake of the drug into systemic circulation. To avoid ‘dumping’ medication into the pump pocket, one should always aspirate drug after partial filling to assure that there is no sanguinous material in the aspirate. Programming errors that lead to serious consequences include programming wrong concentrations or wrong rates of administration. Also, remember that it is important to correctly calculate a ‘bridge bolus’ after changing concentrations of the drug infused.
Catheter tip granuloma In 1991, North et al. first reported a granulomatous region associated with the intrathecal catheter tip causing mass effect and neurologic dysfunction.122 In a literature review on the subject by Coffey and Burchiel, in November of 2000, 41 cases, 16 from the literature and 25 reported to Medtronic, Inc. and to the FDA, were identified.35 The mean duration of therapy in these cases was 24.5 months. Most cases were located in the thoracic region. Intrathecal drugs involved included morphine or hydromorphone, either alone or mixed with other drugs in 39 out of the 41 cases. Thirty patients underwent surgery to relieve spinal cord or cauda equina compression. Eleven of the patients were nonambulatory and one died due to pulmonary embolism. Microscopically, the masses were composed of chronic inflammatory cells with variable degrees of granuloma formation. In these cases, there was a region of central necrosis resembling an abscess that contained no polymorphonuclear leukocytes. Although tissue stains for microorganisms were uniformly negative, intraoperative cultures were positive in three cases, thought to be a secondary process. Yaksh et al., observing masses in humans and in two species of animals, suggested a probable relationship existing between the mass formation and opioid dose and concentration.123 Some authors have suggested placing catheter tips below the conus medullaris to avoid catastrophic complications caused by granulomatous mass formation over the spinal cord. However, in a case report by Fernandez et al.,124 a patient placed on hydromorphone, 110 mg per day with a concentration of 400 mg/mL, developed a catheter tip granuloma in the sacral region. In this case, the catheter was placed caudally into the lumbosacral region. This patient presented with saddle anesthesia and bowel/bladder incompetence, and after surgery, the patient was left permanently disabled.
References 1. Goldstein A, Lowney LI, Pal PK. Stereospecific and nonspecific interactions of the morphine congenitor levorphanol in subcellular fractions of mouse brain. Proc Natl Acad Sci USA 1971; 68:1742–1747. 2. Pert C, Synder S. Opiate receptor: demonstration in nerve tissue. Science 1973; 48:1011–1014 3. Kuhar MH, Pert CB, Synder SH. Regional distribution and opiate receptor binding in monkey and human brain. Nature 1973; 245:447–450.
363
Part 2: Interventional Spine Techniques 4. Lamotte C, Pert CB, Synder SH. Opiate receptor binding primate spinal: distribution and change after dorsal root section. Brain Res 1976; 11:407–412.
31. Du Pen S, Du Pen A, Hillyer J. Intrathecal hydromorphone for intractable nonmalignant pain: A retrospective study. Pain Med 2006; 7:10–15.
5. Yaksh TL, Rudy TA. Analgesia mediated by a direct spinal action of narcotics. Science 1976; 192:1357–1358.
32. Hildebrand KR, Elsberry DE, Anderson VC. Stability and compatibility of hydromorphone hydrochloride in an implantable infusion system. J Pain Symptom Manage 2001; 22:1042–1047.
6. Wang JK, Naus LA, Thomas JE. Pain relief by intrathecally applied morphine in man. Anesthesiology 1979; 50:149–151. 7. Behar M, Olshwang D, Magora F, et al. Epidural morphine in treatment of pain. Lancet 1979; I:527–528. 8. Ventafrida V, Figliuzzi M, Tamburini M, et al. Clinical observation on analgesia elicited by intrathecal morphine in cancer patients. In: Bonica JJ, Ventafrida V, eds. Advances in pain research and therapy, vol. 2. New York: Raven; 1979:559–565. 9. Krames ES. Intraspinal analgesia for nonmalignant pain. In: Steve D. Waldman. Interventional pain management, 2nd edn. 2001:609–620. 10. Krames ES. Intraspinal opioid therapy for chronic nonmalignant pain: current practice and clinical guidelines. J Pain Symptom Manage 1996; 11:333–352. 11. Winkelmuller M, Winkelmuller W. Long-term effect of continuous intrathecal opioid treatment in chronic pain of nonmalignant etiology. J Neurosurg 1996; 85:458–467. 12. Hassenbusch SJ, Stanton-Hicks MD, Soukup J, et al. Sufentanil citrate and morphine/bupivacaine as alternative agents in chronic epidural infusion for intractable non-cancer pain. Neurosurgery 1991; 29:76–82. 13. Schuchard M, Krames ES, Lanning RM. Intraspinal analgesia for nonmalignant pain: a retrospective analysis for efficacy, safety and feasibility in 50 patients. Neuromodulation 1998; 1:46–56. 14. Borolat G, Schwartzman RJ, Aries L. Chronic intrathecal morphine infusion for intractable pain in reflex sympathetic dystrophy. In: Proceedings of the 8th meeting of the European Society for Steriotatic and Functional Neurosurgery. Budapest, Hungary, 1981:81. 15. Nitescu P, Joberg M, Applegren L, et al. Complications of intrathecal opioids and bupivacaine in the treatment of refractory cancer pain. Clin J Pain 1995; 11:45–62. 16. Krames E. Best practice and research. Clin Anesthesiol 2002; 4:619–649. 17. Macres S, Richeimer S. Successful treatment of erythromelalgia with intrathecal hydromorphone and clonidine. Clin J Pain 2000; 16:310–313. 18. Ong B, Segstro R. Resperatory depression associated with meperidine spinal anesthesia. Can J Anesth 1994; 41:725–727. 19. Mironer YE, Tollison CD. Methadone in the intrathecal treatment of chronic nonmalignant pain resistant to other neuroaxial agents. The first experience. Neuromodulation 2001; 4:25–31. 20. Meininger D, Byhahn C, Kessler P. Intrathecal fentanyl, sufentanil, or placebo combined with hyperbaric mepivacaine 2% for parturients undergoing elective cesarean delivery. Anesth Analg 2003; 96:852–858. 21. Shah FR, Halbe AR, Panshal ID. Good child CS, improvement of postoperative pain relief by the addition of midazolam to an intrathecal injection of buprenorphine and bupivacaine. Eur J Anesthesiol 2003; 20:904–910. 22. Kumar K, Kelly M, Pirlot T. Continuous intrathecal morphine treatment for chronic pain of nonmalignant etiology: long-term benefits and efficacy. Surg Neurol 2001; 55:79–86; discussion 86–88. 23. Deer T, Chapple I, Classen A, et al. Intrathecal drug delivery for treatment of chronic low back pain: report from the National Outcomes Registry for Low Back Pain. Pain Med 2004; 5(1):6–13. 24. Cousins MJ, Cherry DA, Gourlay GK. Acute and chronic pains use of spinal opioids. In: Cousins MJ, Bridenbaugh P, eds. Neural blockade in clinical anesthesia and management of pain, 2nd edn. Philadelphia: JB Lippincott; 1988:955–1029. 25. SJogren P, Thunedborg LP, Christrup L et al. Is development of hyperalgesia, allodynia and myoclonus related to morphine metabolism during long-term administrating: six case histories. Acta Anaesthesiol Scanda 1988; 42:1070–1075. 26. Hemstapat K, Monteith GR, Smith D, et al. Morphine-3-glucoronide’s neuroexcitatory effects are medicated via indirect activation of N-methyl-D-aspartic acid receptors: mechanistic studies in embryonic cultured hippocampal neurons anesthesia, and analgesia. Anesth Analg 2003; 97(2):494–505. 27. Abs R, Verhelst J, Maeyaert J et al. Endocrine consequences of long-term intrathecal administration of opioids. J Clin Endocrinol Metab 2000; 85:2215–2222.
364
33. Brodsky JB, Chaplay SR, Brose WG, et al. Continuous epidural hydromorphone for post phoracotomy pain relief. Ann Thorac Surg 1990; 50:888–893. 34. Johansen MJ, Satterfield WC, Baze WB, et al. Continuous intrathecal infusion of hydromorphone: Safety in the sheep model and clinical implications. Pain Med 2004; 5:14–25. 35. Coffey RJ, Burchiel K. Inflammatory mass lesions associated with intrathecal drug infusion catheters: report and observations on 41 patients. Neurosurgery 2002; 50:78–86; discussion 86–87. 36. Yaksh TL, Hassenbusch S, Burchiel K, et al. Inflammatory masses associated with intrathecal drug infusion: A review of preclinical evidence and human data. Pain Med 2002; 3:300–312. 37. Wright AW, Mather LE, Smith MT. Hydromorphone-3-glucoronide is a more potent neuro-excitant than its structural analogue morphine-3-glucoronide. Life Sci 2001; 69:409–420. 38. Patel D, Janardhan Y, Meri B et al. Comparison of intrathecal meperidine and lidocaine in endoscopic urologic procedures. Can J Anesthes 1990; 37:567–570. 39. Thi TV, Orliaguet G, Liu N et al. A dose range study of intrathecal meperidine combined with bupivacaine. Acta Anaesthesiol Scand 1992; 36:516–518. 40. Sharma SK, McIntire DD, Wiley J, et al. Labor analgesia and cesarean delivery: an in patient meta-analysis of nulliparous women. Anesthesiology 2004; 100:142–148. 41. Cozian A, Pinand M, Lepage JY et al. Effects of meperidine spinal anesthesia on hemodynamics, plasma catecholamines, angiotensin I, aldosterone, and histamine concentrations in elderly men. Anasthesia 1986; 64:815–819. 42. Harvey SC, O’Neil MG, et al. Continuous intrathecal meperidine via an implantable pump for chronic, nonmalignant pain. Ann Pharmacother 1997; 31(11):1306–1308. 43. Mironer YE, Grumman S. Experience with alternative solutions in intrathecal treatment of chronic nonmalignant pain. Pain Dig 1999; 9:299–302. 44. Chrubasik J, Chrubasik S, Friedrich G et al. Long-term treatment of pain by spinal opiates: an update. Pain Clin 1992; 5:147–156. 45. Mironer YE. Neuraxial opioid therapy. In: Tollison CD, Satterthwaite JR, Tollison JW, eds. Practical pain management, 3rd edn. Philadelphia: Williams & Wilkins; 2002:135–154. 46. Hassenbusch SJ, Portenoy RK. Current practices in intraspinal therapy – a survey of clinical trends and decision making. J Pain Symptom Manage 2000; 20:S4–S11. 47. Gorman AL, Elliot KJ, Inturrisi CE. The D and L isomers of methadone bind to the noncompetitive site on the N-methyl-D-aspartade (NMDA) receptor in rat forebrain and spinal cord. Neurosci Lett 1997; 223:5–8. 48. Davis AM, Inturrisi CE. d-Methadone blocks morphine tolerance and N-methyl-Daspartate-induced hyperalgesia. J Pharmacol Exp Ther 1999; 289:1048–1053. 49. Shir Y, Shapiras S, Shenkman Z, et al. Continuous epidural methadone treatment for cancer pain. Clin J Pain 1991; 7:339–341. 50. Mironer YE, Haasis J C III, Chapple ET, et al. Successful use of methadone in neuropathic pain: a multicenter study by the national forum of independent pain clinicians. Pain Dig 1999; 9:191–193. 51. Mironer, YE, Tollison CD. Methadone in the intrathecal treatment of chronic nonmalignant pain resistant to other neuroaxial agents: the first experience. Neuromodulation 2001; 4:25–31. 52. Reynold L, Ked Laya D. Spinal administration of opioids. Anesthesiology 1984; 61:276–310. 53. Loper KA, Ready BL, Downey M et al. Epidural and intravenous fentanyl infusion are clinically equivalent after knee surgery. Anesth Analg 1990; 70:72–75. 54. Kamran S, Wright BD. Complications of intrathecal drug therapy. Neuromodulation 2001; 4:111–115. 55. Willis KD, Doleys DM. The effects of long-term intraspinal infusion therapy with noncancer pain patients: evaluation of patient, significant-other, and clinic staff appraisals. Neuromodulation 1999; 2:241–253.
28. Shulman MS, Walkerlin G, Yamaguchi L, et al. Experience with epidural hydromorphone for post thoracotomy pain relief. Anesthes Analges 1987; 66:567–570.
56. Hansdottir V, Hedner T, Woestenborghs R, et al. The CSF and plasma pharmacokinetics of sufentanil after intrathecal administration. Anesthesiology 1991; 74:264– 269.
29. Mahler PL, Forest W. Relative analgesic potencies of morphine and hydromorphone in postoperative pain. Anesthesia 1975; 42:602–607.
57. Ionescu TI, Drost RH, Roelofs JM, et al. The pharmacokinetics of intradural morphine in major abdominal surgery. Clin Pharmacokinet 1988; 14:178–186.
30. Anderson VC, Cooke B, Burchiel K. Intrathecal hydromorphone for chronic nonmalignant pain: a retrospective study. Pain Med 2001; 2:287–297.
58. Sosnowski M, Yaksh TL. Differential cross-tolerance between intrathecal morphine and sufentanil in the rat. Anesthesia 1990; 73:1147.
Section 2: Interventional Spine Techniques 59. Camann WR, Denny RA, Holby ED et al. A comparison of intrathecal, epidural, and intravenous sufentanil for labor analgesia. Anesthesia 1992; 77:351–353. 60. Rawal N, Nuutinen L, Raj PP, et al. Behavioral and histologic effects following intrathecal administration of butorphanol, sufentanil, and nalbuphine in sheep. Anesthesia 1991; 75:1029–1034. 61. Hildebrand KR, Elsberry DD, Deer TR. Stability, compatibility, and safety of intrathecal bupivacaine administered chronically via an implantable delivery system. Clin J Pain 2001; 17;239–244. 62. Trissel LA, Pham L. Physical and chemical stability of low and high concentrations of morphine sulfate and bupivacaine hydrochloride packaged in plastic syringes. Intl J Pharm Compounding 2002; 6:70–73. 63. Li DF, Hahar M, Cole G, et al. Neurological toxicity of the subarachnoid infusion of bupivacaine, lignocaine, or 2-chloroprocaine in the rat. Br J Anaesth 1985; 57:424–429. 64. Dahm P, Lundborg C, Janson M, et al. Comparison of 0.5% intrathecal bupivacaine with 0.5% intraspinal ropivacaine in the treatment of refractory cancer and noncancer pain conditions: Results from a prospective, crossover, double-blind, randomized study. Reg Anesth Pain Med 2000; 25:480–487. 65. SJoberg M, Karlsson PA, Nordborg C, et al. Neuropathologic findings after longterm intrathecal infusion of morphine and bupivacaine for pain treatment in cancer patients. Anesthesia 1992; 74: 424–429. 66. Rigler ML, Drasner K, Krejcie TC et al. Cauda equina syndrome after continuous spinal anesthesia. Anesth Analg 1991; 72:275–281. 67. Dupen SL, Williams AR. Management of patients receiving combined epidural morphine and bupivacaine for the treatment of cancer pain. J Pain Symp Manage 1992; 27:125–127. 68. Krames ES, Lanning RM. Intrathecal infusional analgesia for nonmalignant pain: analgesic efficacy of intrathecal opioid with or without bupivacaine. J Pain Symp Manage 1993; 8:539–548. 69. Deer TR, Caraway DL, Kim CK, et al. Clinical experience with intrathecal bupivacaine in combination with opioid for the treatment of chronic pain related to failed back surgery syndrome and metastatic cancer pain of the spine. Spine J 2002; 2:274–278. 70. van Dongen RTM, Crul BJP, von Egmond J. Intrathecal coadministration of bupivacaine diminishes morphine dose progression during long-term intrathecal infusion in cancer patients. Clin J Pain 1999; 15:166–172. 71. Mironer YE, Haasis JC, Chapple I, et al. Efficacy and safety of intrathecal opioid/bupivacaine mixture in chronic nonmalignant pain: a double-blind, randomized, crossover, multicenter study by the National Forum of Independent Pain Clinicians (NFIPC). Neuromodulation 2002; 5:208–213. 72. Lundborg C, Dahm P, Nitescu P, et al. Clinical experience using intrathecal (IT) bupivacaine infusion in three patients with complex regional pain syndrome type I (CRPS-I). Acta Anaesthesiol Scand 1999; 43:667–678.
84. Siddall PJ, Molloy AR, Walker S, et al. The efficacy of intrathecal morphine and clonidine in the treatment of pain after spinal cord injury. Anesth Analg 2000; 91:1493–1498. 85. Uhle EI, Becker R, Gatscher S, et al. Continuous intrathecal clonidine administration for the treatment of neuropathic pain. Stereotact Funct Neurosurg 2000; 75:167–175. 86. Kroin JS, McCarthy RJ, Penn RD. Continuous intrathecal clonidine and tizanidine in conscious dogs: analgesic and hemodynamic effects. Anesth Analg 2003; 96:776–782. 87. Kawamata T, Omote K, et al. Antihyperalgesic and side effects of intrathecal clonidine and tizanidine in a rat model of neuropathic pain. Anesthesiology 2003; 98(6):1480–1483. 88. Mathur VS, et al. Neuronal N-type calcium channels: new prospect in pain therapy. Pharmaceutical News 1999; 5:25–29. 89. Atanassoff PG, Hartmannsgruber MW, et al. Ziconotide, a new N-type calcium channel blocker, administered intrathecally for acute postoperative pain. Regional Anesthes Pain Med 2000; 25:274–278. 90. Presley RW, Yearwood TL, Charapata SG, et al. Intrathecal ziconotide in the treatment of opioid-refractory neuropathic and nonmalignant pain: a controlled clinical trial. Submitted to Anesthesia and Analgesia. 91. Staats PS, Yearwood T, Charapata SG, et al. Intrathecal ziconotide in the treatment of refractory pain in patients with cancer or AIDS: a randomized controlled clinical trial. JAMA 2004; 291:63–70. 92. Staats PS, Luthardt F, Shipley J, et al. Long-term intrathecal ziconotide therapy: a case study and discussion. Neuromodulation 2001; 4:121–126. 93. Penn RD, Paice JA. Adverse effects associated with the intrathecal administration of ziconotide. Pain 2000; 85:291–296. 94. Valentine JM, Lyons G, Bellamy MC. The effect of intrathecal midazolam on postoperative pain. Eur J Anaesthes 1996; 13:589–593. 95. Goodchild CS, Guo Z, Masgreave A. et al. Antinociception by intrathecal midazolam involves endogenous neurotransmitters acting at spinal cord delta opioid receptors. Br J Anaesth 1996; 77(6):758–763. 96. Nishiyama T. Hanaoka K. The synergistic interaction between midazolam and clonidine in spinally mediated analgesia in two different pain models in rats. Anesthes Analg 2001; 93:1025–1031. 97. Nishiyama T, Gyermek L, Lee C, et al. Synergistic analgesic effects of intrathecal midazolam and NMDA or AMPA receptor antagonists in rats. Can J Anesth. 2001; 48:288–294. 98. Nishiyama T, Matsukawa T, Hanaoka K. Acute phase histopathological study of spinally administered midazolam in cats. Anesthes Analg 1999; 89:717–720. 99. Johansen MJ, Gradert TL, Satterfield WC, et al. Safety of continuous intrathecal midazolam infusion in the sheep model. Anesthes Analg 2004; 98(6):1528–1535.
73. Spaulding TC, Fielding S, Venafro JJ et al. Antinociceptive activity of clonidine and its potentiation of morphine analgesia. Eur J Pharmacol 1979; 58:19–25.
100. Erdine S, Yucel A, Ozyuvaci E, et al. Neurotoxicity of midazolam in the rabbit. Pain 1999; 80:419–423.
74. Wilcox GL, Carlson KH, Jochim A, et al. Mutual potentiation of anti-nociceptive activity of morphine and clonidine on motor and sensory responses in rat spinal cord. Brain Res 1987; 405:84–93.
101. Yaksh TL, Allen JE. The use of intrathecal midazolam in humans: a case study of process. Anesth Analg 2004; 98:1536–45.
75. Hodgson P, Neal J, Pollock J, et al. The neurotoxicity of drugs given intrathecally. Anasth Analg 1999; 88:797–809. 76. Thompson’s physicians desk reference. Montvale, NJ: Duraclon;.2003:1254–1255. 77. Coombs DW, Sanders RL, LaChance D, et al. Epidural clonidine analgesia; use of clonidine, DADLE, and intraventricular morphine. Anasthesia 1985; 62: 358–363. 78. Eisenach JC. Overview; first international symposium on alpha-2 adrenergic mechanisms of spinal anesthesia. Regional Anesthes 1993; 18:I–V. 79. Rauck RL, Eisenach JC, Kackson KE, et al. Epidural clonidine for refractory reflex sympathetic dystrophy. Anesthesia 1991; 75:A657. 80. Hildebrand KR, Elsberry DD, Hassenbusch SJ. Stability and compatibility of morphine–clonidine admixtures in an implantable infusion system. J Pain Symptom Manage 2003; 25:464–471. 81. Classen AM, Wimbish GH, Kupiec TC. Stability of admixture containing morphine sulfate, bupivacaine hydrochloride, and clonidine hydrochloride, in an implantable infusion system. J Pain Symptom Manage 2004; 28(6):603–611. 82. Hassenbusch SJ, Gunes S, Wachsman S, et al. Intrathecal clonidine in the treatment of intractable pain: a phase I/II study. Pain Med 2002; 3:85–91. 83. Ackerman LL, Follett KA, Rosenquist RW. Long-term outcomes during treatment of chronic pain with intrathecal clonidine or clonidine/opioid combinations. J Pain Symp Manage 2003; 26:668–677.
102. Rainov NG, Heidecke MD, Burkert W. Long-term intrathecal infusion of drug combinations for chronic back and leg pain. J Pain Symptom Manage 2001; 22:862–871. 103. Goodwin K, Kim N-H, Zuniga R. Stability of a baclofen and clonidine hydrochloride admixture for intrathecal administration. Hospital Pharm 2001; 26:950–954. 104. Lauretti GR, Reis MP, Prado WA, et al. Dose–response study of intrathecal morphine versus intrathecal neostigmine, their combination or placebo for postoperative analgesia in patients undergoing anterior and posterior vaginoplasty. Anesth Analg 1996; 82:1182–1187. 105. Klamt JG, Dos Reis MP, Neto JB, et al. Analgesic effect of subarachnoid neostigmine in two patients with cancer pain. Pain 1996; 66:389–391. 106. Kekesi G, Dobos L, Benedek G, et al. The antinociceptive potencies and interaction of endogenous ligands during continuous intrathecal administration: adenosine, agmatine and endorphine-1. Anesth Analg 2004; 98:420–426. 107. Eisenach JC, Rauck RL, Curry R. Intrathecal, but not intravenous adenosine reduces allodynia in patients with neuropathic pain. Pain 2003; 105:65–70. 108. Scwetz I, Naliboff B, Munakata J, et al. Antihyperalgesic effect of octreotide in patients with irritable bowel syndrome. Aliment Pharmacol Ther 2004; 19:123–131. 109. Paice JA, Penn RD, Kroin JS. Intrathecal octreotide for relief of intractable nonmalignant pain: 5-year experience with two cases. Neurosurgery 1996; 38:203–207. 110. Yaksh TL, Dirksen R, Harty GJ. Antinociceptive effects of intrathecally injected cholinomimetic drugs in the rat and cat. Eur J Pharmacol 1985; 117:81–88.
365
Part 2: Interventional Spine Techniques 111. Han BF, Zhang C, Qi JS, et al. ATP sensitive potassium channels and endogenous adenosine are involved in spinal antinociceptive produced by locus coeruleus stimulation. Acta Physiol Sinica 2002; 54:139–144. 112. Bennett G, Burchiel K, Buchser E, et al. Clinical guidelines for intraspinal infusion: report of an expert panel. J Pain Symptom Manage 2000; 20;S37–S43. 113. Hassenbusch S, Portenoy R, et al. Polyanalgesic Consensus Conference 2003: an update on the management of pain by intraspinal drug delivery – report of an expert panel. J Pain Symptom Manage 2004; 27(6):540–563. 114. American Society of Health System Pharmacists ASHP. Guideline on quality assurance for pharmacy-prepared sterile products. Am J Health Syst Pharmacol 2003; 60:1440–1446. 115. USP. General chapter 797: pharmaceutical compounding sterile preparations. US Phamacopeia 2004; Jan 1. 116. Naumann C, Erdine S, et al. Drug adverse events and system complications of intrathecal opioid delivery for pain: origins, detection, manifestations and management. Neuromodulation 1999; 2:92–107. 117. Wang SC. Emetic and antiemetic drugs. In: Root WS, Hofmann FG, eds. Physiological pharmacology, II. New York: Academic Press; 1965:255–328.
366
118. Barnes NM, Bunce KT, Naylor RJ, et al. The actions of fentanyl to inhibit druginduced emesis. Neuropharmacology 1991; 30:1073–1083. 119. Aldrete JA, da Silva JMC. Leg edema from intrathecal opiate infusions. Eur J Pain 2000; 4:361–365. 120. Freye E, Latasch L. Development of opioid tolerance – molecular mechanisms and clinical consequences. Anasthesiol Intensivemed Notfallmed Schmerzther 2003; 38(1):14–26. 121. Hsu MM, Wong CS. The roles of pain facilitatory systems in opioids tolerance. Acta Anaesthesiol Sin 2000; 38(3):155–166. 122. North RB, Cutchis PN, Epstein JA, et al. Spinal cord compression complicating subarachnoid infusion of morphine: case report and laboratory experience. Neurosurgery 1991; 29:778–784. 123. Yaksh TL, Hassenbusch S, Burchiel K, et al. Inflammatory masses associated with intrathecal drug infusion: a review of preclinical evidences and human data. Pain Med 2002; 3:300–312. 124. Fernandez G, Madison-Michael L, Feler CA. Catheter tip granuloma associated with sacral region intrathecal drug administration. J Neuromodulation 2003; 6:225–228.
PART 2
INTERVENTIONAL SPINE TECHNIQUES
Section 2
Interventional Spine Techniques
CHAPTER
Vertebroplasty
32
Amit S. Bhargava and Curtis W. Slipman
SCREENING OF PATIENTS REFERRED FOR VERTEBROPLASTY Before considering vertebroplasty, one must perform a through history, physical examination, and review appropriate investigations including radiographic analysis. This information should be able to differentiate between the source of pain being vertebral compression fracture or other back problems such as disc herniation, facet arthropathy, or spinal stenosis.1 History should include the site of pain, cause, inciting event, date of origin, exacerbating factors, alleviating factors, analgesic use, and activities of daily living. The patient should be screened for allergies, medications, medical problems, and conditions which may prevent the patient from lying prone during the procedure. The origin of pain may coincide with minor trauma and is typically exacerbated during activity, movement, or while weight bearing, and is relieved by lying down. Physical examination will reveal a tender site corresponding with the fracture level. If multiple vertebral compression fractures are present, the origin of pain will be elicited by careful clinical examination and analysis of radiographic studies.1,2 Magnetic resonance imaging (MRI) is helpful in patients with multiple fractures and usually reveals edema within the marrow space of the vertebral body that is best visualized on sagittal T2-weighted images. Bone scans can also differentiate the symptomatic level from incidentally discovered fractures.3 Bone scan imaging may be indicated when considering vertebroplasty therapy for patients suffering from multiple vertebral compression fractures of uncertain age or in patients with nonlocalizing pain patterns. We do not, however, routinely perform bone scans.4 Blood investigations should include complete blood and platelet counts, measurement of prothrombin time, partial thromboplastin time, International Normalized Ratio, activated clotting time, and complete metabolic panel.5,6
CONSULTATION Because most vertebral compression fractures occur in the older age group, the initial consultation should include family members involved in the patient’s care. The time of reporting for the procedure, postprocedure care, and time of discharge from the hospital should be explained. Informed consent must include a through explanation of the procedure, methods, the physician’s prior history of complications, and the expected outcome based on the physician’s own outcome data. The patient should also be informed that the addition of material (barium, tungsten or tantalum) to make the bone cement material opaque technically makes the cement a non-FDA-approved material.1,7
One should carefully temper unrealistic patient expectations. In general, the patient can be told to expect a higher chance of a favorable outcome if his or her fracture is subacute, but a diminished success rate if the fracture is old.
Timing Early studies performed vertebroplasty only after conventional treatment (medication and rest) had failed.8 Later series have advocated treatment as early as weeks or days if the patient requires narcotic medication or admission to hospital secondary to pain. Others have recommended vertebroplasty within 4 months.3 Although late treatment is unlikely to be successful, there are case reports of patients being successfully treated after a few years.9 Even though some believe it is a reasonable indication,1 there are insufficient data to categorically support the treatment of painful tumor infiltration without fracture. In addition, it is unclear whether to treat before or after radiation therapy. Injection of cement into the vertebral body will likely dislodge marrow elements that could potentially be absorbed into the blood stream. This concern for causing metastatic dissemination suggests that vertebroplasty should be performed only after radiation therapy. Prophylactic vertebroplasty is neither widely accepted nor approved for osteoporotic vertebral compression fractures and no studies have been done to substantiate the utility of this practice.1
TECHNIQUE 1. Pre-procedure planning. MRI, computed tomography (CT), and X-ray images of the fracture are evaluated in all views specifically looking for the angle of approach to the vertebra through the pedicle. Because normal anatomy (Fig. 32.1) is altered by the fractures, the approach to the body of the vertebra through the pedicle is altered. This altered bone architecture must be carefully analyzed by reviewing all the available radiological films. Specifically, the cortical margins of the bone are reviewed in anteroposterior (AP), lateral, and axial views to preplan the pathway of the trocar to the exact target area within the vertebral body. The angle will be altered based on the characteristics of the fractured vertebra. The vertebra may be approached through one pedicle or both pedicles. If the angle of insertion is achieved in such a way that the tip of the trocar is in the center of the body, then one may use a single-pedicle approach. If the trocar lies on one side of the body of vertebrae, then the other pedicle may be used to approach the other side of the vertebral body. 2. Prior food and medication. For procedure performed in the morning, the patient is informed not to eat or drink after midnight, but is allowed to take medications. When conscious, sedation is used
367
Part 2: Interventional Spine Techniques
A
Thoracic vertebra
Lumbar vertebra
B
Thoracic vertebra
Lumbar vertebra
for a procedure to be done later in the day, and the patient should not drink or eat for a minimum of 4 hours beforehand. Diabetics and other chronic medical illness management including the timing of anticoagulants should be coordinated with the primary care physician. 3. Prophylactic antibiotics. Intravenous antibiotics (cefazolin 1 g) are given 30 minutes before the procedure. Ciprofloxacin 500 mg orally twice a day may be given, if the patient is allergic to other medications and should be started 12 hours before the procedure and continued 24 hours after completion of the procedure.6 We do not give any prophylactic antibiotics and prescribe antibiotics postoperatively for a week. 4. Position of patient. The patient is placed in a prone position for surgery in the thoracic and lumbar region and supine for cervical region.3 It is critical to confirm the level of pain and fracture under fluoroscopy before beginning vertebroplasty.1 Applying pressure with the thumb or palm of the hand over each spinous process or side-to-side movement of the spinous process will often elicit tenderness. As the patient is awake during the procedure and placed in a prone position, the patient should be made comfortable with padding and arm supports. 5. Anesthesia. Percutaneous vertebroplasty is performed using local anesthesia typically combined with neuroleptanalgesia2,3,5,10,11 or general anesthesia.10,11,12 The authors use a combination of intravenous midazolam (Versed; Roche, Manate, Puerto Rico) and fentanyl (Sublimaze; Abbott Laboratories, North Chicago, IL).13,14 Dosages are based on patient size and condition and can be titrated during the procedure based on the patient’s response. 368
Fig. 32.1 Pedicles. (A) Axial view. (B) Lateral view.
General anesthesia is rarely used for this procedure. Two to 3 ml of 1% solution of lidocaine injected into the marrow through the needle will relieve pain, which some patient may experience when cement is injected into the bone.6,15 6. Prepping and draping. The skin is prepared with iodine and then draped. As the position is checked many times in AP and lateral views, the field of procedure should be well protected with sufficient drapes. 7. CT scan versus C-arm fluoroscopy. Vertebroplasty is performed using biplanar fluoroscopy,3,11 C-arm fluoroscopy, and dual-guidance CT.3,16 CT is only used for extremely difficult cases, such as tumor destruction of the posterior vertebral wall6 or vertebra plana.17 When using a single-plane C-arm fluoroscopy all the movements during the procedures should be confirmed in two planes, AP and lateral. 8. Approach to the vertebral body. Cervical vertebroplasty has been done with transoral approach,18,19 lateral, and anterolateral approach.20 The authors do, however, have concerns about the transoral approach. This technique necessitates traversing the oropharynx which is riddled with bacteria ready to flourish in the vertebral body. Consequently, we prefer the anterolateral approach used by Deramond in the first described vertebroplasty procedure.21 As osteoporotic fractures are rare in the cervical area, vertebroplasty is rarely done in the cervical region except for conditions such as tumors. During the needle placement one must be careful to avoid the carotid artery and internal jugular vein.6 Both structures are displaced laterally and the esophagus and trachea medially to reach the body of cervical vertebrae (Fig. 32.2).
Section 2: Interventional Spine Techniques Approach to vertebral body Trachea Esophagus ICA Jugular vein
Fig. 32.2 Cervical body, anterior.
The thoracic and lumbar vertebral bodies are usually approached through one or, most commonly, both pedicles.2,8,21–27 Various approaches are used including a costovertebral,5 paravertebral, posterolateral, or anterolateral (cervical) approach. The parapedicular or transcostovertebral28 approach is used when a transpedicular approach cannot be used because of small pedicles, a fractured pedicle, or tumor invading the pedicle. Like most physicians, the authors prefer the transpedicular approach instead of the parapedicular approach, which may increase the chance of both a pneumothorax and that a paraspinous hematoma may not be controlled with application local pressure.6 The posterolateral approach increased the risk of injuring the exiting nerve root and segmental artery,6 and has largely been abandoned although some authors recommend it for lumbar vertebrae.20,23,28 There are many companies which supply cement and delivery equipment: Parallax Medical Inc./Arthrocare Corporation; Cook Group Inc.; Interpore Cross International Inc.; Interpore Cross International Inc./American OsteoMedix Corp.; Medtronic Inc./ Medtronic Sofamor Danek; Orthofix International NV/Orthofix Inc.; Stryker Corp.; Tecres SPA.29 These sets contain stylets, needles, tubing, injectors, and injector barrels, but the end result is the same. The equipment allows one to inject cement into the anterior part of the vertebral body. Some authors have, however, modified the equipment and technique,30–33 and before these sets were available, operators recommended using 1 mL syringes for injection of cement.7,11,17,24
Fig. 32.3 Injecting local anesthetic.
Fig. 32.4 Needle is inserted and viewed on the monitor with the clamp holding the needle.
9. Needle insertion. Mark a point on the skin after viewing the fractured vertebra in the anteroposterior and lateral views. This is the planned insertion site of the cannula. The initiation site should correspond with superolateral aspect of the pedicle. It should not be near the inferior or medial margins of the pedicle. Local anesthetic is infiltrated into the skin, subcutaneous tissue, and up to the periosteum of the pedicle. We inject 2–3 mL of lidocaine 1% with 25-gauge 1.5 inch needle for local anesthesia (Fig. 32.3). A small incision is made using a No. 11 knife blade and the introducer needle from the set is inserted (Fig. 32.4). A 15-gauge needle is used for cervical vertebrae and 10-gauge for thoracic and lumbar vertebrae.3 Currently, even thinner needles (13-gauge) are being used.6 The needle entry site is localized in the AP view. The authors use a diamond-tipped needle to start the entry. During the procedure, one must confirm all the movements and steps in both the AP and lateral fluorosopic views. The needle is held with forceps to minimize radiation exposure to the operator.6 After confirming the position, the vertebroplasty needle is advanced through the superior-lateral cortex of the pedicle (Fig. 32.5).
Fig. 32.5 Initial tap into the pedicle.
369
Part 2: Interventional Spine Techniques
The vertical and horizontal diameter of the pedicle increases from upper thoracic to lower lumbar vertebrae (Table 32.1). Proximally, in the sagittal plane, the direction of the pedicle is more oblique. (Fig. 32.6) The authors start with a diamond-tipped needle and then change it to beveled needle to make directional adjustments.7 The bevel of the needle is directed so that the tip is pointed laterally to avoid the spinal canal. The needle is directed anteriorly, medially, and inferiorly through the pedicle to reach the anterior third of the vertebral body in the midline in the sagittal plane. Incremental changes in position of the needle are observed in the AP and lateral views to ensure that the proper pathway is being pursued. In osteoporotic bones it may be easy to advance the needle by hand, but in cases where the bone is dense, as in pathologic fractures, a mallet is necessary to advance the needle.6 While advancing the needle by hand the direction of needle may change, and using the mallet may keep the needle advancing in the direction wanted. We invariably use
Table 32.1: Vertical and horizontal pedicle diameter Pedicles
T3
L4
Vertical diameter
0.7 cm
1.5 cm
Horizontal diameter
0.7 cm
1.6 cm
A
B
370
Thoracic vertebra
Thoracic vertebra
a mallet to advance the needle as this provides much greater control of the needle direction. As the needle is slowly advanced through the pedicle, we are hypervigilant about the location of the needle tip and the orientation of the needle. At no point do we want to breach the medial wall and subject the patient to the risk of cement extravasation into the spinal canal. When we reach the anterior part of the pedicle on lateral view, the trocar should be just lateral to the medial border of the pedicle on anteroposterior view. This ensures we are not going to break the medial wall of the pedicle. In addition, we do not want to fracture the roof or the base of the pedicle and inadvertently pierce an exiting nerve root. Advancing the needle through the lateral border of the pedicle will deposit cement intramuscularly. We have experienced this latter scenario on a few occasions and it is not associated with any adverse effects. Theoretically, it is conceivable that the needle could be placed too close to the aorta if the needle breaks through the lateral margin of the left pedicle, but this is a highly unlikely event. It is also important to be sure that the angle of inclination will allow the needle to ultimately rest in the anterior one-third of the vertebral body. To obtain ideal terminal position, it is critical that one repeatedly rechecks the cephalocaudal tilt while traversing through the pedicle. It is very difficult to re-orient the angle of inclination once the needle has passed through the pedicle and enters the vertebral body. If the angle of inclination is too steep then gentle downward pressure on the hub will minimize this angle, especially if the needle is still within the pedicle. We emphasize the term ‘gentle’ since osteoporotic bone can easily fracture if aggressive motions are used. If such gentle pressure does not achieve the intended result, a beveled needle can be
Lumbar vertebra
Lumbar vertebra
Fig. 32.6 (A) Direction of insertion of the trocar and cannular (axial view). (B) Approach to vertebra on lateral view.
Section 2: Interventional Spine Techniques
substituted for the diamond-tipped needle. The bevel can be rotated so that the needle courses in the direction of choice. After the needle is observed to enter the vertebral body using a lateral view, the AP perspective does not need to be checked until the cement is injected. An AP view is needed at three points during the procedure: when planning where to insert he needle, checking the progress of the needle as it courses through the pedicle, and then later when cement is injected. Once the needle is in the vertebral body it should be rotated so that the tip is opening medially. 10. Biopsy. If a biopsy is required, it is done by introducing the needle coaxially34 or thorough the needle. The biopsy is done before the cement is injected.1 The authors introduce a thinner biopsy cannula through cannula already through the pedicle. Biopsy kits are commercially available and the biopsy needle size is compatible with the vertebroplasty cannula. After the trocar and cannula have been placed in the vertebral body through the pedicle, the trocar is removed. The biopsy needle is inserted through the vertebroplasty cannula. The biopsy needle is longer than the vertebroplasty cannula and precaution should be taken not to pierce the anterior cortex. The authors initially stop the vertebroplasty cannula in the posterior third of the vertebral body. The biopsy needle is then inserted and advanced through the vertebroplasty cannula in a rotating motion and then pulled out. After the biopsy is obtained, the trocar is reinserted into vertebroplasty cannula and it is advanced anteriorly to the target area. 11. Another needle may be placed in the contralateral pedicle in the manner mentioned above for bipedicular approach. 12. Venography can be done after achieving the correct position with the needle.10,28 Contrast dye is injected into the vertebral body and leakage can be visualized under fluoroscopy. Because the viscosity of the contrast material and bone cement is so different, venography may not be an accurate assessment of the embolization risk.6 In fact, venography is seldom used in Europe and is only done in United States to discover the potential leak sites. Some authors, however, continue to defend its use,2,35,36 while others have either seldom7,37,38 or never used venography.39,40 Embolization of vascular lesions may be done by microfibrillar collagen after venography.2 13. Cement preparation. Bone cement, approved by FDA specifically for vertebroplasty with radio opaque material already incorporated, is available. There are two kinds of cement, slow set or fast set. The authors prefer the fast-set cement. Prior to starting the procedure we place the monomer in a refrigerator. Cooling the liquid slows the set time, allowing a few extra minutes to complete the procedure. Once the monomer and cement powder are mixed, a chemical reaction ensues that cannot be aborted, which ultimately results in hardening of the mixture. Once this reaction has progressed beyond a certain point it becomes impossible to advance cement through the delivery apparatus. So, cooling of the monomer decreases the kinetic energy and slows the chemical reaction time, thereby providing a few extra minutes to the potential cement delivery time. Some interventional spine physicians have suggested altering the monomer to powder ration as a method of altering the set time. We do not do this and do not advocate such a solution. Using polymethyl methacrylate (PMMA) for vertebroplasty is considered off-label use although it is off-label only because of the ratio of monomer to cement powder. But before one modifies the cement preparation, one must first understand that the mechanical properties of the cement would be inextricably altered. Second, and probably most important, is that the amount of free or unbound monomer would likely increase, which could lead to increased complication due to intravascular monomer uptake.
The typical concentration is 0.40 mL of PMMA powder (SimplexP; Stryker-Howmedica-Osteonics) combined with 6 g of sterile barium sulfate powder, tantalum,3,11 or tungsten (Figs 32.7, 32.8).10 The barium sulfate powder is included to better visualize the PMMA under fluoroscopy. The safety of the procedure depends on cement leakage rather than the type of cement used.41 In addition, before adding the 10 mL liquid monomer, one can add 1 g of tobramycin antibiotic to reduce the chance of disc space infection.5,25,42,43 Some authors, including ourselves, recommend not adding antibiotics to PMMA unless the patient is immunocompromised.6,17 After the barium is added to the powder, the polymer is added to the monomer using a 10 cc syringe and an 18-gauge, 5” needle. The tube is closed and the mixture is shaken vigorously for 45 seconds. Open mixing should be avoided to maintain a sterile environment. While one is mixing the cement, an assistant connects the long, flexible tube for delivery to the injector barrel. The bone cement preparation is mixed until a doughy, cohesive consistency (similar to toothpaste) is obtained. We delay the polymerization process by
Fig. 32.7 Mixing PMMA and barium.
Fig. 32.8 Preparing cement. 371
Part 2: Interventional Spine Techniques
cooling the polymer in the refrigerator for an hour before the procedure and this gives additional working time.6,44 In limited circumstances, slow-set cement Cranioplastic type 1 Slow Set (Codman/Johnson & Johnson, Berkshire, UK), at room temperature can be used.6,35 Rapid-set material has the advantage as it rapidly sets in case of leaks, as seen with these procedures. If a cement leak is observed on fluoroscopy, one can stop for a few minutes till the fast cement hardens and blocks that area. As the leaking area is blocked by the hardening cement, more cement may be reinjected. One should look for cement flowing into the opposite direction to the area where the previous cement had already hardened. The cement will rapidly polymerize and will plug the leak in 1–2 minutes and further cement can be injected, which is not possible with slow-setting cement. In addition, slow-setting cement stays liquid longer in the body and thus could potentially leak for a longer time and may leak along the needle tract when the needle is pulled out.6 Once mixing is completed, the bone cement is slowly poured into the injector tube (Fig. 32.9). The injector device is attached and rotated till the cement starts pouring from the tip of the flexible tube (Figs 32.10, 32.11). One can see the consistency of the cement
Fig. 32.9 Pouring cement into the chamber.
Fig. 32.10 Connecting the rotator. 372
at the end (Fig. 32.12). The flexible tube is connected to the needle inserted earlier into the vertebral body (Fig. 32.13). 14. Cement injection. The paste-like cement is slowly injected into the vertebral body under constant fluoroscopic control with help of the injector device (Fig. 32.14). The amount of cement injected is monitored under fluoroscopy and the quantity can be measured from the labeled injector tube. The objective is to fill the anterior two-thirds of the vertebral body as seen on the lateral view. If required, further cement can be injected from the contralateral pedicle cannulation.3 At times, the cement does not flow according to the plan. The cement may pool in front of the needle, and the cannula may be repositioned by slightly moving anteriorly or posteriorly. If the cement is moving into the anterior part of the vertebral body, the cannula can be withdrawn slightly and one can then inject more cement. If the cement is flowing to the posterior or lateral part of the vertebral body, the inserting device can be rotated in the opposite direction to create a negative pressure. In some cases, cement may
Fig. 32.11 Connecting the delivery tube.
Fig. 32.12 Checking the consistency of the cement.
Section 2: Interventional Spine Techniques
in both AP and lateral views. If it is considered safe to proceed with the procedure, the needle position should be adjusted. Another needle can also be placed from the contralateral pedicle. 16. Removal of the needle. The stylet should be repositioned into the needle before removal of the needle whenever possible to prevent cement leak.3 The authors prefer not to place the trocar as that may lead to unmonitored injecting of cement. We leave both cannulas in the vertebral body till the cement is injected from the cannula. If one cannula is pulled out before the cement is injected into the second pedicle, then one is potentially providing a route for cement to leak from the first pedicle. 17. Dressing. Local pressure is applied at the skin puncture site to prevent any bleeding. The puncture site is closed with steristrips and a sterile dressing applied.
Postprocedure Fig. 32.13 Connecting the delivery tube to the needle.
The cement polymerizes in 1 hour and the patient remain recumbent in supine position for that duration. The patient may be discharged after an hour of monitoring.5 At our center, we discharge patients after keeping them for 1 hour postprocedure, or if medically required we admit them overnight. The patient is discharged with narcotic medication to be used on an as-needed basis and is prescribed Keflex for a week. If the patient is allergic, ciprofloxacin is prescribed. The patient is not given any brace on discharge.
Multiple compressions Multiple-level vertebral compression fractures may be treated by percutaneous vertebroplasty. It is less cumbersome to stagger needles by alternating between right and left pedicles.2 However, there may be additional stress on the adjacent vertebrae.49 If there are multiple compression fractures, one should treat the most painful fracture first.1 No more than two should be treated on a particular day. It is the authors’ preference to treat a single vertebral fracture per day to ensure monomer toxicity risk is minimized. Incidence of venous extravasation of cement or fat50 increases with multiple-level treatment.
Repeat vertebroplasty Fig. 32.14 Ready to inject with hands out of the radiation field.
fortuitously flow to the opposite side of the vertebral body and injection through the second pedicle may not be required. Vital signs should be monitored looking for hypotension, as cement injection has been known to cause hypotension in patients undergoing joint replacement surgery.45,46 15. Amount of cement. Total volume of cement injected is commonly 2–8 mL.3,6 Outcome, however, is not related to the amount of cement injected, and even 2 mL of cement injected has been reported to provide pain relief.47 Only a small amount of bone cement (≈15% volume of fill) is necessary to restore compressive stiffness of the damaged vertebral body to its value before damage.48 The injection of cement is stopped whenever epidural or paravertebral opacification is observed or when the cement reaches the dorsal quarter of the vertebral body.3 If extravasation of cement is seen, further injection of cement is stopped. The extravasation is evaluated
If the recurrent pain arises from a vertebra previously treated with vertebroplasty, repeat percutaneous vertebroplasty offers therapeutic benefit.37 Repeat vertebroplasties may be approached from the pedicle opposite the previous insertion.37,51
AVOIDANCE OF COMPLICATIONS The complications are minimal if precautions are taken.52
Leakage of cement Leakage of cement can cause neurologic injury or pulmonary emboli.53–56 One can, however, prevent cement leaks by using high-resolution fluoroscopy (or rarely CT), adequate cement opacification, and by interrupting or terminating the procedure on first recognition of a leak. Biplanar fluoroscopy is not required but does make visualization in two projections simpler and faster. One must visualize the vertebra in two planes numerous times. The authors use a uniplanar machine which is rotated at every step to obtain anteroposterior and lateral views. Sterile barium sulfate is added to bring the barium quantity to 30% by weight, making the cement opaque for visualization under fluoroscopy. Presently, FDA approved premixed cement for vertebroplasty is available commercially. Terminating injection when 373
Part 2: Interventional Spine Techniques
early leakage of cement is visualized limits the size of the leak and usually prevents it from becoming significant. Venography has been used to observe leakage but it does not accurately predict the leak of cement.14 If there is leakage into the spinal canal with neurological deficit, a neurosurgeon or spinal surgeon should be consulted.57,58 The cement emboli can leak into the valveless veins of the vertebrae and migrate into the paraspinal plexus which drains into the azygous vein. The azygous veins empty in to the right atrium of the heart, after which blood then flows to the lungs. Asymptomatic leakage of the cement routinely occurs and a patient with mediastinal problem had an MRI of chest done at our center. Small emboli of cement were observed in the lungs and he had previous history of percutaneous vertebroplasty. This patient probably had asymptomatic multiple microemboli of cement. The PMMA cement emboli were not the source of his problem.
Pain exacerbation At times the pain may exacerbate due to local ischemia or increased pressure. A CT scan be immediately obtained to ensure no leakage. Otherwise, the pain usually resolves in a few hours or a few days.14 We discharge all patients with narcotic medication (oxycodone) to be used on an as-needed basis. If radicular pain occurs secondary to leakage into the neural foramen, within 10–20 minutes we inject 10 cc of 0.2% lidocaine followed by 100–200 cc of pressurized saline perfusion.59,60 During the injection, the patient may feel some pressure, but the surgeon should be aware of this and slow or stop injection if significant radicular pain occurs.
Bleeding The cannula is removed after adequate filling of the vertebra. Venous bleeding may be observed at the needle entry sites and local pressure for 3–5 minutes will minimize the bleeding.6
Occupational dose mitigation Secondary radiation, particularly scatter radiation from the patient and leakage radiation from the radiograph tube, is the primary source of operator and medical staff exposure. Techniques to reduce exposure to the operator include shielding devices, which are placed directly on the patient to provide maximum shielding to the operator’s hands and upper body. Additionally, a lead apron can be placed between the surgeon and the patient. Exposure on injecting cement with 1 mL syringe and vertebroplasty kit is the same.61 Through the use of radiation-reducing procedures, such as pulsed fluoroscopic operation at 4 pps, radiograph tube positioning under the patient table, and use of lead sheets on the patients and lead aprons placed between the surgeon and the patient, more than 6700 vertebroplasty vertebrae procedures may be safely performed by a single operator per year. Polymethyl methacrylate vapor levels to which medical personnel are exposed during percutaneous vertebroplasty are well below the level typically considered hazardous. However, it is important to note that some individuals may experience adverse effects, such as asthma, coughing, nausea, and decreased appetite, when exposed to levels6 typically considered to be acceptable.62–64
References 1. Stallmeyer MJ, Zoarski GH, Obuchowski AM. Optimizing patient selection in percutaneous vertebroplasty. J Vascul Intervent Radiol 2003; 14(6):683–696. 2. Amar AP, Larsen DW, Esnaashari N, et al. Percutaneous transpedicular polymethylmethacrylate vertebroplasty for the treatment of spinal compression fractures. Neurosurgery 2001; 49(5):1105–1114; discussion 1114–1115.
374
3. Gangi A, Guth S, Imbert JP, et al. Percutaneous vertebroplasty: indications, technique, and results. Radiographics 2003; 23(2):e10. 4. Maynard AS, Jensen ME, Schweickert PA, et al. Value of bone scan imaging in predicting pain relief from percutaneous vertebroplasty in osteoporotic vertebral fractures. Am J Neuroradiol 2000; 21(10):1807–1812. 5. Hodler J, Peck D, Gilula LA. Midterm outcome after vertebroplasty: predictive value of technical and patient-related factors. Radiology 2003; 227(3):662–668. 6. Mathis JM, Wong W. Percutaneous vertebroplasty: technical considerations. J Vascul Intervent Radiol 2003; 14(8):953–960. 7. Kallmes DF, Jensen ME. Percutaneous vertebroplasty [Review]. Radiology 2003; 229(1):27–36. 8. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. Am J Neuroradiol 1997; 18(10):1897–1904. 9. Kaufmann TJ, Jensen ME, Schweickert PA, et al. Age of fracture and clinical outcomes of percutaneous vertebroplasty. Am J Neuroradiol 2001; 22(10):1860–1863. 10. Barr JD, Barr MS, Lemley TJ, et al. Percutaneous vertebroplasty for pain relief and spinal stabilization [see comment]. Spine 2000; 25(8):923–928. 11. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg 2003; 98(1 Suppl):21–30. 12. White SM. Anaesthesia for percutaneous vertebroplasty. Anaesthesia 2002; 57(12):1229–1230. 13. Brown DB, Gilula LA, Sehgal M, et al. Treatment of chronic symptomatic vertebral compression fractures with percutaneous vertebroplasty. Am J Roentgenol 2004; 182(2):319–322. 14. Mathis JM. Percutaneous vertebroplasty: complication avoidance and technique optimization. Am J Neuroradiol 2003; 24(8):1697–1706. 15. Sesay M, Dousset V, Liguoro D, et al. Intraosseous lidocaine provides effective analgesia for percutaneous vertebroplasty of osteoporotic fractures. Can J Anaesthes 2002; 49(2):137–143. 16. Gangi A, Kastler BA, Dietemann JL. Percutaneous vertebroplasty guided by a combination of CT and fluoroscopy. Am J Neuroradiol 1994; 15(1):83–86. 17. Peters KR, Guiot BH, Martin PA, et al. Vertebroplasty for osteoporotic compression fractures: current practice and evolving techniques. Neurosurgery 2002; 51(5 Suppl):96–103. 18. Gailloud P, Martin JB, Olivi A, et al. Transoral vertebroplasty for a fractured C2 aneurysmal bone cyst [Case Reports. Letter]. J Vascul Intervent Radiol 2002; 13(3):340–341. 19. Martin JB, Gailloud P, Dietrich PY, et al. Direct transoral approach to C2 for percutaneous vertebroplasty. Cardiovasc Intervent Radiol 2002; 25(6):517–519. 20. Cotten A, Boutry N, Cortet B, Assaker R, et al. Percutaneous vertebroplasty: state of the art. Radiographics 1998; 18(2):311–320; discussion 320–323. 21. Galibert P, Deramond H, Rosat P, et al. [Preliminary note on the treatment of vertebral angioma by percutaneous acrylic vertebroplasty]. [French] Neuro-Chirurgie. 1987; 33(2):166–168. 22. Appel NB, Gilula LA. ‘Bull’s-eye’ modification for transpedicular biopsy and vertebroplasty. Am J Roentgenol 2001; 177(6):1387–1389. 23. Cortet B, Cotten A, Boutry N, et al. Percutaneous vertebroplasty in the treatment of osteoporotic vertebral compression fractures: an open prospective study. J Rheumatol 1999; 26(10):2222–2228. 24. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate. Technique, indications, and results. Radiol Clin N Am 1998; 36(3):533–546. 25. Kallmes DF, Schweickert PA, Marx WF, et al. Vertebroplasty in the mid- and upper thoracic spine. Am J Neuroradiol 2002; 23(7):1117–20. 26. Kim AK, Jensen ME, Dion JE, et al. Unilateral transpedicular percutaneous vertebroplasty: initial experience. Radiology 2002; 222(3):737–741. 27. Martin JB, Wetzel SG, Seium Y, et al. Percutaneous vertebroplasty in metastatic disease: transpedicular access and treatment of lysed pedicles – initial experience. Radiology 2003; 229(2):593–597. 28. Garfin SR, Yuan HA, Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the treatment of painful osteoporotic compression fractures. Spine 2001; 26(14):1511–1515. 29. http://sis.windhover. com/windbuy/lpext.dll/ windbuy/iv/2001/ 2001800190.htm 30. Al-Assir I, Perez-Higueras A, Florensa J, et al. Percutaneous vertebroplasty: a special syringe for cement injection. Am J Neuroradiol 2000; 21:159–161.
Section 2: Interventional Spine Techniques 31. Heini PF, Allred C. The use of a side-opening injection cannula in vertebroplasty: a technical note. Spine 2002; 27(1):105–109.
49. Berlemann U, Ferguson SJ, Nolte LP, et al. Adjacent vertebral failure after vertebroplasty. A biomechanical investigation. J Bone Joint Surg [Br] 2002; 84:748–752
32. Murphy KJ, Lin DD, Khan AA, et al. Multilevel vertebroplasty via a single pedicular approach using a curved 13-gauge needle: technical note. Can Assoc Radiol J 2002; 53(5):293–295.
50. Aebli N, Krebs J, Davis G, et al. Fat embolism and acute hypotension during vertebroplasty: an experimental study in sheep. Spine 2002; 27:460–466.
33. Schallen EH, Gilula LA. Vertebroplasty: reusable flange converter with hub lock for injection of polymethylmethacrylate with screw-plunger syringe. Radiology 2002; 222(3):851–855.
51. Gilula L. Is insufficient use of polymethylmethacrylate a cause for vertebroplasty failure necessitating repeat vertebroplasty? [comment]. Am J Neuroradiol 2003; 24(10):2120–2121; author reply 2121–2122.
34. Minart D, Vallee JN, Cormier E, et al. Percutaneous coaxial transpedicular biopsy of vertebral body lesions during vertebroplasty. Neuroradiology 2001; 43(5):409–412.
52. McGraw JK, Cardella J, Barr JD, et al. SIR Standards of Practice Committee. Society of Interventional Radiology quality improvement guidelines for percutaneous vertebroplasty. J Vascul Intervent Radiol 2003; 14(7):827–831.
35. McGraw JK, Heatwole EV, Strnad BT, et al. Predictive value of intraosseous venography before percutaneous vertebroplasty [see comment]. J Vascul Intervent Radiol 2002; 13(2 Pt 1):149–153.
53. Harrington KD. Major neurological complications following percutaneous vertebroplasty with polymethylmethacrylate: a case report [see comment]. J Bone Joint Surg [Am] 2001; 83-A(7):1070–1073.
36. Peh WC, Gilula LA. Additional value of a modified method of intraosseous venography during percutaneous vertebroplasty. Am J Roentgenol 2003; 180(1):87–91.
54. Kang JD, An H, Boden S, et al. Cement augmentation of osteoporotic compression fractures and intraoperative navigation: summary statement. Spine 2003; 28(15): S62–S63.
37. Gaughen JR Jr, Jensen ME, Schweickert PA, et al. The therapeutic benefit of repeat percutaneous vertebroplasty at previously treated vertebral levels [see comment]. Am J Neuroradiol 2002; 23(10):1657–1661. 38. Phillips FM. Minimally invasive treatments of osteoporotic vertebral compression fractures. Spine 2003; 28(15):S45–S53. 39. Vasconcelos C, Gailloud P, Beauchamp NJ, et al. Is percutaneous vertebroplasty without pretreatment venography safe? Evaluation of 205 consecutives procedures. Am J Neuroradiol 2002; 23(6):913–917. 40. Wong W, Mathis J. Is intraosseous venography a significant safety measure in performance of vertebroplasty? J Vascul Intervent Radiol 2002; 13(2 Pt 1):137–138.
55. Mousavi P, Roth S, Finkelstein J, et al. Volumetric quantification of cement leakage following percutaneous vertebroplasty in metastatic and osteoporotic vertebrae. J Neurosurg 2003; 99(1 Suppl):56–59. 56. Yeom JS, Kim WJ, Choy WS, et al. Leakage of cement in percutaneous transpedicular vertebroplasty for painful osteoporotic compression fractures. J Bone Joint Surg [Br] 2003; 85(1):83–89. 57. Lee B-J, Lee S-R, Yoo T-Y. Paraplegia as a complication of percutaneous vertebroplasty with polymethylmethacrylate: a case report. Spine 2002; 27(19):E419–E422.
41. Mathis JM, Barr JD, Belkoff SM, et al. Percutaneous vertebroplasty: a developing standard of care for vertebral compression fractures. Am J Neuroradiol 2001; 22(2):373–381.
58. Shapiro S, Abel T, Purvines S. Surgical removal of epidural and intradural polymethylmethacrylate extravasation complicating percutaneous vertebroplasty for an osteoporotic lumbar compression fracture. Case report. J Neurosurg 2003; 98(1 Suppl):90–92.
42. Hiwatashi A, Moritani T, Numaguchi Y, et al. Increase in vertebral body height after vertebroplasty. Am J Neuroradiol 2003; 24(2):185–189.
59. Jarvik JG, Kallmes DF, Mirza SK. Vertebroplasty: learning more, but not enough. Spine 2003; 28(14):1487–1489.
43. Peh WC, Gilula LA. Percutaneous vertebroplasty: indications, contraindications, and technique. Br J Radiol 2003; 76(901):69–75.
60. Kelekis AD, Martin J-B, Somon T, et al. Radicular pain after vertebroplasty: compression or irritation of the nerve root? Initial experience with the ‘cooling system.’ Spine 2003; 28(14):E265–E269.
44. Chavali R, Resijek R, Knight SK, et al. Extending polymerization time of polymethylmethacrylate cement in percutaneous vertebroplasty with ice bath cooling. Am J Neuroradiol 2003; 24(3):545–546. 45. Kaufmann TJ, et al. Cardiovascular effects of polymethylmethacrylate use in percutaneous vertebroplasty [see comment]. Am J Neuroradiol 2002; 23(4):601–604. 46. Vasconcelos C, Gailloud P, Martin JB, et al. Transient arterial hypotension induced by polymethylmethacrylate injection during percutaneous vertebroplasty. J Vascul Intervent Radiol 2001; 12(8):1001–1002. 47. Belkoff SM, Mathis JM, Jasper LE, et al. An ex vivo biomechanical evaluation of a hydroxyapatite cement for use with vertebroplasty. Spine 2001; 26(14):1542–1546. 48. Liebschner MA, Rosenberg WS, Keaveny TM. Effects of bone cement volume and distribution on vertebral stiffness after vertebroplasty. Spine 2001; 26(14):1547–1554.
61. Kallmes DF, Roy SS, Piccolo RG, et al. Radiation dose to the operator during vertebroplasty: prospective comparison of the use of 1-cc syringes versus an injection device. Am J Neuroradiol 2003; 24(6):1257–1260. 62. Cloft HJ, Easton DN, Jensen ME, et al. Exposure of medical personnel to methylmethacrylate vapor during percutaneous vertebroplasty. Am J Neuroradiol 1999; 20(2):352–353. 63. Kirby BS, Doyle A, Gilula LA. Acute bronchospasm due to exposure to polymethylmethacrylate vapors during percutaneous vertebroplasty. Am J Roentgenol 2003; 180(2):543–544. 64. Nimmagadda U, Salem MR. Acute bronchospasm associated with methylmethacrylate cement. Anesthesiology 1998; 89:1290–1291.
375
PART 2
INTERVENTIONAL SPINE TECHNIQUES
Section 2
Interventional Spine Techniques
CHAPTER
Kyphoplasty Technique
33
Amir H. Fayyazi and Frank M. Phillips
INTRODUCTION Pathologic vertebral compression fractures (VCFs) are a leading cause of disability and morbidity in patients with osteoporosis, multiple myeloma, and bone metastases.1–4 The consequences of these fractures include pain and often progressive vertebral collapse with resultant spinal kyphosis. Osteoporotic VCFs have been shown to adversely affect quality of life, physical function, mental health, and survival.4–6 These effects are related to the severity of the spinal deformity and are, in part, independent of pain.4,5 In recent years, researchers have highlighted the reduced quality of life, functional limitations, and impaired pulmonary function associated with spinal kyphotic deformity from osteoporotic VCFs.3,4,7–9 Kyphosis can lead to reduced abdominal space with poor appetite and resultant nutritional problems.4,10 By shifting the patient’s center of gravity forward, kyphotic deformity not only increases the risk of additional fractures,11 but also may lead to poor balance which potentially increases the risk of accidental falls.12,13 The ideal surgical treatment of VCFs should address both the fracture-related pain and the kyphotic deformity. It should be accomplished in a minimally invasive fashion without subjecting the patient to inordinate risks or excessive surgical trauma. Over the past decade, percutaneous vertebroplasty, involving the injection of polymethylmethacrylate (PMMA) into a fractured vertebral body, has been popularized. Substantial alleviation of pain has been reported in a majority of patients treated with vertebroplasty for osteopenic VCF.14–22 Although effective at relieving vertebral fracture pain, vertebroplasty is not designed to address the associated sagittal plane deformity. Kyphoplasty involves the penetration of the vertebral body with a trochar followed by insertion of an inflatable balloon tamp (IBT). Inflation of the balloon tamp restores the vertebral body back towards its original height, while creating a cavity to be filled with bone void filler. This technique was first performed in 1998. Early results of kyphoplasty suggest significant pain relief as well as the ability to improve the collapsed vertebral body’s height.23–29 The kyphoplasty procedure was designed to address vertebroplasty’s shortcomings such as high rates of cement leakage, although they rarely manifest with symptoms, and inability to correct fracture deformity. As the balloon tamp is inflated in the fractured vertebral body, the vertebral endplates are pushed apart reducing the fracture, and cancellous bone is pushed away from the balloon creating a cavity surrounded by compacted cancellous bone.30–32 The creation of an intravertebral cavity may decrease the potential for cement leakage by allowing for low-pressure, controlled placement of ‘doughy’ cement into the cavity and by creating a dam effect by densely compacting bone around the cavity.
PMMA has been the most common bone void filler used in both vertebroplasty and kyphoplasty. This acrylic cement has a long history of clinical use for the fixation of metal and plastic joint replacements and for the fixation of pathological fractures.33,34 When used to treat vertebral compression fractures, PMMA is usually modified (for example, addition of more barium sulfate, addition of antibiotics, alteration of monomer to powder ratio), in part to attain a viscosity that allows percutaneous insertion into vertebrae while minimizing risk of extravertebral leaks. In April, 2004, the United States FDA approved a formulation of PMMA for use in kyphoplasty procedures.
KYPHOPLASTY PATIENT SELECTION Indications and contraindications The main indications for kyphoplasty are painful or progressive osteoporotic or osteolytic vertebral compression fractures. Contraindications include systemic pathologies such as sepsis, prolonged bleeding times, or cardiopulmonary conditions that would preclude the safe completion of the procedure. In certain vertebra plana fracture configurations with height loss greater than 80% of the prefracture height, kyphoplasty may be technically difficult. The feasibility of the procedure should be assessed on the merits of the case. Patients with true burst fractures or fractures associated with neurologic findings are not candidates for percutaneous vertebral augmentation procedures. Generally, we do not advocate cementing more than three vertebral levels in one procedure because of the potential for deleterious cardiopulmonary effects related to pulmonary embolization (fat or cement) or to cement monomer.
Surgical timing The optimal timing of kyphoplasty treatment is uncertain. In a patient with an acute VCF and relatively minor vertebral collapse, the senior author (F.M.P.) will attempt a trial of conservative care during which serial radiographs are obtained. Kyphoplasty is recommended if there is progressive collapse of the vertebral body, if the pain attributed to the VCF is incapacitating, or if the pain attributed to the VCF does not respond to a reasonable period of conservative care. With advanced kyphosis at the time of presentation after a VCF, immediate kyphoplasty treatment may be considered to improve sagittal alignment. In the authors’ experience, earlier kyphoplasty may also be warranted for fractures at the thoracolumbar junction, fractures due to steroid-induced osteoporosis, and fractures occurring in vertebra with extremely low bone mineral density (i.e. a T score of ≤ 4 SD), which are predisposed to progressive collapse and deformity. To improve reliability and the extent of fracture reduction, one might consider performing kyphoplasty soon after fracture. Some studies
377
Part 2: Interventional Spine Techniques
suggest improved fracture reduction when kyphoplasty is performed earlier.24,26 However, the appropriate duration of nonoperative treatment prior to consideration of kyphoplasty has not yet been established.
the pedicle allowing cannulation through an extrapedicular approach. Despite the smaller size of the thoracic pedicle, the costovertebral attachment results in a much larger effective pedicle size (Fig. 33.2)
Preoperative evaluation
KYPHOPLASTY SURGICAL TECHNIQUE
Before proceeding with kyphoplasty, the physician must confirm that the patient’s back pain is indeed caused by a VCF. This determination requires careful correlation of the patient’s history and clinical examination with radiographic documentation of an acute or nonhealed VCF. The possibility of other spinal pathologies such as tumors or degenerative spondylosis must be considered as potential causes of back pain and deformity. A thorough neurologic examination is essential to rule out neurologic compromise. Pain radiating around the trunk in a dermatomal manner may accompany VCFs. Pulmonary function should be evaluated in those patients in whom advanced kyphosis may have led to respiratory difficulty. Preoperative planning for kyphoplasty includes imaging studies to confirm the fracture, estimate the duration of the fracture, and define the fracture anatomy. Lateral radiographs are particularly useful to plan the trajectory for any percutaneous procedure. Magnetic resonance imaging (MRI) can visualize bony edema, which indicates acute fracture, as well as help rule out infection or tumor involvement. Malignant causes of VCF are usually characterized by an illdefined margin, signal enhancement, and pedicle involvement as well as by paravertebral soft tissue mass.35 Sagittal MRI images with short tau inversion recovery (STIR) sequences highlight the marrow edema changes associated with acute VCFs. STIR sequence MRI has proven useful in determining the acuteness of a VCF.
Anesthesia
SURGICAL ANATOMY Understanding the anatomy of the spinal column and correlating spinal anatomy with intraoperative fluoroscopic images is essential to performing kyphoplasty. The mediolateral pedicle diameter is significantly smaller than the superior–inferior diameter. In the thoracic spine, the pedicle diameters are smallest in the midthoracic region especially at T5–7. The pedicle size appears to decrease as one descends from the upper thoracic segment to the middle segment and later increases in the lower segments. In the lumbar spine, the pedicle diameter increases gradually in the caudal segments. Also, in the majority of patients, the L1 pedicle diameter is smaller than the T11 or T12 pedicle diameter. The orientation of the pedicle is important in planning an appropriate trajectory for kyphoplasty. The medial inclination in the transverse plane appears to be greatest in the upper thoracic segments (T1–3), and becomes a straight anterior trajectory in the middle to lower thoracic spinal segments (Fig. 33.1). In the lumbar spine, the medial orientation of the pedicles increases slightly from L1 to L5. In the thoracic spine, the attachment of the ribs to the corresponding vertebral body (i.e. costovertebral joint) protects the lateral side of
Fig. 33.1 In the thoracic spine, the pedicles have less of a medial inclination (arrows), so that an extrapedicular approach will allow for better medialization of the IBTs. 378
Although the procedure may be performed under conscious sedation, the authors prefer to use general anesthesia for patients undergoing kyphoplasty. Advantages of general anesthesia include easier airway management, elimination of patient discomfort during the procedure, and elimination of patient motion that might impair fluoroscopic imaging.
Intraoperative positioning The patient is positioned prone on a table in the operating room or on a spinal frame with cushioned bolsters in the radiology suite. We prefer to use a Jackson frame which enhances the natural extension of the spine and also allows for biplane fluoroscopy. Alternatively, the patient can be placed on a radiolucent table with rolls placed beneath the chest and hips. The face, elbows, and legs should be well padded.
Fluoroscopic imaging The authors have found simultaneous biplanar fluoroscopy to be advantageous by allowing orthogonal visualization without having to move the C-arm. The ability to visualize the pedicles in both anteroposterior (AP) and lateral views is essential to performing the procedure. Fluoroscopic images confirming the patient’s anatomy must be obtained prior to initiating vertebral cannulation. In the AP view, the superior and inferior endplates are parallel to the fluoroscopic beam and are each
Costovertebral attachment
Fig. 33.2 The costovertebral attachment results in a much larger effective pedicle size in thoracic vertebrae.
Section 2: Interventional Spine Techniques
visualized as a single cortical shadow, the spinous process is centered in the vertebral body, and the pedicles are symmetric and positioned in the upper half of the vertebral body (Fig. 33.3A). In the lateral view, the endplates are also parallel and the pedicles are superimposed (Fig. 33.3B), Alternatively, the fluoroscope can be rotated 10– 20° for a pedicle en-face view, the view down the path of the pedicle (Fig. 33.3C) In this position, the pedicle is visualized directly and can be cannulated by paralleling the pathway of the X-ray beam.
spine, the transpedicular route may not allow for adequate medial placement of the instruments, which may limit optimal IBT inflation. The extrapedicular approach is an alternative that may allow for better medialization of the tools. The extrapedicular approach takes advantage of the costovertebral complex and allows entry through a more lateral starting point. An alternative far lateral approach to the lumbar vertebra has also been described; however, this technique has not been widely adopted.
Surgical approaches
Surgical technique
Bilateral transpedicular and extrapedicular approaches have been described for accessing the vertebral body during kyphoplasty. Most kyphoplasty procedures are performed by accessing the vertebral body through a transpedicular approach. In the upper and midthoracic
When using the transpedicular approach, the initial instrument should dock on the lateral aspect of the facet joint overlying the lateral aspect of the pedicle on the AP fluoroscopic image (Fig. 33.4). With
Starting position
Pedicles in upper half of vertebral body Endplates parallel Spinous process equidistant between pedicles
A
Endplates parallel
Pedicles superimposed
B
C Fig. 33.3 (A) In a centered AP view, each endplate is visualized as a single cortical shadow, the spinous process is centered in the vertebral body, and the pedicles are symmetrical and positioned in the upper half of the vertebral body. (B) In a centered lateral view, the endplates are parallel, and the pedicles are superimposed. (C) When the fluoroscope is rotated 10–20°, a pedicle en-face view, the view down the path of the pedicle, is visualized. Figures A and B courtesy of Kyphon Inc., Sunnyvale CA, USA.
Fig. 33.4 With the transpedicular approach, the initial instrument should dock on the lateral aspect of the facet joint overlying the lateral aspect of the pedicle on the AP view (center). Lateral and axial views are shown (top and bottom, respectively). 379
Part 2: Interventional Spine Techniques
the extrapedicular approach, the initial instrument is docked at the junction of the transverse process, rib head, and lateral pedicle wall (Fig. 33.5). The tip of the instrument appears outside of the lateral pedicle wall on the AP image. Unless an appropriate starting point is chosen, the balloon tamps cannot be positioned correctly, decreasing the success of the reduction. Once the docking position is selected on the AP view, the position of the starting point must be checked on the lateral view to confirm the appropriate trajectory toward the collapsed vertebral body.
Transpedicular
Pedicle cannulation During a transpedicular approach, the Jamshidi needle is advanced down the pedicle and into the posterior aspect of the vertebral body. At first, resistance to the passage of the needle is noted because of the cortical bone of the facet. As the needle enters the cancellous bone of the pedicle, the resistance decreases. Orthogonal fluoroscopic views are required as the needle advances through the pedicle. With both transpedicular and extrapedicular approaches, as the needle is advanced, the tip should remain lateral to the medial pedicle wall on the AP image until it reaches the posterior aspect of the vertebral body on the lateral image (Fig. 33.6). This technique ensures that the instrument remains outside of the spinal canal. Once the vertebral body is entered, the tip of the instrument may be medialized as Midpedicle
Final position
Extrapedicular
Midpedicle
Final position
Fig. 33.6 With both transpedicular and extrapedicular approaches, as the needle is advanced (Midpedicle), the tip should remain lateral to the medial pedicle wall on the AP image (center) until it reaches the posterior aspect of the vertebral body on the lateral image (Final position, top). Axial views are also shown (bottom). Fig. 33.5 With the extrapedicular approach, the initial instrument is docked at the junction of the transverse process, rib head, and lateral pedicle wall. Lateral, AP, and axial views are shown (top, center, and bottom, respectively). 380
Section 2: Interventional Spine Techniques
is appropriate but should not cross the midline. The Jamshidi needle should be advanced 1–2 mm past the posterior vertebral body margin.
Placement of working cannulae Fig. 33.9 On the AP view, the tip of the drill should approach the middle of the vertebral body but not cross midline. Courtesy of Kyphon Inc., Sunnyvale CA, USA.
The inner stylet is removed from the introducer needle, and a guide wire is placed into the vertebral body. After the working cannula is advanced over the guide wire into the posterior aspect of the vertebral body under biplanar fluoroscopic guidance, the guide wire is removed (Fig. 33.7). It is important to limit the number of passes through the pedicle as multiple attempts at cannulation create potential paths for cement leakage.
Vertebral body preparation A drill or bone tamp is used to prepare the vertebral body for placement of the IBTs. Under lateral fluoroscopy, the drill or tamp should be advanced to within 2–4 mm of the anterior cortex without perforating the cortex (Fig. 33.8). On the AP view, the tip of the drill should approach the middle of the vertebral body (Fig. 33.9). Once the drill is removed, a dull guide pin can be used to palpate the anterior cortex to confirm that there is no perforation. The vertebral body is now ready for expansion.
Fig. 33.7 The working cannula is advanced over the guide wire into the posterior aspect of the vertebral body under biplanar fluoroscopic guidance, and the guide wire is removed. Courtesy of Kyphon Inc., Sunnyvale CA, USA.
Inflatable balloon tamp inflation The bilateral IBTs are placed anteriorly in the vertebral body. To create a cavity within the vertebra and to reduce the fracture deformity, the IBTs are inflated in 0.5 cc increments while using visual (radiographic), volume, and pressure controls (digital manometer). Inflation continues until vertebral body height is restored, the IBT contacts a vertebral body cortical wall, the IBT reaches the maximal pressure rating without spontaneous decay, or maximal balloon volume is reached (Fig. 33.10). Four- or six-millimeter-sized balloons are available. We prefer to use 6 mm balloons in larger vertebral bodies (T12–L5) and 4 mm balloons in the midthoracic spine.
Cement application After the IBTs are withdrawn, a bone filler cannula is used to place partially cured PMMA into the cavity within the fractured vertebral body. To minimize the risk of cement extravasation, the authors allow the cement to become quite viscous prior to placement in the vertebral body. The bone filler device (BFD) filled with cement is positioned anteriorly in the intravertebral cavity created by IBT inflation. As the plunger is advanced, cement is expelled and fills the intravertebral cavity in a retrograde fashion. Cementing should be discontinued if extravertebral extravasation occurs or when cement reaches the posterior 25% of the vertebral body. The cement volume should approximate the volume of the intravertebral cavity. The judicious use of live fluoroscopic imaging is critical during cementing (Fig. 33.11). If cement extravasation occurs, usually through a fractured endplate or vertebral cortex, placing a small amount of viscous cement into the cavity and reinflating the balloon can salvage this situation. This maneuver will line the cavity walls with cement, effectively preventing further extravasation when the remainder of the cavity is filled with cement.
Postoperative care Postoperatively, the authors prefer to keep patients prone until they are alert. Once the patients have recovered from the anesthesia, they are mobilized by first sitting on the side of the bed and ambulating later that evening. Most patients are discharged home within a day of the procedure.
A
B
Fig. 33.8 Under lateral fluoroscopy, the drill (A) or tamp (B) should be advanced to within 2–4 mm of the anterior cortex without perforating the cortex. Courtesy of Kyphon Inc., Sunnyvale CA, USA.
COMPLICATIONS AND PREVENTIVE MEASURES Errors in patient selection Poor clinical outcomes may be predicted for kyphoplasty unless careful attention is given to patient screening and work-up. Treating old, healed VCFs is unlikely to affect the patient’s symptoms. The VCF must be confirmed as the likely pain generator if either 381
Part 2: Interventional Spine Techniques
Fig. 33.11 The cement volume should approximate the volume of the intravertebral cavity. The judicious use of live fluoroscopic imaging is critical during cementing. Courtesy of Kyphon Inc., Sunnyvale CA, USA.
A
by activity or changing positions and that is localized to the area of the radiographically documented fracture suggests the fracture to be responsible for the patient’s symptoms. In contrast to acute fracture pain, the back pain of chronic kyphosis typically worsens as the patient remains erect for periods of time and is not typically exacerbated by changes in position. The existence of multiple fractures may complicate the diagnosis, so that advanced imaging studies such as MRI or computed tomography (CT) with bone scans are usually required to identify recent fractures. Sagittal T1-weighted MR sequences can distinguish acute or nonhealed fractures from healed fractures. Edema associated with acute VCFs produces low signal intensity, whereas more chronic fractures tend to produce signals that are similar to those of nonfractured vertebrae. As mentioned in the Preoperative Evaluation section, sagittal STIR (heavily T2-weighted) MRI sequences are the most sensitive way to distinguish marrow fat from marrow edema. In STIR-MR images, edema in acute fractures produces high-intensity signal.36–38 On bone scan analyses, recently fractured vertebrae show an increased uptake of 99mTc compared to nonfractured vertebrae. CT plus bone scans may be used when MR images cannot be obtained.
B
C
Fig. 33.10 Inflation continues (A–C) until vertebral body height is restored, the IBT contacts a vertebral body cortical wall, the IBT reaches maximal pressure rating without spontaneous decay, or the maximal balloon volume is reached. Courtesy of Kyphon Inc., Sunnyvale CA, USA.
vertebroplasty or kyphoplasty is being considered. This determination usually requires a combination of clinical findings suggestive of fracture pain and confirmatory imaging studies. VCF pain often increases with weight-bearing activities and eases with recumbency. On history, the presence of abrupt onset of pain that is aggravated 382
Vertebral body access complications With either the transpedicular or the extrapedicular approach, care must be taken to avoid injuring surrounding tissues while accessing the vertebral body. The risk of injury to the neural elements increases if the medial pedicle wall is breached. Accessing the vertebral body caudal to the pedicle may place the segmental vessels and nerve roots at risk. Anterior or lateral perforation of the vertebral cortices with instruments may result in vascular injury or injury to structures in the thoracic or retroperitoneal spaces. Multiple attempts at cannulating the vertebral body should be avoided because of the increased risk of cement leaks through these additional tracts.
Cement complications The majority of complications reported for vertebral augmentation procedures relate to extravertebral cement extravasation. Cement may leak out of the vertebral body directly through deficiencies in the vertebral body cortex or via the venous system. If PMMA extravasates
Section 2: Interventional Spine Techniques
outside of the vertebral body, complications related to mechanical or thermal injury of adjacent anatomic structures may occur. The risk of local cement leakage is likely affected by cement injection pressure and cement viscosity as well as the ability of the bone, particularly the vertebral body cortex, to resist cement leakage. In addition to the risks of local cement leakage, systemic exposure to cement has been associated with cardiovascular collapse.39,40 It has been hypothesized that pressurization of PMMA into cancellous bone predisposes to embolization of cement, methylmethacrylate monomer, and bone marrow contents to the lungs with resulting adverse cardiopulmonary sequelae.39–42 This theorized result is certainly a cause for concern during vertebral augmentation procedures when high-pressure PMMA injection into vertebral bodies is performed. Extravertebral cement extravasation commonly occurs during vertebroplasty with reported leak rates of up to 65%;14 however, clinical sequelae of the leakage have been infrequently reported. In contrast, the reported rate of cement extravasation with kyphoplasty is typically less than 10%.23,26–29,43 With kyphoplasty, the creation of an intravertebral cavity surrounded by compacted bone allows for the placement of higher-viscosity cement under lower pressure compared to the injection conditions needed for vertebroplasty.
Failure of reduction The deleterious effects of spinal kyphosis on physical function, mental, respiratory, and gastrointestinal health are well established.3–5,9,44–46 Kyphoplasty attempts to reduce the fracture and associated deformity in a reliable and predictable fashion. Some degree of fracture reduction has been achieved in more than 60% of treated fractures.27,28 Factors that seem to limit reduction achieved with kyphoplasty include partial healing of bone, suboptimal placement of the IBT, and collapse of vertebral endplates after IBT removal and before cement placement. In cases where healed bone limits IBT expansion and fracture reduction, high IBT pressures at low balloon volumes and distorted IBT inflation shapes will be observed. To improve reduction of partially healed bone, the authors have developed a technique combining kyphoplasty with percutaneous osteotomy. Regarding positioning, if the IBT is placed too far laterally in the vertebral body, balloon contact with the lateral vertebral body cortex early during inflation limits the surgeon’s ability to continue inflation and optimize vertebral endplate elevation. This difficulty may be salvaged by the use of directional balloon tamps that preferentially inflate in a medial direction; however, this situation is best prevented by creating an appropriate channel for IBT placement. In cases where loss of endplate reduction occurs with balloon deflation, it may be possible to maintain reduction with unilateral bone tamp inflation elevating the endplate while placing cement on the opposite side.
SUMMARY Kyphoplasty is a technically demanding procedure offering a much needed treatment option for patients with symptomatic VCFs that do not respond to medical therapy or that are associated with progressive kyphosis. Rapid pain reduction, improved quality of life, and often fracture reduction have been observed in several consecutive case series.23,25–28,43,47 Further study is required to determine the optimal time for surgical intervention, to refine the patient selection criteria, and to delineate specific long-term effects of correcting vertebral deformity.
References 1. Barrick MC, Mitchell SA. Multiple myeloma. AJN 2001; 101(Suppl)(4):6–12. 2. Schachar NS. An update on the nonoperative treatment of patients with metastatic bone disease. Clin Orthop 2001; (382):75–81.
3. Lyles KW, Gold DT, Shipp KM, et al. Association of osteoporotic vertebral compression fractures with impaired functional status. Am J Med 1993; 94(6):595–601. 4. Silverman SL. The clinical consequences of vertebral compression fracture. Bone 1992; 13(Suppl 2):S27–S31. 5. Gold DT. The clinical impact of vertebral fractures: quality of life in women with osteoporosis. Bone 1996; 18(3 Suppl):185S–189S. 6. Gold DT, Lyles KW. Fractures: effects on quality of life. In: Rosen CJ, Glowacki J, Bilezikian JP, eds. The aging skeleton. San Diego, CA: Academic Press; 1999:632. 7. Leidig G, Minne HW, Sauer P, et al. A study of complaints and their relation to vertebral destruction in patients with osteoporosis. Bone Miner 1990; 8(3):217–229. 8. Pluijm SM, Tromp AM, Smit JH, et al. Consequences of vertebral deformities in older men and women. J Bone Miner Res 2000; 15(8):1564–1572. 9. Schlaich C, Minne HW, Bruckner T, et al. Reduced pulmonary function in patients with spinal osteoporotic fractures. Osteoporos Int 1998; 8(3):261–267. 10. Ross PD, Davis JW, Epstein RS, et al. Pain and disability associated with new vertebral fractures and other spinal conditions. J Clin Epidemiol 1994; 47(3):231–239. 11. Lindsay R, Silverman SL, Cooper C, et al. Risk of new vertebral fracture in the year following a fracture. JAMA 2001; 285(3):320–323. 12. White AA 3rd, Panjabi MM, Thomas CL. The clinical biomechanics of kyphotic deformities. Clin Orthop 1977 128:8–17. 13. Keller TS, Harrison DE, Colloca CJ, et al. Prediction of osteoporotic spinal deformity. Spine 2003; 28(5):455–462. 14. Cortet B, Cotten A, Boutry N, et al. Percutaneous vertebroplasty in the treatment of osteoporotic vertebral compression fractures: an open prospective study. J Rheumatol 1999; 26(10):2222–2228. 15. Cortet B, Cotten A, Boutry N, et al. Percutaneous vertebroplasty in patients with osteolytic metastases or multiple myeloma. Rev Rhum Engl Ed 1997; 64(3):177–183. 16. Cyteval C, Sarrabere MP, Roux JO, et al. Acute osteoporotic vertebral collapse: open study on percutaneous injection of acrylic surgical cement in 20 patients. AJR Am J Roentgenol 1999; 173(6):1685–1690. 17. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate. Technique, indications, and results. Radiol Clin North Am 1998; 36(3):533–546. 18. Evans AJ, Jensen ME, Kip KE, et al. Vertebral compression fractures: pain reduction and improvement in functional mobility after percutaneous polymethylmethacrylate vertebroplasty: retrospective report of 245 cases. Radiology 2003; 226(2):366–372. 19. Gangi A, Kastler BA, Dietemann JL. Percutaneous vertebroplasty guided by a combination of CT and fluoroscopy. AJNR Am J Neuroradiol 1994; 15(1):83–86. 20. Grados F, Depriester C, Cayrolle G, et al. Long-term observations of vertebral osteoporotic fractures treated by percutaneous vertebroplasty. Rheumatology 2000; 39(12):1410–1414. 21. Hodler J, Peck D, Gilula LA. Midterm outcome after vertebroplasty: predictive value of technical and patient-related factors. Radiology 2003; 227(3):662–668. 22. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the treatment of osteoporotic vertebral body compression fractures: technical aspects. AJNR Am J Neuroradiol 1997; 18(10):1897–1904. 23. Rhyne A 3rd, Banit D, Laxer E, et al. Kyphoplasty: report of eighty-two thoracolumbar osteoporotic vertebral fractures. J Orthop Trauma 2004; 18(5):294–299. 24. Wong WH, Reiley MA, Garfin SR. Vertebroplasty/kyphoplasty. J Women’s Imaging 2000; 2(3):117–124. 25. Theodorou DJ, Theodorou SJ, Duncan TD, et al. Percutaneous balloon kyphoplasty for the correction of spinal deformity in painful vertebral body compression fractures. Clin Imaging 2002; 26(1):1–5. 26. Phillips FM, Ho E, Campbell-Hupp M, et al. Early radiographic and clinical results of balloon kyphoplasty for the treatment of osteoporotic vertebral compression fractures. Spine 2003; 28(19):2260–2265. 27. Lieberman IH, Dudeney S, Reinhardt MK, et al. Initial outcome and efficacy of ‘kyphoplasty’ in the treatment of painful osteoporotic vertebral compression fractures. Spine 2001; 26(14):1631–1638. 28. Ledlie JT, Renfro M. Balloon kyphoplasty: one-year outcomes in vertebral body height restoration, chronic pain, and activity levels. J Neurosurg 2003; 98(1 Suppl):36–42. 29. Dudeney S, Lieberman IH, Reinhardt MK, et al. Kyphoplasty in the treatment of osteolytic vertebral compression fractures as a result of multiple myeloma. J Clin Oncol 2002; 20(9):2382–2387. 30. Garfin SR, Yuan HA, Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the treatment of painful osteoporotic compression fractures. Spine 2001; 26(14):1511–1515.
383
Part 2: Interventional Spine Techniques 31. Lane JM, Johnson CE, Khan SN, et al. Minimally invasive options for the treatment of osteoporotic vertebral compression fractures. Orthop Clin North Am 2002; 33(2):431–438, viii. 32. Phillips FM, Wetzel FT, Lieberman I, et al. An in vivo comparison of the potential for extravertebral cement leak after vertebroplasty and kyphoplasty. Spine 2002; 27(19):2173–2178; discussion 2178–2179. 33. Jang JS, Lee SH, Rhee CH. Polymethylmethacrylate-augmented screw fixation for stabilization in metastatic spinal tumors. Technical note. J Neurosurg 2002; 96(1 Suppl):131–134. 34. Bauer TW, Schils J. The pathology of total joint arthroplasty. I. Mechanisms of implant fixation. Skeletal Radiol 1999; 28(8):423–332.
40. Rudigier JF, Ritter G. Pathogenesis of circulatory reactions triggered by nervous reflexes during the implantation of bone cements. Res Exp Med (Berl) 1983; 183(2):77–94. 41. Markel DC, Femino JE, Farkas P, et al. Analysis of lower extremity embolic material after total knee arthroplasty in a canine model. J Arthroplasty 1999; 14(2):227–232. 42. Orsini EC, Byrick RJ, Mullen JB, et al. Cardiopulmonary function and pulmonary microemboli during arthroplasty using cemented or non-cemented components. The role of intramedullary pressure. J Bone Joint Surg Am 1987; 69(6):822–832.
35. Shih TT, Huang KM, Li YW. Solitary vertebral collapse: distinction between benign and malignant causes using MR patterns. J Magn Reson Imaging 1999; 9(5):635–642.
43. Coumans JV, Reinhardt MK, Lieberman IH. Kyphoplasty for vertebral compression fractures: 1-year clinical outcomes from a prospective study. J Neurosurg 2003; 99(1 Suppl):44–50.
36. Do HM. Magnetic resonance imaging in the evaluation of patients for percutaneous vertebroplasty. Top Magn Reson Imaging 2000; 11(4):235–244.
44. Leech JA, Dulberg C, Kellie S, et al. Relationship of lung function to severity of osteoporosis in women. Am Rev Respir Dis 1990; 141(1):68–71.
37. Mathis JM, Barr JD, Belkoff SM, et al. Percutaneous vertebroplasty: a developing standard of care for vertebral compression fractures. AJNR Am J Neuroradiol 2001; 22(2):373–381.
45. Kado DM, Browner WS, Palermo L, et al. Vertebral fractures and mortality in older women: a prospective study. Arch Intern Med 1999; 159(11):1215–1220.
38. Phillips FM, Pfeifer BA, Lieberman IH, et al. Minimally invasive treatments of osteoporotic vertebral compression fractures: vertebroplasty and kyphoplasty. Instr Course Lect 2003; 52:559–567.
384
39. Pinto PW. Cardiovascular collapse associated with the use of methylmethacrylate. AANA J 1993; 61(6):613–616.
46. Cooper C, Atkinson EJ, Jacobsen SJ, et al. Population-based study of survival after osteoporotic fractures. Am J Epidemiol 1993; 137(9):1001–1005. 47. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful vertebral body fractures in cancer patients. J Neurosurg 2003; 98(1 Suppl):21–30.
PART 3
SPECIFIC DISORDERS
Section 1
Medical Spinal Disorders
CHAPTER
Medical Radiculopathies
34
Andrew J. Haig
Sciatica – This is often associated with rheumatism and gout, but is also frequently brought on by catching cold. Occasionally it is due to accumulations in the bowels, or to diseases of the bones through which the nerve makes its exit. The painful points are usually found back of the trochanter or most projecting point of the thigh bone, at certain spots in the thigh about the knee and ankle joints. Medicology, a medical text published in 1905.1 How dumb could those old guys have been? Sciatica is caused by the spine. Disc herniation, spinal stenosis, fracture, tumor … Didn’t they ever examine the patient? This chapter will show that they were not so dumb. Despite our obsession with spinal imaging and spinal injections, all that radiates does not come from the spine. All that denervates does not come from the spine, either. The author will follow through on the history of sciatica, look at the differential diagnosis, and then take a look at the clues on history and physical examination that can give us a hint. Finally, the author will evaluate diagnostic tests that might help detect causes of sciatica and denervation.
HISTORY AND EPIDEMIOLOGY Sciatica is a constant. It has been present throughout the ages. With humility, it should be noted that it is not sciatica, but the medical theories and treatment that have changed over the years … and not always to the benefit of the patient. Theories of etiology are varied across cultures and time. The equivalent of Medline in the late 1800s was an annual compilation of published research presented by the United States Surgeon General. A search on the term sciatica results in numerous ‘hits’ – articles discussing the presentation and treatment of sciatica as a self-limiting cold ‘settling’ in the back, or flu ‘residing’ in the sciatic nerve. The 1905 general medical text Medicology doesn’t even mention trauma as an etiology.1 Around the turn of the last century the field of physical medicine and rehabilitation was born. A fringe group who espoused electrical treatments of medical problems ranging from cancer to the common cold held their first annual meeting in 1890.2 Though scorned by the medical establishment, this specialty gained popularity with the people, in part due to its apparent success in treating sciatica and back problems. As medicine advanced, management of back pain became more focused on basic scientific theory than pragmatic outcomes. New theoretical ‘causes’ for back pain and sciatica resulted in alarmingly unchallenged treatments. For example, long before the disc was implicated in sciatica, it was popular to blame sciatica on entrapment of the nerve in the piriformis muscle or on irritation from the sacroiliac joint. In 1928, Yeomans claimed success with surgical treatment of hundreds of people with sciatica and nerve damage that he
related to the sacroiliac joint.3 Almost certainly, a number of these people – at least the ones with neurologic deficits – had lumbar disc herniation, a syndrome that would not be discovered for more than a decade. His patients typically recovered and were ‘cured’ in spite of his well-meaning, but wrong, interventions. Mixter and Barr are rightly credited with proving that sciatica comes from disc herniations.4 But there is history behind this history. In the authors’ first years of practice at the University of Vermont, his senior partner Phillip Davis would often tell the story of Mixter and Barr’s first patient. This Vermonter had excruciating pain down the leg. His small-town doctor told him that it was likely ‘one of those cartilage tumors in the spine’ but that he would get better if he only waited. The disgusted patient ignored his doctor and went for a second opinion at the prestigious Harvard Medical School, where Mixter and Barr performed the first of millions of possibly unnecessary operations, paving their way to fame. More recent literature on the natural history of sciatica show us that, even today, physicians with high-sounding theoretical constructs and a big podium often win out over common sense and clinical insight. The NHANES survey of American health indicates that about 13% of noninstitutionalized adults have back pain of more than 2 weeks duration, and about 9% of these have sciatica with back pain.5 A lifetime prevalence of 1.5% can be calculated from these studies. But other studies show that up to 40% of people suffer from sciatica in their lifetime.6,7 Regardless of the numbers, from a physician standpoint, sciatica is a very common patient complaint. The author will present numerous nonspinal causes for sciatica. Since back pain is so common, there is a good chance they could coincide with sciatica. Since one-third or more of the population has abnormalities on an MRI, there is even a good chance that back pain, disc changes, and an unrelated cause of sciatica coincide. The risk of error is even greater when one realizes that MRI also misses some spinal causes of sciatica.
DIFFERENTIAL DIAGNOSIS Jeffrey Saal coined the term ‘pseudo-radicular syndrome’ for the nonspinal disorders that cause sciatica-like pain.8 The causes of pseudoradicular syndrome can be divided into musculoskeletal causes, focal neuropathies, and neuromuscular diseases. Among the musculoskeletal causes (Table 34.1), Galm et al.9 have shown that sacroiliac pain occurs in about one-third of persons with disc herniations, and that treatment of the sacroiliac joint in these people results in relief of pain. Trochanteric bursitis is another cause of similar pain that often occurs after onset of sciatica from disc herniation.10 Swezy11 found trochanteric bursitis in 31 of 70 persons referred for evaluation of sciatica or back pain. Most think of hip arthritis in the differential diagnosis of radiculopathy in older persons. In younger persons, avascular necrosis of the femoral head, 385
Part 3: Specific Disorders
Table 34.1: The Differential Diagnosis of Radiculopathy INTRINSIC SPINAL CAUSES
FOCAL NEUROMUSCULAR CAUSES—Cont’d
Cord compression at or above the suspected area Disc herniation Spinal stenosis Spondylolisthesis Segmental hypermobility Ganglion cyst Tumor Fracture Failed spine surgery syndrome Arachnoiditis Facet joint Bent spine syndrome Posterior primary ramus syndrome
Vibration hand (‘white finger’) syndrome Lumbar plexus Tumor Aneurysm Pelvic organ enlargement Sciatic nerve lesions Piriformis syndrome Blunt, sharp, or chronic trauma Baker’s cyst Peroneal nerve lesion at the fibular head Tarsal tunnel syndrome Anterior tarsal tunnel syndrome Femoral neuropathy Lateral femoral cutaneous (meralgia paresthetica) Obturator, gluteal, cluneal, and other odd neuropathies
MUSCULOSKELETAL CAUSES Neck Myofascial pain Glenohumeral joint pain Acromioclavicular joint pain Lateral epicondylitis Low back Sacroiliac joint pain Trochanteric bursitis Anserine bursitis Hip arthritis Avascular necrosis of the femoral head Diffuse arthritis Shin splints Hamstring strain FOCAL NEUROMUSCULAR CAUSES Brachial plexus Tumor Stretch Thoracic outlet syndrome Upper limb focal neuropathies Carpal tunnel syndrome Ulnar neuropathy Multiple radial nerve locations
slipped capital femoral epiphysis, and other unusual hip arthritides can fool the unwary. Paraspinal muscle inadequacy-related to previous surgery,12 deconditioning, stretch of the dorsal root,13 or focal myopathy14,15 is increasingly being reported as a cause of pain. Focal neuromuscular disorders are not uncommon. Most worrisome are tumors and infections causing compression of the nerves or plexus. Bicknell and Johnson16 pointed out a number of characteristics of neoplastic plexopathies. They are characteristically painful; in the brachial plexus, more than 70% involve the lower trunk and are mainly due to axillary lymph node infiltration. In contrast, lumbosacral plexus neoplasms cause neuropathy by direct infiltration. They also favor the lower plexus, with 31% lumbar and 51% sacral plexus. With a history of cancer treatment the differential diagnosis is often radiation plexopathy versus tumor.17,18 Painless and progressive weakness is the hallmark of radiation plexopathies, which typically occur in the upper trunk of the brachial plexus and in the lower part of the lumbosacral plexus. In the lumbar area, radiation plexopathy is usually bilateral but asymmetrical.16 The presence of lymphedema suggests that there has been radiation damage, but does not rule out tumor. The classic electrodiagnostic finding of myokymia is related to radiation, but again does not rule out tumor. 386
NEUROMUSCULAR DISEASES Diffuse polyneuropathy Mononeuritis multiplex Inflammatory radiculopathy/plexopathy Myopathy Myoneural junction disorder SYSTEMIC CAUSES Cardiac ischemia Aortic aneurysm Pulmonary embolism and other lung diseases Gastrointestinal disorders Genitourinary disorders Metabolic disorders (e.g. sickle cell, porphyria) Fibromyalgia Polyarthritis PSYCHIATRIC DISORDERS Anxiety/hyperventilation Hysteria Malingering Munchausen syndrome
Infectious causes are typically obvious because of their systemic presentation. But they can be missed. Tuberculosis deserves special attention because of the rise in immune disorders such as AIDS and the increasing resistance to antibiotics. The slow-growing nature of tuberculosis may result in a missed diagnosis.19 Focal neuropathies masquerading as radiculopathy are not uncommon. Some, such as carpal tunnel syndrome, meralgia paresthetica, or peroneal nerve lesion at the fibular head, are relatively straightforward to diagnose once the clinician is aware of the possibility. The association of these lesions with neck and back pain is termed the ‘double crush syndrome.’ It is debated whether the presence of two compressions (e.g. neck and ulnar nerve) is coincidental or whether one lesion predisposes to the other.20 Other focal neuropathies such as thoracic outlet syndrome or piriformis syndrome are quite controversial. For both of these disorders part of the controversy has to do with language. For example, some will call a tender tight piriformis muscle ‘piriformis syndrome’ while others reserve this term for nerve irritation caused by the muscle. Thoracic outlet syndrome should properly be divided into ‘true neurogenic thoracic outlet syndrome’ in which there is objective electrodiagnostic evidence of nerve involvement, vascular thoracic outlet syndrome in which a vein or artery is clearly causing dysvascular pain,
Section 1: Medical Spinal Disorders
and ‘disputed thoracic outlet syndrome’ in which there is a subjective sense that the thoracic outlet is involved. Even when language is clear, the diagnosis of these disorders is not simple. Despite its long history in the literature, as late as 1989 there had not been a single unequivocal, electrodiagnostically proven case of piriformis syndrome.21 Subsequent cases have shown that the syndrome exists.22 Fishman believes that it is very common, based on a somewhat circuitous but reasonable argument that electrodiagnostic F-waves disappear in certain positions in people with certain complaints.23 Thoracic outlet syndrome clearly exists, based on a number of electrodiagnostic, vascular, and surgical observations. Nerves, arteries, or veins can be entrapped by a number of structures in the neck and shoulder, ranging from the classic cervical rib to the scaleneus muscles to anomalous fibrous bands. But some think it is exceedingly rare, while others think it is common. The controversy is further befogged by the fact that a key article published by Urschel,24 one of the great proponents of thoracic outlet surgery, has been found to include misrepresentations.25 Many of the focal neuropathies that can mimic radiculopathy are uncommon. They are typically found when an alert clinician detects a classic presentation or when the MRI is negative despite neurogenic complaints. Neuromuscular diseases are frequently confusing to spine clinicians. In the author’s prospective masked study of 150 older persons with low back pain, spinal stenosis, or no spinal symptoms prescreening was conducted for polyneuropathy, alcohol, and diabetes. Despite this, eight subjects thought by a clinician to have spinal stenosis were found on electrodiagnostic testing to have a neuromuscular disease.26 These included undetected diabetic neuropathy, but also a statin myopathy and Charcot-Marie-Tooth disease. Similar to spinal disorders, neuromuscular diseases can cause weakness, sensory loss, and pain. They may actually predispose to back pain due to their effect on spinal stability and limb biomechanics.27 Even when there is a spinal disorder, the prognosis from invasive treatment is poorer in these people.28 It is beyond the scope of this chapter to review all neuromuscular diseases. Some observations are useful, however. Diabetes and alcohol are the two most common causes of polyneuropathy in developed countries. Diabetes can present with neuropathy before the disease itself is detected. Alcohol use is notoriously underreported, especially among women with back pain.29 Congenital neuropathies and myopathies are often unrecognized by the back pain patient, as they develop slowly, and family members often have the same impairments. Inflammatory and congenital myopathies often present with back and hip pain.30 One interesting myopathy requires special attention by spine clinicians. The ‘bent spine syndrome,’ also called camphylocormia or, in the cervical region, ‘dropped head syndrome’ is a focal myopathy of the paraspinal muscles.14,15 The typical presentation sounds strangely like spinal stenosis, as the patient can ambulate for a short time, but the back begins to ache and tire. After a rest the patient can continue ambulation. Attentive inspection of the MRI will show fatty replacement (as opposed to atrophy) of the paraspinal muscles. Electromyogram of the paraspinal muscles will confirm the diagnosis. It has been shown by the author that the disability caused by bent spine syndrome actually relates to the presence of a hip flexion contracture. Correction of hip flexion contracture in one patient allowed him to assume a more typical myopathic extended spine posture, and increased his ambulation ability tenfold.31 Systemic disorders commonly present to the primary care physician as back pain. The spine physician does not see these very often, probably because of good screening on the part of the primary care
physician. While any of the disorders listed in Table 34.1 could be detected by the specialist, most interesting are a number of disorders that can cause both pain and psychiatric disease. Chronic pain with psychiatric presentation is so common in the spine clinician’s practice that a medical tie between the two is often not considered. The prototype disease is acute intermittent porphyria. But thyroid disease, chemical toxicities, sickle cell disease, metabolic derangements, and numerous other disorders can cause both psychiatric and peripheral nerve complaints. Of course, purely psychiatric complaints such as hysteria or malingering do occur, as well. Although high lumbar disc herniations – L2, 3, or 4 nerve root irritation – are really spinal disorders, they deserve special attention. They are often missed because the physician is looking solely for sciatica as the complaint from disc herniations. These lesions comprise only about 5% of disc herniations. They seldom present with pain below the knee, but instead typically cause anterior thigh pain. Albert et al.32 collected 141 surgically proven high lumbar disc herniations. They found that the examination for weakness is often negative, although the iliopsoas can be of some help. The only accessible high lumbar reflex, the patellar reflex, remains intact in about 50% of surgically proven lesions. The straight leg raise test is negative, and the ‘reverse straight leg raise’ test thought to be specific for high lesions is also negative in about half of cases. More concerning, MRI misses about half of these lesions, which are more often hidden in the lateral recess. Fortunately, electromyography including a systematic paraspinal examination appears to miss very few upper lumbar lesions.33
PHYSICAL EXAMINATION Many, but not all, useful physical examination tests for back pain have been subjected to validation trials.34–36 Most components of the ‘manual physical examination’ used to evaluate segmental changes in the spine have not shown good reliability, despite the fact that the manual therapy which is based on such evaluations probably is effective.37 While this is specifically true, in general it is not difficult to find a musculoskeletal diagnosis. Finding peripheral musculoskeletal causes is a matter of thinking and taking the time to examine the patient. One simply asks the patient where he or she is tender, and confirms this location by palpation. The problem comes in patients who have been told that their problem is spinal. They attribute bone, joint, or ligament findings to the spine. Some hints include lateral hip pain or pain on lying on the side (trochanteric bursitis), groin pain, especially getting in and out of a car (hip arthritis), and complaints of pain emanating from the sacral sulcus when combined with five or more sacroiliac joint provocation maneuvers38 and point towards the sacroiliac joint as a cause of pain.39 Focal neuropathies are somewhat more difficult to differentiate from radiculopathies on physical examination, especially when they are not severe. Classically, hand pain that does not go above the wrist is more likely a focal median or ulnar neuropathy. If the problem is neurologically severe enough, the physical examination should be normal in muscles that share the same nerve root, but not the same nerve. A comprehensive strength examination should find these contradictions. Table 34.2 lists selected muscles that share the same root, but not the same nerve. Perhaps the most important pair is the extensor hallucis longis and the tensor fascia lata. L5 is the most common lumbar radiculopathy. Toe weakness in the presence of back pain suggests an L5 radiculopathy. Since polyneuropathy, peroneal neuropathy, bunions, and discoordination can affect extension of the great toe, it is important to always test the tensor fascia lata to see if the lesion is proximal and in another nerve. This is done by having the patient sit with knees 387
Part 3: Specific Disorders
Table 34.2: Selected Muscles that Share the Same Root but Different Nerves Root
Muscle 1
Confirmation Muscle
C5
Biceps, musculocutaneous N
Rhomboids, nerve to rhomboids
C6
Biceps, musculocutaneous N
Supraspinatus, suprascapular N
C7
Triceps, radial N
Flexor carpi radialis, median N
C8
Extensor indicis, radial N
Flexor pollicis longus, anterior interosseous N
T1
Abductor digiti quinti, ulnar N
Abductor pollicis brevis, median N
L2–4
Quadriceps, femoral N
Adductors, obturator N
L5
Extensor hallucis longis, peroneal N
Tensor fascia lata, superior gluteal N
S1
Gastrocnemus, tibial N
Gluteus maximus, inferior gluteal N
N, nerve.
together and ankles apart. Resisted pressure laterally and simultaneously on the ankles is a remarkably sensitive finding. While it is true that a recovering radiculopathy may have good hip muscle strength, but still have distal weakness, this pattern of weakness should raise suspicion. The physical examination for neuromuscular diseases may be clear or may still result in confusion. Numbness in a stocking distribution or symmetrical weakness may be helpful. In congenital neuropathies the classic high arches, and in myopathies the proximal weakness and myalgia, may be appreciated. More useful is a high index of suspicion based on history. In persons with diabetes, alcoholism, or other disorders known to cause polyneuropathy, there should be a presumption that any neurologic deficit is not caused by the spine until proven otherwise.
DIAGNOSTIC TESTING The single most important test in differentiating nonspinal causes of radiculopathy is electrodiagnostic consultation (EDX). It is the only test that can diagnose polyneuropathy, myopathy, or neuromuscular junction disorders. EDX is also sensitive to spinal causes of radicular pain, and in fact may be more sensitive and specific than MRI to the clinical syndrome of spinal stenosis.40,41 In contrast to imaging studies, there is little overlap between the asymptomatic and symptomatic populations. EDX costs less than MRI and patients tolerate it as well as or better than MRI, with essentially no long-term side effects. EDX findings that suggest a nonspinal cause for radicular pain include needle examination showing findings in a nonroot distribution and nerve conduction studies showing slowing, either diffusely or across an area of possible nerve damage. Axonal neuropathies have distal, rather than radicular findings. Mononeuritis multiplex will show lesions outside of the area in question. Nonanatomic radiculopathies will often show diffuse, rather than focal paraspinal abnormalities. Where there is a question of polyneuropathy, study of an uninvolved limb and of the thoracic paraspinal muscles should be considered. There are some cautions about EDX. Since S1 probably does not innervate the paraspinal muscles it is impossible to differentiate an S1 radiculopathy from a mild sacral plexopathy. A more severe peripheral nerve lesion anywhere would result in decreased sensory nerve amplitude. Classically, radiculopathies are proximal to the dorsal root ganglion, but contrary to common thought, about 10% of S1 radiculopathies due to spinal disorders may be distal to the S1 ganglion. The EDX consultant must build an index of suspicion about possible peripheral nerve causes of radiculopathy. A good screen includes 388
5 lower limb muscles plus quantified paraspinal needle exam for the low back, or 7 upper limb muscles for the neck.42,43 Work the author has recently concluded shows the great importance of a quantified paraspinal examination, which is the single most sensitive and specific electrodiagnostic test for spinal stenosis and probably other spinal disorders.21,26 It also includes a sensory and a motor study, or alternatively an H-wave. With any index of suspicion, a test of the upper limbs (for a lumbar complaint) or lower limbs (for a cervical complaint), or the thoracic paraspinals (for a difficult radicular complaint) is useful. Imaging of the apparently affected part may be useful. Anesthetic injections into the affected part may also confirm a diagnosis. Blood tests such as a blood count and sedimentation rate are useful, but often need to be followed by a more detailed rheumatologic or metastatic work-up.
SUMMARY All that radiates is not sciatica, and all that is neurogenic is not discogenic. Given the high prevalence of back pain along with the high prevalence of disorders that can mimic sciatica, the spine clinician must remain constantly aware of the possibility of a cause outside of the spine. The key is to have a high index of suspicion. An abnormal MRI is not proof that the complaint emanates from the spine. Some warning signs include: ● ● ● ● ● ● ● ●
History suggesting a comorbid disorder that can cause neuropathy; Distal bilateral pain; High arches; Pain that does not go above the wrist or ankle; Diffuse hyporeflexia; Tenderness away from the spine; Groin pain; Pain that does not go away with spinal treatments. Sciatica – apply belladonna ointment to seat of pain. Poultices applied very hot. Sulpher applied to painful part is very effective, after which the limb or part should be enveloped in flannel. … also amenable to treatment with electricity … have fifty of these pills made: Sulphate iodine … phosphate iron … Strychnine. … Take one after each meal. … The use of these tonics will tend towards a cure, but the disease is very obstinate, and strict observances of hygiene precautions is imperative.1 Medicology
Section 1: Medical Spinal Disorders
References 1. Wood JP. Medicology (or) home encyclopedia of health. A complete family guide. New York: University Medical Society; 1905. 2. Gritzer G, Arluke A. The making of rehabilitation. A political economy of medical specialization, 1890–1980. Berkeley, CA: University of California Press; 1985. 3. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica. Lancet 1928; 2:1119–1122. 4. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211:210. 5. Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low back pain and its related medical care in the United States. Spine 1987; 12:264. 6. Svensson HO, Anderson GBJ. Low back pain in 40–47 year old men: I. Frequency of occurrence and impact on medical services. Scand J Rehabili Med 1982; 14:47. 7. Frymoyer JW, Pope MH, Clements JH, et al. Risk factors in low-back pain. An epidemiological survey. Bone Joint Surg (Am) 1983; 65(2):213–218. 8. Saal JA, Dillingham MF, Gamburd RS, et al. The pseudo-radicular syndrome: lower extremity peripheral nerve entrapment masquerading as lumbar radiculopathy. Spine 1988; 13:926–930. 9. Galm R, Frohling M, Rittmeister M, et al. Sacroiliac joint dysfunction in patients with imaging-proven lumbar disc herniation. Eur Spine J 1998; 7(6):450–453. 10. Tortolani PJ, Carbone JJ, Quartararo LG. Greater trochanteric pain syndrome in patients referred to orthopedic spine specialists. Spine J 2002; 2(4):251–254. 11. Swezey RL. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil 1976; 57(8):387–390.
23. Fishman LM, Anderson C, Rosner B. BOTOX and physical therapy in the treatment of piriformis syndrome. Am J Physical Med Rehabil 2002; 81(12):936–942. 24. Urschel HC Jr. Management of the thoracic-outlet syndrome. N Engl J Med 1972; 286(21):1140–1143. 25. Wilbourn AJ, Lederman RJ. Evidence for conduction delay in thoracic-outlet syndrome is challenged. N Engl J Med 1984; 310(16):1052–1053. 26. Haig AJ, Tong HC, Yamakawa KSJ, et al. Spinal Stenosis, back pain, or no symptoms at all? A masked study comparing radiologic and electrodiagnostic diagnoses to the clinical impression. Arch Phys Med Rehabil 2006; 87(6):897–903. 27. Ingram CM, Harris MB, Dehne R. Charcot spinal arthropathy in congenital insensitivity to pain. Orthopedics 1996; 19(3):251–255. 28. Cinotti G, Postacchini F, Weinstein JN. Lumbar spinal stenosis and diabetes. Outcome of surgical decompression. J Bone Joint Surg (Br) 1994; 76(2):215–219. 29. Booker EA, Haig AJ, Geisser ME, et al. The relationship between alcohol use and performance in persons with chronic back pain disability. Am J Phys Med Rehabil 2001; 80:8. 30. Haig AJ. The complex interaction of myotonia and low back pain. Spine 1991; 16:580–581. 31. Haig AJ, Tong HC, Kendall R. The bent spine syndrome: myopathy + biomechanics = symptoms. In review, Spine J, October, 2004. 32. Albert TJ, Balderston RA, Heller JG, et al. Upper lumbar disk herniations. J Spinal Disord 6(4)351–359. 1993; 33. Haig AJ, Yamakawa K, Hudson DM. Paraspinal electromyography in high lumbar and thoracic lesions. Am J Phys Med Rehabil 2000; 79(4):336–342.
12. Sihvonen T, Herno A, Paljarvi L, et al. Local denervation atrophy of paraspinal muscle in postoperative failed back syndrome. Spine 1993; 18(5):575–581.
34. van den Hoogen HM, Koes BW, van Eijk JT, et al. On the accuracy of history, physical examination, and erythrocyte sedimentation rate in diagnosing low back pain in general practice. A criteria-based review of the literature. Spine 1995; 20(3): 318–327.
13. Fisher MA, Kacr D, Houchin J. Electrodiagnostic examination, back pain, and entrapment of posterior rami. Electromyogr Clin Neurophysiol 1985; 25:187.
35. Andersson GBJ, Deyo RA. History and physical examination in patients with herniated lumbar discs. Spine 1996; 21(24S):105–185.
14. Ricq G, Laroche M. Acquired lumbar kyphosis caused in adults by primary paraspinal myopathy. Epidemiology, computed tomography findings, and outcomes in a cohort of 23 patients. Joint, Bone, Spine: Revue du Rhumatisme 2000; 67(6): 528–532.
36. Deyo RA, Rainville J, Kent DL. The rational clinical examination: What can the history and physical examination tell us about low back pain? JAMA 1992; 268: 760–765.
15. Laroche M, Ricq G, Delisle MB, et al. Bent spine syndrome: computed tomographic study and isokinetic evaluation. Muscle Nerve 2002; 25(2):189–193. 16. Bicknell JM, Johnson SF. Widespread electromyographic abnormalities in spinal muscles in cancer, disc disease, and diabetes. Univ Mich Med Center J 1976; 42:124–127. 17. Kori SH, Foley KM, Posner JB. Brachial plexus lesions in patients with cancer: 100 cases. Neurology 1981; 31:45–50. 18. Jaeckle KA, Young DF, Foley KM. The natural history of lumbosacral plexopathy in cancer. Neurology 1985; 35:8–15. 19. Myllyla VV, Sutinen S, Kotaniemi A. Radicular symptoms in tuberculosis. A case report. European Neurology 1976; 14(2):90–96. 20. Bednarik J, Kadanka Z, Vohanka S. Median nerve mononeuropathy in spondylotic cervical myelopathy: double crush syndrome? J Neurology 1999; 246(7):544–551. 21. Haig AJ, Wallbom A. Low back pain and electromyography. New England J Med 2001; 344(12):1644. 22. Papadopoulos EC, Khan SN. Piriformis syndrome and low back pain: a new classification and review of the literature. Orthoped Clin N Am 2004; 35(1):65–71.
37. Najm WI, Seffinger MA, Mishra SI, et al. Content validity of manual spinal palpatory exams – A systematic review. Complement Alternat Med 2003; 3(1):1. 38. Fortin JD, Falco FJ. The Fortin finger test: an indicator of sacroiliac pain. Am J Orthoped (Chatham, NJ) 1997; 26(7):477–480. 39. Slipman CW, Sterenfeld EB, Chou LH, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79(3):288–292. 40. Haig AJ, Tong HC, Yamakawa KSJ, et al. The sensitivity and specificity of electrodiagnostic testing for the clinical syndrome of lumbar spinal stenosis. Spine 2005; 30(23):2667–2676. 41. Haig AJ, Geisser ME, Tong HC, et al. Electromyographic and magnetic resonance imaging measurements in older persons with lumbar spinal stenosis, low back pain, and no back complaints. (In revision, JBJS August 2005.) 42. Dillingham TR, Lauder TD, Andary M, et al. Identifying lumbosacral radiculopathies: an optimal electromyographic screen. Am J Phys Med Rehabil 2000; 79(6):496–503. 43. Dillingham TR, Lauder TD, Andary M, et al. Identification of cervical radiculopathies: optimizing the electromyographic screen. Am J Phys Med Rehabil 2001; 80(2):84–91.
389
PART 3
SPECIFIC DISORDERS
Section 1
Medical Spinal Disorders
CHAPTER
Spondyloarthropathies
35
Joanne Borg-Stein and Bonnie Bermas
INTRODUCTION
GENERAL CLINICAL FEATURES
Spondyloarthropathy (SpA) refers to the clinical family of disorders that are characterized as inflammatory rheumatic disorders with manifestations in the vertebral column, peripheral joints, and extraarticular structures. These disorders frequently manifest initially with back complaints. For example, back complaints are the first symptoms in 75% of patients with ankylosing spondylitis and may be present in 89% of patients with undifferentiated spondyloarthropathy.1,2 Given the high prevalence of axial spine complaints in this population, it is of critical importance to the spine clinician to be aware of these diagnoses. The spine specialist must be familiar with characteristic aspects of the patient history, physical examination, laboratory data, and diagnostic imaging. It is the purpose of this chapter to provide a comprehensive overview of the different categories of spondyloarthropathy, including pathology, diagnostic criteria, imaging, extra-articular manifestations, and treatment.
In general, spondyloarthropathies demonstrate the following clinical features:
DEFINITION AND CLASSIFICATION The spondyloarthropathies are a cluster of overlapping and interrelated chronic inflammatory rheumatic disorders which include ankylosing spondylitis (often considered the prototype), reactive arthritis, arthritis associated with psoriasis, arthritis associated with Crohn’s disease and ulcerative colitis, Reiter’s syndrome, and undifferentiated spondyloarthropathy.3 These disorders are often referred to as the seronegative spondyloarthropathies, which are considered together since they share clinical, epidemiologic, and imaging features. The spondyloarthropathies usually have a negative rheumatoid factor (seronegativity), association with HLA-B27, familial clustering, predominant axial and peripheral joint involvement, and extra-articular manifestations.4
EPIDEMIOLOGY AND GENETICS Spondyloarthropathies are a group of diseases heavily influenced by genetic factors, particularly HLA. There is a clinical spectrum of these disorders. Undifferentiated spondyloarthropathy is the most common disorder; with ankylosing spondylitis (AS) being second most common. The estimated incidence is likely more common than previously realized as newer classification systems have been developed. Prevalence of SpA is correlated with the presence of HLA-B27 in a particular population.5,6 Both men and women are affected. In ankylosing spondylitis, males are disproportionally affected in a 3:1 ratio.7 Psoriatic arthritis affects men and women equally.8 Postvenereal Reiter’s syndrome is more common in men, whereas postdysenteric Reiter’s syndrome equally affects men and women.9,10
● ● ● ● ● ●
A tendency to affect spinal joints, causing sacroiliitis and spondylitis; Peripheral arthritis, typically oligoarticular and asymmetric; Inflammation of bony insertions for tendons and ligaments (enthesitis or enthesopathy); Usually a young age at onset; Negative tests for rheumatoid factors; and Familial predisposition and a strong association with a genetic polymorphism of the major histocompatibility complex (MHC), HLA-B27.7,11,12
PATHOLOGY Enthesopathy The ‘enthesis’ is the region of insertion of a tendon, ligament, capsule, or fascia into bone. The enthesis is now understood to be a complex structure that extends into the bone and marrow cavity.13 Recent work suggests that the entheseal fibrocartilage is the major target of the immune response and the primary site of the immunopathology.14 The bone marrow demonstrates edema and contains cellular infiltrates. T lymphocytes are abundant in these areas with a preponderance of CD8+ cells.15 Pathologic studies have demonstrated inflammatory infiltration and destruction which affect the whole anulus fibrosus, not just the enthesis of the intervertebral disc.16
Synovitis Patients with spondyloarthropathy may have peripheral arthritis, typically mono- or oligoarticular, and often affecting one or both knees. Microscopic analysis reveals fibrin, synovial cell proliferation, lymphocytes, and plasma cells in the synovium.17 A more recent hypothesis suggests that bacterial antigens and microorganisms in a susceptible HLA-B27-postitive patient may interact to produce inflammation and arthritis in ankylosing spondylitis.18 It is well established in reactive arthritis that synovial fluid demonstrates bacteria-specific T-cell responses to the bacterium that causes the arthritis.19,20
Sacroiliitis Studies of the sacroiliac joint reveal evidence of synovitis, osteitis, and enthesitis. Biopsy and autopsy specimens demonstrate pannus formation, myxoid marrow, superficial cartilage destruction, intra-articular fibrous strands, new bone formation, and bony ankylosis. Biopsy 391
Part 3: Specific Disorders
samples demonstrate cellular infiltrates of T lymphocytes, with both CD4+ and CD8+ cells.21,22 Contrast-enhanced magnetic resonance imaging (MRI) studies of the sacroiliac joints in inflammatory back pain can demonstrate the following: sacroiliitis is more often bilateral in AS (84%) than in undifferentiated SpA (48%); the dorsocaudal parts of the synovial joint and the bone marrow are the most frequently inflamed structures early in the disease; in contrast, the entheses and ligaments are more commonly involved in later stages.23
DIFFERENTIAL DIAGNOSIS The differential diagnosis of sacroiliitis is narrow and is summarized in Table 35.1.7 Spinal pain and restriction may also be caused by diffuse idiopathic skeletal hyperostosis (DISH). In contrast to SpA, DISH usually presents with later age of onset, normal sedimentation rate, larger and more flowing ligamentous ossifications (syndesmophytes), and the absence of sacroiliitis.24
DIAGNOSIS The classification criteria for AS were reassessed in 1984 and are referred to as the ‘modified New York criteria for ankylosing spondylitis.’ The criteria include both clinical and radiographic categories.25,26 The three clinical criteria include:
● ●
Low back pain and stiffness of longer than 3 months’ duration, improved with exercise but not relieved by rest; Limitation of motion of the lumbar spine in both the sagittal and frontal planes; and Limitation of chest expansion relative to normal values corrected for age and sex.
The two radiologic criteria include: ● ●
Sacroiliitis with more than minimum abnormality bilaterally; and Sacroiliitis of unequivocal abnormality unilaterally.
‘Definite AS’ is present in the presence of one clinical criterion and one radiologic criterion. ‘Probable AS’ is diagnosed if three clinical criteria are present or one radiologic criterion.
Table 35.1: Spondyloarthropathies SPONDYLOARTHROPATHIES AS Reiter’s syndrome (reactive arthritis) Psoriatic arthritis Inflammatory bowel disease Acne-associated arthritis or SAPHO syndrome Intestinal bypass arthritis INFECTIOUS Pyogenic infections Tuberculosis Brucellosis Whipple’s disease OTHER Hyperparathyroidism Paraplegia Sarcoidosis (rare)
392
Clinical features of AS are heralded by chronic low back pain and stiffness as the initial symptoms in 75% of patients.27 Often, the symptoms develop spontaneously and progress insidiously. Buttock pain that radiates into the thigh may be erroneously blamed on sciatica. This pain may reflect involvement of the sacroiliac joints.28,29 A history of nocturnal back pain, diurnal variation with prolonged morning stiffness, and improvement with exercise should raise the suspicion of an inflammatory etiology to chronic back pain. A good response to nonsteroidal antiinflammatory drug (NSAID) therapy and an age younger than 40 also increase the likelihood of inflammatory back pain.30 Another, less common presentation of AS may be enthesitis or peripheral arthritis, mono- or oligoarticular.31 The enthesitis may involve the Achilles or plantar tendon insertions. The knee is often involved in the arthritis. These findings are not unique to AS. The differential diagnosis may include Reiter’s syndrome or reactive arthritis.
Physical examination
Ankylosing spondylitis
●
Clinical features
The earliest physical examination finding is often tenderness in the region of the sacroiliac joints or pain on provocative test maneuvers such as hip hyperextension and sacral compression tests. The two most sensitive maneuvers are pressure over the anterior-superior iliac spines and pressure over the lower half of the sacrum.32 As the disease progresses, physical examination findings will reflect restricted ranges of motion. As an example, reduced chest expansion is measured from maximal exhalation to maximal inhalation at the level of the fourth intercostal space. An expansion of less than 2.5 cm is considered abnormal.27 The restricted motion reflects fusion of the costovertebral joints. Schober’s test and finger-to-floor test will also become abnormal. The Schober’s test is performed by marking the fifth lumbar vertebra and a point in the midline 10 cm above. The patient is then asked to flex forward maximally while maintaining the knees straight. The distance between the two points exceeds 15 cm in normal individuals.1
Laboratory studies Laboratory studies in AS are often non-specific. Acute-phase reactants such as erythrocyte sedimentation rate and C-reactive protein are often elevated, but are not specific for AS and do not necessarily reflect disease activity.33,34 A mild normochromic normocytic anemia may be present. Serologic tests for lupus and rheumatoid arthritis should be negative. HLA-B27 is present in approximately 90% of Caucasian patients and 50–60% of African-American patients with AS.3 It is present in only 6% of the general population.
Undifferentiated spondyloarthropathy, Reiter’s syndrome, and reactive arthritis The spondyloarthropathy family of diseases share common features. As a spine specialist, it is most important to diagnose the presence of a spondyloarthropathy, rather than the specific type. The classification criteria for SpA is based on clinical features, as there are no specific confirmatory blood tests. There are two sets of clinical criteria that have been developed and validated in Europe and are used widely. These are the European Spondyloarthropathy Study Group (ESSG) and the multiple-entry criteria by Bernard Amor.1
Section 1: Medical Spinal Disorders
The European Spondyloarthropathy Study Group criteria To consider the diagnosis of spondyloarthropathy according to the ESSG criteria, a patient must demonstrate one of two entry criteria: ● ●
Inflammatory spinal pain; or Synovitis, either asymmetric or predominantly in the lower limbs.
Table 35.2: Clinical features scored in the Amor classification
● ● ● ●
Onset before 40 years of age; Insidious onset; Duration longer than 3 months; Morning stiffness; and Improvement with exercise.
Indications for the designation of synovitis are: ● ● ● ● ●
Soft tissue swelling; Warmth over a joint; Joint effusion; Decreased active and passive range of motion; and Symptoms are worse after rest.
There are other features which can be considered if a patient has one or two of the entry criteria. These include: ● ● ● ● ● ● ●
Positive family history; Psoriasis; Inflammatory bowel disease; Urethritis, cervicitis, acute diarrhea; Alternating buttock pain; Enthesopathy; and Sacroiliitis.
The ESSG criteria have been evaluated in many studies, including those in Europe, Brazil, and Alaska.35–38
The Amor criteria The Amor criteria are a series of items which are weighted with a point scoring system.1,39,40 In order to qualify for a diagnosis of spondyloarthropathy, a patient must score a total of at least six from among the list of features detailed in Table 35.2.
Specific diagnoses The Amor and ESSG criteria are for the diagnosis of spondyloarthropathy in general. The criteria for the subtypes of spondyloarthropathy are less well defined.
Reactive arthritis Inflammatory arthritides developing after a distant infection are labeled reactive.41 Inciting organisms may be: Chlamydia, Yersinia, Salmonella, Shigella, Campylobacter, Clostridium difficile, Brucella, and Giardia.42 The infection should have occurred within 6 weeks of clinical presentation of the arthritis. The presence of HLA-B27 renders the host susceptible; however, there is an interplay between HLA-B27 and environmental/infectious triggers in the development of reactive arthritis.43
Reiter’s syndrome Reiter’s syndrome represents one example of reactive arthritis. The classic triad of uveitis, urethritis, and arthritis defines Reiter’s syndrome. The pathogenesis is similar to reactive arthritis since both
Score
Night pain or morning stiffness of the thoracic or lumbar spine
1
CLINICAL
Indications for the designation of spinal pain as ‘inflammatory’ are: ●
Feature
Asymmetrical oligoarthritis
2
Buttock pain (uni- or bilateral)
1 or 2
Sausage-like toe or digit
2
Heel pain
2
Iritis
2
Nongonococcal urethritis or cervicitis within 1 month prior to arthritis
1
Acute diarrhea within 1 month prior to arthritis
1
Presence or h/o psoriasis, balanitis, inflammatory bowel disease
2
Sacroiliitis (grade >2 if bilateral; grade >3 if unilateral)
2 or 3
HLA-B27 present and/or family h/o spondyloarthropathy
2
Clear-cut response to NSAIDs
2
RADIOLOGIC
GENETIC
RESPONSE TO TREATMENT
are triggered by an infectious agent and are more common in those patients with the HLA-B27 gene.44 Not all patients present with all three features of the triad. The American College of Rheumatology requires peripheral arthritis (longer than 1 month’s duration) in association with urethritis or cervicitis.45
Undifferentiated spondyloarthropathy Among patients who meet ESSG or Amor criteria for spondyloarthropathy, there is a large group that does not fit into the above discrete categories. These patients are labeled as undifferentiated spondyloarthropathy.1 In a recent study from Spain,46 68 patients with the diagnosis of undifferentiated spondyloarthropathy (uSpA) were followed for 2 years. At the end of this period, 75% retained the diagnosis of uSpA; disease remission occurred in 13%; ankylosing spondylitis 10%; and psoriatic arthritis 2%. In addition, a subset of patients with uSpA may be found to have reactive arthritis.47
Arthritis associated with psoriasis Psoriasis is a chronic autoimmune disorder affecting the skin and can be associated with inflammatory arthritis. Ten to forty percent of patients with psoriasis develop a chronic inflammatory arthritis. Psoriatic arthritis (PSA) occurs as a result of interplay of genetic, immunologic, and environmental factors.48,49 Clinically, PSA may resemble RA, except that PSA patients are seronegative and express cytokines preferentially at the enthesis in addition to the synovium. The most common presentation is either oligoarthritis or symmetric polyarthritis. There are several proposed subtypes: monoarthritis and 393
Part 3: Specific Disorders
oligoarthritis, polyarthritis, arthritis of distal interphalangeal joints with nail changes, arthritis mutilans, and spondylitis.6,50 This is often associated with flexor tenosynovitis. Axial spinal involvement of sacroiliitis and spondylitis does occur in PSA but usually occurs after years of illness, and is not a common presenting complaint.8
Enteropathic arthritis Enteropathic arthritis refers to inflammatory arthritis in association with inflammatory bowel disease, ulcerative colitis, or Crohn’s disease.51 Conversely, two-thirds of patients with spondyloarthropathy show subclinical histologic signs of gut inflammation and approximately 6% will go on to develop inflammatory bowel disease.52 In a study by de Vlam et al.,53 39% of 103 consecutive patients followed in a gastroenterology clinic for ulcerative colitis or Crohn’s disease had enteropathic arthritis. Ninety percent met criteria for spondyloarthropathy, while 10% fulfilled criteria for ankylosing spondylitis. An additional 18% had asymptomatic sacroliliitis.6 Approximately 25% of patients with enteropathic arthritis have axial disease. Peripheral joint arthritis occurs more frequently in patients with enteropathic colitis compared with AS. Please refer to Table 35.3 which represents a summary of some of the key clinical aspects of the differential diagnosis of systemic causes of arthritis. This may clarify the recognition of systemic arthritis for the practicing spine specialist.1
Radiographic imaging in spondyloarthropathies Seronegative spondyloarthropathies including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, Reiter’s syndrome, enteropathic arthritis, and undifferentiated spondyloarthropathy share common clinical and radiographic features. Synovial joint inflammation and enthesitis may involve the axial or appendicular skeleton, or both. The main musculoskeletal features include: sacroiliitis, spondylitis, and peripheral joint lesions. Sacroiliitis is the hallmark feature which unifies the group.54 The distribution of joint involvement may give a clue to diagnosis. For example, ankylosing spondylitis primarily involves the axial joints and enthesis, with less consistent findings in the appendicular skeleton,55 and psoriatic arthritis distinctively may involve the interphalageal joints.56 Multiple imaging modalities are available to assess seronegative spondyloarthropathies, provide early diagnosis, and possibly follow disease activity.
Radiographic assessment Standard radiographs are still the appropriate first images to obtain in practice. Radiographic features common to all spondyloarthropathies include: erosion, periostitis, bone proliferation at the entheses, and normal bone mineralization.54 Radiographic analysis of early sacroiliitis may demonstrate erosions on the iliac side of the joint. Latestage radiographic appearance is one of SI fusion and ankylosis.57 The shortcomings of plain radiography for the diagnosis of sacroiliitis include the large variability in interpretation among radiologists, and the relative insensitivity in early sacroiliitis.58
Scintigraphy (bone scan) Bone scanning is well documented as a modality to identify hyperemia and joint inflammation that may not be apparent radiographically. Quantitative bone scanning has approximately 80% predictability for detection of active sacroiliitis. This compares to 100% for MRI.59 Periarticular radionuclide uptake around peripheral joints and at the entheses are demonstrated with bone scan.60 The problem with scintigraphy is that it is non-specific and must be correlated with other clinical and radiologic investigations. Single photon emission computed tomography (SPECT) has improved localization of areas of increased uptake and may be a useful supplement.54
Computed tomography Computed tomography (CT) scanning is superior to plain radiography for visualization of early sacroiliac erosions and sclerosis.61 The true synovial sacroiliac joint is the inferior two-thirds, with the superior one-third being ligamentous. Comparison of CT with MRI scanning suggests that CT is superior for evaluation of chronic bone changes in the ligamentous portion of the joint; however, it is insensitive for detection of inflammatory changes in the subchondral bone.62 In addition, CT should be considered if further information about spinal fracture or bony canal stenosis is needed. A recent study demonstrates efficacy of CT-guided sacroiliac injections for treatment of sacroiliitis.63
Magnetic resonance imaging Magnetic resonance imaging (MRI) has emerged as a sensitive and detailed modality for imaging of spondyloarthropathy. MRI is excellent at depicting the normal sacroiliac joint and clearly separates the
Table 35.3: Differential diagnosis of some systemic causes of arthritis
394
Reiter’s syndrome
Rheumatoid arthritis
Gonococcal arthritis
Psoriatic arthritis
Age
Young
Middle
Young
Middle
Gender
Male > female
Female > male
Female > male
No effect
Onset
Abrupt
Insidious
Abrupt
Insidious
Joint number
Oligoarthritis
Polyarthritis
Monoarthritis or oligoarthritis
Oligoarthritis
Symmetry of arthritis
No
Yes
No
No
Sausage digits
Yes
No
No
Yes
Back pain
Yes
No
No
Yes
Urethritis
Yes
No
Yes
No
Skin lesions
Palms and soles in 10%
Subcutaneous nodules
Pustular, nodular, or vesicular
Psoriasis
Gonococcus
No
No
Yes
No
Section 1: Medical Spinal Disorders
3. Check specialized tests of chest expansion and lumbar range of movement; and 4. Take specific imaging.
synovial and ligamentous compartments. The tissue resolution permits visualization and evaluation of bone marrow, synovium, articular cartilage, ligaments, tendons, muscles, entheses, and various stages of inflammation. MRI can identify joint effusion, synovitis, bone marrow edema, and bone erosions.54 In patients with a high clinical likelihood of spondyloarthropathy and negative standard radiography, MRI (especially with gadolinium enhancement) provides excellent radiation-free evidence of sacroiliitis and enthesitis.64
Systemic features of spondyloarthropathies One of the distinguishing features of the spondyloarthropathies is their systemic nature. In contrast to other etiologies of back pain, patients with spondyloarthropathies may experience systemic symptoms such as fever, malaise, and weight loss. Patients may have increased levels of inflammatory markers such as an erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Moreover, they may have extra-articular manifestations of their disease. Below is a discussion of the most common extra-articular findings in patients with spondylitis.
Musculoskeletal ultrasound Currently, ultrasound is best applied to the evaluation of small peripheral joints since they are superficial and accessible. Early enthesitis may be demonstrated on ultrasound.54
DIAGNOSIS OF SPONDYLOARTHROPATHIES
Ocular Eye involvement can occur in all of the spondylotic variants. The most common finding is uveitis, and this can be seen in 25–40% of patients who have ankylosing spondylitis.65 Symptoms include eye pain, blurred vision, and photosensitivity. The eye can appear red and injected. In cases in which uveitis is suspected, patients should immediately be referred to an ophthalmologist, as the diagnosis can
As an overview, there are four basic steps to follow if a clinician suspects the diagnosis of spondyloarthropathy (Fig. 35.1): 1. Suspect the disease if back pain characteristics are ‘inflammatory;’ 2. Take additional history, physical examinations, labs;
Inflammatory arthritis that is asymmetric or predominantly lower extremity? and/or Back pain of insidious onset of >3 months’ duration associated with morning stiffness and improvement with activity?
No
Unlikely to be a spondyloarthropathy
Yes
Evidence of psoriasis or inflammatory bowel disease? No
Yes
One or more of the following? Radiographic evidence of sacroiliitis Enthesopathy Dactylitis Buttock pain (unilateral or alternating) Urethritis or cervicitis Family history Iritis Acute diarrhea or nongonococcal urethritis within 1 month of onset
Consider enteropathic or psoriatic arthritis
Yes
No Unlikely to be a spondyloarthropathy
Likely to be a spondyloarthropathy
Evidence of spondylitis? (inflammatory spinal pain and limitation of movement) No Evidence of chlamydial infection? (i.e. elevated antichlamydial antibody titers) No Reactive arthritis/ Reiter’s syndrome
Probably reactive arthritis/Reiter’s syndrome
Yes Probably ankylosing spondylitis
Yes Chlamydial-associated reactive arthritis
Fig. 35.1 An algorithm of the four basic steps to follow if a clinician suspects the diagnosis of spondyloarthropathy. 395
Part 3: Specific Disorders
only be made by slit-lamp examination. The treatment generally includes topical nonsteroidal eye drops or steroid drops. In severe or refractory cases, systemic immunosuppression and aggressive treatment with disease-modifying agents is necessary. While most patients will recover, severe cases can result in visual loss. A less common ocular manifestations of the spondylotic variants includes Sjögren’s syndrome and optic neuritis.66
Spondylitis Functional Index (BASFI) and the Dougados Functional Index (DFI).77 More recently, the World Health Organization Disability Assessment Schedule II (WHODAS II) was shown to be useful for evaluating functional capacity in patients with ankylosing spondylitis.78 The BASDAI focuses on pain, joint involvement, and swelling while the BASFI, DFI, and the WHODAS II assess functional impairment.
Gastrointestinal
Prognostic indicators
Gastrointestinal involvement, in particular bowel inflammation and ulceration, can be seen in all of the spondylotic variants. Up to 44% of patients with ankylosing spondylitis have gastrointestinal involvement.67 Gut inflammation in patients with ankylosing spondylitis is histologically similar to the lesions found in Crohn’s disease.68 Moreover, in one series subclinical sacroiliitis was found in 24% of patients with inflammatory bowel disease.69 Therefore, patients with spondylitis should be monitored for symptoms suggestive of occult inflammatory bowel disease and, conversely, patients with documented inflammatory bowel disease should be monitored for spondylitis.
In addition to functional assessment, various disease characteristics portend prognostic outcome. In particular, worse outcome is found in persons who have disease onset prior to age 16, hip joint involvement, peripheral joint involvement (in particular a sausage digit), decreased range of motion of the lumbar spine, high ESR, and poor response to nonsteroidal antiinflammatory drugs.79 One should examine patients for active inflammation of the peripheral joints. Laboratory testing should include ESR and CRP, CBC with differential, platelet count, and an assessment of baseline renal and liver function. The renal and liver function should be assessed because of the potential of hepatorenal toxicity of many of the medications in use. An elevated ESR and CRP suggest that ongoing active inflammation is occurring.
Cardiac Aortitis and aortic root disease that can sometimes lead to valvular dysfunction is the most common cardiac lesion found in patients with ankylosing spondylitis. In one case series, 82% of patients with ankylosing spondylitis had evidence of either aortic root disease or valvular disease. Valve regurgitation was found in close to half of the patients and many of these patients went into heart failure or required valve replacement therapy.70 Conduction abnormalities affecting the atrioventricular node and myocardial involvement are found less commonly.71
Skin There have been reports of an association between vitiligo and the spondyloarthropathies. In men, circinate balanitis can also occur.72,73
Pulmonary In patients who have thoracic spine and costovertebral joint involvement, decreased chest wall expansion during inspiration can lead to decreased lung capacity and dyspnea. This can lead to recurrent infections as well.74 In addition, patients can develop fibrobullous disease of the upper lobes.75
Genitourinary tract In both male and female patients with ankylosing predominately spondylitis, Chlamydia trachomatis infection is common and seen in patients who are HLA-B27 positive.76
Patient management The management of patients with spondylotic variants should first include a functional evaluation. Treatment modalities include physical therapy, pharmacologic agents, spinal injections, surgery, and complementary therapies.
Functional assessment This functional evaluation should include a functional assessment and an evaluation of how much fixed damage has been done to the spine and the joints. Patients with spondylitis can develop functional impairment leading to long-term disability. Various assessment tools can be used but the most common are the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), the Bath Ankylosing 396
Physical therapy One of the mainstays of therapy for spondylitis is exercise and physical therapy. The theory is that even in cases of spinal fusion and severe restriction in range of motion of the spine, physical therapy and exercise can maximize function and maintain as much mobility as possible. In Europe, spa therapy is included as part of the treatment regimen.80 Unfortunately, there are few well-designed studies that clearly demonstrate long-term efficacy of physical therapy. In one metaanalysis, group physical therapy was better than home exercise in decreasing pain and stiffness.81 In another study, recreational exercise for longer than 200 minutes a week was shown to decrease pain and stiffness, but not to improve HAQ scores in patients with disease for less than 15 years. In patients with longer-standing disease, 5–7 days a week of back exercises decreased pain and had a modest improvement of HAQ scores.82
Pharmacologic management For many years, treatment of the spondylotic variants, in particular ankylosing spondylitis and Reiter’s syndrome, was almost exclusively limited to nonsteroidal antiinflammatory drugs, analgesics, and occasionally steroids. Other disorders that present with spondylitis as part of the disease, such as inflammatory bowel disease and psoriatic arthritis, were more likely to be treated with systemic agents for the extraspinal manifestations. Occasionally, disease-modifying antirheumatic drugs such as sulfasalazine and methotrexate were used, but with limited enthusiasm. More recently, however, with the advent of biologics, there has been interest in being more aggressive with the treatment of the spondylotic variants. There is growing evidence that these agents may arrest the progression of these disorders. Below is a discussion of the treatment of spondylotic disorders with NSAIDs, sulfasalazine, methotrexate, biologics, and the more experimental therapies such as palidronate and thalidomide.
Nonsteroidal antiinflammatory drugs and COX-2 inhibitors Historically, the most commonly used NSAID has been indometacin.83 This was based upon the sense that this medication was more
Section 1: Medical Spinal Disorders
effective than other antiinflammatory agents although controlled studies have failed to substantiate this finding.84 In general, any of the nonsteroidals may be used to treat the pain and inflammation of the spondylotic variants. Phenylbutazone was once used with high frequency in patients with ankylosing spondylitis but is no longer used secondary to its high toxicity. In those patients who are intolerant of NSAIDs or who have had gastrointestinal toxicity from NSAIDs, the COX-2 inhibitors can be used. Both the NSAIDs and the COX-2 inhibitors can unmask occult colitis in these patients, so the treating healthcare provider should be aware of the potential for gastrointestinal toxicity. Moreover, the COX-2 inhibitors have been associated with increased risk of cardiovascular disease and should be used judiciously.
Sulfasalazine Sulfasalazine has been used for many years in the treatment of inflammatory bowel disease and for rheumatoid arthritis. The data on its utility in spondylitis are murkier. While inflammatory markers such as the C-reactive protein clearly improve with sulfasalazine it is unclear whether the spondylitis and those symptoms benefit. It is particularly beneficial for patients who have extraspinal manifestations of spondylitis such as psoriatic arthritis, peripheral arthritis, and inflammatory bowel disease. Dosing is in the range of 2000–3000 mg a day. The major toxicity is bone marrow or liver toxicity.85
Methotrexate Methotrexate was approved in the early 1980s for use in rheumatoid arthritis. It has also been used for the treatment of inflammatory bowel disease and psoriatic arthritis. The efficacy of this medication in spondylitis is less clear. In one double-blind, placebo-controlled study of ankylosing spondylitis, there was no benefit of methotrexate treatment compared with placebo.86
Tumor necrosis factor-alpha antagonists The new biologic agents, especially those directed against tumor necrosis factor-alpha, have only been used recently for the treatment of spondylotic variants but represent a large advance in the pharmacologic therapy of ankylosing spondylitis. Those that are approved include etanercept, infliximab, and adalimumab. These agents have been shown to be effective in the treatment of patients with ankylosing spondylitis. Both infliximab and etanercept have been shown to cause a rapid and significant improvement in BASDAI scores and improvement in morning stiffness, spinal pain, and inflammatory markers such as the ESR and CRP.87,88 As these agents are used with greater frequency and earlier in the course of the disease, it will be interesting to see whether they can impact disease outcome. They do have significant toxicities including either the exacerbation of underlying demyelinating processes or the reactivation of tuberculosis, including atypical forms.
Corticosteroids Systemic corticosteroids are of limited use in patients with ankylosing spondylitis and are generally not used.85
Corticosteroid injections Sacroiliac injections can provide short-term relief in patients with AS.89 Improvement can last up to 15 months and in one study the average length of improvement in 66 patients receiving CT-guided intra-articular corticosteroids was 10±5 months.90
Experimental therapy Thalidomide has been used for refractory ankylosing spondylitis. In one open label study minimal improvement in joint symptoms and function was observed. Further studies need to be performed before this medication is used on a regular basis.91 Pamidronate has been studied in a few open label trials. Long-lasting improvement in pain, stiffness, and function were found although several patients developed arthralgias and myalgias after the infusions. Further studies need to be done before accepting the utility of this medication in treating spondylitis.92
Complementary therapy There are limited data on the use of complementary therapy in the treatment of spondylitis. In one case study, chiropractic manipulation was helpful in a patient with advanced ankylosing spondylitis. However, given the degree of fusion found in patients’ spines, caution should be used.93
Surgery Some patients with spondylotic variants will require surgery. Hip arthroplasty and spinal surgery are the most common. Risks particular to persons with ankylosing spondylitis are postoperative heterotopic ossification. Spinal surgery is rarely used for the treatment of ankylosing spondylitis because the auto-fusion the patients experience circumvents the benefit of many spinal surgical procedures. In the case of instability, fusion has been used. Persons presenting for evaluation of lower back pain, especially in the area of the sacroiliac joints, may be presenting with spondylitis. Morning stiffness and systemic symptoms may be present. Once the diagnosis of spondylitis is suspected, patients should be monitored for extra-articular manifestations. While standard therapy has included physical therapy and nonsteroidal antiinflammatory drugs, more recently the biologics and other agents are being evaluated. These newer therapies may hopefully lead to earlier treatment that will circumvent the spinal fusion that can be so debilitating in these disorders.
CASE STUDIES Case study 1 A 28-year-old male who has a 10-year history of ankylosing spondylitis comes to the office. He has ongoing pain in his neck and the feeling of malaise. He has shortness of breath with walking short distances. He also has new onset of eye pain and blurry vision. His family history is notable for a mother with AS. On exam, Schober’s reveals an expansion of 1 mm, chest expansion is 1 cm, and he has minimal rotation (30° in either direction) of his neck. He is currently taking nonsteroidals but is wondering about other treatment options. Laboratory testing reveals an elevated ESR and CRP. What further work-up needs to be done? This case illustrates the systemic nature of ankylosing spondylitis and the spondylotic variants. The key features of his presentation are the shortness of breath and eye symptoms. These should prompt further work-up. He needs to have a chest X-ray to rule out pulmonary fibrosis and possibly pulmonary function tests. He also needs to be referred to an ophthalmologist for a slit-lamp examination because of the risk of uveitis. After these extraspinal conditions are ruled out, one could consider therapy with a disease-modifying agent such as sulfasalazine or tumor necrosis factor blockade. 397
Part 3: Specific Disorders
Case study 2 A 33-year-old woman is referred for pain in her lumbar area. The pain is not radiating and she has no neurological symptoms. She feels that after she gets up in the morning and showers, she loosens up. She feels better as the day goes on and she moves around. She is concerned because she is recently married and would like to start a family and she is not sure that she would be able to handle an infant with her current level of pain. On examination, her Schober’s test shows her lumbar spinal extension is 3 cm, chest expansion is normal, and she has no peripheral joint involvement. Plain radiographs of her back are negative. What should the next diagnostic work-up be? MRI of the sacroiliac joints is more sensitive than plain radiographs in detecting erosions. In this case, her history of profound morning stiffness and improvement with activity in conjunction with the findings on physical examination are quite suggestive of a spondylotic variant. This patient should have MRI of her sacroiliac joints.
SUMMARY
16. Bywaters EGL. Pathology of the spondyloarthropathies. In: Calin A, ed. Spondyloarthropathies. Orlando: Grune & Stratton; 1984:43–68. 17. Chang CP, Schumacher HR. Light and electron microscopic observations on the synovitis of ankylosing spondylitis. Semin Arthritis Rheum 1992; 22:54. 18. Granfors K. Do bacterial antigens cause reactive arthritis? Rheum Dis Clin North Am 1992; 18:37–48. 19. Hermann E. T cells in reactive arthritis. APMIS 1993; 101:177–186. 20. Urgrinovic S, Mertz A, et al. A single monamer from the Yersinia 60-kD heat shock protein is the target of HLA-B27 restricted CTL response in Yersinia-induced reactive arthritis. J Immunol 1997; 159:5715–5723. 21. Braun J, Bollow M, Neure L, et al. Use of immunohistologic and in situ hybridization techniques in the examination of sacroiliac joint biopsy specimens from patients with ankylosing spondylitis. Arthritis Rheum 1995; 38:499. 22. Bollow M, Fischer T, Reisshauer H, et al. Quantitative analyses of sacroiliac biopsies in spondyloarthropathies: T cells and macrophages predominate in early and active sacroiliitis – cellularity correlates with the degree of enhancement detected by magnetic resonance imaging. Ann Rheum Dis 2000; 59:135.
Spondyloarthropathies are a family of disorders that frequently manifest with back and spine complaints. These disorders are associated with psoriasis and inflammatory bowel disease. Other systemic symptoms are seen, including uveitis and lung disease. Practitioners who treat patients with spine disorders should be aware of these diseases and consider them in the differential diagnosis of patients who present with back pain. Systemic symptoms, the presence of an elevated CRP and ESR, and a positive HLA-B27 can be helpful in diagnosing these disorders. Imaging studies such as radiographs and magnetic resonance imaging may be helpful in establishing the ankylosing spondylitis. These patients may be treated with traditional NSAIDs and, in some cases, patients may benefit from rheumatic disease-modifying antirheumatic drugs.
23. Muche B, Bollow M, Francois RJ, et al. Anatomic structures involved in earlyand late-stage sacroiliitis in spondylarthritis: a detailed analysis by contrastenhanced magnetic resonance imaging. Arthritis Rheum. 2003; 48:1374–1384.
References
30. Maksymowych WP. Ankylosing spondylitis. Not just another pain in the back. Can Fam Physician 2004; 50:205–207, 213–215.
1. Yu DT, Wiesenhutter CW. Clinical manifestations and diagnosis of ankylosing spondylitis. UpToDate. on line 12.1:1–21. 2. Yu DT, Wiesenhutter CW. Definition and diagnosis of undifferentiated spondyloarthropathy, Reiter’s syndrome, and reactive arthritis. UpToDate. online 12.1: 1–18. 3. Espinoza L. Spondyloarthropathies. Lippincotts Prim Care Pract 1998; 2:81–86. 4. Grigoryan M, Roemer FW, Mohr A, et al. Imaging in spondyloarthropathies. Curr Rheumatol Rep 2004; 6:102–109. 5. Reveille JD. The genetic basis of spondyloarthritis. Curr Rheumatol Rep 2004; 6:117–125. 6. Khan MA. Update on spondyloarthropathies. Ann Intern Med 2002; 136:896–907. 7. Arnett FC. Ankylosing spondylitis. In: Koopman WJ, Moreland LW, eds. Arthritis and allied conditions – a textbook of rheumatology. Philadelphia: Lippincott, Williams & Wilkins; 2001:Chap. 66. 8. Bennett RB. Psoriatic arthritis. In: Koopman WJ, Moreland LW, eds. Arthritis and allied conditions-a textbook of rheumatology. Philadelphia: Lippincott, Williams & Wilkins; 2001:Chap. 68. 9. Kvien TK, Glennaos A, Melby K, et al. Reactive arthritis: incidence, triggering agents and clinical presentation. J Rheumatol 1994; 21:115–122. 10. Michet CJ, Machado EB, Ballard DJ, et al. Epidemiology of Reiter’s syndrome in Rochester, Minnesota: 1950–1980. Arthritis Rheum 1996; 39:1172–1177. 11. Miceli-Richard C, et al. Spondyloarthropathy for practicing rheumatologists: diagnosis, indication for disease-controlling antirheumatic therapy, and evaluation of the response. Rheum Dis Clin North Am 2003; 29:449–462. 12. Dougados M, van der Heijde D. Ankylosing spondylitis: how should the disease be assessed? Best Pract Res Clin Rheumatol 2002; 16:605–618. 13. Granfors, K, Marker-Hermann E, de Keyser F, et al. The cutting edge of spondyloarthropathy research in the millennium. Arthritis Rheum 2002; 46:606. 14. Benjamin M, McGonagle D. The anatomical basis for disease localization in seronegative spondyloarthropathy at spondylotic and related sites. J Anat 2001; 199:503–526.
398
15. Laloux L, Voisin MC, et al. Immunohistological study of entheses in spondyloarthropathies: comparison of rheumatoid arthritis and osteoarthritis. Ann Rheum Dis 2001; 60:316–321.
24. Mader R. Diffuse idiopathic skeletal hyperostosis: a distinct clinical entity. Isr Med Assoc J 2003; 5:506–508. 25. van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. Arthritis Rheum 1984; 27:361. 26. Gran JT, Husby G. The epidemiology of ankylosing spondylitis. Semin Arthritis Rheum 1993; 22:319. 27. Gran JT. An epidemiologic survey of the signs and symptoms of ankylosing spondylitis. Clin Rheum Dis 1985; 4:161–169. 28. Calin A, Porta J, Fries JF, et al. Clinical history as a screening test for ankylosing spondylitis. JAMA 1977; 237:2613–2614. 29. Blackburn WD Jr, Alarcon GS, Ball GV. Evaluation of patients with back pain of suspected inflammatory nature. Am J Med 1988; 85:766–770.
31. Olivieri I, Barozzi L, Padula A. Enthesopathy: clinical manifestations, imaging and treatment. Baillieres Clin Rheumatol 1998; 12:665–681. 32. Bower PW, Griffin AJ. Clinical sacroiliac tests in ankylosing spondylitis and other causes of low back pain – 2 studies. Ann Rheum Dis 1984; 43:192–195. 33. Ruof J, Stucki G. Validity aspects of erythrocyte sedimentation rate and C-reactive protein in ankylosing spondylitis: a literature review. J Rheumatol 1999; 26:966–970. 34. Spoorenberg A, van der Heijde D, et al. Radiological scoring methods in ankylosing spondylitis: reliability and sensitivity to change over one year. J Rheumatol 1999; 26:997. 35. Cury SE, Vilar MJ, Ciconelli RM, et al. Evaluation of the European spondyloarthropathy study group preliminary classification criteria in Brazilian patients. Clin Exp Rheumatol 1997; 15:79–82. 36. Gomariz EM, Guijo VP, et al. The potential of ESSG spondyloarthropathy classification criteria as a diagnostic aid in rheumatologic practice. J Rheumatol 2002; 29:326–330. 37. Collantes-Estevez E, Cisnal del Mazo A, Munoz-Gomariz. Assessment of 2 systems of spondyloarthropathy diagnostic and classification criteria (Amor and ESSG): a Spanish multicenter study. European Spondyloarthropathy Study Group. J Rheumatol 1995; 22:246–251. 38. Boyer GS, Templin DW, Goring WP. Evaluation of the European spondyloarthropathy group preliminary classification criteria in Alaskan Eskimo populations. Arthritis Rheum 1993; 36:534–538. 39. Amor B, Dougados M, Listrat V, et al. Are classification criteria for spondyloarthropathy useful as diagnostic criteria? Rev Rhum Engl Ed 1995; 62:10–15. 40. Amor B, Dougados M, Mijiyawa M. Criteria of the classification of spondyloarthropathies. Rev Rhum Mal Osteoartic 1990; 57:85. 41. Toivanen P, Toivanen A. Two forms of reactive arthritis? Ann Rheum Dis 1999; 58:737–741. 42. Hill Gaston JS, Lillicrap MS. Arthritis associated with enteric infection. Best Pract Res Clin Rheumatol 2003; 17:219–239.
Section 1: Medical Spinal Disorders 43. Cush JJ, Lipsky PE. Reiter’s syndrome and reactive arthritis. In: Koopman WJ, Moreland LW, eds. Arthritis and allied conditions – a textbook of rheumatology. Philadelphia: Lippincott, Williams & Wilkins; 2001:1–37. 44. Parker CT, Thomas D. Reiter’s syndrome and reactive arthritis. J Am Osteopath Assoc 2000; 100:101–104. 45. Willkens RF, Arnett FC, Bitter T, et al. Reiter’s syndrome: evaluation of preliminary criteria for definite disease. Arthritis Rheum 1981; 24:844–849. 46. Sampaio-Barros PD, Bertolo MB, et al. Undifferentiated spondyloarthropathies: a 2-year follow-up study. Clin Rheumatol 2001; 20:201–206. 47. Aggarwal A, Misra R, Chandrasekhar S, et al. Is undifferentiated seronegative spondyloarthropathy a forme fruste of reactive arthritis? Br J Rheumatol 1997; 36:1001–1004. 48. Scarpa R, Cosentini E, Manguso F, et al. Clinical and genetic aspects of psoriatic arthritis ‘sine psoriasis.’ J Rheumatol 2003; 30(12):2638–2640. 49. Gladman DD. Psoriatic arthritis: recent advances in pathogenesis and treatment. Rheum Dis Clin North Am 1992; 18:247–256. 50. Hohler T, Marker-Hermann E. Psoriatic arthritis: clinical aspects, genetics, and the role of T cells. Curr Opin Rheumatol 2001; 28:3–5. 51. Holden W, Orchard T, Wordsworth P. Enteropathic arthritis. Rheum Dis Clin North Am 2003; 29:513–530. 52. De Keyser F, Baeten D, et al. Gut inflammation and spondyloarthropathies. Curr Rheumatol Rep 2002; 4:525–532. 53. de Vlam K, Mielants H, et al. Spondyloarthropathy is underestimated in inflammatory bowel disease; prevalence and HLA association. J Rheumatol 2000; 27:2860– 2865. 54. Grigoryan M, Roemer FW, Mohr A, et al. Imaging in spondyloarthropathies. Curr Rheumatol Rep 2004; 6:102–109. 55. Bennett DL, Ohashi K, El-Khoury GY. Spondyloarthropathies: ankylosing spondylitis and psoriatic arthritis. Radiol Clin North Am 2004; 42:121–134. 56. Taylor WJ, Porter GG, Helliwell PS. Operational definitions and observer reliability of the plain radiographic features of psoriatic arthritis. J Rheumatol 2003; 30:2645–2658. 57. Muche B, Bollow M, et al. Anatomic structures involved in early- and late-stage sacroiliitis in spondylarthritis: a detailed analysis by contrast-enhanced magnetic resonance imaging. Arthritis Rheum 2003; 48:1374–1384. 58. van Tubergen A, Heuft-Dorenbosch L, Schulpen G, et al. Radiographic assessment of sacroiliitis by radiologists and rheumatologists: does training improve quality? Ann Rheum Dis 2003; 62:519–525. 59. Battafarano DF, West SG, et al. Comparison of bone scan, computed tomography and magnetic resonance imaging in the diagnosis of active sacroiliitis. Semin Arthritis Rheum 1993; 23:161–176. 60. Baumgarten DA, Taylor AT Jr. Enthesopathy associated with seronegative spondyloarthropathy: 99mTc-methylene diphosphonate scintigraphic findings. Am J Roentgenol 1993; 160:1249–1250. 61. Yu W, Feng F, Dion E, et al. Comparison of radiography, computed tomography and magnetic resonance imaging in the detection of sacroiliitis accompanying ankylosing spondylitis. Skeletal Radiol 1998; 27:311–320.
69. Queiro R, Maiz O, Intxausti J, et al. Subclinical sacroiliitis in inflammatory bowel disease: a clinical and follow-up study. Clin Rheumatol 2000; 19:445–449. 70. Roladan CA, Chavez J, Wiest PW, et al. Aortic root disease and valve disease associated with ankylosing spondylitis. J Am Coll Cardiol 1998; 2:1397–1404. 71. Lautermann D, Braun J. Ankylosing spondylitis – cardiac manifestations. Clin Exp Rheumatol 2002; 20:S11–S15. 72. Padula A, Ciancio G, La Civita L, et al. Association between vitiligo and spondyloarthritis. J Rheumatol 2001; 28:313–314. 73. Angualo J, Espinoza LR. The spectrum of skin, mucosa and extra-articular manifestations. Baillieres Clin Rheumatol 1998; 12:649–666. 74. Hunningnake GW, Fauci AS. Pulmonary involvement in the collagen vascular diseases. Ann Rev Respir Dis 1979; 119:471–503. 75. Rumanak WM, Firooznia H, Davis MJ, et al. Fibrobullous disease of the upper lobes: an extraskeletal manifestations of ankylosing spondylitis. J Comput Tomogr 1984; 8:225–229. 76. Lange U, Teichmann J. Ankylosing spondylitis and genitourinary infection. Eur J Med Res 1999; 4:1–7. 77. Ruof J, Sangha O, Stucki G. Comparative responsiveness of 3 functional indices in ankylosing spondylitis. J Rheumatol 1999; 26:1959. 78. Van Tubergen A, Landewe R, Heuft-Dorenbosch L, et al. Assessment of disability with the World Health Organization Disability Assessment Schedule II in patients with ankylosing spondylitis. Ann Rheum Dis 2003; 62:140–145. 79. Amor B, Santos RS, Nahal R. Predictive factors for the long-term outcome of the spondyloarthropathies. J Rheumatol 1994; 21:1883. 80. Van Tubergen A, Hidding A. Spa and exercise treatment in ankylosing spondylitis: Fact or fancy? Best Pract Res Clin Rheumatol 2002; 16:653–666. 81. Dagfinrud H, Kvien TK, Hagen K. Physiotherapy interventions for ankylosing spondylitis. Cohrane Database Syst Rev 2004; (4)CD002822. 82. Uhrin A, Kuzis S, Ward M. Exercise and changes in health status in patients with ankylosing spondylitis. Arch Intern Med 2000; 160:2969–2975. 83. Harrison TR, Wilson JD. Ankylosing spondylitis and reactive arthritis. In: Jeffers HD, Boynton SD, eds. Principles of internal medicine, 12th ed. New York: McGraw-Hill: 1991:1453. 84. Barlle-Gualda E, Figueroa M, Ivorra J, et al. The efficacy and tolerability of aceclofenac in the treatment of patients with ankylosing spondylitis: a multicenter controlled clinical trial. Aceclofenac Indomethacin Study Group. J Rheum 1996; 23:1200–1206. 85. Dougados M, Dijkmans B, Khan M, et al. Conventional treatments for ankylosing spondylitis. Ann Rheum Dis 2002; 61:11140–11150. 86. Roychowdhury B, Bintly-Bagot S, Bulgen DY, et al. Is methotrexate effective in ankylosing spondylitis? Rheumatology 2002; 41:1330–1332. 87. Braun J, Brandt J, Listing J, et al. Long-term efficacy and safety of infliximab in the treatment of ankylosing spondylitis: an open, observational, extension study of a three-month, randomized, placebo-controlled trial. Arthritis Rheum 2003; 42:2224–2233. 88. Gorman JD, Sack KE, Davis JC. Treatment of ankylosing spondylitis by inhibition of tumor necrosis factor alpha. N Engl J Med 2002; 246:1349–1356.
62. Puhakka KB, Jurik AG, Egund N, et al. Imaging of sacroiliitis in early seronegative spondyloarthropathy: assessment of abnormalities by MR in comparison with radiography and CT. Acta Radiol 2003; 44:218–229.
89. Karabackakoglu A, Karakose S, Ozerbilo M, et al. Fluoroscopy-guided intra-articular corticosteroid injections into the sacroiliac joints in patients with ankylosing spondylitis. Acta Radiol 2002; 43:425–427.
63. Pulisetti D, Ebraheim NA. CT-guided sacroiliac joint injections. J Spinal Disord 1999; 12:310–312.
90. Bollow M, Braun J, Taupitz M, et al. CT-guided intra-articular corticosteroid injection into the sacroiliac joints in patients with spondyloarthropathy: indication and follow-up with contrast-enhanced MRI. J Comput Assist Tomogr 1996; 20:512– 521.
64. Braun J, Bollow M, Sieper J. Radiologic diagnosis and pathology for the spondyloarthropathies. Rheum Dis Clin North Am 1998; 24:697–735. 65. Maksymowych WP, Chou CT, Russell AS. Matching prevalence of peripheral arthritis and anterior uveitis in individuals with ankylosing spondylitis. Ann Rheum Dis 1995; 54:28. 66. Brandt J, Rudwaleit M, Eggens U, et al. Increased frequency of Sjögren’s syndrome in patients with spondyloarthropathy. J Rheum 1998; 25:718. 67. Leirisalo-Repo M, Turenen U, Stenman S, et al. High frequency of silent inflammatory bowel disease in spondyloarthropathy. Arthritis Rheum 1994; 37:23. 68. Baeten D, De Keyser F, Mielants H, et al. Ankylosing spondylitis and bowel disease. Best Pract Res Clin Rheumatol 2002; 16:537–549.
91. Wei JC, Chan TW, Lin HS. Thalidomide for severe refractory ankylosing spondylitis: a 6-month open-label trial. J Rheumatol 2003; 30:2627–2632. 92. Maksymowych WP, Jhangri GS, Leclercq S, et al. An open study of pamidronate in the treatment of refractory ankylosing spondylitis. J Rheumatol 1998; 25:714– 717. 93. Rose KA, Kim WS. The effect of chiropractic care for a 30-year-old male with advanced ankylosing spondylitis: a time series case report. J Manip Phys Ther 2003; 26:E1–E9.
399
PART 3
SPECIFIC DISORDERS
Section 1
Medical Spinal Disorders
CHAPTER
Spine Infections: An Algorithmic Approach
36
Gregory A. Day and Ian B. McPhee
INTRODUCTION Late diagnosed or misdiagnosed spine infections may have serious consequences. The commonest organisms causing spine infection are pyogenic bacteria. Other bacteria, Mycobacterium species, and fungi are infrequent causes of spine infection. Adverse outcomes can be anticipated in spine infections involving more virulent organisms or immunocompromised hosts. The range of spinal infections from hematogenous spread includes childhood discitis, spondylodiscitis and epidural abscess, and excludes open trauma to the spine. Other iatrogenic spinal infections including adult discitis, spondylodiscitis, and facet (zygapophyseal) joint septic arthritis resulting from postdiscectomy/laminectomy, postinjection/aspiration, or instrumentation of the spine are discussed separately. Successful management encompasses early diagnosis, appropriate antimicrobial medication, and surgical management if the patient develops neurological deficit, has an unstable spine, or fails conservative management. This algorithmic approach to the management of spinal infections presents the clinician with clinical paths to aid in the management of a potentially serious condition.
CHILDHOOD DISCITIS Pathogenesis, etiology, and natural history The natural history of childhood discitis varies from neonates/infants to young children to teenagers.1
Neonate/infant and young children discitis A high proportion of negative disc cultures in infants and toddlers has prompted some authors to state that childhood discitis may be either inflammatory or infective. Infective childhood discitis usually results from hematogenous seeding of organisms. The intervertebral disc is avascular even in infants.2 It has been postulated that pediatric spine infections commence in the microarterioles of the vertebrae3 because the nutrient arteries have been demonstrated to be a more direct route for the spread of infection to the vertebral column than its venous drainage.3 This theory proposes that spinal infection in infants and toddlers starts in a very similar way to the development of metaphyseal osteomyelitis in long bone infection. Terminal arterioles arising from the circumferential vessels fed from the extraperichondrial arterial plexus and from nutrient metaphyseal arteries penetrate the hyaline cartilage endplates of the vertebral bodies and terminate adjacent to the intervertebral disc in neonates up to 1 year of age.2,4,5 Venous drainage follows the same route. Blood-borne bacteria can be delivered directly to the intervertebral disc during bacteremia.6 The pediatric host cannot mount a response to invading organisms within an avascular disc, allowing the organisms to multiply unim-
peded. Pyogenic bacteria release proteolytic enzymes, leading to destruction of the intervertebral disc. Spread of infection to the vertebral body in infants is limited by the cartilage-capped endplates. However, with further progression, the hyaline cartilage-capped endplates may be destroyed, allowing the invading organisms direct access to the vertebral body.7 Infants have widespread anastomotic connections between intraosseous arterioles within the vertebral body.8 Disappearance of these anastomoses later in childhood increases the risk of vertebral bone necrosis and subsequent osteomyelitis through microthrombosis. Vertebral osteomyelitis is present in 25% of cases. Spread to the epidural space is rare in young children but has been reported in previously well males.9
Early teenage discitis The anatomy of the adolescent spine is similar to a skeletally mature spine after the growth plates fuse to the vertebral body, and spine infections follow a similar pathogenesis.
Clinical presentation – history and clinical features Childhood discitis is uncommon. The clinical presentation can be subdivided into three distinct age groups – neonates/infants, young children, and early teenagers. Infants and young children present acutely with malaise and a limp or refusal to bear weight on one leg.10 Brown et al.11 report an insidious onset of symptoms in young children with typical late presentation. Viral or bacterial infections often precede childhood discitis. A history of recent mild spinal trauma is sometimes elicited. Seventy-eight percent of cases involve the lumbar spine.12 Fifty percent to 57% of young children present with backache.10,13 Teenagers present with spinal and occasionally abdominal pain.14 The commonest clinical signs are trunk stiffness and a loss of the normal lumbar lordosis.11 Paravertebral muscle spasm and hamstring tightness are common. Some children may present with a totally rigid lumbar spine. Spinal tenderness is easier to detect in children old enough to communicate verbally. A minority (28%) of children with discitis are febrile (>37.9°C).12 If the disease progresses to spondylodiscitis (which includes vertebral osteomyelitis), up to 79% have an elevated temperature.12 Neurological deficit in this age group is rare.
ADULT PYOGENIC SPONDYLODISCITIS Pathogenesis, etiology, and natural history Spondylodiscitis may complicate generalized septicemia or result from a distant focus such as vegetation of a heart valve or florid skin infection. Blood-borne adult pyogenic spondylodiscitis originates in the endplate of the vertebra (rather than the intervertebral disc), 401
Part 3: Specific Disorders
most likely in the capillary loop or postcapillary venous channels, spreading secondarily to the intervertebral disc. Pyogenic bacteria secrete proteolytic enzymes, causing necrosis of bone and intervertebral disc. Individuals at risk include those affected by: ● ● ● ● ● ● ● ● ● ●
Postprocedural, including postspinal injection and postdiscectomy; Advancing age – more than one-half of recently reported spinal infections involve subjects 50 years and older; Chronic malnutrition and chronic alcoholism; Diabetes; Immune deficiency including HIV infection, steroid and cancer therapy, immunosuppression and organ transplantation; Intravenous drug abuse; Chronic disease such as rheumatoid arthritis, psoriasis, and sickle cell disease; History of malignancy; Renal failure; Distant infection, including endocarditis/heart valve vegetation and skin infection.
Infection of males has a slight preponderance,15 with a male:female ratio ranging up to 1.8:1. If the patient has been previously well and the organism is indolent, the spondylodiscitis can be arrested at an early stage with nonoperative management. If the patient has been previously unwell and the organism is more virulent, the natural history of spondylodiscitis is of worsening local sepsis, sometimes spreading paravertebrally. Infection may spread to form a psoas abscess and extend to its insertion at the lesser trochanter of the proximal femur. Epidural spread also occurs. The spinal cord or cauda equina may be compressed by an enlarging abscess, usually at one spinal level. The microvascular circulation from the anterior spinal artery to the spinal cord/cauda equina is also disturbed by the presence of microvascular thrombosis as a result of persisting adjacent infection.16 Prolonged immobilization with osteopenia and progressive vertebral osteomyelitis with bone destruction predispose to pathological fracture. The resultant angular kyphosis or posteriorly displaced bone fragments into the spinal canal may contribute to neurological compromise. Mortality has been reported in 10–16% of adults with pyogenic spondylodiscitis.17–19
Clinical presentation – history and clinical features Patients typically present with insidious onset of unremitting spinal pain and loss of spinal movement. The clinical presentation can be classified into acute, subacute and chronic, depending on the virulence of the organism and the ability of the affected individual to mount a response.20 A history of malaise, anorexia, fevers, weight loss, and night or resting spinal pain is common. Most have a diminished range of movement and mild tenderness over the spinous process of the affected vertebra early in the disease. Paravertebral muscle spasm is common. Torticollis in cervical spine infection and bizarre posturing from thoracic and lumbar spine infection may be related to psychological factors, but a large psoas abscess or neurological compromise should be excluded. Rigors are uncommon and are manifest by a spiking elevation in temperature. With more-advanced spinal infection, neurological deficit is present in 29–51% of spondylodiscitis.17,18,21–23 Two-thirds of patients with paralysis from spinal infection have central cord syndrome and onethird have anterior cord syndrome.21 Neurological deficit is most common at the cervical spine level and least common at the lumbar level. 402
Factors associated with neurological deficit include diabetes mellitus, advancing age, steroid therapy, organ transplantation, chronic inflammatory conditions, and intravenous drug abuse.18
ADULT PYOGENIC DISCITIS Pathogenesis, etiology, and natural history True adult pyogenic discitis usually follows surgical intervention. The incidence following discography is 0.5–1% and following any type of spinal procedure 0.4–4%.24 It has been reported after every type of spinal procedure including laminectomy, discectomy, arthrodesis, discography, chemonucleolysis, myelography. and lumbar puncture. Discitis complicates discectomy in 0.4–2.8% of patients.24,25 Microdiscectomy using a microscope was reported to reduce the rate of discitis24 but others have found no difference in infection rate.26 It is probably due to direct inoculation of the organism into the avascular intervertebral disc although some believe that it results from aseptic inflammation.24 During the stage of suppuration, the invading organisms multiply and a surrounding inflammatory response is mounted by the host. In a similar manner to spondylodiscitis, the bacteria secrete proteolytic enzymes, leading to necrosis of the intervertebral disc and endplates. Again, the amount of disc destruction depends on the virulence of the invading organism and the resistance of the host. In a previously well patient, the discitis may be locally contained with little treatment, when the invading organism is indolent. However, the infection may spread to the vertebral endplates and beyond if the organism is virulent or in an immunocompromised individual. Should this occur, the pathogenesis and natural history of discitis is similar to that of adult pyogenic spondylodiscitis (Fig. 36.1).
Clinical presentation – history and clinical features Pain is expected following a surgical procedure or injection.24 The clinical course of postprocedural discitis is often reflected by early relief of symptoms due to the surgical procedure, typically Potential pathological seguence Hematology (embolic or bacteremic) spread
Primary source: Kidney Upper respiratory tact Skin Bowel
Infection
Disc
Iatrogenic: Discography Nucleotomy Myelography Metal/material insertion into the intervertebral disc Vertebral bodies
Destruction
Spread
Paravertebral
Epidural space
Psoas abscess
Epidural abscess
(Extra spinal)
Surgical implantation
Neuology
Fig. 36.1 Potential pathological sequence.
Collapse
Fracture
Deformity Kyphosis Instability
Section 1: Medical Spinal Disorders
followed by recurrence of similar spinal pain 1–4 weeks after the procedure (range, 2 days to 10 weeks).27 The constant, throbbing pain that subsequently develops is often out of proportion to the clinical picture. Unlike postoperative deep wound infection, the surgical skin incision/scar is normal in more than 90% of cases.24 Most patients with postprocedural discitis have only a very mildly elevated temperature. They eventually develop malaise, anorexia and weight loss. Clinically, patients develop marked paravertebral muscle spasm and stiffness of the affected spine. Fewer than 15% of patients develop a new or worsening neurological deficit from the spread of infection.24,28
Prolonged surgical time may result in excess wound edema or ischemic/necrotic wound edges from prolonged skin edge retraction. Both complications allow virulent bacteria or normal skin flora to enter the wound. Skin flora of low virulence including Acinetobacter baumani, Peptiostreptococcus, Corynebacterium, coagulase-negative Staphylococcus, and Propionibacterium acnes have been cultured from postoperative surgical wounds in elective orthopedic surgery.34 Although S. aureus and methicillin-resistant S. aureus (MRSA) are the commonest hospital-based organisms responsible for early deep wound infection, some wound infections involve more than one organism and include indolent types of bacteria from normal skin flora.
POSTOPERATIVE DEEP WOUND INFECTION Pathogenesis, etiology, and natural history Early wound complications of spine surgery Early postoperative infections occur less frequently following discectomy (0.5–1%) than instrumented posterior spine arthrodesis (up to 12.9%).29 Laminectomy alone has been reported to result in a 1.5% wound infection rate. When arthrodesis is added, the risk increases 50%, and with the addition of instrumentation it increases 100%.29 The preoperative nutritional status of the patient is an important factor in the incidence of wound dehiscence and subsequent infection.30–32 Generally, patients have a better chance of uncomplicated postoperative wound healing with a plasma albumin level of greater than 3.5 g/dL and a total lymphocyte count of greater than 2000 cell/ mm3.12 Preoperative radiation increases the risk of early wound complication in patients with spinal tumours.29,32 Risk factors for early wound complications include prolonged intraoperative time (>4 hours), massive blood loss, blood transfusions, large wound hematomas, posterior rather than anterior approach, and large numbers of operating theater personnel.33 Staphylococcus aureus accounts for approximately 60% of all infections. Other organisms implicated in primary and postprocedural pyogenic spinal infections are shown in Table 36.1. Patients with immune deficiency are susceptible to the rarer fungal organisms including those shown in Table 36.2. Superficial wound infection may extend to involve deeper tissues, including the intervertebral disc, following spinal surgery.
Table 36.1: Other Organisms Implicated in Primary and Postprocedural Pyogenic Spinal Infections Actinomyces
Aerobacter
Bacteroides
Brucella
Enterobacter
Escherichia coli
Klebsiella
Proteus
Pseudomonas
Salmonella
Serratia
Streptococcus
Table 36.2: Rarer Fungal Organisms Aspergillus
Candida
Coccidioides
Cryptococcus
Histoplasma
Nocardia
Late infection and late hematogenous seeding The range of organisms isolated from late infection of the spine following instrumented spine arthrodesis is similar to that of early wound infection. Embolization or bacteremia from the bladder, kidney, respiratory tract, skin, or bowel may result in hematogenous seeding in spinal instrumentation some time after surgery. Late infection can also follow intravenous drug abuse.35 The bacteria remain dormant for a period of time and secrete a glycocalyx which promotes their adherence to the metal of the spinal instrumentation and shields the organisms from lymphocytes and antibiotics.36–38 When the host develops an intercurrent illness and natural immunity is depressed, late spinal infection may develop. It is manifest as an initial suppurative phase with abscess formation, followed by reactive granulation tissue when the host mounts a response to the infection. Pyogenic bacteria secrete proteolytic enzymes, leading to necrosis of surrounding soft tissue and bone. Symptoms have usually developed by this stage and the patient may develop a painful swelling about the spinal instrumentation. Should the infection remain undiagnosed, a sinus may develop. Superficial drainage to the skin is not common in late pyogenic infection.
Sterile inflammation Hematoma formation and sterile bursae are frequently evident between prominent metal and the skin in thin patients with posteriorly instrumented spinal arthrodesis. Corrosion and metal fretting with release of particulate metal from micromotion between coupled spinal instrumentation results in a sterile inflammatory response, even after solid arthrodesis.39,40 In most cases, cultures of the fluid and tissue adjacent to the metal implants are negative. Where bacteria can be cultured from the interface membrane, it is hypothesized that the metal particles and resultant inflammation may potentiate late infection due to activation of indolent organisms or hematological embolization.
Clinical presentation – history and clinical features Deep spinal wound infection can be manifest in three clinical scenarios – early, delayed, and late. Early deep wound infection may follow a superficial wound infection from anterior or posterior spine surgery. The incidence of erythema, cellulitis, wound dehiscence, or purulent discharge before the onset of deep wound infection is up to 93%.29 Less than a one-third are noted to have a temperature of greater than 37.5°C at diagnosis. Delayed and late deep wound infections are reportedly due to or associated with intraoperative inoculation of indolent bacteria/fungi in the presence of metal fretting or from true late hematogenous seeding in spinal instrumentation. When intraoperative inoculation of indolent organisms occurs, some early wound erythema is often noted.29,41,42 Diagnosis is often made by exclusion. 403
Part 3: Specific Disorders
Clinical symptoms include spinal pain, malaise, anorexia, and subjective swelling within the spinal wound.43
EPIDURAL SPACE INFECTION Pathogenesis, etiology, and natural history Epidural infection is relatively rare but the incidence may be increasing due to a greater number of spinal procedures, epidural catheterization for pain control, intravenous drug abuse, and immunocompromised patients.23,44 Although they are distributed circumferentially around the spinal cord/cauda equina, anterior epidural space infection is more likely to be associated with spondylodiscitis than a posterior infective focus. Posterior foci usually result from hematogenous spread and are associated with frequent venous puncture for steroid or antiinflammatory injection and acupuncture.45 Epidural space infections are more common in the thoracic and lumbar spines, and tend to spread rapidly, often spanning a number of spinal segments at the time of diagnosis. Neurological compromise and even paralysis can occur early in the course of the infection, being manifest in days rather than in weeks, as is sometimes the case in spondylodiscitis. A combination of neural compression and microvascular thrombosis of the vessels of the spinal cord are thought to be responsible. Neurological deficit has been described in 19–80% of cases.23,45 Rarely, other infections occur within the spinal canal, including subdural abscess and spinal cord abscess.
Clinical presentation – history and clinical features Epidural infections affect patients of all ages (including children) and may present with signs of overwhelming infection including septicemia, bleeding diathesis, abrupt onset of paraplegia, and even adult respiratory distress syndrome with minimal overt signs of spinal infection. In contrast to spondylodiscitis, high fevers and rigors are noted early in the course of the infection. Affected individuals often have severe constitutional symptoms of malaise and anorexia. Neck rigidity is often seen in cervical epidural space infection. Meningeal irritation and radicular pain are often present. Classically, neurologic deficit is evident within 7–10 days of the onset of infection. Progressive neurologic deficits are present in 19–37% of cases,23,46 and are commoner in the thoracic spine (60% of these cases) than the cervical spine (33.3% of cases),46 although McHenry et al. report a higher incidence from cervical spine infection.18
PRIMARY AND POSTPROCEDURAL FACET JOINT INFECTION Pathogenesis, etiology, and natural history Even though the capsule of the lumbar facet joint has anterior perforations, paraspinal and intradural extension of the abscess is exceedingly rare.47,48 The sepsis is contained within the joint in most cases and causes localized spinal pain until drained. Severe neurological sequelae have not been reported in joint sepsis following facet joint infection.
Clinical presentation – history and clinical features Suppurative facet joint arthritis is rare with less than 50 reported cases.47 The clinical features can mimic spondylodiscitis. It is a very rare complication following facet joint injection with only three cases 404
reported to date.49 Because facet joint injection is gaining popularity in the therapeutic management of low back pain in Western medicine, an increase in incidence should be expected. Most patients undergoing this procedure have localized spinal pain with or without radiation. Often, the patient will have immediate benefit of pain relief while the local anaesthetic is effective. Postinjection suppurative arthritis is difficult to diagnose in the early stages because it is recognized that under normal circumstances, it may take up to 10 days for locally injected steroids to have a dampening effect on the pain. Pain localization usually occurs only when the infection is established. Patients with undiagnosed postinjection suppurative facet joint arthritis continue to deteriorate, with severe unremitting back pain.
DIAGNOSIS There is no single diagnostic test for spinal infection.
Plain radiology Childhood discitis In the earliest stages of infection, loss of cervical or lumbar lordosis is seen on lateral plain radiographs.7 A reduced disc height and erosion of adjacent vertebral endplates is present in up to 76% childhood discitis of 2 weeks duration.7,12 Long-standing infection leads to scalloping of the vertebral endplates. Late angular kyphosis may develop from destruction of either the vertebral body or the growth plates or both. The differential diagnosis of childhood discitis includes vertebra plana secondary to eosinophilic granuloma, bone tumors, and Scheuermann’s kyphosis in adolescents. Plain radiographs of the spine can distinguish among these conditions at presentation in most cases.
Pyogenic spondylodiscitis Depending on the nature of the invading organisms and the general condition of the patient, plain radiological changes appear from 2 weeks to 3 months after the onset of infection.50 Progressive narrowing of the disc space and irregularity and loss of the sharp, straight outline of the adjacent vertebral endplates is demonstrated better on lateral radiographs.51 Subchondral endplate lysis or defects may follow. Evidence of bone repair is manifest by hypertrophic or sclerotic bone formation adjacent to the vertebral endplate. With progression of the disease, paravertebral soft tissue swelling is evident on anteroposterior (AP) radiographs. A psoas abscess may form, changing the profile of the psoas shadow on AP radiographs. If gas is demonstrated in the soft tissues, anaerobic bacteria are usually responsible. With progressive osteomyelitis, bone destruction of the vertebral bodies may cause a pathological fracture,50 acute angular kyphosis or, less commonly, scoliosis. Pyogenic spondylodiscitis may heal by late bony or fibrous ankylosis (Fig. 36.2).
Axial and spiral CT Pyogenic spondylodiscitis The demonstration of end-plate irregularities, erosions, and sclerosis in adjacent vertebral bodies helps to differentiate spondylodiscitis from most secondary spine tumors. Secondary spinal tumors usually involve the pedicle or the posterior aspect of one or sometimes many vertebral bodies. Apart from multiple myeloma, primary spine tumors (osteoid osteoma, osteoblastoma, and giant cell tumor) usually involve the posterior elements of a vertebra. Multiplanar (spiral) CT is the investigation of choice to demonstrate the presence and extent of paraspinal/psoas abscesses, because MRI sagittal plane sequences are usually limited laterally to the tips of the transverse processes. Spiral CT imaging has the added advantage
Section 1: Medical Spinal Disorders
A
B
of providing the clinician with a 3-D view of the vertebral bodies of the infected spine.50,51 CT-guided percutaneous spinal biopsy allows for precise direction and localization of the infected disc or paravertebral abscess. MR imaging is superior in differentiating among epidural blood, pus, or tumor (Fig. 36.3).
Nuclear medicine (scintigraphy) Nuclear medicine studies are very sensitive in identifying spinal infection before changes occur on plain radiographs. Increased blood flow to soft tissue and bone occurs as the host mounts a vascular response to an invading spinal organism. Nuclear medicine studies are sensitive to this vascular response 2–3 days after a pyogenic infection commences. They are also useful in identifying remote infections in bone, joint, and soft tissue, especially in childhood infection. Techniques include Technetium 99 (Tc-99m), Gallium 67 citrate (Ga-67), and Indium 111 labeled leukocyte (In111-WBC) scan. Gallium is an analog of ferritin which is secreted by leukocytes. In111-WBC scans have a low sensitivity (17%).50,51 Ga-67 SPECT images are accurate in diagnosing spinal osteomyelitis in up to 91% of cases. Combined accuracy of Technetium 99 and Gallium 67 citrate scans is as high as 94%.50 Technetium 99 scanning is recommended in very young children when discitis is suspected and exact localization is difficult from history and clinical examination. The scan appearance may show a high probability of infection as early as 3–5 days after clinical symptoms develop.52,53 During the healing phase
Fig. 36.2 A 67-year-old female. Staphylococcus L1–2 spondylodiscitis. Pathological fractures of each vertebra with resultant slight angular kyphosis.
of infection, the Gallium-67 scan may become negative although the Technetium-99 scan remains positive.54 For this reason, Gallium-67 scan alone has been recommended for follow-up studies of disc space infections.55 The authors’ preferred recommendation is follow-up MRI with gadolinium, except when general anesthesia is required for children. Under these circumstances, follow-up Technetium-99 and Gallium-67 scans are both considered (Fig. 36.4)
Magnetic resonance imaging Magnetic resonance imaging (MRI) is the investigation of choice in assessment of early spondylodiscitis.50 It allows for multiplanar imaging. It has a specificity of up to 94% in distinguishing among discitis, vertebral osteomyelitis, epidural, paraspinal and prevertebral abscess, transverse myelitis, and spinal cord or intradural suppuration with a sensitivity of up to 97%,56,57 when gadolinium is added for enhancement. Early infection can be detected on T1-weighted sequences, in which decreased signal intensity in the intervertebral disc and the adjacent vertebral bodies from edema is evident. The intranuclear cleft is nearly always demonstrable (94%)51 in normal discs and is not visible in discitis. Signal hyperintensity of the disc on T2-weighted images, combined with loss of disc height, is useful in identifying the infected disc. After discography or facet joint blocks, injected fluids demonstrate low signal intensity on T1-weighted sequences and high signal intensity on T2-weighted sequences, occasionally mimicking purulent fluid. T2-weighted images demonstrate increased signal 405
Part 3: Specific Disorders
A
B
Fig. 36.3 Staphylococcus spondylodiscitis. Endplate irregularity and lytic erosion of vertebra, and disc destruction.
Fig. 36.4 Scintigraphy. Staphylococcus L1–2 spondylodiscitis. (The same 67-year-old female as in Fig. 36.2.) 406
Section 1: Medical Spinal Disorders
intensity within the bone marrow of adjacent vertebral endplates in spondylodiscitis due to inflammatory changes. Axial plane gradient echo sequences are useful in distinguishing between normal and infected vertebral bodies. Fat suppression techniques are useful for differentiating inflammatory areas in the vertebral bodies from fatty marrow in older individuals. Fat suppression also distinguishes between epidural suppuration and epidural fat. Epidural abscesses demonstrate high signal on T2-weighted sequences and may be isointense with cerebrospinal fluid (CSF). Proton densityweighted sequences demonstrate a darker image for CSF than pus. Gadolinium enhances images when tissue is hypervascular, and can help distinguish infection from scar tissue, tumor, CSF, and chronic degenerative changes. Enhancement of the disc, vertebral endplates, and bone marrow on postgadolinium sequences is highly suggestive of pyogenic spondylodiscitis.50,58,59 Gadolinium is especially useful when the spinal cord or dural sac is compressed by abscess, distinguishing pus from surrounding edema fluid.50 The signal from the spinal cord may be hyperintense under compression but acute changes are felt to be reversible. Persisting spinal cord hyperintensity usually reflects cord ischemia or myelomalacic change.60 One favored protocol for MRI of cervical spine infections involves:60 ● ● ● ●
Sagittal T1-weighted sequences; Sagittal fast spin-echo fat-saturation T2-weighted sequences; Axial T1-weighted sequences; and Gadolinium-enhanced sagittal and axial fat-saturation T1-weighted images.
MRI is more difficult to interpret following surgery which involves bone grafting. Also, postoperative enhancement of the uninfected disc is common.50 In the first few days after surgery, paravertebral edema and slight enhancement of the bone graft–vertebra interface is evident on T2-weighted sequences. By 4 weeks postsurgery, a noninfected bone graft and adjacent vertebrae enhance irregularly. The bone graft normally demonstrates high signal intensity on
A
B
T2-weighted sequences for 1 year following surgery. This enhancement eventually reduces as the bone graft incorporates into the adjacent vertebral bodies. When infection intervenes, the bone graft usually displays a hyperintense, uniform enhancement. Stainless steel causes more artifact than titanium on all sequences, and its use may preclude MRI as a useful tool for diagnosing postoperative infection. Some conditions are difficult to distinguish from spondylodiscitis on MRI. Severely degenerative discs with acute fibrovascular infiltration demonstrate decreased signal on T1-weighted images and increased signal on T2-weighted sequences in the subchondral endplates. These degenerate discs, however, demonstrate reduced T2-weighted disc signals in the less hydrated nucleus pulposus. Inflammatory spinal conditions have similar signal changes to infection on all MRI sequences. They include ankylosing spondylitis, rheumatoid arthritis, sarcoid disease, gout, and calcium pyrophosphate crystal deposition. Gouty lesions (very rare) are usually sharply delineated and are associated with punched-out lesions of the endplate. If a spinal infection is less vascular, for example a granuloma, then MRI may not distinguish the infection from tumors which rarely cross a disc space (multiple myeloma and lymphoma).60 In these cases, there is an indication to perform spinal biopsy (Figs 36.5, 36.6).
Laboratory studies Leukocytosis is usually indicative of infection but can often be absent or minimal in patients with pyogenic vertebral osteomyelitis. Elevated leukocyte counts are evident in 13–60% of cases.46 Elevation of erythrocyte sedimentation rate (ESR) is sometimes minimal in spine infection, but a vast majority of patients with discitis demonstrate a raised ESR at some stage.24 The sensitivity for using ESR as a postprocedural index of infection ranges 73–100%.24,46 The specificity ranges 38–62%.24 The ESR peaks 4 days after surgery and returns to normal levels between 14 and 42 days after surgery, depending on the extent of surgery and the amount of spinal instrumentation.24
Fig. 36.5 MRI T2-weighted sequence. A 71-year-old male. Early T12–L1 staphylococcal spndylodiscitis, reported as acute Schmorl’s node. 407
Part 3: Specific Disorders
A
B
Fig. 36.6 CT coronal, axial. The same 71-year-old male as in Fig. 36.5, 6 months after the previous MRI, demonstrating disc and vertebral destruction, minor epidural abscess.
C-reactive protein (CRP) is nearly always elevated when inflammation or infection occurs and is an excellent indicator of the degree of infection/inflammation. The sensitivity for using CRP as a postprocedural index of infection is 64–100%;24 the specificity is 62–96%.24 CRP levels demonstrate a faster return to normal following surgery compared to ESR.24 CRP levels fall with the leukocyte count. The magnitude of spinal surgery/instrumentation also determines how quickly the CRP level returns to normal. It is recommended that both ESR and CRP be serially monitored to gauge the efficiency of treatment of spinal infections.24 Blood cultures are reported to be positive in 25% of spinal infections61 in adults and up to 50% in childhood discitis,62 if taken at the time of a rigor.
Diagnostic procedures CT-guided percutaneous biopsy accurately predicts the invading organism in 37% of childhood discitis7 and 60–70% of adult cases.62 Cultures may be negative if the patient has been previously administered antibiotics. Histological examination will exclude tumors and foreign body granulomas. Gram stain and acid-fast stain as well as cultures for aerobic, anaerobic, fungal, and TB cultures of fresh material will maximize the chances of an accurate diagnosis. Bacterial cultures should be maintained for a minimum 10 days to detect indolent organisms. The volume of material obtained reflects the degree of accuracy in diagnosis. A tissue core obtained through a Craig biopsy needle or a TruCut (Baxter Travenol) needle generally provides more material than a fine needle aspiration, unless forced aspiration is applied as the needle is withdrawn. An open surgical
408
biopsy has a higher yield for the confirmation of a positive bacterial culture62 and is obligated if CT-guided aspiration fails to grow an organism and the patient does not respond to antistaphylococcal antibiotics (Fig. 36.7)
MANAGEMENT Nonoperative The management of spinal infection changed in the 1940s and 1950s with the introduction of penicillin and other antibiotics. The traditional treatment prior to this was rest in bed and immobilization. Today, treatment of individual spinal infections depends on the nature of the invading organism, the host resistance, and the stage of spinal infection at the time of diagnosis (acute, subacute, chronic). Ideal nonoperative management involves establishing the diagnosis, isolating the causative organism, providing or restoring nutrition to the host to fight the infection, maintaining spinal stability, eliminating the invading organism initially with intravenous antibiotics, and detecting early neurological deficit. Broadly, definitive antibiotic medication management commences after procuring positive cultures and sensitivities of the invading organisms. The duration of antibiotic therapy is variable. For pyogenic infections, intravenous antibiotics are continued empirically for approximately 6 weeks. The patient’s reaction to the infection is monitored by serial white cell count, ESR, and C-reactive protein. Oral antibiotics are generally ceased when the ESR has returned to less than 20.63 Failure of nonoperative treatment is high in immunocompromised patients –18/57 HIV positive and 42/57 intravenous drug abusers.64
Section 1: Medical Spinal Disorders
Suspected infection of spine
Haematologic investigations White cell count ESR CRP
+
Secondary imaging: CT MRI
Plain x-ray
+
–
Scintigraphy
–
Discharge
CT guided biopsy Histology Gram stain C/8 – up to 1+ days to include anaerobic cultures + Fig. 36.7 Diagnosis of spine infection.
Probable/confirmed infection
Specific infections Childhood discitis Childhood discitis can usually be treated nonoperatively. In the past, no difference has been reported in the outcome for infants receiving antibiotics and those treated with bed rest alone.65–69 Immunocompetent infants who are systemically well are more likely to respond to this management. However, prolonged or recurrent symptoms can occur in children not initially receiving intravenous antibiotics.70 For this reason, intravenous antibiotics are now recommended for initial management.2,5,11,71,72 Recommendations for the ideal length of an intravenous antibiotic course range from 1 to 8 weeks.5,6,11,12 Generally, intravenous antibiotics are administered for up to 2 weeks followed by oral antibiotics for up to 6 weeks. Response to antibiotic treatment is monitored by weekly white cell count, ESR, and C-reactive protein. Patients should be followed up for at least 12–18 months after resolution of spinal pain and malaise. The indications for repeat radiological assessment include a recurrence of symptoms or failure of the ESR and CRP to return to normal. Narrowing of the disc space and vertebral endplate sclerosis are expected;5 however, 20% infants and 30% older children demonstrate spontaneous fusion.10,66 If an infant develops vertebral osteomyelitis, an extreme form of angular kyphosis may develop.1 As bone necrosis is rare in infantile discitis, the only explanation is that the vertebral growth plates are destroyed as a result of the infection. The indications for considering surgical debridement of the disc/vertebrae are continuing septicemia during an antibiotic course or progressive neurological deficit.11,73 An updated algorithm for investigating/managing childhood discitis is: 1. Initial leukocyte count, differential, ESR and CRP; 2. Blood cultures;
3. Spinal biopsy recommended only for failure of conservative management or for immunocompromised or immunosuppressed patients; 4. Rest in bed without spinal immobilization for immunocompetent infants; 5. Empiric antistaphylococcal parenteral antibiotics for 2–6 weeks (or when the CRP returns to 4.5 mm translation, >15° angulation)
Flexion/extension X-rays
No gross movement
Flexion-biased L/S stabilization, core conditioning, NSAID
Surgery
Instability
No gross movement [refer to A)]
Surgery
SXs persist
SXs improve
D/C Involved segment not clearly indicated clinically
Th SNRB @ level indicated by pain distribution, myotomal deficit, or reflex change
EDX evaluation [refer to *] Improvement
C
D/C
examinations must verify this angle, and that the weakness is stable or improving. If weakness continues to progress, surgery may be indicated. If pain is minimal, and the patient’s chief complaint is weakness and sensory changes, a neurocompressive lesion might be illuminated by advanced imaging. Under such circumstances, decompressive surgical intervention may be necessary to successfully treat the condition. As has already been detailed, magnetic resonance imaging is very sensitive in detecting spinal abnormalities. Plain radiography can be useful to evaluate osseous alignment. Thus, the authors routinely order both imaging modalities to initiate the work-up of the L/S radiculopathy patient. Lateral flexion–extension views evaluate for segmental instability of levels of degenerative facet joint disease. If gross instability, >4.5 mm of translation at L5–S1 or >4 mm at higher lumber levels; or >15 degrees of sagittal angulation; or >2 degress of rotation is present, surgical care is prescribed. Intervertebral disc
SXs persist
Surgery
Fig. 82.4—Cont’d
height can be assessed prior to performing intradiscal procedures, such as percutaneous discectomy. If MRI displays a corroborative lesion such as HNP, or central or lateral canal stenosis, affecting the clinically suspected nerve root, therapeutic interventions are initiated. The authors employ a tiered treatment approach when addressing L/S radiculopathy. The initial step involves prescribing physical therapy (PT) with passive modalities for pain relief and graduated exercises that do not increase extremity complaints, oral nonsteroidal antiinflammatory medications (COX-2-specific agents with celebrex 100 mg b.i.d. as drug of choice), avoidance of aggravating activities, and a soft L/S corset if needed. Passive modalities such as cryotherapy, heat, and transcutaneous electrical nerve stimulation help modulate the patient’s pain to allow participation in PT. Lumbosacral stabilization and core conditioning exercises are prescribed in PT to stabilize the L/S spine. William’s flexion-biased L/S stabilization is utilized in 903
Part 3: Specific Disorders Radialopathy 2°
Lateral recess stenosis
Foraminal stenosis
Extraforaminal stenosis
Explosive onset
Gradual onset
MRI
MRI
$ Corroborative IVD extrusion/ sequestration
Corroborative IVD protrusion
Intraspinal cyst No evidence [may present with decreased of HNP sitting or standing tolerance]
[refer to C]
Emanating from chronic spondylolysis
Flex/Ext. X-rays
Emanating from posterior longitudinal ligament, duramater, IVD
[ refer to D ]
No instability
SXs moderate
SXs severe
Improvement
Compression by lumbosacral ligaments [refer to $]
SXs persist
D/C SXs moderate and not disruptive
SXs severe & disruptive
L/S stabilization, NSAID
Improvement L/S stabilization, NSAID D/C
SXs improve
SXs persist
D/C
Th SNRB × 3–4, PT, NSAID
SXs Th SNRB × 3–4, improve PT, NSAID
SXs persist
DC
Surgery
SXs persist
Th SNRB x 3-4, PT, NSAID
Surgery Improvement
SXs persist
D/C
Cyst aspiration
D Fig. 82.4—Cont’d
Surgery
Cyst puncture
Surgery
Apposition of transverse process to sacral ala [refer to $]
Th SNRB × 3–4, PT, NSAID
Surgery
904
Exit-zone stenosis d/t hyperostosis of vertebral body endplates [refer to $]
SXs severe
SXs moderate and do not disrupt work/ ADL’s
Flexion-biased L/S stabilisation, core conditioning, NSAID Instability
Loss of intervertebral canal fat, compression of exiting root, loss of disc height [refer to $]
EDX evaluation
[ refer to B ]
Emanating from arthritic facet joint
FJA/ Ligamentum flavum hypertrophy
May or may not present as neurogenic claudication
Section 5: Biomechanical Disorders of the Lumbar Spine Postoperative radiculopathy
MRI
Epidural hematoma
E) Pseudomeningocele compressing involved root
Central/peripheral clumping of nerve roots c/w arachnoiditis
Seroma
refer to E) (refer to E) Doesn’t corroborate clinical findings
EDX evaluation
Corroborates clinical SXs
Corroborative
Non-corroborative
Surgery
EDX evaluation
Anti-epileptic medications (AED), NSAID, PT
Conclusive for clinically involved root
Non-conclusive
Conclusive for radialopathy
Refer to stenosis flow-chart
Inconclusive
DX SNRB Surgery
DX SNRB
Positive Positive
E
Unaffected lateral recess, foraminal, or extra-foraminal stenosis
Negative
Negative
AEDs, NSAID, Repeat D×L SNRB PT @ alternate level
Repeat DX SNRB @ alternative level Somatic referral
cases of stenosis; McKenzie evaluation and treatment is employed in cases of disc herniation. If the patient does not improve over 1–3 weeks, or the patient presents with disruption of the ADLs, insomnia, inability to perform work-related duties due to severe pain, the authors will offer fluoroscopically guided therapeutic injections once the diagnosis has been confirmed. These minimally invasive injection procedures in addition to the aforementioned conservative measures constitute the second tier. The third treatment tier is defined by the use of percutaneous discectomy using the Dekompressor, coblation technology (nucleoplasty) or automated percutaneous discectomy (APLD), in addition to the measures offered in the first two tiers. The authors typically perform percutaneous discectomy in conjunction with a selective nerve root corticosteroid injection to address both the biomechanical and biochemical insults. Percutaneous disc decompression offers a minimally invasive percutaneous treatment, short of surgery, that has been shown to effectively treat L/S radiculopathy.101 In certain cases, however, nucleoplasty102 may be offered earlier in the treatment algorithm. APLD is preferred when there is a need to extract a larger volume of tissue or in cases of recurrent disc herniation.
Fig. 82.4—Cont’d
If a patient presents with unilateral or bilateral neurogenic claudication after acute onset, and MRI reveals a central focal disc protrusion causing functional stenosis, as can occur in a congenitally small canal due to short pedicles, the authors will incorporate both biomechanical and biochemical treatment pathways. In the authors’ experience, percutaneous disc decompression combined with therapeutic SNRB has been successful in treating such stenosis cases, and if not, the patient is referred to a surgical colleague. In instances of a more gradual onset of claudicating symptoms due to spinal stenosis, its etiology helps guide treatment. Amundsen et al. advocated bracing and physical therapy as initial treatment of stenosis patients presenting with unilateral or bilateral neurogenic claudication.103 The authors found that moderate pain would satisfactorily decrease in 50% of the patients after 3 months of conservative care. The other 50% nonresponders and those with severe pain benefited from surgical decompression; however, their treatment algorithm did not encompass therapeutic SNRBs. Botwin et al. documented a 50% reduction in visual analog scale scores in 75% of elderly stenosis patients who underwent therapeutic SNRBs 12 months prior, to treat unilateral neurogenic claudication, in addition to therapy and oral antiinflammatory medications.104 The Penn Spine 905
Part 3: Specific Disorders
Center approach blends the findings of both of these studies. The first tier offers PT, oral antiinflammatory medications, bracing, and activity modification. If symptoms do not abate, therapeutic SNRBs are offered unless there is a superimposed disc protrusion in a tight canal, and a subsequent surgical referral if improvement is unsatisfactory. If, however, a patient complains of lower limb fatigue, cramping, or heaviness with ambulation, or pain not alleviated by sitting, the threshold for a surgical referral is lowered. Spinal stenosis due to degenerative facet joint cysts may require percutaneous aspiration or puncture. Therapeutic SNRBs can be effective because an inflammatory process is probably present. The authors have observed perineural enhancement on fat-suppression sagittal MRI with gadolinium consistent with perineural venous engorgement and/or inflammation in cases of facet joint cystmediated radiculopathy (Fig. 82.5). The third treatment tier in facet joint cyst-related radiculopathy involves attempted aspiration of the cyst via an intra-articular approach through the joint. Involution of the cyst wall can be achieved via suction through a 20-gauge needle with a 10 cc syringe.105 If aspiration proves unsuccessful, cyst puncture can be attempted, again utilizing an intra-articular approach. As many as 50% of successfully treated facet joint cyst-related radiculopathies may require aspiration or puncture.106 In disc herniation-induced radiculopathy, treatment options again follow the tiered protocol, incorporating minimally invasive procedures, if necessary. Regardless of whether the herniation is a protrusion, extrusion, or sequestration, therapeutic SNRBs are offered if more conservative efforts fail. If therapeutic SNRBs are not curative, nucleoplasty, Dekompressor, or APLD can be employed to treat contained herniations. The authors have used the Dekompressor and APLD for disc extrusions with excellent outcomes, but those results have not been published as of yet. Nucleoplasty ought not be performed in the setting of a disc extrusion. If the patient’s pain improves but his or her weakness persists, as has been witnessed in cases of disc sequestration, surgical decompression has often been necessary. Seventy percent of patients will experience significant reduction in pain at 12 months after undergoing 1–4 therapeutic SNRBs107,108 A smaller proportion, who have disc sequestrations, will experience a similar outcome.25
A
906
B
CASE REPORT The following case report exemplifying the Penn Spine Center approach to a complicated L/S radiculopathy case. A 59-year-old female presented with a 6-month history of right paramidline lumbosacral pain referring to her superior buttock and posterior thigh to her midcalf. Her symptoms started gradually, were sharp, burning, and achy in nature, and her VAS rating was a 5 out of 10. Exacerbating factors included sitting, bending forward, driving, sneezing, and coughing. Ambulation consistently alleviated her symptoms. Her pain had not lessened despite physical therapy and Bextra 20 mg b.i.d. Physical examination revealed a mildly obese female ambulating with a nonantalgic gait pattern without demonstration of Trendelenburg gait or truncal list. Lumbosacral range of motion was full but painful in flexion. Mild tenderness to palpation was noted over the right paraspinal region. Straight leg raising to 50° produced right lumbar and gluteal pain. Sustained bilateral hip flexion reproduced her lumbar and gluteal pain. Manual muscle testing did not detect weakness, and muscle stretch reflexes were intact and symmetric. Sensory examination for light touch, pin-prick, and proprioception were intact. Upper motor neuron signs were absent. Magnetic resonance imaging revealed intra-articular fluid and joint gapping in the right L4–5 zygapophyseal joint (Fig. 82.6). Subarticular stenosis was noted on the right at this level, and a small central focal protrusion was observed at L5–S1. Flexion–extension plain radiography did not reveal gross instability. An electrodiagnostic evaluation demonstrated normal sural sensory and peroneal motor nerve conduction studies. However, the H-reflex latencies were asymmetric with the right latency 1.45 ms longer than the left. The differential diagnoses included right S1 versus L5 radicular pain, L4–5 versus L5–S1 Z-joint synovitis, and lumbosacral internal disc disruption syndrome with somatic pain referral. Advanced imaging revealed evidence to support each of these conditions. However, the electrodiagnostic findings suggested a right S1 radiculopathy. The authors’ algorithmic approach employed an initial right S1 diagnostic selective nerve root injection. An L5 diagnostic block followed by diagnostic intra-articular injections of the Z-joints would ensue.
Fig. 82.5 (A) Sagittal view of T1-weighted fat suppressed images illustrating increased perineural signal around the L5 nerve root due to edema or venous congestion (white arrow). In contrast, the nonenhanced L4 nerve root exits its foramen one segment above (gray arrow). (B) Axial T2-weighted image of the same segment demonstrating the cyst emanating from the right L5–S1 zygapophyseal joint (gray arrow).
Section 5: Biomechanical Disorders of the Lumbar Spine
A
B
However, the S1 diagnostic root injection was positive, and she subsequently underwent two therapeutic right S1 selective nerve injections with complete resolution of her pain. Purposely withheld from this case report was the history of an ineffective intra-articular steroid injection into the right L4–5 Z-joint months prior to the evaluation of this patient. Increasing the volume within this joint would not be expected to relieve this patient’s symptoms. Although intra-articular injection of antiinflammatory medication might be expected to alleviate the symptoms, the S1 nerve root was the inflamed structure both clinically and electrodiagnostically. Hence, the most appropriate target for treatment was the S1 nerve root, rather than the Z-joint or intervertebral disc.
Fig. 82.6 (A) Sagittal T2-weighted view of the right paramidline lumbosacral spine demonstrating increased signal (black arrow) within the right L4–5 Z-joint. (B) The corresponding axial segment displays intraarticular gapping and increased signal (black arrow).
4. Fortin JD, Washington WJ, Falco FJE. Three pathways between the sacroiliac joint and neural structures. Am J Neuroradiol 1999; 20(Sept):1429–1434. 5. Yeoman W. The relation of arthritis of the sacro-iliac joint to sciatica with an analysis of 100 cases. Lancet 1928; 2:1177–1180. 6. Fishman LM, Zybert PA. Electrophysiologic evidence of piriformis syndrome. Arch Phys Med Rehabil 1992; 73:359–364. 7. Slipman CW, Vresilovic EJ, Palmer MA, et al. Piriformis muscle syndrome: a diagnostic dilemma. J Muscul Pain 1999; 7(4):73–83. 8. Fishman LM, Dombi GW, Michaelsen C, et al. Piriformis syndrome: diagnosis, treatment, and outcome – a 10-year study. Arch Phys Med Rehabil 2002; 83: 295–301. 9. Faraj AA, Kumaraguru P, Kosygan K. Intra-articular bupivacaine hip injection in differentiation of coxarthrosis from referred thigh pain: a 10-year study. Acta Orthop Belg 2003; 69(6):518–521.
CONCLUSION
10. Tortolani PJ, Carbone JJ, Quartararo LG. Greater trochanteric pain syndrome in patients referred to orthopedic spine specialists. Spine J 2002; 2(4):251–254.
Lumbosacral radiculopathy is most commonly managed successfully by conservative treatment measures.25,47,56,67,68 Among these tools are therapeutic SNRBs or transforaminal epidural steroid injections. The mechanism of action of these interventions is not completely understood but it appears to involve both local (W. D. Chow, personal communication, San Francisco, 2003) and systemic effects.109 Thus, clinical improvement may occur after the instillation of steroids at the incorrect nerve root level or inaccurate site of pathology due to a nonspecific systemic steroid effect. Maximizing the therapeutic benefits of axial steroid injections requires accurate placement of these medications. Therefore, appropriate diagnosis is requisite, and warrants the judicious use of visual anatomic, electrophysiologic, and functional diagnostic testing guided by a sound algorithm.
11. Swezey RL. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil 1976; 57:387–390.
References 1. Kimura J. Radiculopathies and plexopathies. In: Kimura J, ed. Electrodiagnosis in diseases of nerve and muscle: principles and practice. New York: Oxford University Press; 2001.
12. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211(5):210–215. 13. Verbiest H. A radicular syndrome from developmental narrowing of the lumbar vertebral canal. J Bone Joint Surg [Br] 1954; 36;230–237. 14. Porter RW. Spinal stenosis and neurogenic claudication. Spine 1996; 21(17): 2046–2052. 15. Kao C, Uihlein A, Bickel W, et al. Lumbar intraspinal extradural ganglion cyst. J Neurosurg 1968; 29:168–172. 16. Abdullah AF, Chambers RW, Daut DP. Lumbar nerve root compression by synovial cysts of the ligamentum flavum: report of four cases. J Neurosurg Psychiatry 1984; 60:617–620. 17. Lin R, Wey K, Tzeng C. Gas-containing ganglion cyst of lumbar posterior longitudinal ligament at L3. Spine 1995; 18:2528–2532. 18. Schreiber F, Nielson A. Lumbar spinal extradural cysts. Am J Surg 1950; 80: 124–126. 19. DePalma MJ, Strakowski JA, Mandelker EM, et al. An instance of an atypical intraspinal cyst presenting as an S1 radiculopathy. A case report and brief review of pathophysiology. Arch Phys Med Rehabil 2004; 85(6):1021–1025.
2. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: asymptomatic volunteers. Spine 1994; 19(13):1475–1482.
20. Tarlov IM. Perineural cysts of the spinal nerve roots. Arch Neurol Psychiatry 1938; 40:1067–1074.
3. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.
21. Kikta DG, Breuer AC, Wilbourn AJ. Thoracic root pain in diabetics: the spectrum of clinical and electromyographic findings. Ann Neurol 1982; 11;80–85.
907
Part 3: Specific Disorders 22. Olsewski JM, Simmons EH, Kallen FC, et al. Evidence from cadavers suggestive of entrapment of fifth lumbar spinal nerves by lumbosacral ligaments. Spine 1991; 16:336–347. 23. Howe JF, Loeser JD, Calvin WH. Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 1977; 3:25–41.
50. Vroomen PC, de Krom MC, Knotterus JA. Diagnostic value of history and physical examination in patients suspected of sciatica due to disc herniation: a systematic review. J Neurol 1999; 246:899–906.
24. Hitselberger WE, Witten RM. Abnormal myelograms in asymptomatic patients. J Neurosurg 1968; 28:204–206.
51. Nasseri K, Strijers RL, Dekhuijzen LS, et al. Reproducibility of different methods for diagnosing and monitoring diabetic neuropathy. Electromyog Clin Neurophysiol. 1998; 38(5):295–299.
25. Saal JA, Saal JS. The nonoperative treatment of herniated nucleus pulposus with radiculopathy: an outcome study. Spine 1989; 14:431–437.
52. Young A, Getty J, Jackson A, et al. Variations in the pattern of muscle innervation by the L5 and S1 nerve roots. Spine 1983; 8(6):616–624.
26. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography: I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984; 9(6):549–551.
53. Slipman CW, Palmitier RA. Diagnostic selective nerve root blocks. Crit Rev Phys Med Rehabil Med 1998; 10(2):123–146.
27. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg 1990; 72A(3):403–408.
54. Modic MT, Masaryk T, Boumphrey F, et al. Lumbar herniated disk disease and canal stenosis: prospective evaluation by surface coil MR, CT, and myelography. AJNR 1986; 7:710–717. 55. Ross JS, Glicklich M, Buchesneau PM. Imaging of the lumbar spine. In: Hardy RW, ed. Lumbar disc disease. 2nd edn. New York, NY: Raven Press; 1993.
28. Maigne JY, Rime B, Delinge B. Computed tomographic follow-up study of fortyeight cases of nonoperatively treated lumbar intervertebral disc herniation. Spine 1992; 17:1071–1074.
56. Williams AL, Haughton VM, Daniels DL, et al. CT recognition of lateral lumbar disc herniation. AJNR 1982; 3:211–213.
29. Delauche-Cavallier MC, Budet C, Laredo JD, et al. Lumbar disc herniation: computed tomography scan changes after conservative treatment of nerve root compression. Spine 1992; 17:927–933.
57. Haueisen C, Smith B, Myers SR, et al. The diagnostic accuracy of spinal nerve injection studies. Their role in the evaluation of recurrent sciatica. Clin Orthop 1985; 198:179–183.
30. Mixter WJ, Ayer JB. Herniation or rupture of the intervertebral disc into the spinal canal. N Engl J Med 1935; 213:385–395.
58. Anand AK, Lee BCP. Pain and metrizamide CT of lumbar disc disease: comparison with myelography. AJNR 1982; 3:567–571.
31. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15(7):674–678.
59. Sotiropoulos S, Chafetz NI, Lang P, et al. Differentiation between postoperative scar and recurrent disc herniation: prospective comparison of MR, CT, and contrast enhanced CT. AJNR 1989; 10:639–643.
32. Lindahl O, Rexed B. Histologic changes in spinal nerve roots of operated cases of sciatica. Acta Orthop Scand 1951; 20:215–225. 33. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 331(2):69–73.
60. Ross JS, Masaryk TJ, Schrader M, et al. MR imaging of the postoperative spine: assessment with gadopentate dimeglumine. AJNR 1990; 11:771–776. 61. Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990; 15(7):683–686.
34. Bobechko WP, Hirsch C. Auto-immune response to nucleus pulposus in the rabbit. J Bone Joint Surg 1965; 47B(3):574–580.
62. Mcnab I. Negative disc exploration: an analysis of the causes of nerve-root involvement in sixty-eight patients. J Bone Joint Surg 1971; 53:891–903.
35. McCarron RF, Wimpee MW, Hudkins PG, et al. The inflammatory effects of nucleus pulposus: a possible element in the pathogenesis of low back pain. Spine 1987; 12:760–764.
63. Tajima T, Furukawa K, Kuramochi E. Selective lumbosacral radiculopathy and block. Spine 1980: 5:68–77.
36. Saal JS, Franson R, Myers R, et al. Human disc PLA2 induces neural injury: a histolomorphometric study. Presented at the International Society for the Study of the Lumbar Spine, Annual Meeting, May 20–24, 1992. 37. Chen C, Cavanaugh JM, Ozaktay C, et al. Effects of phospholipase A2 on lumbar nerve root structure and function. Spine 1997; 22:1057–1064.
64. Kikuchi S, Hasue M, Nishiyama K. Anatomic and clinical studies of radicular symptoms. Spine 1984; 9:23–30. 65. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988; 13:79–83. 66. Herron LD. Selective nerve root blocks in patient selection for lumbar surgery – surgical results. J Spinal Disord 1989; 2:75–79.
38. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6, and prostaglandin E2. Spine 1996; 21(3):271–277.
67. van Akkerveeken PF. The diagnostic value of nerve sheath infiltration. Acta Orthop Scand 1993; 64:61–63.
39. Byrod G, Olmarker K, Konno S, et al. A rapid transport route between the epidural space and the intraneural capillaries of the nerve roots. Spine 1995; 20:138–143.
68. Stanley D, McLoren MI, Evinton HA, et al. A prospective study of nerve root infiltration in the diagnosis of sciatica. A comparison with radiculopathy, computed tomography and operative findings. Spine 1990; 15:540–543.
40. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies. Phys Med Rehabil Clin N Am 2002; 13:697–711. 41. Rydevik B, Brown MD, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984; 9:7–15. 42. Murphy RW. Nerve roots and spinal nerves in degenerative disk disease. Clin Orthop Rel Res 1977; 129:46–60. 43. Goddard MD, Reid JD. Movements induced by straight leg raising in the lumbosacral roots, nerves and plexus, and in the intrapelvic section of the sciatic nerve. J Neurol Neurosurg Psychiatr 1965; 28:12. 44. Howe JF, Loeser JD, Calvin WH. Mechanosensitivity of dorsal root ganglia and chronically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain 1977; 3:25–41. 45. Bradley KE. Stress–strain phenomena in human spinal nerve roots. Brain 1961; 84:120. 46. Bora FW, Pleasure DE, Didizian NA. A study of nerve regeneration and neuroma formation after nerve suture by various techniques. J Hand Surg 1976; 1: 138–143.
908
49. Fortin JD. Sacroiliac joint dysfunction. A new perspective. J Back Musculoskel Rehabil 1993; 3(3):31–43.
69. Lauder TD, Dillingham TR, Andary M, et al. Effect of history and exam in predicting electrodiagnostic outcome among patients with suspected lumbosacral radiculopathy. Am J Phys Med Rehabil 2000; 79(1):60–68. 70. Pease WS, Johnson EW, Charles M. Recruitment interval in L5 radiculopathy: a preliminary report. Arch Phys Med Rehabil 1984; 65:654. 71. Colachis SC, Pease WS, Johnson EW. Polyphasic motor unit action potentials in early radiculopathy: their presence and ephaptic transmission as an hypothesis. Electromyogr Clin Neurophysiol 1992; 32:27–33. 72. Johnson EW, Melvin JL. Value of electromyography in lumbar radiculopathy. Arch Phyl Med Rehabil 1971; 52(6):239–243. 73. Johnson EW, Fletcher FR. Lumbosacral radiculopathy: review of 100 consecutive cases. Arch Phys Med Rehabil 1981; 62(7):321–323. 74. Braddom RI, Johnson EW. Standardization of H-reflex and diagnostic uses in S1 radiculopathy. Arch Phys Med Rehabil 1974; 55:161–166. 75. Strakowski JA, Redd DD, Johnson EW, et al. H-reflex and F-wave latencies to soleus normal values and side-to-side differences. Am J Phys Med Rehabil 2001; 80(7):491–493.
47. Bush K, Cowan N, Katz DE. The natural history of sciatica with associated disc pathology: a prospective study with clinical and independent radiologic follow-up. Spine 1992; 17:1205–1212.
76. Shea PA, Woods WW, Werden DH. Electromyography in diagnosis of nerve root compression syndrome. Arch Neurol Psychiat 1950; 64:93–104.
48. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21(22):2594–2602.
77. Nardin RA, Patel MR, Gudas TF, et al. Electromyography and magnetic resonance imaging in the evaluation of radiculopathy. Muscle Nerve 1999; 22:151–155.
Section 5: Biomechanical Disorders of the Lumbar Spine 78. Kellegren JH. On the distribution of pain arising from deep somatic structures with charts of segmental pain. Clin Sci 1939; 3:35–46. 79. Kuslich SD, Ulstrom CL, Michael CL. The tissue origin of low back pain and sciatica: a report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Ortho Clin N Am 1991; 22(2):181–187. 80. Schwarzer AC, Aprill CN, Derbry R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20(17):1878–1883. 81. Kokmeyer DJ, Van der Wurff P, Aufdemkampe G, et al. The reliability of multitest regimens with sacroiliac pain provocation tests. J Manip Phsiol Ther 2002; 25(1):42–48. 82. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79:288–292. 83. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome. Spine 1996; 21(19):2251–2254. 84. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21(16):1889–1892. 85. Revel M, Poiraudeau S, Auleley GR, et al. Capacity of the clinical picture to characterize low back pain relieved by facet joint anesthesia: proposed criteria to identify patients with painful facet joints. Spine 1998; 23(18):1972–1977. 86. Slipman CW, Plastaras C, Palmitier RA, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation: are dynatomal maps identical to dermatomal maps? Spine 1998; 23(20):2235–2242. 87. Moriishi J, Otani K, Tanaka K, et al. The intersegmental anastomoses between spinal nerve roots. Anat Rec 1989; 224(1):110–116. 88. Neidre A, MacNab I. Anomalies of the lumbosacral nerve roots. Spine 1983; 8:294–299. 89. Bogduk N. Nerves of the lumbar spine. In: Bogduk N, ed. Clinical anatomy of the lumbar spine and sacrum. 3rd edn. London: Elsevier Science; 2002. 90. Krempen JD, Smith B. Nerve root injection: a method for evaluating the etiology of sciatica. J Bone Joint Surg 1974: 56A:1435–1444. 91. Schutz H, Lougheed WM, Wortzman G, et al. Intervertebral nerve-root in the investigation of chronic lumbar disc disease. Can J Surg 1973; 16:217–221. 92. Kikuchi S, Hasue M. Combined contrast studies in lumbar spine diseases: myelography (peridurography) and nerve root infiltration. Spine 1988; 13:1327–1331. 93. White A. Injection techniques for the diagnosis and treatment of low back pain. Orthop Clin N Am 1983; 14:553–567.
94. Huston CW, Slipman CW, Garvin, C. Complications and side effects of cervical and lumbosacral selective nerve root injections. Arch Phys Med Rehabil 2005; 86(2):277–283. 95. Botwin KP, Gruber RD, Bouchlas CG, et al. Complications of fluoroscopically guided transforaminal lumbar injections. Arch Phys Med Rehabil 2000; 81(8):1045–1050. 96. Schwarzer AC, Aprill CN, Bogduk M. The sacroiliac joint in chronic low back pain. Spine 1995; 20(1):31–37. 97. Durranti A, Winnie AP. Piriformis muscle syndrome: an underdiagnosed cause of sciatica. J Pain Symp Manage 1991; 6:374–371. 98. Solheim LF, Siewers P, Paus B. The piriformis muscle syndrome. Acta Orthop Scand 1981; 52:73–75. 99. Slipman CW, El Abd OH, Brandys EB, et al. The prevalence of referred abdominal and inguinal pain in patients with lumbar internal disruption syndrome. In press. 100. Alo KM, Wright RE, Sutcliffe J, et al. Percutaneous lumbar discectomy: clinical response in an initial cohort of fifty consecutive patients with radicular pain. Pain Pract 2004; 4(1)19–29. 101. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Medicine 2002; 3(3):200–207. 102. Maillefert JF, Aho S, Huguenin MC, et al. Systemic effects of epidural dexamethasone injections. Rev Rhum [Engl Edn] 1995; 62(6):429–432. 103. Sharps LS, Isaac Z. Percutaneous disc decompression using nucleoplasty. Pain Phys 2002; 5(2):121–126. 104. Amudsen T, Weber H, Nordal HJ, et al. Lumbar spinal stenosis: conservative or surgical management?: a prospective 10-year study. Spine 2000; 25(11): 1424–1436. 105. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transforaminal epidural steroid injection in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 81(12):898–905. 106. Lutz GE, Shen T. Fluoroscopically guided aspiration of a symptomatic lumbar zygapophyseal joint cyst: a case report. Arch Phys Med Rehabil 2002; 83(12): 1789–1791. 107. Slipman CW, Lipetz JS, Yusuke W, et al. Nonsurgical treatment of zygapophyseal joint cyst-induced radicular pain. Arch Phys Med Rehabil 2000; 81(8):973–977. 108. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: an outcome study. Arch Phys Med Rehabil 1998; 79:1362–1366. 109. Riew KD, Yin Y, Gilula L, et al. The effect of nerve-root injections on the need for operative treatment of lumbar radicular pain. J Bone Joint Surg 2000; 82A: 1589–1593.
909
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ ii: Lumbar Radicular Pain
CHAPTER
Injection Procedures
83
Jaro Karppinen and Jukka-Pekka Kouri
PATHOPHYSIOLOGY OF RADICULAR LUMBAR PAIN Lumbar radicular pain, i.e. sciatica, in this context is defined as pain referred from the back into the dermatome of the affected nerve root along the femoral or sciatic nerve trunk. This has to be differentiated from nonradicular pain, which refers symptoms into the leg in a nondermatomal pattern.1 Radicular pain is shooting and bandlike, whereas somatic referred pain is usually constant in position but poorly localized and diffuse, and is aching in quality. True radiculopathy is defined as radicular pain in the presence of a neurological deficit.2 The prevalence of lumbar disc syndrome (herniated disc or typical sciatica) was studied as part of the Mini-Finland Health Survey.3 A diagnosis of lumbar disc syndrome was made for 5.1% of men and 3.7% of women aged 30 years or over. In a Finnish longitudinal birth cohort study, symptomatic lumbar disc disease (herniated nucleus pulposus or sciatica) appeared around the age of 15 years, and the incidence rose more sharply from the age of 19 years.4
Tissue origin of lumbar radicular pain The tissue origin of sciatic pain has been studied during decompression operations performed with local anesthesia. In these studies, sciatic pain could be produced only by pressure on the compressed, swollen nerve root, or on the dorsal root ganglion (DRG). Pressure on normal nerve roots or on other tissue did not produce sciatica.5,6
Intervertebral disc Disc herniation is the single most common cause of radicular pain.2 Mixter and Barr7 discovered that soft tissue ‘tumours’ were actually derived from the intervertebral discs, and that their surgical removal relieved sciatica symptoms. The causal link between herniated nucleus pulposus (HNP) and radicular pain is, however, not so straightforward since (1) HNP can be found in 20–36%, depending on the age, of asymptomatic subjects,8–11 and (2) internal disc ruptures (without HNP) may also induce disabling radicular pain,12,13 indicating the existence of an alternative mechanism to neural compression. Even though this chapter does not cover the clinical diagnosis of lumbar radicular pain, the authors stress that nerve root tension signs, assessed by the straight leg-raising test, can be positive in sciatica patients without HNP in MRI.14
Central and lateral stenosis Spinal stenosis is a condition associated with degenerative changes of the disc and zygapophyseal joints at multiple levels, which may include degenerative spondylolisthesis.15 Spinal stenosis has both structural and dynamic components. When the spinal canal is
structurally narrowed, slight extension can cause compression of the nerves.16,17 Extension can also cause an increase in epidural pressure.18 Flexion has the reverse effect, widening the spinal canal and foramina and reducing the epidural pressure. These typical features can be used in the practical clinical diagnosis of spinal stenosis and also in the algorithm of radicular pain. Lateral lumbar spinal stenosis due to osteoarthritis can be divided into entrance zone, midzone and exit zone stenosis.19 When a nerve root is laterally entrapped, it gives unilateral pain that is worse on walking. When central canal is narrow, pain radiates to one or both legs while walking and is relieved with flexion postures.20,21 Midzone stenosis is clinically the most relevant entity, because the DRG occupies a large part of the midzone.19 Recent experimental data also support the critical role played by the DRG in the pathophysiology of painful stenosis.22 The authors found that neither demyelinization nor axonal degeneration in the cauda equina induced mechanical allodynia, i.e. neuropathic pain, whereas lesions distal or immediately proximal to it are painful. They concluded that DRG apoptosis may be important for the production and maintenance of mechanical allodynia.22
Pathophysiological mechanisms of radicular pain Evidence of other mechanisms that can elicit lumbar radicular pain other than nerve root compression comes from many directions. We have already cited the findings of experimental surgery in anesthesia, existence of HNP in asymptomatics, and on the other hand, sciatica syndromes in those without an HNP. Additional evidence comes from animal experiments. McCarron et al.23 demonstrated that nuclear material of the intervertebral disc is chemically inflammatory and neurotoxic. Olmarker et al. showed that nuclear material – without any compression – can induce structural and functional changes in porcine nerve roots.24 The functional changes included focal degeneration of myelinated fibers and focal Schwann cell damage in nondegenerated axons. The damage to the Schwann cells resulted in a disintegration of Schmidt-Lantermann incisures, which represent connections of Schwann cell cytoplasm inside and outside the myelin sheath.25 Additional evidence supporting inflammation comes from the finding that nucleus pulposus is chemotactic, attracting leukocytes, and it may also induce macromolecular leakage and spontaneous firing of axons in vitro.26 Inflammation-induced capillary leakage increases endoneural pressure and reduces blood flow, thereby causing a ‘compartment syndrome’ in the DRG.27 A similar decrease in blood flow has been observed also in the canine nerve root. This reduction correlated with decrease in nerve conduction velocity, and was maximal within 1 week and recovered within 1 month. The pattern of nucleus-exposed DRG was, however, different, showing no clear recovery.28 These findings suggest that DRG irritation may lead into 911
Part 3: Specific Disorders
a different – perhaps more conservative treatment-resistant – radicular pain entity than nerve root involvement only. An additional, important landmark study is that of Kawakami et al.29 They nicely showed that leukocytes are essential in experimental radicular pain. In a rat model of mechanical hyperalgesia induced by application of nucleus pulposus to nerve roots, depletion of leukocytes with nitrogen mustard inhibited the generation of hyperalgesia. This indicated that the leukocytes are important in the production of pain-related behavior. The cells first appearing in and around the HNP on nerve–nuclear interface were polymorphonuclear leukocytes. Macrophages, originating from monocytes, did predominate a few days later and then remain in the affected region until the inflammation subsided.29 The implication of the observations is that lumbar radicular pain is a systemic disease, at least in the early stages of the disease. What is the leukotactic signal(s) of extruded nuclear material? Many substances, including hydrogen ions and glycoproteins, have been suspected of causing chemical radiculitis.30–32 A crucial finding was the one reported by Olmarker et al.33 They noted that the neurotoxicity of the nucleus seems to be associated with disc cells, as freezing prevented the neuronal damage. This observation limited the number of possible inflammatory candidates, but several were still ‘without alibi.’ Phospholipase A2 (PLA2) was a promising suspect, as it is the ratelimiting enzyme in the synthesis of proinflammatory lipid mediators (prostaglandins, leukotrienes, lipoxenies, and platelet-activating factor). It is calcium-dependent, adsorbing tightly to plasma membranes and intact cells. PLA2 liberates arachidonic acid from the membrane phospholipids, and is secreted extracellularly by activated phagocytes in response to cytokines.34 Additionally, it is released from rabbit chondrocytes in response to interleukin (IL)-1.35 It was found in extraordinarily high concentrations in herniated and painful discs,36 although this finding has since been questioned.37 It is also itself inflammatory38 and neurotoxic.39 When PLA2 was injected epidurally, motor weakness, demyelinization, and increased sensitivity of dorsal roots to mechanical stimulation were observed 3 days after the injection, but not beyond 3 weeks.40 Tumor necrosis factor alpha (TNF-α) is another potential candidate in HNP-induced nerve root irritation. TNF-α is a cytokine produced mainly by activated macrophages and T cells in response to inflammation, and by mast cells and Schwann cells in response to peripheral nerve injury.41,42 It activates the transcription factors NF-κB and AP-1 by binding to its p55 TNF-receptor (TNFR1), thereby inducing the production of proinflammatory and immunomodulatory genes.43 Endoneurial TNF-α causes demyelinization, axonal degeneration, and hyperalgesic pain states.44 In thermal hyperalgesia, two peaks have been associated with Wallerian degeneration, and can be reproduced in chronic injury to peripheral nerves.45 These peaks are also related to changes in TNF-α expression. It seems that the first peak, 6 hours after the nerve injury, is due to the local expression of the cytotoxic transmembrane 26 kDa TNF-α protein released by the resident Schwann cells. The second peak occurs 5 days after the injury, and may represent TNF-α protein released by hematogenously recruited macrophages.45 It has been shown immunohistochemically that TNF-α is expressed in the porcine nucleus pulposus.46 In a rat model, the concentration of TNF-α was found to be approximately 0.5 ng per herniated rat disc.47 Moreover, exogenous TNF-α produced neuropathological and behavioral changes (Wallerian degeneration of nerve fibers, macrophage recruitment to phagocytoze the debris, splitting of the myelin sheath) that mimicked those of the nucleus pulposus.47 Application of TNF-α on porcine nerve roots induced a reduction of the nerve conduction velocity that was even more pronounced than for nucleus pulposus, whereas application of IL-1β and IFNδ induced slight reductions of conduction velocity compared with fat, 912
but they were not statistically significant.48 Additional evidence for a crucial role of TNF-α comes from an animal study in which soluble TNF-α receptor (etanercept, Enbrel™) reversed nucleus pulposusinduced nerve conduction block and nerve root edema.49 However, TNF-α is not just a ‘bad guy’ as it also has an important role in the resorption of disc herniations. Macrophages secrete matrix metalloproteinase (MMP)-7 (=matrilysin) enzyme, which liberates soluble TNF-α from macrophage cell membranes. Soluble TNF-α induces disc chondrocytes to secrete MMP-3 (stromelysin), required for the release of a macrophage chemoattractant and subsequent macrophage infiltration of the disc.50,51 In addition to TNF-α, other inflammatory mediators may take part in the inflammatory component of radicular pain. These mediators could be either proximal to TNF-α, i.e. increase the expression of TNF-α, or distal to TNF-α, i.e. they are upregulated by TNF-α. Kang et al.52 observed increased matrix metalloproteinase activity, and increased levels of nitric oxide, prostaglandin E2, and IL-6 in HNP culture media compared with the control discs. Similarly, Burke et al.53 also detected increased levels of IL-6 in disc extracts from patients undergoing fusion for discogenic pain. They found additionally increased levels of a chemokine, IL-8. Interleukin-6 is an interesting interleukin, as it regulates to a large extent the hepatic acute phase and cachectic responses to an acute inflammatory stimulus.54 Recently, it was found that sciatica patients have an elevated acute phase response.55 Mean sensitized C-reactive protein (CRP) levels were significantly higher in sciatica patients compared to age- and sex-matched controls (1.68 versus 0.74 mg/L; p=0.002). We have genotyped sciatica patients with regard to some inflammatory genes and compared these patients to asymptomatic subjects. A genotype leading to increased production of IL-6 was overexpressed in sciatica patients.56 Additionally, in the HNP homogenates IL-1α, IL-1β and granulocyte-macrophage colony stimulating factor are detectable.57 The exact role of IL-1 in HNP-induced radicular pain is not known but it may have separate activity as it has in experimental arthritis.58
Natural course of lumbar radicular pain The long-term prognosis of lumbar radicular pain is considered to be good59 although in one study only one-third of sciatica patients recovered fully within 1 year, whereas one-third underwent surgery and one-third had residual symptoms.60 This study by Balague60 is in concordance with a systematic review on the long-term course of low back pain (LBP).61 Sixty-two percent of LBP patients still experienced pain at 12 months, 16% were sick-listed 6 months after inclusion into the study, and 60% experienced relapses of pain. A cohort of primary care patients with sciatica was followed in the Netherlands.62 An unfavorable outcome was predicted by a disease duration of more than 30 days, increased pain on sitting, pain upon coughing, and straight leg raising restriction. Magnetic resonance imaging (MRI) follow-up examinations have shown that HNP tends to regress over time, with partial to complete resolution after 6 months in two-thirds of people.63 We have recently rescanned 21 patients with HNP-induced severe sciatica at 2 weeks, 3 months, and 6 months in an intervention trial. Significant resorption seemed to occur already as early as 3 months in most patients.64 There is a predilection for large extrusions to resorb well.65,66 The resorption process seems to associate with HNP-encircling rim enhancement,67 which is thought to represent a neovascularized zone with macrophage infiltration.68 Neovascularization probably remains high in extrusions, as these have ruptured the posterior longitudinal ligament and entered the epidural space, allowing small vessels to penetrate the disc tissue more easily, whereas subligamentous herniations are more or less immunoprivileged.69 This is supported
Section 5: Biomechanical Disorders of the Lumbar Spine
by the higher resorption rate for extrusion-type disc herniations.70 We have recently analyzed determinants of HNP resorption.71 In the final model, the only significant determinants for resorption were thickness of rim enhancement and Komor classification, i.e. herniation extending above or below 67% of the adjacent vertebra.72
INTERVENTIONAL TREATMENT OPTIONS FOR LUMBAR RADICULAR PAIN Evidence on substantiating the best method to achieve successful treatment of lumbar radicular pain is still sparse. A recent systematic review found only 19 randomized, controlled trials (RCTs), of which eight met the three major requirements (comparability of groups, observer blinding, and intention-to-treat analysis).73 From the perspective of this review, no significant effect was demonstrated for nonsteroidal antiinflammatory agents (NSAIDs), traction, or intramuscular steroids. Considering the, at least partial, inflammatory nature of lumbar radicular pain, blocking of the cytokine cascade by local or systematic corticosteroids might, however, be effective. It is known from animal experiments that methylprednisolone injected within 2 days after the application of the nucleus pulposus inhibits the nucleus-induced vascular permeability and functional impairment, i.e. decrease of nerve conduction velocity.74 Any clinically useful intervention for radicular pain should be (1) effective in pain alleviation, (2) safe (i.e. no harmful complications), and (3) the technical details of the procedure or the equipment used should not be too complicated so that the intervention can be used widely in clinical practice. Moreover, if two different interventions are found equally effective and safe on radicular pain, the more cost-effective procedure should be chosen. When designing and using interventions for radicular pain, one should not tamper with the benign natural course of sciatica. In the ensuing, epidural injections, selective nerve root blocks, and anticytokine therapy are discussed in more extensive detail.
Epidural injections Epidural injections in the cervical, thoracic, and lumbosacral spine have been used for both diagnostic and therapeutic purposes in modern interventional spine practice. Epidural injections should preferably be combined with other therapeutic modalities, e.g. physical training and musculoskeletal rehabilitation. Epidural injection of medication allows a concentrated amount of the treatment agents (i.e. mostly corticosteroids) to be deposited and retained, thereby exposing the nerve roots to the medication for a prolonged period of time. The ability of steroids injected through an epidural route to reach their target in the anterior or anterolateral epidural compartment has been questioned. Indeed, even in experienced hands 25–45% of blind interlaminar or caudal epidural needle placements may be incorrect.75–77
Technical procedure There are two different routes to perform epidural injections: a caudal route through the sacral hiatus, and a lumbar interlaminar route. Epidural injection can be done with fluoroscopy or without it. Many specialists recommend fluoroscopy, because without fluoroscopy the needle is not always placed in the epidural space. Additionally, fluoroscopy prevents accidental intravascular injection. The incidence of intravascular uptake during lumbar spinal injection procedures was found to be approximately 8.5%. Absence of flashback of blood upon preinjection aspiration did not predict extravascular needle placement.78 Recently, fluoroscopic guidance has evolved into the standard approach in the US, although some clinicians stubbornly perform blind injections (Curtis Slipman, personal communication). Typically, blind injections are reserved for pregnant women and heavy patients who exceed the weight limits of the fluoros-
copy table. It is easiest and safest to insert the needle at L2–3 or L3–4, close to the superior spinous process. The standard technique used in epidural injections is the loss of resistance technique, where a controlled and well-defined loss of resistance occurs upon entering the epidural space through the ligamentum flavum. One study found that in the non-obese patient, lumbar interlaminar injections can be accurately placed without X-ray screening, in contrast to caudal injections, which require X-ray screening independent of the weight of the patient.79 In the caudal epidural injection, the quantity of corticosteroid that is possible to apply near to the inflamed nerve root is usually small. As well, the precise application is always uncertain, because anatomical structures such as septas may interfere with the flow of the injectate. However, caudal epidural route is useful in cases when the lesion is at L5–S1, but the interspinous route is preferable if the lesion is located at L4–5 or above.
Efficacy Epidural steroid injections are found to have a high success rate when evaluated in terms of long-term alleviation of radicular symptoms due to lumbar HNP.80,81 One published meta-analysis concluded that epidural corticosteroids are effective in both the short and long term in low back pain and sciatica.82 In contrast, the systematic review by Koes et al. that included higher-quality trials, found at most a shortterm effect on sciatica.83 To further complicate the matter, the systematic review by Vroomen et al. on treatment of sciatica concluded that epidural steroids may produce a short-term benefit for lumbar radicular pain.73 Following these aforementioned studies, two RCTs on epidural steroids for sciatica have been published. In the trial of Buchner et al.,84 patients with lumbar radicular pain consequent to a confirmed HNP were randomized into the epidural group (3 injections of 100 mg methylprednisolone in 0.25% bupivacaine; n=17) and control group (n=19). At 2 weeks, patients receiving methylprednisolone injection showed a significant improvement in straight leg raising test results and a tendency for a greater pain relief. At 6 weeks and 6 months, no significant differences were observed in any of the outcomes. In the trial of Valat and colleagues,85 three epidural injections of 50 mg prednisolone acetate (n = 43) were compared to epidural saline injections (n = 42) in HNP-induced sciatica. A significant improvement was observed in both groups, but epidural steroid injections provided no additional benefit over saline. Our conclusion, which stems from the reviews and subsequent RCTs, is that epidural steroids may have, at best, a short-term beneficial effect on lumbar radicular pain. Additionally, cost minimization analysis suggests that epidural injections under fluoroscopy may not be justified on the basis of the current literature.86 The authors’ personal preference is to use selective nerve root blocks (SNRB) in lieu of interlaminar epidurals for lesions at L4–5 or above. At L5–S1, our present view is to prefer computed tomography (CT)-guided SNRBs over caudal epidurals, and caudal epidurals over fluoroscopy-guided SNRBs. We do acknowledge that there is no uniform consensus regarding the approach at L5–S1.
Safety A major concern when administrating anesthetics into the epidural space is systemic toxicity. There is the theoretical risk of cardiovascular toxicity and central nervous system (CNS) effects. These complications can be avoided by adhering to careful technique and using lower doses of less concentrated anesthetics as discussed in the spinal injections technique chapter (Ch. 23). The maximum epidural dose recommended for a single injection is 500 mg for lidocaine and 225 mg for bupivacaine. The amount of local anesthetic agent used for SNRBs is much less. Epidural injections are usually considered to be extremely safe when performed with the proper technique.87 Nevertheless, the interlaminar 913
Part 3: Specific Disorders
route may be prone to complications, which include dural puncturecaused spinal headache, transient hypotension, Cushing’s syndrome, bacterial meningitis, chemical meningitis, epidural abscess, sinus arrhythmia, respiratory distress from spinal anesthesia, transiently increasing back or leg pain, numbness, transient dizziness, and cardiopulmonary arrest.88 In the meta-analysis of Watts and Silagy, which was based on seven trials with 431 patients, 2.5% suffered from dural taps, 2.3% transient headache, 1.9% transient increase in pain, and 0.2% irregular menstrual cycle.82 Long-term complications were not covered in the original reports, but, according to data from the American Society of Anesthesiologists Closed Claims Project database (1970– 1999), epidural steroid injections accounted for 40% of all chronic pain management claims. Serious injuries, involving brain damage or death, occurred, especially with local anesthetics and/or opioids.89
Selective nerve root blocks Derby et al.90 have postulated that the transforaminal approach may get corticosteroid more reliably in the anterior epidural space, where most of the pain-sensitive structures are located. In the procedure, the pharmaceutical agents are injected between the nerve root and the epidural sheath, depicting the nerve root in tubular fashion.91 Hereafter, we use the term selective nerve root block (SNRB), but synonymous terms
include selective nerve root injection, periradicular infiltration, transforaminal injection, and perineural injection. The mechanism of therapeutic effect is postulated to rely on mainly on the antiinflammatory effect of corticosteroid, which blocks the afferent impulses from the periphery.91 However, the anesthetic component may have an effect on its own, as lidocaine has been shown to increase intraradicular blood flow identical to the responses of a sympathetic ganglion block.92 SNRBs are useful in the diagnosis of radicular pain in atypical presentations. They have an accuracy of 85–94% in identifying a single symptomatic root, sensitivity of 100%, and a positive predictive value of 93–95% has been presented for root blocks.1,91,93,94 Indications are: (1) atypical extremity pain; (2) when imaging studies and clinical presentation do not correlate; (3) when electromyography and MRI do not correlate; (4) anomalous innervations, such as conjoint nerve roots or furcal nerves; (5) failed back surgery syndrome with atypical extremity pain; and (6) transitional vertebrae.88 A diagnostic SNRB is usually done without any antiinflammatory drug such as steroid in order to confirm the identity of the affected nerve root, whereas in therapeutic injections the ultimate goal is a therapeutic effect (typically achieved with a corticosteroid with or without local anesthetic). See the algorithm on diagnostic SNRBs and treatment of lumbar radicular pain, Figures 83.1A and 83.1B, respectively.
−
Positive SLR
SNRB
+
Pain worsened with extension and better when sitting
Pain below the knee Radicular pain: Back pain:
Radicular pain: Back pain: no influence
No influence on radicular pain nor on back pain
Possible HNP or disc rupture
Repeat 2–4 times if necessary
Facet or SI-joint injections
+
Severe symptoms, duration 0–2 wks Active noninvasive pain therapy, activity modifications, conservative therapy
Sympathetic blockade
A
−
+
+
SNRB of L2 nerve root
Pain radiating mainly above the gluteal fold
Unilateral pain
Bilateral pain, pain mainly proximally
Confirm with CT or MRI
− +
+
Possible spinal stenosis
Possible lateral stenosis
Confirm with CT or MRI
Confirm with CT or MRI
+ Possible SIor facet joint pathology + SI- or facet joint injection
+
+
SNRB irrespective of symptom duration
Mild symptoms Conservative therapy
+
+ Severe symptoms, >2 wks
Severe or persisting symptoms
SNRB +
− Refer to surgery
B Fig. 83.1 Algorithms for diagnosis (A) and treatment (B) of lumbar radicular pain. 914
+ Repeat 2 or more times
+ −
Repeat 2–4 times
SNRB
Refer to foraminotomy
Epidural injection
−
Mild but persisting symptoms
−
Refer to surgery anticytokine therapy??
Repeat SNRB 1 or more times
Repeat 1–2 times
Refer to decompressive surgery
Section 5: Biomechanical Disorders of the Lumbar Spine
Technical procedure Fluoroscopy-guided SNRB is typically the simplest, most rapid, and cost-effective technique. The details of this procedure have been thoroughly explained in Chapter 23. There are, however, two other techniques to confirm the proper needle insertion and placement: CT and MRI guidance.
CT guidance During CT-guided SNRBs, patients are in prone position on the scanner table. Axial slides are taken and analyzed before the procedure. The safe triangle described within the numerous technique chapters is the targeted area. The trajectory of the injection can be preplanned according to the information obtained from the CT scans. The entry point is marked on the skin with ink and can be controlled with a new CT scan (Fig. 83.2). Injection angle and the distance between skin and target area can be measured accurately. The interventionalist can check the correct angle of the injection needle with an angle measurement device and thus guide the clinician throughout the procedure. The correct injection site can also be controlled with contrastenhanced CT scans when needed. For postoperative radicular pain, CT-guided injection seems to be superior to fluoroscope-assisted injection for both its visualization and a longer-lasting effect.95
MRI guidance MRI guidance is another method, though it has not gained wide popularity because of the expensive MRI equipment required. The technical details of the MRI imaging system include an openconfiguration c-arm magnet, an MR-compatible in-room console, large screen display unit, and optical navigator.96 An MRI-guided procedure lacks the disadvantages of the other two methods. There is no ionizing radiation risk, and because of its ability to provide superior soft tissue contrast detail, contrast agent is not required. MRI guidance offers three-dimensional information during the nerve root injection, which is particularly advantageous for S1 infiltrations,96 which tend to produce unsatisfactory results by fluoroscopy.97
Efficacy It was observed in diagnostic studies that patients with lumbar spinal stenosis due to spondylosis or degenerative spondylolisthesis had
Fig. 83.2 An axial view of a CT-guided SNRB. The red line indicates the correct angle of the injection needle.
experienced a better therapeutic benefit from SNRBs than those with radicular symptoms referable to a disc herniation or to spondylolytic spondylolisthesis.91,98 Several uncontrolled follow-up studies confirmed these observations of a therapeutic effect.99,100 In HNPinduced radiculopathy, there was a 75% long-term recovery after an average of 1.8 transforaminal injections per patient of betamethasone acetate combined with Xylocaine. The outcome was better for symptom duration of less than 36 weeks.100 Weiner and Fraser used fluoroscopy-guided SNRB for patients with severe lumbar radiculopathy secondary to foraminal and extraforaminal disc herniation, which had not resolved with rest and nonsteroidal antiinflammatory agents. They observed a considerable and sustained pain relief in 22 out of 28 (79%) patients.99 Derby and colleagues observed that a successful SNRB is a good prognostic sign for a positive surgical result for those with symptomatology of at least 1-year duration.101 Fluoroscopically guided transforaminal steroid injections seem to be beneficial in radicular pain due to lumbar spinal stenosis in terms of both pain reduction and improved walking tolerance.102 However, a prospective cohort study involving radicular patients with a disc herniation or spinal stenosis indicated that the response was significantly better in patients with a HNP.103 So far, only 6 RCTs comparing perineural corticosteroid injection to a nonsteroid regimen have been published. Kraemer et al.104 used an interlaminar injection of triamcinolone and lidocaine (n=47), which was compared to paravertebral local anesthetic (n=46). Actually, they did not use SNRB but an oblique interlaminar method. This injection method, however, is somewhat similar to the SNRB precision technique and therefore it is reviewed in this context. Three injections were given with 1-week intervals. They used a composite score and prevention of back surgery in the assessments. Their results indicated that epidural perineural injections were more effective than conventional posterior epidural injections. Devulder et al.105 used transforaminal injections for failed back surgery. The combination of methylprednisolone, bupivacaine, and hyaluronidase (n=20) was compared to a combination of saline, bupivacaine, and hyaluronidase (n=20). Their main outcome measure was at least 50% reduction in leg pain. No statistical differences were found between the treatment groups, although it is unlikely that SNRBs are effective in postoperative radicular syndromes with a high probability of neuropathic pain component. Riew et al.106 used transforaminal injections for degenerative lumbar radicular pain in patients indicated for surgery. Patients had either a disc herniation or central or lateral stenosis confirmed in MRI and/or CT. Patients were randomized to a selective nerve root injection with either bupivacaine alone or bupivacaine with betamethasone. Nineteen patients received multiple injections. Eighteen out of 27 patients in the control group underwent back surgery, as compared to 8 out of 28 patients in the active group. The difference in the operative rates between the two groups was statistically and clinically significant (p back pain Physical examination providing objective corroborative evidence If physical examination is not corroborative then objective evidence is obtained with electrodiagnostic testing and/or diagnostic selective nerve root block Magnetic resonance imaging (MRI) or computed tomography (CT) evidence of a corroborative disc protrusion or extrusion If there is evidence of a disc extrusion, coblation technology should be avoided At least 50% of disc height remaining for the involved disc Intensive conservative therapy for 2–3 months that has failed to provide substantial symptom relief. This program should includes active physical therapy, oral antiinflammatory agents, activity modification, patient education, and at least one epidural space steroid instillation
Absolute contraindications include systemic infection, cellulitis, discitis, osteomyelitis, collapse of disc space, sequestered herniations, cauda equina syndrome, uncorrectable bleeding diathesis, and gross instability. One the other hand, relative contraindications include noncontained disc herniation, disc extrusion, and spinal stenosis. FDA approval of the techniques to perform disc decompression has been
for contained disc protrusions at the exclusion of noncontained disc herniations or extrusions. Our experience, as well as that of some leaders in the technique of percutaneous disc decompression, disputes that notion (Personal communications: Guiseppe Bonaldi; Mark Brown). In the instance of spinal stenosis, narrowing of the canal is a multifactorial process, representing a combination of disc protrusion, ligamentum flavum buckling, and zygapophyseal joint hypertrophy. In cases where the disc appears to be the predominant contributor to the stenosis, it may be an effective intervention, whereas it is less likely to be successful in cases of bony or ligamentous causes of stenosis. There has been no reported permanent nerve injury or great vessel damage with these techniques. In contrast, open surgical procedures have a small yet palpable risk of a major adverse event. Ramirez and Thisted4 reported that in 28 000 open discectomies, there was a major complication in 1 in 64 patients, neurological complication in 1 in 334 patients, and 1 in 1700 patients died from the procedure. Pappas et al.5 reported outcome analysis in 654 surgically treated lumbar disc herniations; there were two major vascular injuries, one of which resulted in death. It seems that the safety profile of percutaneous disc decompression is superior to that of open surgery.6
CHEMONUCLEOLYSIS Introduction Chemonucleolysis is a medical procedure that involves the dissolving of the gelatinous cushioning material in an intervertebral disc by the injection of an enzyme such as chymopapain. In 1956, Thomas7 injected papain into the vein of a rabbit’s ear, observed the floppiness of that ear (compared with the erect state of the control ear), and confirmed softening of the cartilage attributable to papain. Chemonucleolysis with chymopapain was introduced by Smith and Brown8,9 in 1964 as an effective therapy for some types of intervertebral disc herniation. However, because of the protein nature of chymopapain, anaphylactic reactions and neurotoxicity have limited the use of this therapy. Although it has demonstrated long-term success rates between 66% and 88%,10,11 a controlled study initiated by the US Food and Drug Administration12 (FDA) found chymopapain no more effective than placebo. Though it has become commercially unavailable in the US, it is still widely used outside of the US. Two enzymes have been described as effective when used in vivo: chymopapain, which catalyzes the hydrolytic cleavage of glycosaminoglycans from proteoglycan aggregates in the disc, and collagenase, which splits the type 2 collagen fibers with relative particularity. The basic collagenase enzyme synthesized by Clostridium histolyticum consists of varied subenzymes that split the collagen fibers at different locations. The purified collagenase is relatively specific for type 2 collagen, seen mainly in the nucleus pulposus, which consists of 15–20% collagen in its dry weight. Wittenberg et al.13 did a 5-year 927
Part 3: Specific Disorders
clinical follow-up assessment of a prospective, randomized study of chemonucleolysis using chymopapain (4000 IU) or collagenase (400 ABC units). At 5 years, good and excellent results were observed in 72% of the chymopapain group and 52% of the collagenase group. If conservative treatment in patients with recurrent disc herniation after chemonucleolysis fails, surgery is usually recommended. Historically, a second injection was considered contraindicated because of the fear of allergic or anaphylactic reactions. Schweigel and Berezowskyj14 suggested a second injection of chymopapain generally is contraindicated. They observed five major anaphylactic reactions in a review of 35 patients. Due to the high incidence of anaphylaxis, they considered repeat use of chymopapain to be an unacceptable alternative to surgery until a definitive test for chymopapain sensitivity is available. Sutton15 did not observe an anaphylactic reaction when patients were premedicated with histamine receptor blockers. The effect of histamine, released by the immunoglobulin E mediated mast cells, will be blocked. Van de Belt et al.16 reviewed 85 patients who received a second injection of chymopapain because of a recurrent disc herniation between 1980 and 1996. All patients were pretreated for 3 days with H1 and H2 receptor blockers. Immediate sensitivity reactions were not seen. Four type 1 and one type 2 reactions were seen after the second injection, and no other complications were seen. Age can be a factor in choosing patients for chemonucleolysis. Patients older than 60 years may lack sufficient mucoprotein in the offending disc to be hydrolyzed. Patients younger than 20 years have not been studied as frequently as older patients, but 80–90% satisfactory results are reported even though stiffness of the back may persist for a year or more. Single-level involvement with leg pain greater than back pain, corroborative physical findings, and imaging studies represent the ideal chemonucleolysis candidate.17 A successful intervention depends on the chymopapain reaching the mucoprotein of the herniated nucleus pulposus to hydrolyze it, so there must not be a sequestrated fragment surrounded by fibrosis or a posterior ligament defect closed by fibrosis to prevent the enzyme reaching an extrusion. If the offending herniation is primarily composed of annular tissue, its collagenous content will not be reduced by chymopapain. Spinal stenosis, whether central or lateral, may be exacerbated by chemonucleolysis rather than helped. Deburge et al.18 reported lateral recess stenosis in 16 patients and two cases of sequestrated discs in 38 patients who had not been successfully treated with chymopapain. For the diagnosis of disc abnormalities, MRI is superior to CT scan However, MRI is not as effective in the diagnosis of bony lesions, which makes CT scan essential in the preoperative evaluation of chemonucleolysis. With CT scan, information regarding chronic degenerative disc abnormalities, such as lateral recess stenosis and facet hypertrophy, as well as bony spurs and calcified discs, may be obtained. If a soft protrusion is demonstrated without spinal stenosis on CT scan, the success rate is expected to be better (Table 85.1).19
Complications Between 1982 and 1991, 121 adverse events in 135 000 patients were reported to the FDA and investigated. Seven cases of fatal anaphylaxis, 24 infections, 32 bleeding problems, 32 neurological events, and 15 miscellaneous occurrences were found. The overall mortality rate was 0.019%.17 A major disadvantage of chemonucleolysis is the occurrence of back spasm, which can be quite severe in approximately 10% of patients.17 Comparing the complications of laminectomy reported by Ramirez and Thisted.4 in 1989 with those of chemonucleolysis, Nordby et al.17 reported that he found anaphylaxis to be unique to chemonucleolysis; infection occurred 17 times as often with laminectomy as with chemonucleolysis, neurologic and hemorrhagic events 928
Table 85.1: Contraindications for chemonucleolysis ABSOLUTE Allergy to chymopapain or papaya derivatives Central/lateral spinal stenosis Cauda equina syndrome Sequestered disc fragment Fibrosis due to prior surgery Failed back surgery syndrome Arachnoiditis Multiple sclerosis Pregnancy Profound or rapidly progressive neurological deficit Severe spondylolisthesis Spinal cord tumor Spinal instability RELATIVE Polyneuritis of diabetes Hypertension Morbid obesity Stroke Patients on beta blockers are at increased risk, should anaphylaxis occur, because beta blockade inhibits the effects of epinephrine
six times as often with laminectomy, and mortality rates incidental to the procedures occurred three times as frequently with laminectomy. Other potential complications include overdecompression, disc collapse, or instability of the motion segment. These side effects can result from excess ‘digestion’ of disc material. More serious complications have been reported, including lumbar subarachnoid hemorrhage and paraplegia. When chymopapain is inadvertently injected into the subarachnoid space, a cauda equina syndrome results.20 Wittenberg et al.13 reported cauda equina syndrome in two patients using collagenase. A case of acute transverse myelitis (ATM) was observed 21 days after an injection in 1982, and an additional five cases were subsequently reported to the FDA.21 Since no case of ATM has occurred in nearly 60 000 cases since 1984, an association between ATM and chemonucleolysis probably does not exist. Consequently, as of 1992, the FDA approved removing even the mention of ATM from the detailed chymopapain package Full Prescribing Information.21
Long-term results Following chemonucleolysis, relief of leg pain is immediate; however, in up to 30% of patients, maximal relief of symptoms may take up to 6 weeks. There are some specific measures that can be utilized during chemonucleolysis to reduce the incidence of low back pain which includes infiltrating the needle track with local anesthetic and the use of antiinflammatory medications after the procedure.22 A prospective, placebo-controlled, double-blind, multicenter, crossover trial of 88 patients demonstrated a 73% success rate in the
Section 5: Biomechanical Disorders of the Lumbar Spine
chemonucleolysis group and a 42% success rate in the placebo group The failures in the placebo group later underwent chemonucleolysis and had a 90% success rate.23 The primary end point for considering a patient a failure was if the patient had pain severe enough to consider another intervention for treatment. Nordby et al.17 reported that in a 7–10-year follow-up of 3130 patients with chemonucleolysis, overall satisfactory results were reported from 71–93% among the 13 contributors for an average of 77%. The use of chymopapain has been greater in Europe and Australia than in the United States since the acute transverse myelitis scare, and intrathecal complications have been rare there. A combined long-term report of 1736 patients in 1992 from the United Kingdom, France, and Germany showed good to excellent results of 66–84%, with an overall average of 75.3%. A prospective, randomized, controlled trial comparing automated percutaneous lumbar discectomy (APLD) to chemonucleolysis for the treatment of sciatic pain reported a 1-year outcome of 66% success in the chemonucleolysis group and 37% in the APLD group.24 The most compelling evidence that chemonucleolysis is a safe and effective treatment for herniation of the nucleus pulposus is found in well-designed and conducted prospective, randomized, double-blind studies in the United States and Australia.25 One of these double-blind studies has been carried through for 10 years without code break or loss of follow-up. Success persisted in 77% of patients with chemonucleolysis compared with only 38% for the placebo group (p=0.004). Only six of the patients with chemonucleolysis had required laminectomy compared with 14 in the placebo group (p=0.028). Launois et al.26 reported the success rate at 1 year for chemonucleolysis at 88% and for laminectomy at 76%. Chemonucleolysis continued to be superior to surgery after an additional year. In a 9–11-year prospective, randomized study comparing patients with these two methods, Wilson et al.27 concluded that ‘surgically treated patients that had done well initially deteriorated with time, whereas those who did well following chemonucleolysis maintained a successful outcome in the long-term cost savings.’ A major consideration in cost savings is the absence of epidural scarring or adhesive arachnoiditis with chemonucleolysis, thus avoiding the frequent ‘failed back syndrome’ seen with laminectomy, which has become an ever-increasing health and economic burden.28 When the results of surgery after chemonucleolysis failure were compared with the results from microdiscectomies performed without prior injections, slightly more good and excellent results were observed in the primary surgery patients.29 Other authors such as McCulloch and MacNab30 stated that open surgery was easier after prior chemonucleolysis. Norton31 obtained very poor results in patients treated either surgically or with chymopapain. All of his patients were claiming workmen’s compensation. Others have shown that on treatment with chymopapain such patients do not respond as well as those who are more highly motivated and covered by private insurance. Nordby and Wright32 reported that 45 studies were analyzed, some including comparisons of chemonucleolysis to open laminectomy/discectomy and others to percutaneous discectomy. Individual success rates exceeded 60%, whereas cohort total averaged 76%. In studies comparing chemonucleolysis with open discectomy, success rate averaged 76.2% as compared with 88% for open surgery. In two other studies, percutaneous discectomy was less successful than chemonucleolysis. Where included, duration of hospitalization showed less time and thus less costs for chemonucleolysis. Return to work compilations showed time off slightly less for chemonucleolysis than for laminectomy. Wittenberg et al.13 reported a 5-year clinical follow-up assessment of a prospective, randomized study of chemonucleolysis using chymopapain (4000 IU) or collagenase (400 ABC units); patients in the chymopapain group started work in the same job an average of
8 weeks after injection, whereas patients in the collagenase group returned to work after an average of 11 weeks. Kim et al.19 reported that three thousand patients with herniated lumbar disc were treated with chemonucleolysis between 1984 and 1999 and found that the clinical success rate in their series was 85%. The patient group with the chief complaint of leg pain achieved a better clinical outcome than the patient group with low back pain (88% versus 59%), and a positive straight leg raising test was strongly correlated with good clinical outcome. Patients manifesting a soft, protruded disc had a better outcome than those manifesting diffuse bulging disc. Other prognostic factors favoring a good outcome were young age, short duration of symptoms, and no bony spur or calcification on radiological study. Revel et al.33 conducted a randomized clinical trial to compare the results of automated percutaneous discectomy with those of chemonucleolysis in 141 patients with sciatica caused by a disc herniation; 69 underwent automated percutaneous discectomy and 72 were subjected to chemonucleolysis. The principal outcome was the overall assessment of the patient 6 months after treatment. Treatment was considered to be successful by 61% of the patients in the chemonucleolysis group compared with 44% in the automated percutaneous discectomy group. At 1-year follow-up, overall success rates were 66% in the chemonucleolysis group and 37% in the automated percutaneous group. Within 6 months of treatment, 7% of the patients in the chemonucleolysis group and 33% in the discectomy group underwent subsequent open surgery. The complication rates of both treatment groups were low, with the exception of a high rate of low back pain in the chemonucleolysis group (42%). In another prospective study, 22 patients with painful disc herniations were randomized either to chemonucleolysis or APLD; at 2 years the chemonucleolysis-treated patients were significantly better, based upon outcomes as measure with the Oswestry Disability Index, back pain and leg pain recurrence.34 The combination of low-dose chemonucleolysis with 500 IU chymopapain followed by an automated percutaneous nucleotomy of the cervical spine has been performed. A follow-up of at least 1 year of the first 22 patients showed in 19 patients good or excellent results. In one patient a fair result was obtained and in two patients the symptoms were unchanged.35
AUTOMATED PERCUTANEOUS LUMBAR DISCECTOMY Introduction In 1975, Hijikata et al.2 performed the first percutaneous discectomy using modified pituitary rongeurs. A decade later in 1985, Onik and colleagues24 developed the nucleotome, an automated suction shaver that allows for the performance of an automated percutaneous lumbar discectomy (APLD). The shaver functioned by drawing the nucleus pulposus into a small cutting port and eliminated a portion of the nucleus via a reciprocating ‘guillotine-like’ blade. APLD utilized a 20.3 cm needle inserted through a 2.8 mm diameter cannula. Onik and Helms36 reported an 85% success rate independent of the amount of disc material removed. It is believed that the removal of nuclear material from the center of the disc results in disc decompression. Ultimately, it is believed this decreases pressure transmitted through the rent in the anulus to the herniation. This results in decreased pressure on the affected nerve.
Indications Different morphological and pathophysiological parameters are used to define criteria for selecting candidates for APLD. Some clinicians 929
Part 3: Specific Disorders
stress the value of CT discography. Mochida and Arima37 demand the absence of perforation of the posterior longitudinal ligament and degenerative canal stenosis detected by CT or MRI along with other clinical guidelines including age and disturbance of innervated muscles. APLD is efficacious for patients whose herniations are still contained by the anulus or the posterior longitudinal ligament. Patients with sequestered fragments are not candidates because there is no biomechanical mechanism by which that fragments would be resorbed. MRI can be extremely helpful in excluding obviously migrated fragments and large disc extrusions.36 An absolute contraindication of APLD is the migration of a disc fragment. When small degrees of migration are present (3 mm or less) the possibility of a good result from APLD is not precluded. The success rate for APLD is about 43% in those patients who had fragments that migrated more than 3 mm from the disc space. In a study by Carragee and Kim examining outcomes of open discectomy, it had been shown that herniations larger than 6 mm generally did well with discectomy, whereas smaller herniations were associated with a poor outcome (26% success).38 These studies suggest that patients with smaller herniations are ideal candidates for APLD and probably with other techniques that effect percutaneous disc decompression. A CT discogram is the most definitive procedure for selecting patients for APLD which demonstrate complete tears of the anulus and posterior longitudinal ligament. A CT discogram also allows the assessment of the size of the rent in the anulus that is communicating with the herniation. Besides the characterization of the herniation on imaging studies, patients should clinically have the symptoms of radiculopathy.36 APLD is not a procedure for those patients with vague or equivocal symptoms or simply a bulging disc. APLD can be an excellent procedure for patient who has had a reherniation at the site level of previous disc surgery. These patients who are reoperated at the same level obtain lower success rates, as well as being exposed to a much higher morbidity due to lack of tissue planes caused by epidural fibrosis. APLD takes a posterolateral course that avoids the epidural space and does not create epidural fibrosis. Mirovsky and Neuwirth39 reported 10 patients with lumbar disc reherniation at the same level as a previously open operation with follow-up of 2.5 years They report that 70% of their patients showed complete or significant pain relief avoiding reoperation. Sixty percent showed motor deficit improvement. Failure was primarily relegated to those with spinal stenosis or segmental instability. Onik et al.40 reported that patients whose herniations occur in the lateral location beyond the intervertebral foramen are candidates for APLD. Such patients are difficult to treat with the traditional interlaminar approach of microdiscectomy, which requires the removal of all or a large portion of the facet. APLD showed excellent results in those patients because the percutaneous discectomy instrumentation drives over the herniation itself. The poor results occurred in patients with concomitant stenosis.41 ALPD can be the procedure of choice for those patients suspected of infectious discitis. The first principles of treatment for disc space infection are to make the diagnosis and isolate the organism. Diagnosis may be delayed because patient’s complaints are relatively non-specific. Imaging studies may direct one to the diagnosis, but tissue must be obtained for the confirmation and isolation of the organism. APLD biopsy is a minimally invasive procedure for obtaining sufficient material for histological analysis and culture. The rate of secondary surgical intervention may be reduced if infected disc material is removed by percutaneous biopsy; however, surgical treatment is indicated in all patients who develop neurological deficits as well as in the presence of epidural or retroperitoneal abscess.42 930
Gebhard and Brugman43 reported a case in which nucleotome was used to remove 5 ml of disc material and the disc space was irrigated with 75 ml of normal saline containing cefazolin, the patient reported immediate relief of his back and thigh pain. Fouquet et al.44 obtained bacteriologic diagnosis in only nine of 25 patients biopsied with a Mazabraud trocar. Krodel et al.45 reported seven positive cultures of 15 patients who underwent needle biopsy. Yu et al.46 described two cases in which automated biopsy was used to diagnose unusual infections include Candida discitis and tuberculosis. Percutaneous discectomy has been used also in the treatment of cervical disorders. Theron et al.,47 in 1992, reported preliminary experience in 23 cases. All patients complained of neck pain or brachialgia due to single, soft herniated disc at a single level; the success rate was 80%. They later reported 78 treated cases, including 68 with follow-up of at least 6 months and overall success rate of 70.6%, and no complication was reported (Table 85.2).
Complications Complications result from periprocedural issues or from the technique. Periprocedural complications may involve adverse reactions to anesthetic, sedative/analgesic medications, perioperative antibiotic prophylaxis, or intravenous fluid management. Technique-related complications include nerve root injury, discitis, osteomyelitis, cellulitis, uncontrolled bleeding, dural puncture, annular injury, and vertebral endplate injury. Matsui et al.48 reported a rare complication of a case of lateral disc herniation which occurred soon after percutaneous discectomy. In that case, it appeared that the extrusion occurred through the hole in the anulus made during the procedure.
Long-term results Mochida and Arima37 reported that the postoperative pain relief and patient satisfaction that can be achieved by APLD is related to patient age, motor function of the lower limbs, and the length of preoperative
Table 85.2: Contraindications for APLD ABSOLUTE Cauda equina syndrome Sequestered disc fragment Arachnoiditis Pregnancy Profound or rapidly progressive neurological deficit Severe spondylolisthesis Bleeding dyscrasia Spinal instability or fracture Spinal tumor RELATIVE Previous open surgery at proposed treatment level Central stenosis Significant bony spurs that could block percutaneous entry into the disc space
Section 5: Biomechanical Disorders of the Lumbar Spine
conservative treatment. Hijikata49 reported poorer results at the level L5–S1. Others reported that the only significant predictive factor for a positive outcome with respect to pain relief and satisfaction was age. Outcome is also influenced by physical activity. Patients who are active in sports are significantly more satisfied compared to patients who are not, but sporting activity is not in itself a predictive factor for a positive outcome.50 Sahlstrand and Lonntoft51 evaluated the size of the disc herniation with MRI before, on the day, and 6 weeks after APLD and compared the MRI findings with the early clinical outcome. The development of pain, nerve root tension sign, and neurological findings were analyzed and no significant difference in the maximum protrusion of the disc herniation among the three measurements was reported. The sciatic pain improved significantly on the first day after the procedure, but not at 1 week or 6 weeks after the procedure. There was no correlation between the MRI findings and the early clinical outcome. It has been reported that with APLD approximately 2–7 g of human disc has been removed. The amount of disc material retrieved is superior to any the other methods of percutaneous discectomy. In a study by Chatterjee et al.52 comparing APLD with microdiscectomy for contained herniations, the microdiscectomy group had an 80% success rate. The risk of reoperation was reported by Bernd et al.50 to be 25% while Nachemson53 reports that 6.6% of patients in his study required reoperation. Stevenson et al.54 did a cost-effectiveness study of APLD versus microdiscectomy in the treatment of contained lumbar herniation in a randomized, controlled trial and found that APLD is less cost-effective than microdiscectomy. In summary, APLD has a positive effect in patients suffering from pain related to disc herniation. Outcome is influenced by the natural course, patient age, the extent of nerve involvement, and physical activity.
PERCUTANEOUS LASER DISCECTOMY Introduction In 1984, percutaneous laser disc decompression was pioneered in America by Choy et al.,55,56 who were intrigued by the principle that a small change in volume in a contained area results in a large change in pressure. This pressure reduction was demonstrated by Choy and coworkers in 18 cadavers. They measured intradiscal pressure using a pressure transducer that was inserted into the lumbar discs. Afterwards, 1000 J from an Nd:YAG, 1.32-ym laser was delivered through a quartz fiber. The mean intradiscal pressure after loading (pre-treatment) was 2419 mmHg. After laser treatment, the mean pressure decreased by 1073 mmHg, a decrement of 44%. The laser (Light Amplification by Stimulated Emission of Radiation) transmits energy in the form of light. This light is transformed into heat, which can simultaneously cut, coagulate, and vaporize tissue. The primary advantage of laser energy is its ability to focus at a single point. Several types of laser are available. The most commonly used are the KTP laser (potassium-titanyl-phosphate), Nd:YAG (neodymium:yttrium-aluminum-garnet) and Ho:YAG (holmium:YAG). The choice of laser type is dependent on the ability of energy to be delivered through a fiberoptics system, tissue absorption/ablation properties, and the amount of thermal generation and spread.57 Hellinger et al.58 reported that percutaneous laser discectomy with the Nd:YAG laser (1064 nm) markedly reduces the postoperative density by 20% in protrusion and extrusion of the intervertebral discs. Percutaneous laser discectomy of the cervical disc herniation spine can be done under X-ray fluoroscopy. CT-guided technique also provides safe and accurate position of the needle tip during puncture of the needle on axial images, permitting accurate laser ablation of the
intervertebral disc. The use of CT also avoids damage to adjacent and visceral structures since it is superior in spatial and soft tissue resolution to X-ray fluoroscopy (Table 85.3).59 Ohnmeiss et al.57 found that patients who met the following criteria, which included leg pain, positive physical examination finding, discographic confirmation of contained disc herniation, and no stenosis or spondylolisthesis, found that the success rate was 70.7% and the success rate was only 28.6% among patients who did not meet all the criteria. The advantage of performing discography immediately before laser disc discectomy is that it could be performed through the same needle placement to be used for the laser discectomy. The advantage of performing discography 1 or more days prior the laser discectomy that it allows more time to evaluate the discogram results and increases the allotted time for a patient to consider alternative treatments. The contraindications of this procedure are paralysis, hemorrhagic diathesis, spondylolisthesis, spinal stenosis, previous surgery at the indicated level, significant psychological disorders, significant narrowing of disc space, and industrial injuries with monetary gain. For 2 weeks after the procedure, any position that could induce hyperkyphosis as well as athletic activities should be restricted.61 The use of percutaneous laser disc decompression for the treatment of erectile dysfunction caused by herniated disc disease has been reported in two patients.62 In addition to the early return of the erectile function in both patients, immediate pain relief was achieved in the second case. Follow-up visits confirmed continued normal sexual function and lack of pain.62
Complications Choy et al. reported one case of discitis. Bosacco et al.63 reported one minor complication involving a single patient, who had acute urinary retension and reflex ileus, out of 63 patients who underwent laser disc decompression with KTP 532 laser. There were no complications involving infection, hematoma, neurological injury, myelitis, or great vessel disease. Nerubay et al.64 reported complications with symptoms and signs of root irritation in 4 of 50 patients who underwent CO2 laser discectomy which were probably caused by thermal damage to the root caused by warming the cannula. Ohnmeiss et al.57 reported
Table 85.3: Contraindications for percutaneous laser discectomy ABSOLUTE Central stenosis Significant bony spurs that could block percutaneous entry into the disc space Facet hypertrophy Sequestrated disc fragment. Ruptured posterior longitudinal ligament ( epidural leak of contrast medium in discography) RELATIVE Progressive neurological deficit Involvement in workers’ compensation cases Previous surgery at the same disc level
931
Part 3: Specific Disorders
one case of reflex sympathetic dystrophy and 12 cases of postoperative dysesthesia among 164 patients who underwent leaser disc discectomy. Hellinger65 reported bowel necrosis, subsequently requiring resection, resulting from inadvertent perforation of the anterior anulus and two cervical cases of infections with succeeding neurological deficits. In one case there was a reversible paresis of the arm and in the other case there was paraplegia. Hellinger and Hellinger describe their outcomes and complications in greater detail in Chapter 29.
Long-term results Percutaneous laser discectomy has been performed on both cervical and thoracic disc but the numbers are so small as to make their reporting anecdotal. The advantages of laser discectomy include short recovery time, it is performed under local anesthesia, it reduces the soft tissue and bone injury, there is no epidural fibrosis, lessened chance of creating instability since only a small amount of tissue is removed, and reduced missed time from work.57 Disadvantages include the relative expense of the procedure and inadequate temperature control causing nerve root, vertebral body, and endplate damage.73 Choy et al.67 reported the results of 333 patients in whom they performed laser discectomy with the Nd:YAG laser and obtained 78.4% good results and poor responses for 21.6%. One hundred and sixty patients experienced immediate pain relief during the procedure. Choy also reported in another study that there is no association between outcome and sex, age, duration of symptoms, or disc level.74 Liebler60 reported that the success rate of the KTP laser based on 2 years’ follow-up was 72% and the success rate with the Nd:YAG laser was very similar, at 70%. For all patients, the average overall pain index declined immediately after the procedure. Pain intensity had a tendency to decrease as the duration of the follow-up continued, but this was not the case for the neurological findings. There were no statistical differences noted in knee jerk, ankle jerk, pin prick and Lasague’s sign as a function of disc level and follow-up for all patients. Nerubay et al.66 reported the results of 50 patients in whom they performed laser discectomy with the carbon dioxide laser and obtained 74% good results. Chronic effects of laser discectomy have been evaluated in animals. Using a CO2 laser for cervical discectomies in a canine model, Gropper et al.69 found that the disc, easily and safely ablated, was replaced by dense, fibrous tissue in 10 weeks. Using Ho:YAG laser, Black et al.70 noted a similar effect in pigs. Laser discectomy yields results comparable to those of manual or automated percutaneous discectomy,47 but is considerably more expensive. Percutaneous laser nucleolysis can damage endplates from excess thermal energy,66 and also has been shown to be significantly less effective than chemonucleolysis.71 Dangaria72 reported 15 cases where laser was used as a second attempt to relieve the symptoms of lumbar disc herniation in patients having undergone prior percutaneous discectomy with unsuccessful outcome. He found that only three out of 15 patients had good results, while none had excellent results. Chiu et al.73 reported that cervical discectomy with laser thermodiscoplasty is safe and effective for the treatment of cervical disc herniation. A 94.5% success rate was obtained in 200 patients selected through diagnostic MRI, CT, and electromyogram (EMG) correlated with signs and symptoms. Knight et al.74 also reported that cervical laser disc decompression produces sustained and significant clinical benefit in over 51% of patients observed for a mean period of 43 months. In a further 25%, functional benefit was achieved. Paresis, sensory deficits, neck pain, brachialgia, and headache improved considerably in most patients. 932
NUCLEOPLASTY (COBLATION) Introduction Coblation is a new minimally invasive procedure, using radiofrequency (RF) energy to remove nucleus material and create small channels within the disc. With coblation technology, RF energy is applied to a conductive medium, causing a highly focused plasma field to form around the energized electrodes. The plasma field is composed of highly ionized particles. These ionized particles have sufficient energy to break organic molecular bonds within tissue and form a channel. The by-products of this non-heat-driven process are elementary molecules and low molecular weight inert gases, which are removed from the disc via the needle. On withdrawal of the Perc-DC® Spine Wand, the newly created channel is thermally treated, producing a zone of thermal coagulation. Thus, nucleoplasty combines coagulation and tissue ablation to form channels in the nucleus and decompress the herniated disc. The temperature is kept below 70°C to minimize tissue damage. Unlike chemonucleolysis, nucleoplasty is not dose dependent, and pressure changes seem to occur quicker. Chen et al.75 assessed the intradiscal pressure change after disc decompression with nucleoplasty in human cadavers, and found that intradiscal pressure was markedly reduced in the younger, healthy disc cadaver. In the older, degenerative disc cadavers, the change in intradiscal pressure after nucleoplasty was very small. There was an inverse correlation between the degree of disc degeneration and the change in intradiscal pressure. The limitation of this study was that pressure measurements were performed on cadavers and not in vivo. Chen et al.76 also reported that after histological examination of disc and neural tissue in two pigs that underwent coblation there was no evidence of direct mechanical or thermal damage to the surrounding tissues and there were clear evidence of coblation channels with clear coagulation borders of the nucleus pulposus. Normal histological findings of the anulus and endplate with normal neural elements of the spinal cord and nerve roots at the level of the procedure were observed. Since its first application in July 2000, the DISC Nucleoplasty procedure has been used to treat over 55 000 patients in the USA and around the world. Other techniques used for percutaneous disc decompression have suffered from the following limitations: Removal of too much tissue – Decompressing the disc in most cases requires the removal of only a small amount of tissue. Excessive tissue removal can cause the disc to lose height, possibly leading to disc degeneration. DISC Nucleoplasty allows controlled removal of a precise amount of tissue by the surgeon. Indiscriminate removal of tissue – removing tissue beyond a small, targeted area can cause injury to the anulus of the disc, or to other surrounding structures in the spine. DISC Nucleoplasty provides the surgeon with full control over which tissue is removed. Thermal injury to the disc – high temperature (>100°C) tissue removal systems (including laser) remove tissue by exploding molecules with extreme temperatures, but with the result that remaining tissue can be severely burned or charred. This is particularly of concern in the disc where there are no blood vessels to allow necrotic tissue to be resorbed into the body. DISC Nucleoplasty does not rely on heat for tissue removal, and does not introduce excessive heat to cause such tissue damage in the disc. Aggressive access into the disc – introduction of large instruments into the nucleus of the disc can cause irreparable damage to the anulus. Such damage has been shown to lead to the onset or acceleration of disc degeneration. DISC Nucleoplasty uses a small 17-gauge needle to access the disc; no technique uses a narrower needle to decompress the disc.
Section 5: Biomechanical Disorders of the Lumbar Spine
Coblation can be performed from either side of the affected disc, not just from the ipsilateral, symptomatic side. Thus, treatment approaches are not limited to one site only.
Indications The inclusion criteria for cervical or lumbar coblation are leg and back pain with MRI evidence of contained disc protrusion with a disc height >50%, after failed medical rehabilitation, and interventional spine therapy for 4 weeks. The exclusion criteria are disc height 50 years of age demonstrate degenerative SIJ changes on plain radiographs,21,22 and similar degenerative findings in aging asymptomatics have been demonstrated utilizing computed tomography (CT) imaging.23 Similarly, no specific pathology has been described in patients undergoing surgical intervention for chronic sacroiliac joint pain.24 Sacroiliac joint pain referral patterns often localize to the sacral sulcus and buttock,12 but patients can also describe symptom referral to the medial thigh and groin,13,25–28 posterior thigh, and calf.9,13,29–31 Physical exam maneuvers utilized to detect motion irregularities have demonstrated poor intertester reliability32,33 and have been
observed to be positive in 20% of asymptomatics.34 The detection of joint motion abnormalities by physical examination,29 response to pain provocation tests such as Faber’s and Gaenslen’s maneuvers,17,29,35 and historical findings13,29 have all correlated poorly with the response to fluoroscopically guided diagnostic intra-articular injections, which have come to be recognized as the gold standard for diagnosing SIJ pain. As specific history, examination, and imaging findings have all correlated poorly with a positive response to a diagnostic intra-articular injection, it is more likely a combination of presenting factors which might lead the treating clinician to suspect the SIJ as an active pain generator and warrant introduction into the SIJ diagnostic and therapeutic algorithm. Suggestive symptoms include pain predominantly below the L5 level in the region of the sacral sulcus, with or without referral to the groin13 or more distal lower limb, and sacral sulcus tenderness to palpation.29,35,36 Additionally, patients with unilateral symptoms and a positive response to multiple provocative maneuvers may be more likely to demonstrate a positive diagnostic injection response and subsequently benefit from targeted therapeutic approaches.29,35,36 While a previous history of a fall upon the affected buttock, recent pregnancy, pelvic trauma, or an antecedent gait alteration37 also prompt this author to consider the SIJ as a pain generator, these historical points have not been demonstrated to be predictive by the available literature. For those patients who are believed to be reasonable candidates, an algorithmic approach to the SIJ (Fig. 89.2) can be initiated and a confirmatory diagnostic SIJ injection performed. Diagnostic intraarticular injections were initially described in 1938,38 and the utilization of fluoroscopic guidance was first introduced in 1979.39 It has been estimated that successful intra-articular SIJ entry is achieved in only 22% of injections performed without image guidance,40 and such blind injections performed for either diagnostic or therapeutic purposes are not included in an algorithmic approach to SIJS. Given the complexity of the anatomy and configuration of the SIJ, it would seem that this 22% figure may even be an overestimate, further amplifying the requirement of using fluoroscopic guidance. If a positive response to a guided diagnostic injection is realized, therapeutic injections should follow. Therapeutic SIJ corticosteroid injections have been advocated as an appropriate treatment for patients with persistent SIJ pain.41 A retrospective and uncontrolled study of SIJ injections in 31 patients with chronic pain of SIJ origin has suggested a lasting resultant improvement in pain, work status, and disability.42 The efficacy of these injections has been more clearly demonstrated, both prospectively and retrospectively and in a controlled fashion, in the seronegative spondyloarthropathy population.43,44 The mechanism of action of injections in patients with presumed SIJS outside of the spondyloarthropathy population remains less clear, but is presumed to arise from the well-known antiinflammatory properties of corticosteroids.28,45 The role of inflammation in SIJS remains unconfirmed. The role of injection therapy in this patient population therefore remains poorly defined. Injection therapy can be combined with a targeted physical therapy regimen which emphasizes pelvic stabilization techniques and SIJ-specific therapies. For those patients who fail to respond to therapeutic injections, a more recently described and evolving radiofrequency denervation approach to the SIJ might then be considered. The nerves which can be targeted for this approach include the L5 dorsal ramus and the lateral branches of S1–3.46 The ability to reliably target and anesthetize these nerves with fluoroscopic guidance remains less clear.47 In those patients who demonstrate a positive diagnostic response to anesthetization of these innervating branches or who demonstrate a concordant response48 with lateral branch stimulation, a denervation procedure can be trialed. The ability of such a denervation approach to successfully anesthetize the SIJ remains less clear with only 977
Part 3: Specific Disorders SIJ suspected as primary pain generator
Fluoroscopically guided diagnostic SIJ injection
Negative response
Positive response
Consider alternative pain generator
Therapeutic fluoroscopically guided SIJ injections performed in conjunction with targeted SIJ/pelvic stabilization therapies
Persistent pain
Satisfactory outcome: algorithm concluded
Consider fluoroscopically guided diagnostic L.5 dorsal ramus and sacral lateral branch block
Negative response
Positive response
Radiofrequency denervation procedure of dorsal ramus and lateral branches
Persistent pain
Satisfactory outcome: algorithm concluded
Confirmatory fluoroscopically guided diagnostic intra-articular SIJ injection
Negative response
Positive response
Consider alternative pain generator
SIJ arthrodesis
Satisfactory outcome: algorithm concluded
Persistent pain
More chronic pain management paradigm
978
Fig. 89.2 General algorithmic approach to the sacroiliac joint.
Section 5: Biomechanical Disorders of the Lumbar Spine
small and uncontrolled studies suggesting a significant therapeutic response.49–52 For those patients with persistently debilitating SIJ pain who either fail to respond to denervation techniques or who demonstrate an initial negative response to L5 dorsal ramus and sacral lateral branch anesthetization, surgical arthrodesis of the SIJ can be considered as a final treatment option.50,53 In selecting candidates for SIJ fusion, those patients who demonstrated both a positive lateral branch response and an initial diagnostic intra-articular injection may be considered less likely to be false-positive SIJ patients. In these cases, it would appear that a confirmatory diagnostic injection has been employed to lessen the likelihood of an initial placebo response. As the approach to and efficacy of lateral branch anesthetization remains less well defined, any patient contemplating SIJ fusion should first demonstrate a second positive response to a confirmatory diagnostic intra-articular injection utilizing an anesthetic of different duration or a blind and placebo-controlled diagnostic injection protocol. As well, the candidacy of such individuals for surgical intervention might be further strengthened by a negative response to provocation discography.
ZYGAPOPHYSEAL JOINT The zygapophyseal joints (Z-joints) have been recognized as a potential source of lumbar pain since 1911.54 The lumbar Z-joints are paired synovial joints with an intra-articular volume capacity of 1–2 mm.55 While the more cephalad lumbar Z-joint orientation tends to be in the sagittal plane, the lower joints are more coronally situated.56 Each lumbar Z-joint is innervated by the medial branch of the dorsal ramus at the level of the joint and by the medial branch arising from the dorsal ramus of the next cephalad level.57 In 1976, Mooney and Robertson58 demonstrated that lumbar axial pain and symptoms referred to the extremity could arise from intra-articular injections of normal saline in asymptomatic volunteers. McCall et al.59 later corroborated these findings and observed a more intense pain response with injection into the capsular tissues when compared with injection into the joint’s intra-articular space. Utilizing progressive local anesthesia during surgery, Kuslich et al.60 demonstrated a pain response with stimulation of the Z-joint capsule, but the pain described by patients was often not concordant with their more debilitating axial pain. Z-joint pain, or ‘facet syndrome,’ is presumed to arise from osteoarthritic change, chondromalacia, or occult fractures.61–66 Less common conditions affecting the Z-joints including infection, ankylosing spondylitis, and villonodular synovitis have also been reported.67,68 Lumbar Z-joint fractures, capsular tears, hemorrhage, and cartilaginous injury have been observed in postmortem studies of trauma patients with normal radiographs.66 A study of 176 consecutive patients presenting with chronic lumbar pain, in which lidocaine and confirmatory bupivacaine medial branch or intra-articular diagnostic injections were employed, suggests that the Z-joint represents the primary pain generator in 15% of cases.69 Plain radiographs often reveal degenerative arthrosis of the Z-joints which strongly correlates with age, but not with symptoms of axial pain.70,71 Utilizing diagnostic intra-articular injections, degenerative Z-joint change detected by CT imaging has also demonstrated a poor correlation with pain arising from the lumbar Z-joints.72 Several studies73–75 have specifically investigated the historical and physical examination findings which might predict the Z-joint as a pain generator. In one of these studies74 a second and confirmatory diagnostic Z-joint injection was included to establish a diagnosis, and in two73,75 a positive response to only a single diagnostic injection was utilized. Patients with confirmed primary Z-joint pain were noted to describe lumbar discomfort, but pain could similarly be referred to the lower limb. Patients generally did not describe central lumbar
pain. While no particular symptoms or historical findings demonstrated a significant correlation with a positive response to diagnostic injections, patients with Z-joint pain tended to be older, without exacerbations during coughing, and without described provocation with forward flexed postures. The L5–S1 Z-joints were found to be more likely symptomatic than L4–5, with pain arising from the L3–4 and L2–3 joints much less commonly observed.69 While eliciting a concordant pain response by direct articular palpation has been described as a potential screening mechanism in patients with suspected Z-joint pain,61 the utility of this examination technique was not clearly substantiated by the aforementioned studies. Deciding which patients to introduce into the Z-joint algorithm presents a challenge to the treating clinician quite similar to that described in patients with SIJS. Radiographic evidence of degenerative change is typically not a reliable indicator, and historical and physical examination findings do not clearly correlate. As in the case of SIJS, it is neither practical or economical to subject each patient with chronic axial pain to a confirmatory diagnostic injection without a reasonable clinical suspicion. Older patients, i.e. greater than 60 years of age, presenting with uni- or bilateral axial lumbosacral pain, and with an absence of provocation during flexion and coughing, may be more likely to demonstrate pain of Z-joint origin. In the author’s practice, a Z-joint pain generator is more suspect in older patients who describe pain which is most reliably provoked by standing, ambulating, or ipsilateral extension, and relieved by sitting. These latter historical features are not supported as clearly reliable by the available literature. In the patient with suspected Z-joint pain, an algorithmic approach can be initiated (Fig. 89.3) and a confirmatory diagnostic intra-articular injection performed.69,74 There is no standard protocol for the selection of joints to anesthetize. It has been suggested that the joints with maximal tenderness during palpation can be marked and identified under fluoroscopic inspection. Alternatively, in patients with unilateral lumbosacral pain, the L4–5 and L5–S1 joints can be investigated. If more isolated posterior element arthrosis is observed radiographically, a single joint can be studied. In patients with bilateral lumbosacral pain, these joints can be bilaterally addressed in a diagnostic fashion. If the diagnostic response from the L4–5 and L5–S1 injections is negative and a midlumbar pain complaint is reported, the L2–3 and L3–4 joints can then be studied in a similar coupled and unilateral or bilateral fashion. If the patient presents with midlumbar rather than lumbosacral pain, the L2–3 and L3–4 joints might be studied first. In the author’s practice, while a radiographic correlate to Z-joint pain has yet to be defined, MRI or CT scan evidence of more advanced arthrosis is also considered in selecting joints for further study when these imaging findings correspond to the patient’s pain location. Following a positive diagnostic response, therapeutic intra-articular injections could follow. Similar to the treatment of SIJS, the therapeutic response arising from intra-articular injection with corticosteroid has not been more definitively revealed by controlled studies, and an inflammatory injury component has only been theorized. While intra-articular effusions can be observed on MRI, histologic studies have not revealed inflammatory cells in patients with spondylotic joints.61 Similarly, clinical studies have yet to identify a therapeutic effect from intra-articular injections in patients with inflammatory rheumatologic spinal conditions.61 A randomized, controlled study investigating the therapeutic benefits of intra-articular methylprednisolone, utilizing an initial single diagnostic injection screen and an intra-articular saline control, have suggested up to 46% of patients can realize significant pain relief at 6 months’ follow-up.76 Open and uncontrolled studies of fluoroscopically guided intra-articular injections suggest an 18–63% therapeutic effect for more than 6 months following injection.61,77–80 979
Part 3: Specific Disorders Zygapophyseal joint suspect as primary pain generator
Fluoroscopically guided diagnostic intra-articular z-jt injection
Negative response
Positive response
Consider alternative pain generator
Therapeutic fluoroscopically guided intra-articular Z-joint injections performed in conjunction with manual or mechanical spine rehabilitative therapies
Persistent pain
Anatomy prevents successful intra-articular injection
Satisfactory outcome: algorithm concluded
Diagnostic medial branch block followed by confirmatory diagnostic injection with second anesthetic or placebo controlled diagnostic screen
Confirmatory medial branch block
Positive response
Negative response
Radiofrequency denervation procedure to address innervating medial branches/branches
Persistent pain
Consider alternative pain generator
Satisfactory outcome: algorithm concluded
Consider more chronic pain management paradigm Fig. 89.3 General algorithmic approach to the zygapophyseal joint.
Pain relief realized following intra-articular injection might provide a window of opportunity to progress the patient in a spine rehabilitation program and graduate mechanical and manual therapies. If the patient failed to realize relief following therapeutic intra-articular injections or spondylotic anatomy prevented the performance of a diagnostic intra-articular injection, a diagnostic medial branch block81 could be utilized to confirm a diagnosis of Z-joint-mediated pain. In the setting of a positive response to medial branch block, radiofrequency neurotomy can be considered. In the patient who initially demonstrated a positive response to an intra-articular injection, the medial branch block can serve as a confirmatory diagnostic measure. For patients in whom a diagnostic intra-articular injection was not previously performed, a positive response to medial branch block should be confirmed with an additional diagnostic screen to address 980
the estimated 38% false-positive response rate with single uncontrolled blocks.74 A second and confirmatory medial branch block can be performed with a local anesthetic of different duration of action. In this scenario, the patient’s analgesic response with each test should correlate with the duration of action of the anesthetic utilized. Alternatively, the confirmatory injection can be performed with an informed patient in a blind fashion with either a saline placebo or anesthetic injected and the patient monitored for an appropriate response. The difficulty with employing local anesthetics of different duration is that the patient is required to accurately record and communicate their pain response over a period of hours which extends beyond the time spent in the office of the evaluating team. Additional response interpretation difficulties can arise in the patient who describes marked symptomatic relief after the injection of the
Section 5: Biomechanical Disorders of the Lumbar Spine
longer-acting anesthetic, but whose response does not last for as long as one would predict based upon the agent’s half-life. To avoid these confounding factors, only shorter-acting anesthetics can be utilized and the response assessed in the office setting by an independent observer. Patients who demonstrate a positive response to either variant of this double diagnostic screen can then be considered for medial branch radiofrequency denervation. While radiofrequency denervation represents a minimally invasive approach to the patient with chronic posterior element pain and localization of the innervating medial branches appears to be reliable, outcome studies are limited. Modest therapeutic responses have been described, uncontrolled small patient populations have been studied,82 and such procedures likely need to be repeated to offer sustained relief as reinervation to the painful joints can occur. A double-blind, controlled study of radiofrequency denervation versus sham lesions which employed a single diagnostic injection screen revealed only a two-point reduction in visual analog pain scores with the minority of patients realizing complete relief.83 A meticulously designed but small and uncontrolled study of medial branch neurotomy, which included electromyographic assessment of the paraspinal musculature to confirm denervation, demonstrated pronounced relief in 60% (n=9 of 460 initially screened) of patients at 12 month follow-up evaluation.82 If the denervation procedure proves helpful but the symptomatic response wanes, neurotomy can be repeated. A significant response should first be realized for at least 6–12 months.82 For those individuals with persistent axial pain of Z-joint origin which fails to improve despite the aforementioned therapies, surgical intervention in the form of posterolateral fusion should be considered only with great caution. While studies have yet to address the success of this approach in patients with Z-joint pain confirmed with a double diagnostic screen, the available literature does not suggest a correlation between posterior element pain and successful outcomes following fusion.84–86 While it may be tempting to assume that posterior element pain can be relieved by fusion, this has yet to be demonstrated. The potential remains for the fused joint to serve as an ongoing pain generator, as its painful tissue components remain after a typical posterior fusion approach. The possibility also remains that forces continue to be borne, albeit reduced, by the painful posterior elements following posterior stabilization. Finally, as mentioned in the discussion of SIJS, for any patient considered for fusion for Zjoint pain, preoperative lumbar discography, which will be further addressed in the next section of this chapter, should also be considered to rule out a contributing discogenic pain source. Discography also allows the clinician to better evaluate the anatomy and symptom response from adjacent levels. While a positive response to a double diagnostic screen would appear confirmatory for a primary Z-joint pain generator in these chronic cases, the possibility remains, potentially in a minority, that a concordant pain response will similarly be demonstrated during discography.87
INTERVERTEBRAL DISC While the sacroiliac joint and Z-joints are suspected as primary pain generators in a significant but relative minority of patients with persistent axial lumbosacral pain, the intervertebral disc has stood center stage as the most commonly suspected pain generator in patients with both debilitating chronic and more acute axial pain. Mixter and Barr’s 1934 publication described herniated lumbar discs and their relationship to nerve root compressive syndromes.3 In addition to inducing radicular complaints affecting the lower limb, the degenerative disc is also believed to be a common primary pain generator in patients with axial pain. In a study of 92 consecutive patients presenting with
chronic lumbar pain, provocative discography revealed a concordant pain response in 39%, most commonly at L4–5 and L5–S1.88 In a unique study utilizing progressive local anesthesia and selective tissue stimulation intraoperatively, Kuslich et al. demonstrated that while stimulation of the nerve root typically resulted in buttock and lower limb pain, stimulation of the disc, and in particular the anulus, most commonly resulted in a reproduction of the patient’s lumbar pain in a concordant fashion.60 The innervation of the intervertebral disc has been well defined. Abundant nerve endings with a variety of free and complex terminals have been identified in the outer third to half of the anulus fibrosus.89–91 The posterior plexus of nerves responsible for innervating the posterior anulus and posterior longitudinal ligament (PLL) is derived predominantly from the sinuvertebral nerve. The sinuvertebral nerve arises from both the somatic ventral ramus and autonomic gray ramus communicans and also supplies innervation to the ventral dura mater.92 Discitis represents a well-documented and painful condition arising from intervertebral disc infection.93,94 A noninfectious and degenerative condition labeled internal disc disruption describes a painful condition of the intervertebral disc involving a deterioration of the disc’s internal architecture with a relative maintenance of external contour. This mechanical breakdown leads to painful radial fissures which reach the outer third of the anulus fibrosus.95,96 Painful tears in the anulus are also presumed to arise, in the more acute injury setting and independent of a more gradual degenerative cascade, from flexion–rotation-type injuries.92 While abnormalities of the anulus are often not readily identified by conventional imaging techniques, discography and postdiscography CT can reveal abnormal disc architecture and painful annular tears. Advanced imaging of the lumbar spine in patients with suspected discogenic pain typically does not provide confirmatory diagnostic information. Degenerative discs can be observed in 35% of asymptomatic 20–39 year olds, and 36% of individuals older than 60 years of age will demonstrate MRI evidence of disc herniation.97 With such a high incidence of abnormal findings in patients without axial pain, the observation of degenerative discs on MRI is clearly not diagnostic in isolation. Posterior annular tears, also referred to as high intensity zone (HIZ) lesions, are more commonly observed in patients with lumbar pain but can also be observed in up to 24% of asymptomatics.98 When appreciated in symptomatic patients, those discs with HIZ lesions have been observed to be twice as likely to produce a concordant pain response during discography when compared to discs without such lesions. Lumbar MRI findings might be most telling when disc space height and hydration are observed to be well preserved. Discs with a preservation of morphology have been demonstrated to be considerably less likely to be painful.96,99,100 Patients with discogenic pain can describe unilateral or bilateral axial pain with or without symptom referral to the proximal and distal lower limb.88 In a study of patients with discogenic pain confirmed by lumbar discography, historical findings were not shown to demonstrate statistical significance in predicting a discogenic pain source.88 Patients were equally as likely to describe increased pain with sitting as with standing. Additionally, physical examination findings, including increased pain with forward flexion, did not demonstrate statistical significance to predict a discogenic pain source. In assessing patients for possible discogenic pain, the clinician might consider the findings from two previous studies examining intradiscal pressures in healthy subjects assuming various postures.101,102 If the compromised and well-innervated posterior anulus is presumed to be the primary pain generator in patients with discogenic pain those positions or activities which maximize intradiscal pressure may be most likely to lead to annular stress and activation of nociceptive fibers. In these studies, erect sitting has been demonstrated to increase intradiscal 981
Part 3: Specific Disorders
pressure only slightly more than erect standing. Standing in a forward-flexed posture significantly increases intradiscal pressure and to a greater extent than sitting in a forward-slouched fashion. Reclining while seated reduces intradiscal pressure to a considerable extent, but pressure reductions are not as great as those observed while resting supine. The greatest intradiscal pressures are observed while performing lifting maneuvers in a standing and forward-flexed posture. Valsalva maneuver has been demonstrated to increase intradiscal pressure at least as much as sitting in a forward-flexed fashion. Disc pressures are also noted to more than double during evening hours, presumably secondary to bodily fluid shifts which can lead to a morepressurized disc during morning hours. While statistical significance has not been demonstrated for particular historical findings or physical examination maneuvers, the studies of dynamic disc pressures likely offer clues in identifying patients with discogenic pain. In the author’s experience, while Z-joint pain is more likely to be observed in older patients, discogenic pain can present in patients of all ages but is particularly common in the younger patient population, i.e. 18–65 years of age. Patients might describe an initial symptomatic onset following a defined and more stressful lifting or rotational maneuver. The gardening and snow shoveling seasons are particularly common times for patients to present with acute discogenic pain following a defined stressful maneuver, but often the onset of pain is more gradual and incremental. The discomfort is described as a deepseated ache which is at times profound, forcing the patient to unload the spine and assume a supine position. Coughing and sneezing are often described as provocative and in some cases represent the initial inciting event. Patients realize increased pain with sitting, particularly during car travel or while at work or in a theater, and experience relief while resting supine with the lower extremities elevated. Standing and walking are often not as provocative, and bending and lifting maneuvers are typically avoided. Young parents and grandparents often present with axial pain of suspected discogenic origin, presumably secondary to the repetitive lifting and rotational maneuvers performed while caring for their children. Morning hours can be particularly problematic, likely secondary to increased intradiscal pressures following sleep and a prolonged period of recumbency, with a symptomatic decline after a period of ambulation and increased activity. At times, patients will describe a truncal shift, characterized by the torso being visibly and horizontally displaced relative to the pelvis, during symptomatic exacerbations. This antalgic posture is presumed to arise from asymmetric reactive paraspinal contraction and deeper-seated protective mechanisms arising from the activation of nociceptive fibers within a richly innervated and activated discogenic pain generator.103 Pain referral patterns to the lower limbs is also often reported, with such complaints described as poorly localizable, migratory, and less debilitating than the axial pain component. Some patients will even report a distal complaint of burning in the soles of the feet which coincides with worsening lumbar pain during prolonged sitting postures. For a primary mechanical and discogenic pain generator to remain suspect, the physical examination should not reveal neurologic deficits consistent with radiculopathy. While sitting, the patient is often observed to lean rearward upon the elbows in an effort to reduce the more pain-provoking axial load to the spine. With the patient supine, passive pelvic rocking, during which the examiner maneuvers the patient’s lower limbs while passively flexed at the hips and knees, may prove provocative through the introduction of a torsional load to the intervertebral discs and a painful posterior anulus. Sustained hip flexion maneuvers, during which the patient actively flexes the hips while supine with the knees extended, is also often provocative. The response to this maneuver is often most notable as the limbs are allowed to slowly descend toward the exam table surface, presum982
ably by simulating a valsalva-type maneuver with a resultant increase in intra-abdominal pressures. Sustained hip flexion or pelvic rocking may be more likely to be positive when the painful segment is at the L4–5 and/or L5–S1 levels, and may be less reliable for more cephalad segments. Pain is often reproduced with pressure applied over the lower lumbar spinous processes. In the author’s experience, standing with active forward flexion at waist with the knees extended most often reproduces axial pain in a concordant fashion. At times, transitioning from the flexed to neutral posture is the most pain-provoking maneuver. While standing extension is classically believed to be relieving, and is often observed to be so clinically, some patients will describe similar if not more intense pain during active extension maneuvers. A McKenzie approach to patient assessment has also been demonstrated to be fairly reliable in detecting pain of discogenic origin.104 Through such mechanical assessment, patients who realize symptom centralization or peripheralization following repetitive movements have been demonstrated to be more likely to demonstrate a symptomatic disc during lumbar discography. For those patients with persistent lumbosacral axial pain of suspected discogenic origin, an algorithmic approach (Fig. 89.4) can be initiated and epidural corticosteroid injections trialed. A plethora of literature, which will be more completely detailed in the appropriate chapters of this text, has described the role of transforaminal epidural injections in patients with radicular syndromes. Many uncontrolled studies,105–108 and more recently a meticulously designed randomized, prospective double-blind, controlled study1 have demonstrated the successful treatment of radiculopathy with transforaminal injection therapy. Transforaminal injections performed with fluoroscopic guidance allow for the most reliable means of administering corticosteroid to the ventral epidural space where the posterior anulus, PLL, spinal nerve, and ventral dura mater reside.109 Corticosteroids are believed to offer relief in patients with radicular syndromes by addressing the biochemical and inflammatory component of radiculopathy which has been extensively described in the literature and which will be more completely detailed in the chapters of this text addressing the pathophysiology of nerve root injury.110,111 The utilization of epidural corticosteroids in the treatment of axial lumbosacral pain, without a radicular component, is more speculative as the biochemical and inflammatory component of discogenic pain has yet to be as convincingly demonstrated.92 The pain generating processes at play in the patient with axial discogenic pain may arise from a prevailing mechanical insufficiency.112,113 Clinical studies investigating the role of epidural steroid injections have suggested but not clearly demonstrated success in the treatment of primary axial pain.114–116 The transforaminal injection approach offers the most direct means reaching the posterior anulus. Unlike the treatment of an inflamed spinal nerve where circumferential bathing of the target can be achieved, the possibility remains that the pain-generating fibers of the degenerative disc are not in direct contact with the epidural space. Alternatively, one might theorize that in the setting of a painful and incompetent anulus a component of the pain-generating process arises from the spillage of inflammatory mediators. This could lead to irritation of ventral spinal tissues such as the dura and PLL which are in intimate contact with the affected disc and are more accessible by transforaminal injection. In this author’s practice, due to concerns of iatrogenic discitis, an inability to isolate the painful disc without more interventional diagnostic measures, and a lack of supportive literature,117,118 intradiscal steroids are not offered in the treatment algorithm for discogenic pain. In the patient with a suspected discogenic pain source who presents with central or bilateral lumbosacral symptoms and an MRI which reveals multilevel, i.e. L3–4 through L5–S1, degenerative disc disease, a bilateral S1 transforaminal injection is performed. This
Section 5: Biomechanical Disorders of the Lumbar Spine Suspect persistent axial pain of discogenic origin
Fluoroscopically guided transforaminal injection therapy targeting suspected symptomatic disc(s) either bilaterally or unilaterally – can be performed in conjunction with a mechanical therapy program and spine stabilization techniques
Improved Discharge to home exercise program with appropriate postural precautions
Symptoms persist
Lumbar discography (can follow with post-discogram CT) scheduled in conjunction with pre-surgical psyche screen
Abnormal psychometric scores
Refer for appropiate consultation and psychological care
Negative
Positive one or two levels with relative preservation of disc height (i.e. 80%)
Positive one or two level with more advanced loss of disc height
IDET
Surgical stabilization with inclusion of inter-body fusion at symptomatic levels (or consider evolving technologies such as disc replacement therapy)
Symptoms persist
Consider alternative pain generator
Greater than two level positive response
Chronic, interdisciplinary pain management approach
Symptoms persist Fig. 89.4 General algorithmic approach to the intervertebral disc.
approach is offered in an effort to achieve a multilevel disc bathing effect through a cephalad push of injectate. If isolated degenerative change or a central contained protrusion with an annular tear is noted at L4–5 and disc morphology is preserved at L5–S1, a bilateral L5 transforaminal injection can be performed in an effort to maximally target the L4–5 disc. When targeting a particular disc in a unilateral or bilateral fashion, the foramen of the next caudal disc space is utilized for entry, as medication tends to spread in a cephalad fashion. No more than two injections are performed during a single procedural visit. In the patient with unilateral pain and two-level disc disease, i.e. L4–5 and L5–S1, an ipsilateral S1 and L5 injection approach is performed. Injection therapy can be offered in conjunction with a diagnosis-specific physical therapy program coordinated by a skilled therapist. In the author’s practice, success has been realized when such therapy is directed by a McKenzie certified or experienced mechanical therapist. The rehabilitation regimen should emphasize postural training, truncal strengthening, work ergonomics, and
patient education, rather than promote a more passive and modalitybased approach.119 For the patient with persistent and debilitating axial pain following an injection trial, lumbar discography and postdiscography CT imaging can be considered. The discogenic pain algorithm varies in this regard, as more-definitive diagnostic measures are deferred until initial treatments fail. We proceed in this fashion, as the majority of patients will ultimately not require discography, which is a more invasive approach than the injections previously described. A few important highlights regarding discography are warranted, as the chapters by Richard Derby and Mike Furman cover the topic in superb detail. A commonly referenced 1968 study by Holt120 raised concerns as a 37% false-positive provocative discography rate was demonstrated, and discography was labeled an unreliable diagnostic tool. This early investigation has been challenged on several fronts, and a 1990 study by Walsh et al.121 demonstrated a concordant pain response in 40% of discs studied in a small symptomatic group and a 0% false-positive 983
Part 3: Specific Disorders
rate in asymptomatic subjects. Discography remains an imperfect diagnostic tool, and subsequent studies have similarly revealed the potential for a false-positive response and in particular in patients with abnormal psychological profiles.98,122 Despite these shortcomings, discography represents an important diagnostic tool in the algorithmic approach to the patient with persistent axial pain and offers the only current means of identifying symptomatic discs. Provocative discography can be followed by CT imaging to reveal the nuclear morphology of the disc in the axial plane and further characterize the annular tears observed under fluoroscopy. Without discography, the treating clinician attempting to identify the symptomatic intervertebral disc(s) would need to rely solely upon MRI or CT imaging, which previous studies have convincingly demonstrated to be fraught with a high false-positive rate. Using an aggressive technique such as discography is essential at this point in the treatment algorithm, as the subsequent therapeutic options to be considered are among the most invasive, expensive, and controversial offered in spine care. Ideally, discography reveals a single symptomatic disc with two asymptomatic control discs also studied. In the patient with suspected single-level lower lumbar disc disease at L4–5 or L5–S1, a three-level discogram can be performed. If two-level symptomatic disc disease is suspect, i.e. at L4–5 and L5–S1, a four-level study can be performed which investigates L2–3 through L5–S1. Following such studies, if a painful disc is not identified and suspicion remains that a more cephalad disc is symptomatic, a three- or four-level discogram can be performed to investigate the upper lumbar discs. In the setting of negative discography, alternative pain generators should be pursued. In this scenario, the posterior elements or sacroiliac joints might be reconsidered as potential primary pain generators. It is the patient with discogenic pain demonstrated by discography who epitomizes the challenges before the treating spine clinician. In this more commonly encountered group of patients with chronic and persistently debilitating discogenic pain, the likelihood of successful treatment outcomes becomes quite variable. Further interventions for the patient with discogenic pain should be reserved for those with ideally one and no more than two-level disc disease.123–126 In the author’s practice, patients with greater than two-level disease are not considered appropriate candidates for further intradiscal or surgical therapies. These individuals are directed toward a chronic and interdisciplinary pain modulation approach. In conjunction with lumbar discography and prior to further interventions, and in particular in those patients for whom surgical approaches are being considered, psychological factors must be critically assessed through the use of a screening examination. Patients with abnormal psychological profiles are more likely to demonstrate false-positive findings during provocative discography, and contributing psychosocial stressors can ultimately correlate with treatment failure and ongoing disability.122,127–130 Patients with persistent pain and abnormal psychological profiles can be referred for psychological care as a component of an interdisciplinary pain management program. For those patients with one- or two-level positive discograms, intradiscal electrothermal (IDET) annuloplasty might be considered, but recent literature is now suggesting a therapeutic effect quite inferior to that initially suggested by uncontrolled trials. The potential mechanism of action of IDET remains unclear. Pain relief has been speculated to result from a coagulation of nociceptive fibers within the anulus,131,132 sealing of painful annular tears,132 collagen modulation and stiffening,131 or even a disruption of the chemical inflammatory cascade.132 A randomized, placebo-controlled trial of IDET126 has demonstrated no appreciable benefit in 50% of patients treated. Approximately 38% of patients in the treatment group realized greater that 50% pain relief, and 22% demonstrated 75% or greater reduction in pain. While the treatment group demonstrated a 984
statistically significant overall 2.4 point drop (versus 1.1 in the control group) in the visual analog scale (4.2 at 6 months post treatment versus 6.6 at baseline), the clinical significance of this pain reduction remains less clear. The IDET group demonstrated better pain relief and Oswestry Disability Scores than the control group, but improvements in the Bodily Pain and Physical Functioning scores of the SF36 were similar. These modest results were realized in a highly select patient population. Patients were screened for depression, had no prior spine surgery, had no workers compensation claim or injury litigation issues, and demonstrated no greater than 20% loss of disc space height at the treated levels. A second randomized, controlled trial,133 which studied patients with a greater baseline disability level and included workers compensation cases, demonstrated no clinically significant improvements in the treatment group. Scores from multiple outcome instruments were assessed at 6 month follow-up, and no patient was observed to realize what the authors defined as a successful clinical outcome. In those patients with single- or, at most, two-level, disc disease who fail to realize relief from IDET or who are considered poor candidates, i.e. more-advanced loss of disc space height, surgical intervention in the form of fusion can be considered. Uncontrolled outcome studies investigating lumbar fusion procedures have described varying success rates ranging of 39–93%.125,134,135 In a study of posterolateral fusion in patients with positive preoperative discography, an overall 39% good or excellent outcome was observed.125 Of the 23 patients studied, 10 were workers compensation cases, and 90% of these proved to be treatment failures. Additionally, patients out of work for more than 3 months preoperatively demonstrated poor outcomes. A study of 137 patients123 in whom discography revealed abnormal disc morphology and symptom reproduction revealed an 89% clinical success rate following either anterior or posterolateral fusion. This compared favorably to the 52% clinical success rate in patients whose radiographs revealed disc degeneration with negative preoperative discograms. A 10-year follow-up study128 of anterior fusion patients demonstrated significant or complete pain relief in 78%. A retrospective study of four fusion techniques136 suggests that anterior interbody fusion performed in conjunction with posterior fusion and instrumentation results in superior outcomes to both stand-alone anterior interbody fusion and posterolateral fusion with instrumentation. A study investigating the potential role of preoperative pressure-controlled discography in surgical planning137 demonstrated no significant difference in outcomes in patients following either anterior, posterior, or combined surgical approaches. Patients with highly sensitive discs demonstrated superior outcomes following surgical approaches which included anterior interbody fusion when compared to an isolated posterolateral fusion approach. Studies demonstrating superior outcomes following anterior interbody fusion may be consistent with either superior segmental immobilization following anterior surgery138–142 or a greater likelihood of symptom resolution only following resection of the painful intervertebral disc.143,144 At this time, the treatment algorithm ends at surgical fusion. For those patients who choose not to proceed with surgery or for whom such intervention is inappropriate, i.e. three-level disc disease or a medical history which presents too great a surgical risk, a chronic pain modulation approach can be introduced. Patients considering surgical intervention for discogenic pain should also be educated in the areas of evolving treatments and technologies for the treatment of discogenic pain. These approaches are described in greater detail in dedicated chapters within this text and include intervertebral disc replacement,145 disc nucleus replacement,146,147 disc regenerative therapies,148 and perhaps, if such technology should evolve, percutaneous fusion utilizing the introduction of bone growth factors. Ultimately, well-designed and controlled prospective studies should
Section 5: Biomechanical Disorders of the Lumbar Spine
demonstrate the superiority of these treatments to current fusion techniques in terms of clinical success, invasiveness, complications, and cost for spine clinicians to embrace such technology. As there are many exciting avenues of research in the treatment of discogenic pain, this information, along with available outcome data for current treatments, needs to be shared with patients so that they can remain educated and primary decision-makers in the algorithmic approach.
exam not further suggestive of radiculopathy, the differential needs to be expanded. The patient may be experiencing symptoms arising from a symptomatic nerve root, a primary discogenic pain source, or even pain arising from combined pain generators which include an inflamed nerve root dura and dorsal root ganglion without associated or more overt neural dysfunction. The addition of these diagnostic tools might help to further clarify such a patient’s candidacy for introduction into the axial pain generator algorithms.
EXAMPLE CASES
Case 1
Before proceeding with two cases which exemplify the algorithmic approach to the patient with persistent axial pain, a few clarifications will be highlighted. First, when the data from combined prevalence studies is considered, the three pain generators emphasized in the preceding sections may only account for approximately two-thirds of the chronic lumbar axial pain population. As the therapeutic outcomes remain inferior to one’s diagnostic abilities, an even lower percentage of this population is likely to be successfully treated through the algorithms proposed. The algorithms, though, do not only offer a logical approach through which treatment outcomes may be maximized. They also protect the patient and clinician from proceeding along even lower-yield or inappropriate treatment pathways. In this regard, an algorithm may lead the patient along an appropriate, and actually successful treatment pathway but without a more complete symptomatic resolution. Each algorithm has assumed that a detailed history, physical examination, advanced imaging, and other diagnostic studies, such as blood work-up when appropriate, have been performed prior to a more interventional approach. In this author’s practice, such screening has led to the identification of benign osteoporotic fractures, vertebral body fractures arising from metastatic disease, osteomyelitis and discitis, primary and metastatic pelvic lesions, expansile hemangiomas, renal tumors, ruptured ovarian cysts, symptomatic abdominal aortic aneurysms, cholelithiasis and pancreatic disease, and primary symptomatic osteoarthritis or avascular necrosis of the hip. Finally, before proceeding with the cases, a word about a less malignant, but commonly encountered clinical syndrome which needs to be considered when evaluating the patient with ongoing axial pain. Radicular syndromes must always remain in the differential when evaluating the patient with axial pain. Not all lumbosacral radiculopathies present with classic myotomal strength deficits or dermatomal pain distributions.149 While a consideration of radiculopathy is likely less important in the patient with isolated and central lumbar pain, the patient with lumbar pain radiating the buttock, inguinal region, or proximal limb may in fact be presenting with a less pronounced radicular syndrome. These pain distributions can be quite similar to the symptom referral patterns described for the three primary pain generators above. This possible symptom overlap emphasizes the need to perform a detailed history and physical examination. The revelation of a prior component of more distal pain radiation or weakness might provide valuable clues and elucidate a previously more overt radiculopathy. The examination should include a methodical neurologic examination in which bilateral sensation, strength, and reflexes are assessed for symmetry. If suspicion remains high, the examination and history unrevealing, and an isolated compressive lesion is appreciated on advanced imaging, additional diagnostic tools can be employed. Electrodiagnostic studies and diagnostic selective nerve root injections, which will be addressed in dedicated chapters of this text, can be included in the diagnostic algorithm in an effort to more definitively rule out a symptomatic nerve root. In the patient with radiographic evidence of an isolated compressive injury, i.e. posterolateral protrusion to the right at L4–5 with compression of the L5 root, lumbar and buttock pain on the right, and a history and
A 36-year-old woman presented with the chief complaint of lumbar and right buttock pain. Her symptoms began 8 weeks earlier after lifting a carton in her garage and then falling rearward upon her buttocks. She had initially trialed a period of activity modification, but after 2 weeks began a regular regimen of icing and over-the-counter ibuprofen. At the 1-month juncture, with only mild improvement, she visited her internist who diagnosed her with a ‘lumbar sprain’ and prescribed physical therapy and a regimen of naproxen twice daily. Four weeks later, as her symptoms persisted, an MRI of the lumbar spine was ordered, and the patient was referred to the author’s practice. Her pain diagram depicted right lower lumbar discomfort which radiated to the superior and midbuttock without involvement of the more distal limb. She described no significant past medical or surgical history. She complained of pain with prolonged sitting as well as during forward-flexed postures and lifting maneuvers. Her physical examination revealed preserved right lower extremity reflexes at the patella, Achilles, and medial hamstring tendons, intact sensation, and full strength. Active lumbar flexion while standing was pain provoking as were pelvic rocking and sustained hip flexion maneuvers. Sacral sulcus tenderness was appreciated to local palpation on the right but not on the left. Faber’s testing and Gaenslen’s maneuver were also positive on the right side. Her MRI of the lumbar spine was notable only for disc desiccation with preservation of height at L4–5 where a small right paracentral protrusion and annular tear was observed. The protrusion was not noted to compress the evolving right L5 nerve root, and no significant central or foraminal stenosis was appreciated at this or other levels. At the conclusion of her initial visit, the patient’s differential diagnosis included lumbar pain of discogenic origin and right sacroiliac joint syndrome. Her radiographs suggested an L4–5 disc pain generator, and her mechanism of injury and exacerbations with sitting, forward flexion, and provocative physical examination maneuvers were supportive of discogenic pain. Her described fall upon the buttocks, tenderness over the sacral sulcus, superior buttock pain, and response to provocative maneuvers were also potentially consistent with a sacroiliac joint process. At this point she felt that she had exhausted physical therapy and refused a further trial of therapy with a skilled therapist affiliated with the author’s practice. She wished to pursue a more interventional and definitive approach, and a diagnostic sacroiliac joint injection was planned prior to proceeding with a more empiric therapeutic injection approach. Her response to the fluoroscopically guided diagnostic intra-articular injection was negative. Minimal relief, approximately 20%, was described 30 minutes after the intra-articular injection of 2 cc of 2% xylocaine. It was then decided to proceed with a working diagnosis of discogenic pain and fluoroscopically guided right L5 transforaminal injections were planned in an effort to maximally bathe the right L4–5 intervertebral disc and protrusion to the right. Two weeks after two therapeutic injections, she described an approximate 60% reduction in her level of lower lumbar pain, and her radiating pain to the buttock was resolved. A third therapeutic injection was then performed without additional appreciable benefit. As an incremental response was not realized, no further injection therapy was planned. 985
Part 3: Specific Disorders
The patient then decided to proceed with further physical therapy with an experienced mechanical therapist and realized some additional relief after 3 weeks of treatment and the introduction of a home exercise regimen. Five months after her initial injury, describing an overall 75% improvement, but with residual lumbar discomfort which prohibited her from lifting or sitting for extended periods without pain, she requested further information regarding her treatment options. The role of lumbar discography was reviewed as a potential precursor to intradiscal annuloplasty, fusion, or, at some point in time, evolving techniques such as disc replacement therapy. The pertinent literature and range of therapeutic outcomes was referenced in our discussion. We also reviewed the option of living with her discomfort along with activity and postural modifications or trialing a more chronic pain management approach and medication trials. She decided to proceed with discography from L3–4 through L5–S1. A concordant pain response was elicited at L4–5 where an annular tear was observed without resultant pain or annular disruption at the adjacent control discs. She then wished to proceed with IDET. After her procedure and 6 weeks of graduating activity and the tapering use of an external orthosis, only mild additional relief was described, with the patient then reporting an overall 80% improvement. While her pain was as easily provoked through similar activities, her localized lumbar discomfort was not as sharp in nature. She chose to continue her home program, addressed her seating system and work station, and continued the intermittent use of nonsteroidal antiinflammatory agents. She decided that she would rather live with her current level of discomfort than pursue further interventions. The patient revealed that she was satisfied with the pain relief obtained and was pleased with her decision to undergo the IDET procedure considering the outcome realised.
Case 2 A 72-year-old male presented with the chief complaint of right lower lumbar pain. His symptoms evolved gradually over 4 months and began without a particular inciting event. He had trialed a course of COX-2-specific nonsteroidal antiinflammatory agents for 3 weeks without relief. His primary care physician suggested he was suffering from a ‘degenerative spine,’ and physical therapy was prescribed. After 6 weeks of therapy, he realized minimal relief and was graduated to a home exercise program. An MRI was ordered, and he presented with these films to his initial visit at the author’s office. He described right lower lumbar pain which radiated to the superior buttock and rarely to the inguinal region. He denied symptom radiation to the more distal lower limb. His symptoms were typically exacerbated by prolonged standing more so than during ambulation and were relieved by sitting. The past medical history was significant for benign prostatic hypertrophy and hypertension. Examination revealed intact right lower limb strength and reflexes and easily appreciated distal pulses. Passive range of motion of the right hip was not pain provoking. There was no significant sacral sulcus tenderness, but right lower lumbar paraspinal tenderness was noted to deep palpation. Sacroiliac joint provocative maneuvers were negative. Pain was reproduced with active lumbar extension and relieved with forward-flexed postures. An MRI of the lumbar spine revealed multilevel disc desiccation and a mild grade I-listhesis at L4–5. No foraminal stenosis was observed and the central canal compromise at L4–5 was graded as mild. Z-joint arthrosis was noted bilaterally at L4–5 and L5–S1 but more notably on the right where increased T2-intra-articular signal was observed. Flexion and extension radiographs revealed no translational, rotational, or angular motion abnormality at the level of the L4–5 olisthesis. At the conclusion of his initial visit, his differential diagnosis included lumbar pain of Z-joint or discogenic origin.
986
As his symptoms were not exacerbated by valsalva maneuvers, exacerbated by standing and extension-biased postures, and relieved through assuming the supine, sitting or flexed positions, the posterior elements were considered more likely as his primary pain generators. His localized tenderness to palpation and asymmetric right-sided Z-joint arthroses were also considered supportive. A diagnostic right-sided fluoroscopically guided intra-articular L4–5 and L5–S1 Z-joint injection was performed utilizing 1.0 cc of 2% xylocaine into each joint. During the assessment phase, the patient described complete relief from his baseline pain during typically provocative standing and extension postures. This confirmatory diagnostic injection was followed by a right-sided therapeutic corticosteroid intra-articular injection at L4–5 and L5–S1. The first injection offered him mild relief and was followed by a second 2 weeks later. Two weeks after his second injection, he described an approximate 60% improvement when compared to his initial presentation and improved ambulation endurance. It was decided to proceed with a third. Two weeks later he described a 70% improvement in his level of right-sided axial pain. Over the subsequent 3 months, his improvements waned, but not to his baseline level. He questioned his candidacy for another injection. In the absence of a sustained incremental response, it was explained that another injection would likely also only offer transient relief. The potential outcomes following radiofrequency denervation were reviewed and a diagnostic medial branch block injection was performed on the right at L3 through L5. This confirmatory diagnostic assessment similarly resulted in complete relief from his residual pain. A radiofrequency denervation procedure to address these medial branches was then performed. The patient realized additional relief which was graded as an overall 75% improvement and increased standing and ambulation tolerance. At 10 months following this procedure, a gradual decline in response was described, and discussions were initiated regarding a possible repeat radiofrequency approach.
References 1. Riew KD, Yin Y, Gilula L, et al. The effect of nerve root injections on the need for operative treatment of lumbar radicular pain. A prospective, randomized, controlled, double blind study. J Bone Joint Surg [Am] 2000; 82(11):1589–1593. 2. Manchikanti L. Role of neuraxial steroids in interventional pain management. Pain Phys 2002; 5(2):182–199. 3. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211:210. 4. Bogduk N. Low back pain. In: Bogduk N, ed. Clinical anatomy of the lumbar spine and sacrum. 3rd edn. New York: Churchill Livingstone; 1997:199–200. 5. Albee S. The study of the anatomy and the clinical importance of the sacroiliac joint. JAMA 1909; 16:1273–1276. 6. Alderink GJ. The sacroiliac joint; review of anatomy, mechanics, and function. Orthop Sports Phys Ther 1991; 13:71–84. 7. Wilkinson M, Bywaters EGL. Clinical features and courses of ankylosing spondylitis. Ann Rheum Dis 1958; 17:209–228. 8. Dunn EJ, Bryan DM, Nugent JT, et al. Pyogenic infections of the sacroiliac joint. Clin Orthop 1976; 118:113–117. 9. Bernard TN, Cassidy JD. The sacroiliac joint syndrome: pathophysiology, diagnosis, and management. In: Frymoyer JW, ed. The adult spine: principles and practice. New York: Raven Press; 1991:2107–2130. 10. Fortin JD. Sacroiliac joint dysfunction. A new prospective. J Back Musculoskel Rehabil 1993; 3:31–43. 11. Humphrey SM, Inman RD. Metastatic adenocarcinoma mimicking unilateral sacroiliitis. J Rheum 1995; 22:970–972. 12. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique. Part I: asymptomatic volunteers. Spine 1994; 19:1475–1482. 13. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37.
Section 5: Biomechanical Disorders of the Lumbar Spine 14. Maigne J, Aivalikilis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892.
42. Slipman CW, Lipetz JS, Plastaras CT, et al. Fluoroscopically guided therapeutic sacroiliac joint injections for sacroiliac joint syndrome. Am Jour Phys Med Rehabil 2001; 80:425–432.
15. Egund N, Olsson TH, Schmid H, et al. Movements in the sacroiliac joint demonstrated with roentgen stereophotogrammetry. Acta Radiologica Diagnosis 1978; 19:833–846.
43. Maguars Y, Mathis C, Berthelot J-M, et al. Assessment of efficacy of sacroiliac joint corticosteroid injections in spondyloarthropathies: a double blind study. Br J Rheumatol 1996; 35:767–770.
16. Sturesson B, Selvik G, Uden A. Movements of the sacroiliac joints. A roentgen stereo photogrammetric analysis. Spine 1989; 14:162–165.
44. Maguars Y, Mathis C, Vilon P, et al. Corticosteroid injection of the sacroiliac joint in patients with seronegative spondyloarthropathy. Arthritis Rheum 1992; 35: 564–568.
17. Slipman CW, Sterenfeld EB, Chou LH, et al. The value of radionuclide imaging in the diagnosis of sacroiliac joint syndrome. Spine 1996; 21:2251–2254. 18. Battafarano DF, West SG, Rak KM, et al. Comparison of bone scan, computed tomography, and magnetic resonance imaging in the diagnosis of active sacroiliitis. Semin Arthritis Rheum 1993; 23:161–176. 19. Hanly JG, Mitchell MJ, Barnes DC, et al. Early recognition of sacroiliitis by magnetic resonance imaging and single photon emission CT. J Rheumatol 1994; 21:2088–2095. 20. Russel AS, Lentle BC, Percy JS. Investigation of sacroiliac disease: comparative evaluation of radiological and radionuclide techniques. J Rheumatol 1975; 2: 45–51. 21. Cohen AS, McNeill JM, Calkins E, et al. The normal sacroiliac joint. An analysis of 88 sacroiliac roentgenograms. Am J Roentgenol Radium Ther 1967; 100: 559–563. 22. Jajic I, Jajic Z. The prevalence of osteoarthritis of the sacroiliac joints in an urban population. Clin Rheumatol 1987; 6:39–41. 23. Vogel JB III, Brown WH, Helms CA, et al. The normal sacroiliac joint: a CT study of asymptomatic patients. Radiology 1984; 151:433–437. 24. Moore M. Diagnosis and surgical treatment of chronic sacroiliac artrhopathy. In: Proceedings of the 7th annual meeting of the North American Spine Society. Boston: North American Spine Society; 1992:100.
45. Flower RJ, Blackwell GJ. Anti-inflammatory steroids induce biosynthesis of phospholipase A2 inhibitor which prevents prostaglandin generation. Nature 1979; 278:456–459. 46. Willard FH, Carreiro JE, Manko W. The long posterior interosseous ligament and the sacrococcygeal plexus. In: Proceedings of the Third Interdisciplinary World Congress of Low Back and Pelvic Pain. Vienna: 1998. 47. Dreyfuss P, Akuthota V, Willard F, et al. Are lateral branch blocks of the S1–3 dorsal rami reasonably target specific? In: Proceedings of ISIS 8th Annual Scientific Meeting. San Francisco; 2000:25–30. 48. Yin W, Willard F, Carreiro J, et al. Sensory stimulation-guided sacroiliac joint radiofrequency neurotomy: Technique based on neuroanatomy of the dorsal sacral plexus. Spine 2003; 28:2419–2425. 49. Dreyfuss P, Park K, Bogduk N. Do L5 dorsal ramus and S1–4 lateral branch blocks protect the sacroiliac joint from an experimental pain stimulus? A randomized, double-blinded controlled study. In: Proceedings of ISIS 8th Annual Scientific Meeting. San Francisco; 2000:31–36. 50. Gevargez A, Groenemeyer D, Schirp S, et al. CT-guided percutaneous radiofrequency denervation of the sacroiliac joint. Eur Radiol 2002; 121360–1365. 51. Cohen SP, Abdi S. Lateral branch blocks as a treatment for sacroiliac joint pain: A pilot study. Reg Anesth Pain Med 2003; 28:113–119.
25. Leblanc KE. Sacroiliac sprain: an overlooked cause of back pain. Am Fam Physician 1992; 46:1459–1463.
52. Ferrante FM, King LF, Roche EA, et al. Radiofrequency sacroiliac joint denervation for sacroiliac joint syndrome. Reg Anesth Pain Med 2001; 26:137–142.
26. Norman G. Sacroiliac disease and its relationship to lower abdominal pain. Am J Surg 1958; 116:54–56.
53. Berthelot JM, Gouin F, Glemarec J, et al. Possible uses of arthrodesis for intractable sacroiliitis in spondyloarthropathy. Report of two cases. Spine 2002; 26: 2297–2299.
27. Smith-Peterson MN. Clinical diagnosis of common sacroiliac joint conditions. Am J Roentgenol Radium Ther 1924; 12:546–550.
54. Goldthwait JE. The lumbosacral articulation: An explanation of many cases of lumbago, sciatica, and paraplegia. Boston Med Surg J 1911; 164:365–372.
28. Woodward JL, Weinstein SM. Epidural injections for the diagnosis and management of axial and radicular pain syndromes. Phys Med Rehab Clin N Am. Injection techniques – principles and practice. 1995; 6:691–714.
55. Glover JR. Arthrography of the joints of the lumbar vertebral arches. Orthop Clin North Am 1977; 8:37–42.
29. Dreyfuss P, Michaelsen DC, Pauza K. The value of the medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21:2594–2602.
56. Lewin T, Moffit B, Viidik A. The morphology of the lumbar synovial intervertebral joints. Acta Morphologica Neurologica Scand 1962; 4:299–319.
30. Kirkaldy-Willis WH. A more precise diagnosis for low back pain. Spine 1979; 4:102–109.
57. Bogduk N. Back pain: Zygapophyseal blocks and epidural steroids. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd edn. Philadelphia: Lippincott; 1989:935–954.
31. Slipman CW, Jackson HP, Lipetz JS, et al. Sacroiliac joint pain referral zones. Arch Phys Med Rehabil 2000; 81:334–338.
58. Mooney V, Robertson J. Facet joint syndrome. Clin Orthop 1976; 115:149–156.
32. Carmichael JP. Inter- and intra-examiner reliability of palpation for sacroiliac joint dysfunction. J Manipulative Physiol Ther 1987; 10:164–171.
59. McCall IW, Park WM, O’Brien JP. Induced pain referral from posterior lumbar elements in normal subjects. Spine 1979; 4:441–446.
33. Potter N, Rothstein J. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1981; 11:1671–1675.
60. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: A report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Orthop Clin North Am 1993; 22: 181–187.
34. Deyfuss P, Dreyer S, Griffen J, et al. Positive sacroiliac screening tests in asymptomatic adults. Spine 1994; 19:1138–1143. 35. Slipman CW, Sterenfeld EB, Chou LH, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehabil 1998; 79:288–292. 36. Laslett M, Young SB, Aprill CN, et al. Diagnosing painful sacroiliac joints: A validity study of a McKenzie evaluation and sacroiliac provocation tests. Austral J Physiother 2003; 49:89–97. 37. Dreyfuss P, Cole AJ, Pauza K. Sacroiliac joint injection techniques. Phys Med Rehab Clin N Am. Injection techniques principles and practice. 1995; 6(4): 785–814. 38. Haldeman K, Sotohall R. The diagnosis and treatment of sacroiliac conditions involving injection of procaine (Novacaine). J Bone Joint Surg [Am] 1938; 3: 675–685.
61. Dreyer SJ, Dreyfuss P, Cole AJ. Zygapophyseal (facet) joint injections. Intraarticular and medial branch block techniques. Phys Med Rehab Clin N Am. Injection techniques principles and practice. 1995; 6(4):715–741. 62. Bough B, Thakore J, Davies M, et al. Degeneration of the lumbar facet joints. Arthrography and pathology. J Bone Joint Surg [Br] 1990; 72:275–276. 63. Carrera GF. Lumbar facet joint injection in low back pain and sciatica: Preliminary results. Radiology 1980; 137:665–667. 64. Lewinnek GE, Warfield CA. Facet joint degeneration as a cause of low back pain. Clin Orthop 1986; 213:216–222. 65. Eisenstein SM, Parry CR. The lumbar facet arthrosis syndrome – clinical presentation and articular surface changes. J Bone Joint Surg [Br] 1987; 69:3–7.
39. Miskew DB, Block RA, Witt PF. Aspiration of infected sacro-iliac joints. J Bone Joint Surg [Am] 1979; 61A:1071–1072.
66. Twomey LT, Taylor JR, Taylor MM. Unsuspected damage to lumbar zygapophyseal (facet) joints after motor vehicle accidents. Med J Aust 1989; 151: 210–217.
40. Rosenberg JM, Quint TJ, deRosayro AM. Computerized tomographic localization of clinically-guided sacroiliac joint injections. Clin J Pain 2000; 16:18–21.
67. Campbell AJ, Wells IP. Pigmented villonodular synovitis of a lumbar vertebral facet joint. J Bone Joint Surg 1982; 64A:145–146.
41. Norman G, May A. Sacroiliac conditions simulating intervertebral disc syndrome. Wes J Surg 1956; 64:461–462.
68. Rush J, Griffiths J. Suppurative arthritis of a lumbar facet joint. J Bone Joint Surg 1989; 71B:161–162.
987
Part 3: Specific Disorders 69. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity. Spine 1994; 19:1132–1137.
99. Milette PC, Fontaine S, Lepanto L, et al. Differentiating lumbar disc protrusions, disc bulges, and discs with normal contour but abnormal signal intensity. Magnetic resonance imaging with discographic correlations. Spine 1999; 24 44–53.
70. Lawrence JS, Sharp J, Ball J, et al. Osteoarthritis. Prevalence in the population and relationship between symptoms and X-ray changes. Ann Rheum Dis 1966; 25:1–24.
100. Horton WC, Daftari TK. Which disc as visualized by magnetic resonance imaging is actually a source of pain. A correlation between magnetic resonance imaging and discography. Spine 1992; 17:S164–S171.
71. Magora A, Schwartz TA. Relation between the low back pain syndrome and X-ray findings. Scan J Rehabil Med 1976; 8:115–125.
101. Nachemson A. The load on lumbar disks in different positions of the body. Clin Orthop 1966; 45:107–122.
72. Schwarzer AC, Wang S, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 20:907–912.
102. Wilke HJ, Neef P, Caimi M. New in vivo measurements of pressures in the intervertebral disc in daily life. Spine 1999; 24:755–762.
73. Jackson RP, Jacobs RR, Montesano PX. Facet joint injection in low back pain: A prospective statistical study. Spine 1988; 13:966–971. 74. Schwarzer AC, Derby R, Aprill CN, et al. The false positive rate of single lumbar zygapophyseal joint blocks. Pain 1994; 58:195–200. 75. Revel ME, Listrat VM, Chevalier XJ, et al. Facet joint block for low back pain: Identifying predictors of a good response. Arch Phys Med Rehabil 1992; 73: 824–828. 76. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections into the facet joints for chronic low back pain. N Engl J Med 1991; 325:1002–1007. 77. Carrera GF. Lumbar facet joint injection in low back pain and sciatica: Preliminary results. Radiology 1980; 137:665–667. 78. Destouet JM, Gilula LA, Murphy WA, et al. Lumbar facet joint injection: Indication, technique, clinical correlation and preliminary results. Radiology 1982; 145:321–325.
104. Donelson R, Aprill C, Medcalf R, et al. A prospective study of centralization of lumbar and referred pain. A predictor of symptomatic discs and annular competence. Spine 1997; 22:1115–1122. 105. Weiner BK, Fraser RD. Foraminal injection for far lateral disc herniation. J Bone Joint Surg [Br] 1997; 79:804–807. 106. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal epidural steroids: an outcome study. Arch Phys Med Rehabil 1998; 79:1362–1366. 107. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transforaminal epidural steroid injections in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 81:898–905. 108. Narozny M, Zanetti M, Boos N. Therapeutic efficacy of selective nerve root blocks in the treatment of radicular leg pain. Swiss Med Wkly 2001; 131:75–80.
79. Lau LSW, Littlejohn GO, Miller MH. Clinical evaluation of intra-articular injections for lumbar facet joint pain. Med J Aust 1985; 143:563–565.
109. Bogduk N, Cristophidis N, Cherry D, et al. Epidural steroids in the management of back pain and sciatica of spinal origin. Report of the Working Party on Epidural Use of Steroids in the Management of Back Pain. Nation Health and Medical Research Council. Canberra; 1993.
80. Murtagh FR. Computed tomography and fluoroscopy guided anaesthesia and steroid injection in facet syndrome. Spine 1988; 13:686–689.
110. Lipetz JS. Pathophysiology of inflammatory, degenerative, and compressive radiculopathies. Phys Med Rehab Clin N Am 2002; 13:439–450.
81. Dreyfuss P, Schwarzer AC, Lau P, et al. Specificity of lumbar medial branch and L5 dorsal ramus blocks: a computed tomographic study. Spine 1997; 22:895–902.
111. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies. Phys Med Rehab Clin N Am 2002; 13:697–712.
82. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25:1270–1277.
112. Adams MA, McMillan DW, Green TP, et al. Sustained loading generates stress concentrations in lumbar intervertebral discs. Spine 1996; 21:434–438.
83. Van Kleef M, Barendse G, Kessels A, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999; 24:1937–1942.
113. McNally DS, Shackleford IM, Goodship AE, et al. In vivo stress measurement can predict pain on discography. Spine 1996; 21:2580–2587.
84. Esses SI, Moro JK. The value of facet blocks in patient selection for lumbar fusion. Spine 1993; 18:185–190.
114. White AH, Derby R, Wynne G. Epidural injections for the diagnosis and treatment of low back pain. Spine 1980; 5:78–82.
85. Jackson RP. The facet syndrome: Myth or reality? Clin Orthop 1992; 279: 110–121.
115. Rapp SE, Haselkorn JK, Elam K, et al. Epidural steroid injection in the treatment of low back pain: A meta-analysis. Anesthesiology 1994; 78:A923.
86. Tsang IK. Perspective on low back pain. Curr Opin Rheumatol 1993; 5:219–223.
116. Weinstein SM, Herring SA, Derby R. Contemporary concepts in spine care. Epidural steroid injections. Spine 1995; 20:1842–1846.
87. Schwarzer AC, Aprill CN, Derby R, et al. The relative contributions of the disc and zygapophyseal joint in chronic low back pain. Spine 1994; 19:801–806. 88. Schwarzer AC, Aprill CN, Derby R, et al. The prevalence and clinical features of internal disc disruption syndrome in patients with chronic low back pain. Spine 1995; 20:1878–1883. 89. Malinsky J. The ontogenetic development of nerve terminations in the intervertebral discs of man. Acta Anat 1959; 38:96–113. 90. Rabischong P, Louis R, Vingard J, et al. The intervertebral disc. Anat Clin 1978; 1:55–64. 91. Yoshizawa H, O’Brien JP, Thomas-Smith W, et al. The neuropathology of intervertebral discs removed for low back pain. J Path 1980; 132:95–104. 92. Bogduk N. Clinical anatomy of the lumbar spine and sacrum. 3rd ed. New York: Churchill Livingstone; 1997: 138–207. 93. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg 1987; 69B:26–35. 94. Guyer RD, Collier R, Stith WJ, et al. Discitis after discography. Spine 1988; 13:1352–1354. 95. Bogduk N. The lumbar disc and low back pain. Neurosurg Clin North Am 1991; 2:791–806.
988
103. Suk KS, Lee HM, Moon SH, et al. Lumbosacral scoliotic list by lumbar disc herniation. Spine 2001; 26:667–671.
117. Simmons JW, McMillin JN, Emery SF, et al. Intradiscal steroids. A prospective double-blind clinical trial. Spine 1992; 17:S172–S175. 118. Khot A, Bowditch M, Powell J, et al. The use of lumbar intradiscal steroid therapy for lumbar spinal discogenic pain: a randomized controlled trial. Spine 2004; 29:833–836. 119. Petersen T, Kryger P, Ekdahl C, et al. The effect of McKenzie therapy as compared with that of intensive strengthening and training for the treatment of patients with subacute or chronic low back pain: A randomized controlled trial. Spine 2002; 27:1702–1709. 120. Holt EP. The question of lumbar discography. J Bone Joint Surg [Am] 1968; 50:720–726. 121. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. J Bone Joint Surg [Am] 1990; 72:1081–1088. 122. Carragee EJ, Chen Y, Tanner CM, et al. Provocative discography in patients after limited lumbar discectomy: A controlled randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2001; 25:3065–3071. 123. Colhoun E, McCall IW, Williams L, et al. Provocation discography as a guide to planning operations of the spine. J Bone Joint Surg [Br] 1988; 70:267–271.
96. Bogduk N, Aprill C, Derby R. In: White AH, ed. Spine care. St Louis: Mosby; 1995:219–238.
124. Moore KR, Pinto MR, Butler LM. Degenerative disc disease treated with combined anterior and posterior arthrodesis and posterior instrumentation. Spine 2002; 27:1680–1686.
97. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg [Am] 1990; 72: 403–408.
125. Parker LM, Murrell SE, Boden SD, et al. The outcome of posterolateral fusion in highly selected patients with discogenic low back pain. Spine 1996; 21: 1909–1917.
98. Carragee EJ, Paragioudakis SJ, Khurana S. 2000 Volvo Award winner in clinical studies: Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2001; 23:2987–2992.
126. Pauza KJ, Howell S, Dreyfuss P, et al. A randomized, placebo-controlled trial of intradiscal electrothermal therapy for the treatment of discogenic low back pain. Spine 2004; 4:27–35.
Section 5: Biomechanical Disorders of the Lumbar Spine 127. Block AR, Vanharanta H, Ohnmeiss DD, et al. Discographic pain report: Influence of psychological factors. Spine 1996; 21:334–338.
138. Lee CK, Langrana NA. Lumbosacral spinal fusion: A biomechanical study. Spine 1984; 9:574–581.
128. Penta M, Fraser RD. Anterior lumbar interbody fusion. A minimum 10-year follow up. Spine 1997; 22:2429–2434.
139. Rolander SD. Motion of the lumbar spine with special reference to stabilizing effect of posterior fusion. Acta Orthop Scand Suppl 1966; 90:1.
129. Greenough CG, Peterson MD, Hadlow S, et al. Instrumented posterolateral lumbar fusion. Results and comparison with anterior interbody fusion. Spine 1998; 23:479–486.
140. White AA, Panjabi MM. Clinical biomechanics of the spine: Biomechanical considerations in the surgical management of the spine. 2nd edn. Philadelphia: Lippincott; 1990:529–535.
130. Trief PM, Grant W, Fredrickson B. A prospective study of psychological predictors of lumbar surgery outcome. Spine 2000; 25:2616–2621.
141. Ylinen P, Kinnunen J, Laasonen EM, et al. Lumbar spine interbody fusion with reinforced hydroxyapatite implants. Arch Ortho Trauma Surg 1991; 110:250–256.
131. Saal JS, Saal JA. Management of chronic discogenic low back pain with a thermal intradiscal catheter. A preliminary report. Spine 2000; 25:382–388.
142. Zdeblick TA, Smith GR, Warden KE, et al. Two-point fixation of the lumbar spine. Differential stability in rotation. Spine 1991; 16(S):298–301.
132. Karasek M, Bogduk N. Intradiscal electrothermal annuloplasty: percutaneous treatment of chronic discogenic low back pain. Techniques Reg Anesth Pain Manage 2001; 5:130–135.
143. Saal JS, Franson RC, Saal JA, et al. Human disc PGE2 is inflammatory. Proceedings of the Sixth Annual North American Spine Society Meeting. Colorado; 1991.
133. Freeman BJC. A randomized controlled efficacy study: Intradiscal electrothermal therapy (IDET) versus placebo. Proceedings of the annual meeting of the International Society for the Study of the Lumbar Spine. Vancouver: 2003. 134. Bernard TN Jr. Lumbar discography and post discography computerized tomography: Refining the diagnosis of low back pain. Spine 1990; 15:690–707. 135. Lee CK, Vessa P, Lee JK. Chronic disabling low back pain syndrome caused by internal disc derangements: The results of disc excision and posterior lumbar interbody fusion. Spine 1995; 20:356–361.
144. Weinstein J, Claverie W, Gibson S. The pain of discography. Spine 1988; 13: 1344–1348. 145. Delamarter RB, Fribourg DM, Kanim LE, et al. ProDisc artificial total lumbar disc replacement: introduction and early results from the United States clinical trial. Spine 2003; 28:S167–S175. 146. Klara PM, Ray CD. Artificial nucleus replacement: clinical experience. Spine 2002; 27:1374–1377. 147. Sagi HC, Bao QB, Yuan HA. Nuclear replacement strategies. Ortho Clin North Am 2003; 34:263–267.
136. Vamvanij V, Fredrickson B, Thorpe JM, et al. Surgical treatment of internal disc disruption: An outcome study of four fusion techniques. J Spin Disord 1998; 11:375–382.
148. Kroeber MW, Unglaub F, Wang H, et al. New in vivo animal model to create intervertebral disc degeneration and to investigate the effects of therapeutic strategies to stimulate disc regeneration. Spine 2002; 27:2684–2690.
137. Derby R. et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine 1999; 24:364–371.
149. Nitta H, Tajima T, Sugiyama H, et al. Study of dermatomes by means of selective lumbar spinal nerve block. Spine 1993; 18:782–786.
989
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain
CHAPTER
90
Medical Rehabilitation – Lumbar Axial Pain William Micheo and Carmen E. López-Acevedo
INTRODUCTION Axial low back pain is a common complaint of patients visiting physicians who practice musculoskeletal and pain medicine. The majority of these patients are diagnosed with non-specific back pain, which is presumed to be caused by muscle or ligament soft tissue damage, while many of these patients will actually have pain associated to injury to the posterior elements or the disc. These patients are thought to have a good prognosis for recovery; they improve in 4–12 weeks after the onset of pain, and the strategies of treatment used focus only on short-term management. In reality, many of these patients have future episodes of back pain associated with recurrent injury to the disc and associated structures and some will present with chronic back pain. Patients with unresolved pain may develop significant changes in the quality of their life including reduced health perception, happiness, social participation, and restriction of function.1 In addition, significant direct and indirect healthcare costs are associated with chronic low back pain.2 Low back pain should be considered a symptom of a clinical problem and not a specific diagnosis. Clinicians dealing with the rehabilitation of patients with low back pain should avoid non-specific terminology to describe the patient’s diagnosis such as lumbar strain, lumbago, or myositis. An understanding of the epidemiology of back pain, functional anatomy, and biomechanics of the spine, as well as the pathophysiology of the disease process is required to appropriately manage back pain. In addition, a complete history, physical examination, and appropriate diagnostic studies are paramount for the clinician who rehabilitates patients with this common disorder. Attempts should be made to establish a specific diagnosis for the cause of the axial back pain, which includes the site of injury with the pain generator, the clinical symptoms which require appropriate treatment, biomechanical changes associated to the tissue injury, and finally the functional abnormalities which result from the disease process. The overwhelming majority of patients with back pain will not require surgery and should be managed with conservative treatments which include rehabilitation and functional restoration.3–5 The goals of rehabilitation are to return the individual with low back pain to normal function. This requires achieving control of pain, adequate flexibility, strength, and muscle balance as well as neuromuscular coordination that would allow the return to normal activities. Evaluation, management, and rehabilitation of low back pain also require that the clinician understands the vocational and avocational demands of the patients and their goals. Unfortunately, there is limited positive scientific evidence on the results of a structured rehabilitation program in the management of back pain. In this chapter, the authors will review some of the scientific evidence available that relates to therapeutic interventions used
in rehabilitation such as physical modalities, rest and physical activity, exercise, manual therapy, and education. In addition, the authors will discuss their approach to the patient with back pain, and how they combine the available scientific information with their clinical experience in the management of this very common and often difficult patient problem.
FACTORS INFLUENCING REHABILITATION Epidemiology Understanding the patterns of injury and clinical presentation of low back pain is important for the planning of therapeutic, rehabilitative, and preventive strategies. Low back disorders are prevalent in all societies and the etiology of these disorders is multifactorial including individual/intrinsic as well as external/extrinsic factors. The annual incidence of low back pain in the general population is 5%, with many patients presenting between the ages of 30 and 50 years, and a significant number of cases resolving within 4 weeks of presentation. Of these patients, particularly the ones who present with pain at an early age, a significant number will present with recurrence of the symptoms, and some will develop chronic disability. Therefore, a functional rehabilitation program should be instituted early in the disease process.6–8 Some individual risk factors for pain are modifiable and include obesity, cigarette smoking, and low fitness level.9,10 Occupational factors associated with back pain include vibration, static work posture, flexed posture, frequent bending and twisting, lifting and material handling.11,12 Psychosocial factors associated with back pain and recurrence of symptoms include dissatisfaction with work, long duration of initial treatment, recurrent treatment, and being disabled from work.13–15 Other factors, such as heredity, may not be modifiable but also play a role in the development of low back pain. Familial predisposition to back pain and degenerative disc disease has been described and may be important in patients who present at an early age (Table 90.1).16–19 Sports and recreational activities are also associated with the development of back pain, wherein 10–15% of all sports injuries are related to the spine. Rotational, torsional, and compressive stresses to the spine are associated with the development of intrinsic disc disease.20,21 Activities in daily life that involve frequent bending and lifting may also lead to back pain. Individuals caring for elderly or disabled family members present with an increased prevalence of back pain.22
Functional anatomy and biomechanics A review of the anatomy and biomechanics of the spine is beyond the scope of this chapter; however, an understanding of the functional 991
Part 3: Specific Disorders
Table 90.1: Risk Factors for Axial Low Back Pain Epidemiologic Evidence Individual/Intrinsic
External/Extrinsic
Age
Static work postures
Gender
Prolonged sitting
Abdominal girth
Frequent lifting, pushing and pulling
Smoking
Frequent trunk rotation
Muscle weakness/loss of endurance
Vibration exposure
Reduced/excessive flexibility
Repeated lumbar flexion
Sedentary life style
Activity early in the day
anatomy as well as basic concepts of biomechanics of the lumbar spine is important for the clinician who treats and rehabilitates patients with low back pain. The basic functional unit of the lumbar spine is the three-joint complex formed by two consecutive vertebra, the intervertebral disc, and the zygapophyseal joints. The anterior elements of the lumbar spine sustain the compression loads applied to the vertebral column including body weight and loads associated with contraction of the back muscles. The posterior elements regulate the passive and active forces applied to the vertebral column and regulate motion. The zygapophyseal joints are typical synovial joints endowed with cartilage, capsule, meniscoids, and synovial membrane. The articular facets exhibit variations in both the shape of their articular surfaces and their orientation. In the lumbar spine the only movement permitted is a sliding motion in a vertical direction, executed during flexion and extension.23 Muscle function is very important for the lumbar spine since ligaments provide little static stability and in the absence of muscle activity the spine could buckle with low compressive loads. The erector spinae are composed of two major groups: the longissimus and iliocostalis. They are primarily thoracic muscles that act on the lumbar spine with a long moment arm ideal for lumbar spine extension. The small rotatores and intertransversarii muscles are basically length transducers and position sensors. The multifidi which cross 2 or 3 segmental levels are theorized to work as spinal stabilizers.24 Other muscle groups important for low back function are the quadratus lumborum, which has a direct insertion in the lumbar spine and acts as a weak lateral flexor, and the abdominal muscles which include: the transversus abdominus, internal and external oblique, and rectus abdominus. These muscles are important in flexion of the trunk, lateral bending, but most importantly help to stabilize the lumbar spine. Pelvic muscles also play a role in the kinetic chain by acting on the lumbar spine and transmitting forces from the lower extremity to the trunk and upper extremities and include: the hip flexors such as the iliopsoas, and gluteal hip extensor, as well as abductor muscles.25 The lumbar spine and related structures including ligaments and muscles receive an extensive nerve supply. The vertebral bodies, the intervertebral disc, the zygapophyseal joints, and the ligaments are all innervated and have the capacity to be pain generators, making it difficult for the clinician treating axial back pain to identify the origin of a patient’s symptoms.
Pathophysiology of injury Flexion of the lumbar spine, which involves sagittal rotation and translation, is well tolerated by the lumbar elements. Compression 992
of the lumbar spine occurs by adding body weight, muscular contraction, and the loads that are lifted by the individual. Excessive compression may injure the anterior vertebral elements, particularly the endplates. When flexion and compression are combined with rotation, shear applied to the intervertebral disc results in injury to this structure. Vertebral extension is limited primarily by bony impaction of the spinal processes or the inferior articular facet against the lamina below, and repeated extension as well as rotation activities may lead to injury of the posterior elements such as the pars intercularis.26 Lumbar disc disease associated with axial back pain is multifactorial in origin. Aging, apoptosis, abnormalities in collagen, vascular ingrowth, loads placed on the disc, and abnormal proteoglycan all contribute to disc degeneration.27 Repetitive or continuous axial overloading, associated with disc fatigue, is key in the pathogenesis of lumbosacral degenerative disease.24 Vigorous occupational activity and competitive athletic participation associated with end-range flexion and frequent turning predispose the disc to herniation and accelerated degeneration.28 These changes in the disc, which progress from herniation to subsequent internal disruption and resorption, may affect more than one functional unit and compromise spinal motion. The combined changes in the posterior joint and discs lead to arthritis, lateral recess stenosis, and central stenosis.29–31 Low back pain may result from compression of nerve tissue, inflammation of the nerve root, and the facet joint, as well as damage to the anulus fibrosus. Inflammatory mediators, such as prostaglandins and substance P, have been identified in patients with disc disease and are associated with pain in the absence of a compressive lesion.28,32 Increasing age has been associated with progressive disc degeneration which can be asymptomatic in some individuals. Changes in trabecular bone morphology and inappropriate disc matrix may be related to apoptosis, or programmed cell death, in the patient with disc disease.27,33
Clinical presentation In the individual with axial back pain, the history and physical examination are very important in the planning of a functional rehabilitation program. Pertinent information that should be obtained from the history include: the type of pain, the mechanism of injury, exacerbating and mitigating factors, and previous injuries and response to treatment strategies. The physical examination should identify limitations of motion, direction of pain exacerbation, lack of flexibility, muscle weakness and imbalance, ligamentous laxity, and neurologic as well as proprioceptive deficits. This information combined with pain diagrams, diagnostic imaging, and injection procedures allows the clinician to recognize specific characteristics of different clinical subsets.34 Clinical subsets of axial back pain include patients with acute annular tears, intrinsic disc disease, facet joint degeneration, or posterior element injury. Patients with axial back pain associated with disc disease may present with acute symptoms, chronic symptoms, or acute exacerbation of chronic symptomatology. The patient with an acute annular disc injury will present with axial pain, limited lumbar motion, intolerance to sitting, and exacerbation of symptoms with attempted flexion of the spine. The physical examination of these individuals may reveal a lateral trunk list, pain with flexion of the spine, normal neurologic examination, and typically no evidence of spinal nerve root irritation. The patient with chronic discogenic disease will present with axial back pain, intolerance to sitting as well as pain upon arising from a chair, limited capability to lift, bend, or twist.35 Physical examination will reveal soft tissue inflexibility of paravertebral muscles, fascia and ligaments as well as some muscle spasm. There may be evidence
Section 5: Biomechanical Disorders of the Lumbar Spine
of lumbar segmental hypomobility, loss of lumbar lordosis, and pain with flexion and rotation. The neurologic examination is usually normal with no evidence of root irritation.36 Individuals who present with an acute on chronic injury give the history of an excessive load or sudden trauma superimposed on previous discogenic symptoms. The physical examination is usually similar to patients that presents with an acute annular tear. Patients who present with axial back pain may also have involvement of posterior elements such as the facet joints. These individuals may present with pain in the back which may radiate to the buttocks or thighs that could worsen with extension activities such as walking downhill, prone lying, and prolonged standing. Other patients may present with a different history such as pain with flexion that is not exacerbated by sitting and still have facet joint pathology. The physical examination may reveal inflexibility of the lumbar soft tissues, hypomobility of spine segments, and pain with extension or flexion as well as rotation maneuvers. The neurologic examination and special maneuvers to identify root irritation are usually normal, and injection procedures may be required to clearly identify the facet joint as the pain generator.37 In sports, the patterns of back injury will depend on several factors which include the patient’s age and sport-specific demands. Athletes involved in sports that require trunk rotation and hyperextension usually present with axial back pain associated to posterior element injury. Repeated stresses associated to gymnastics, diving, and wrestling places the athlete at increased risk of pars interarticularis injury such as spondylolisis. These athletes may present with acute or gradual onset of pain and limited motion which restricts activity.38 Older individuals who exercise vigorously or participate in sports will generally present with injuries of the vertebral endplate and the intervertebral discs. These individuals usually present with symptoms associated to repeated flexion and trunk rotation. They may present with episodes of axial back pain and limited motion which may be accompanied by leg symptoms.39
Psychosocial factors Psychologic and social issues should be addressed in the individual with axial back pain because they may affect rehabilitation, and include coexisting anxiety, depression, family or work related stress, and lack of social support. Work dissatisfaction, fear of recurrence of pain with activity, and pending compensation are also factors that may be impediments to return to normal activity.14
BASIC CONCEPTS OF REHABILITATION Complete diagnosis of musculoskeletal injury Prior to starting rehabilitation, attempts should be made to reach a complete diagnosis of the patient with back pain including the pain generator and the biomechanical deficits. In the authors’ practice, a modification of the musculoskeletal injury model described by Kibler is used for this purpose. This model identifies the anatomic site of injury, the clinical symptoms, and the functional deficits (Table 90.2).40
Phases of rehabilitation Musculoskeletal rehabilitation combines therapeutic modalities and exercise in order to return the individual to normal function. It should start early in the disease process in order to reduce the deleterious effects of inactivity and immobilization. A medical rehabilitation program should state the goals and objectives of treatment specific for each phase of rehabilitation. The treatment should focus on optimizing the healing process, restoring the biomechanical relations between the normal and injured tissue, and finally preventing
Table 90.2: Framework for Musculoskeletal Injuries Axial Back Pain CLINICAL ATERATIONS Symptoms Back pain Sitting intolerance Pain with bending ANATOMIC ALTERATIONS Tissue injuries: vertebral end plate, intervertebral disc, facet joints Tissue overload: extensor muscles, interspinal ligaments FUNCTIONAL ALTERATIONS Biomechanical deficits: weak back extensors, tight hip flexors Adaptive behavior: avoidance of trunk flexion, rotation, prolonged sitting
recurrence of pain and chronic disability. A functional rehabilitation program emphasizes therapeutic exercise and physical activity while monitoring for exacerbation of symptoms. Rehabilitation of the patient with back pain can be divided into acute, recovery, and functional phases (Table 90.3). The acute phase addresses the clinical symptom complex and should focus on treating tissue injury. The goal at this stage should be to allow tissue healing while reducing pain and inflammation. Reestablishment of nonpainful range of motion, prevention of muscle atrophy, and maintenance of general fitness should be emphasized. Symptom control and patient education about the condition should be accomplished prior to progressing to the next rehabilitation phase. The subacute or recovery phase should focus on obtaining normal passive and active range of motion, improving muscle control, achieving normal muscle balance, and working on core strength as well as proprioception. Biomechanical and functional deficits including inflexibilities and inability to bend or lift should begin to be addressed. Functional activities should be initiated in this stage and progression without recurrence of symptoms is required prior to advancing to the next stage. The functional or maintenance phase should focus on increasing power and endurance while improving neuromuscular control. Rehabilitation at this stage should work on the entire kinematic chain, addressing specific residual functional deficits. The individual
Table 90.3: Goals in Rehabilitation of Musculoskeletal Injury Acute Phase
Recovery Phase
Functional Phase
Treat clinical symptoms
Allow tissue healing
Correct abnormal biomechanics
Protect injured tissue
Restore normal strength and flexibility
Prevent recurrent injury
993
Part 3: Specific Disorders
should be pain free, exhibit full range of motion, normal strength, and muscle balance prior to returning to full activity. After return to activity, disease prevention and ‘prehabilitation’ strategies to avoid recurrence of symptoms in the previously injured individual should be developed. Exercise programs which combine flexibility, stabilization, dynamic strengthening, and balance training, as well as appropriate biomechanics should be encouraged in the patient who has recovered from low back pain.
REHABILITATION OF AXIAL BACK PAIN The functional rehabilitation model of patient management should be implemented as soon as the patient presents for clinical evaluation of back pain. As previously discussed, identification of the pain generator should be attempted based on the information obtained from the history, physical examination, laboratory studies, imaging data, and diagnostic injections.41 However, in many instances, the pain generator cannot be definitely identified, and a functional approach to the rehabilitation should be undertaken after developing a working diagnosis. Patterns of pain provocation with motion, muscle weakness, inflexibility, abnormal biomechanics, and functional abnormalities can be identified, used as a starting point for treatment, and addressed in a progressive manner.
Acute phase The acute phase of treatment is the period when pain should be addressed, and the injured tissue should be protected from further damage, with the purpose of optimizing the healing process and allowing the patient to progress in the rehabilitation program. It is important to understand that a balance must be achieved between treating the pain with medications, among other passive rehabilitation therapeutic interventions, and encouraging active patient participation in their treatment early in the recovery process (Table 90.4). Medications are an important component of the acute phase of rehabilitation, and basic knowledge of their pharmacology, side effects, and interactions is required for the clinician rehabilitating the patient with back pain. Management of pain is very important at this stage because pain can inhibit muscle contraction, reduce activity tolerance, and limit progression in a rehabilitation program. Some of the therapeutic agents commonly used in the acute phase, about which the treating physicians must be knowledgeable, include nonsteroidal antiinflammatory drugs (NSAIDs), muscle relaxants, nonopioid and opioid analgesics, as well as adjuvant medications such as antidepressants and anticonvulsants. There are multiple clinical studies that show evidence that prescription of various types of NSAIDs at regular intervals provides
Table 90.4: Rehabilitation of Back Injury – Acute Phase 1. NSAIDs and other medications 2. Limited rest 3. General conditioning 4. Cryotherapy 5. Electrical stimulation 6. Protected motion 7. Isometric–static exercise 8. Basic stabilization program 9. Diagnostic and therapeutic injections
994
effective pain relief from acute low back pain.42–45 Use of over-thecounter nonselective NSAIDs can be an initial treatment option, particularly for young patients without a history of gastrointestinal problems.46 In patients with a history of gastrointestinal problems, elderly individuals, or those patients in whom less frequent dosing is important for compliance, COX-2-specific inhibitors offer a therapeutic alternative.47,48 Risk of cardiovascular disease and monitoring fluid retention, blood pressure, and renal and liver function is important for any patient being treated with NSAIDs but particularly those treated with COX-2 inhibitors. In addition, there is clinical and scientific evidence that the different types of muscle relaxants are equally effective in the management of acute low back pain.49–51 However, muscle relaxants have significant adverse effects, such as drowsiness, risk of habituation, and dependency, which require that they be used with caution. The use of low-dose regimens of muscle relaxants offer a good therapeutic alternative with reduced side effects and similar efficacy.52 In many patients, low-dose muscle relaxants are used for a short period of time, particularly at night in patients with sleep dysfunction, since they may aid in sleep. Another treatment alternative to consider in patients with acute exacerbation of chronic symptoms and sleep dysfunction associated with fatigue is antidepressant medications, particularly the tricyclic agents because of their anticholinergic sedative and analgesic effects.53 In patients that do not respond to nonopioid analgesics in combination with the previously mentioned medications, consideration can be given to a short course of opioid analgesics. Formulations which combine acetaminophen with opioid analgesics such as oxycodone or with tramadol offer a treatment alternative for patients with poor response to other treatments or those allergic to aspirin. In the authors’ clinical experience, the use of these agents does not affect participation in the rehabilitation program and, in many instances, facilitates return to activity. During the acute phase, the focus is on reducing pain and protecting injured or inflamed tissue. A common therapeutic intervention in the acute phase of rehabilitation is restricted activity and bed rest. At present, there is scientific evidence that prolonged bed rest is not effective and may be detrimental for patients with acute low back pain.54,55 Based on the best information available, bed rest should be kept to less than 2–3 days for nonradicular low back pain. Hagen et al., from the Cochrane Collaborative Group, reviewed nine clinical trials in which bed rest was used in patients with acute back pain and sciatica and concluded that there is not an important difference in the effects of bed rest when compared to exercise in this patient population and that prolonged bed rest does not appear to be indicated even in the case of sciatica.55 Hilde and colleagues, from the same Cochrane Collaborative Group, reviewed four clinical trials with a total of 491 patients in which advice to stay active was included as a treatment strategy and concluded that the best available scientific evidence suggests that physical activity has a beneficial effect for patients with acute low back pain.56 In the authors’ clinical practice, low-intensity aerobic exercise is routinely prescribed for patients with acute back pain. Walking or swimming are appropriate exercises to prescribe for patients with discogenic pain, while bicycling is adequate for those with posterior element injury. Patient education is very important and should start in the acute phase of rehabilitation. Individuals participating in the rehabilitation program should be educated in the basic concepts of the pathophysiology of their illness, patterns of back pain, and proper spine biomechanics. The patient should be oriented on how to identify changes of intensity, frequency, and duration of pain patterns, how they affect their rehabilitation, and how their medication should be taken. In
Section 5: Biomechanical Disorders of the Lumbar Spine
addition, strategies that allow the patient to cope with their pain are important and should be established early in the management process. The identification of barriers to recovery such as beliefs about the harm of physical activity, comorbid factors such as psychiatric illness, job dissatisfaction, and unemployment is important to prevent the progression to chronic pain.57–59 Physical modalities such as cryotherapy are frequently used in combination with prescribed analgesics at regular intervals. Although the physiologic effects of cold include analgesia, reduction of inflammation, and muscle spasm, making cryotherapy ideal for treatment for acute injury, there is no strong evidence in the medical literature for their benefits in the management of acute back pain.28,60,61 Standard physical therapy treatment has not been shown to be effective in changing long-term outcome of patients with back pain; however, there is a patient-perceived benefit from such treatment.62 It is the authors’ clinical experience that short-term supervised physical therapy early in the clinical course of patients with acute back pain allows a more rapid progression and transition to an activity program, and it is frequently recommended to their patients. Muscle weakness, inhibition, and imbalance particularly of trunk muscles is commonly seen in patients who present with acute or recurrent back pain. Isometric and static exercises should be initiated to retrain proper muscle firing patterns in patients with muscle inhibition and abnormal firing patterns. Identification of the neutral spine position for stabilization exercises is very important at this stage since spine stability is necessary prior to achieving mobility in exercise, work, and activities of daily living. Gradual pain-free range of motion exercises for the back, hips, and lower extremities should be instituted in the acute management. Although, these exercises are commonly used and reported to have good clinical results, there is conflicting scientific evidence that specific back exercises such as flexion, extension, or stretching produce symptomatic improvement in acute low back pain.63 Another modality often recommended in this phase of treatment is electrical stimulation for pain control. Transcutaneous electrical nerve stimulation (TENS) for analgesia has been used in the past by many clinicians treating acute back injury based on the physiologic effects of this modality, which is theorized to block pain perception at the level of the spinal cord and may also cause secretion of endogenous opioids.64 However, there is conflicting evidence for the effectiveness of these treatments in acute back pain, and recent data suggest that subthreshold TENS is not effective treatment for low back pain.65,66 There are additional data that electro-acupuncture is more effective than TENS and classic massage, particularly if indicated in combination with back exercises. This can be an effective option for the treatment of pain and disability associated with chronic low back pain.67 In that group of patients who show poor response to the initial treatment program of medications, modalities, and low-level exercise, consideration should be given to the use of interventional techniques. Injection techniques play a dual role in the acute phase of rehabilitation: that of helping in the diagnosis and identification of the pain generator, and that of an important therapeutic tool to aid in symptom control. In the authors’ treatment algorithm, the use of epidural steroid injections for discogenic pain and facet joint injections or medial branch blocks for posterior element injury is of the utmost importance, since pain control and improved tolerance to physical activity must be achieved prior to progressing to the recovery phase of treatment.
Recovery phase The recovery phase of treatment is the subacute period that focuses on restoring the biomechanical relations between the normal and
Table 90.5: Rehabilitation of Back Injury – Recovery Phase 1. Modalities: superficial heat, ultrasound, electrical stimulation 2. Range of motion exercises, static and dynamic flexibility exercises 3. Dynamic stabilization exercises 4. Closed chain exercises, proprioceptive neuromuscular facilitation 5. Dynamic strengthening exercise 6. Sport- or work-specific functional exercises 7. General conditioning 8. Gradual return to physical activity
injured tissue (Table 90.5). Patients should be advised to gradually increase their physical activity in daily living despite the existence of some pain. Physical modalities such as superficial heat, ultrasound, and electrical stimulation are commonly recommended for treatment of pain in the recovery phase. There is limited evidence in the scientific literature that selected modalities in isolation are effective in this phase of treatment; however, based on their physiologic effects of analgesia, reduction of muscle spasm, facilitation of muscle recruitment, and increased distensibility of soft tissue, they are used in the authors’ practice for a limited period of time in combination with therapeutic exercises such as flexibility training and dynamic strengthening.28,68 Massage and manipulation have been used extensively and are thought to be effective in acute pain when combined with exercises and education. However, Assendelft et al. reviewed randomized clinical trials of spinal manipulation for the treatment of low back pain and concluded that there is no scientific evidence that spinal manipulation therapy is superior to other standard or conventional modalities of treatment for pain relief in patients with acute low back pain.69 The medical literature is not clear and gives conflicting evidence for the use of spinal manipulation for exacerbations of pain or chronic pain, with some studies reporting good short-term results in acute exacerbations.70–72 In the authors’ practice, patients with acute pain or exacerbation of baseline chronic symptoms are referred for manual therapy with good subjective results of pain reduction and increased mobility. In the recovery phase, flexion- or extension-biased exercise should be prescribed based on the identification of the direction that exacerbates the symptoms. The McKenzie approach uses a mechanical assessment of the patient to identify direction of pain exacerbation and has been advocated by many clinicians. The centralization phenomenon or the reduction of pain with preferential direction of motion has been associated with good prognosis for recovery.73 Patients with axial pain secondary to discogenic disease may benefit from extension exercises while patients with posterior element or facet syndrome may benefit from flexion exercises.74 Care should be taken when exercising patients to extreme ranges of motion, since these positions may increase the compressive load to the intervertebral discs.24 There is some evidence that exercises may be effective for patients in the subacute or chronic stage of treatment and may slightly reduce the risk of additional back problems or work disability.75 The intensity of the exercises should be monitored, increased gradually depending on the clinical response, with a specific prescription, and in some instances even in the presence of some pain.76,77 995
Part 3: Specific Disorders
Strengthening of the core musculature has become important in the rehabilitation of patients with back pain. The muscles that are targeted for exercise training include the multifidi, quadratus lumborum, abdominals, and hip girdle muscles. Back stabilization exercises in the neutral spine position are used to initiate strengthening of the back and pelvic core musculature. McGill and others have looked at exercises that could be safely used for strengthening in patients with back pain and these include the curl-up, side bridge, and bird dog or quadruped exercise. Endurance training with a high number of exercise repetitions rather than high-resistance strength training should be emphasized in the patient with back pain at this stage.25,78,79 In the recovery phase, the stabilization program should progress in difficulty, moving from stable to unstable surfaces.80 As the patient’s symptoms improve, inflexibilities and muscle imbalances of specific muscles such as the hip rotators, iliopsoas, and hamstrings should be addressed. Dynamic flexibility training in sagittal, frontal, and transverse planes of motion should be started gradually (Fig. 90.1). Progression of the aerobic and conditioning program is continued during this phase.25 Analgesic and antiinflammatory medications can be prescribed at this point of the treatment program only to facilitate a gradual increase in activities, but should be prescribed for a fixed period of time. Opioid analgesics remain an alternative for patients with no relief from other medications and have been reported to increase back exercise performance in those with intolerance to exercise secondary to pain.81 Local injections and interventional techniques such as epidural, facet, and medial branch blocks or radiofrequency denervation could also be considered at this point in the rehabilitation of patients. When attempting higher levels of activity, symptomatic individuals may benefit from these procedures to control pain and allow participation in the exercise program.82,83 Special patient populations addressed with interventional procedures in this stage include athletes and individuals who need to return to heavy labor. It is the authors’ clinical goal to reduce the fear of activity in these patients.
Complementary medicine approaches to pain management which include acupuncture and relaxation techniques have also been used in this stage of rehabilitation; however, the effectiveness of these treatments in long-term management is not clear.84 The authors recommend using acupuncture to their chronic patients with acute exacerbations who show slow response to treatment, including integrating muscle relaxation and visualization techniques, who present with activity-related anxiety. The functional phase of treatment emphasizes restoration of function for work and activities of daily living (Table 90.6). Another important objective of this phase of treatment is the prevention or reduction of physical or mental disability as well as improving the patient’s quality of life. The final goal is to prevent dependence on medical treatment and allow the patient the transition to exercising on his or her own. At this stage, patients with disabling low back problems who fail to progress in treatment should be referred to a multidisciplinary or behavioral pain management program.85,86 Factors that may predict the failure of an interdisciplinary program in returning the individuals to work include those patients involved in compensation claims and those with a subjective feeling of being disabled.87,88
Functional phase In the functional phase, progression of trunk strengthening is emphasized. Exercises with gym balls, rotational patterns, and eccentric loading of the spine are emphasized (Fig. 90.2). Rainville et al.77 and Cohen and Rainville89 have reported the use of aggressive quota-based exercise programs with the intent of reducing disability and altering fears about functional activities. Their results demonstrate that this is an effective treatment strategy in patients with chronic pain. Improvement in pain intensity and frequency, posture, self-efficacy with activity, and well-being, in addition to increased return to work status, have been documented 6 months to 1 year following rehabilitation.90–92 Finally, normal spine mechanics for sports and work activities and progression of functional training is required prior to allowing the athlete to return to competition or the individual to return to full activity.
Fig. 90.1 Transverse plane rotational exercises. 996
Section 5: Biomechanical Disorders of the Lumbar Spine
Table 90.6: Rehabilitation of Back Injury – Functional Phase 1. Analgesic medications 2. Power and endurance exercises 3. Increase multiple-plane neuromuscular control exercises 4. General flexibility program
low back pain. More studies are required prior to recommending their widespread use.99–101 Another factor to be considered during the rehabilitation process is modification of activity and the work environment. Simple strategies such as establishing a standing rest period after sitting for 50 minutes to 1 hour has been shown to reduce the compressive load on the lumbar spine.102 In addition, avoidance of prolonged flexion and rotation activities during the rehabilitation process should be encouraged.
5. Trunk and extremity strengthening program
SUMMARY
6. Injection techniques
Rehabilitation of axial back pain requires comprehensive knowledge in the areas of epidemiology, anatomy, biomechanics, and pathophysiology of the disease process. This knowledge combined with a thorough history, physical examination, and diagnostic evaluation will allow the clinician to reach a complete diagnosis that includes the suspected pain generator and the functional deficits. This information is necessary to establish a rehabilitation plan that treats the patient’s symptoms, corrects the biomechanical deficits, allows return to normal function, and improves the quality of life. The rehabilitation program is divided in three separate phases with each one having specific goals. The acute phase has the goals of reducing the patient’s symptoms and protecting injured tissues; the recovery phase has the goals of allowing tissue healing as well as achieving normal strength and flexibility; and the functional phase has the goals of correcting abnormal biomechanics as well as returning the patient to normal function and preventing long-term disability. Components of the rehabilitation program that have been shown to be effective in the acute treatment of back pain include a short period of bed rest, low-level physical activity, patient education, and medications. In the recovery phase, flexion and extension exercises, stabilization training, and core strengthening programs have been shown to be clinically successful. Treatment strategies that have been effective in the functional phase include quota-based strengthening exercises and interdisciplinary rehabilitation in patients that fail other treatment options. Therapeutic modalities, manual techniques, and complementary medicine treatments are used based on their clinical effect with reported good results in the short-term management of back pain. However, in well-controlled, randomized clinical trials, there is a lack of scientific validation of their effects in the long-term care of patients with back pain.
7. Work modification 8. Improvement in sports specific techniques
Lumbar supports and braces have been used with the goal of preventing either the onset or recurrence of low back pain. However, the medical literature has not shown effectiveness for this intervention.93–95 In a rehabilitation program, lumbar supports may be used to provide short-term patient comfort, allow participation in an exercise program, and enhance trunk proprioceptive training.96 Special consideration should be given to the use of bracing in patients with axial back pain suspected of having spondylolisis.38 Interventional and injection techniques should also be considered in this stage of patient management. Butterman has used spinal steroid injections for degenerative disc disease in patients with chronic symptoms and acute exacerbations for temporary improvement in pain and function that allows return to activity.97 Zygapophyseal joint injections and radiofrequency denervation for the treatment of patients with zygapophyseal joint-mediated pain can also be considered in the functional phase. Sparse scientific evidence for the long-term effectiveness of these treatments has been evaluated by Slipman et al. in a critical review of the medical literature. However, these treatments remain viable options in the individual with posterior element symptoms and activity intolerance.98 Other techniques that are used for chronic low back pain and have gained recent acceptance include botulinum toxin injections and prolotherapy. Although these treatment are safe, with good anecdotal results when used for addressing the soft tissues as pain generators, there is no scientific evidence documenting their effectiveness in the treatment of chronic
Fig. 90.2 Advanced stabilization exercises. 997
Part 3: Specific Disorders
Interventional techniques should be considered part of the rehabilitation armamentarium and integrated into the different stages of treatment. They should be used to reduce pain in the acute phase, to allow an increase in activity tolerance in the recovery phase, and finally to manage symptoms exacerbation in the functional phase of rehabilitation.
27. Martin MD, Boxell CM, Malone DG. Pathophysiology of lumbar disc degeneration: a review of the literature. Neurosurg Focus 2002; 13(2). Online Available: http://www.medscape.com/viewarticle/442440
References
30. Kirkaldy-Willis WH, Wedge JH, Young-Hing K, et al. Pathology and pathogenesis of lumbar spondylosis and stenosis. Spine. 1978; 3(4):319–328.
29. Van Dieen JH, Weinans H, Toussaint HM. Fractures of the lumbar vertebral endplate in the etiology of low back pain: a hypothesis on the causative role of spinal compression in a specific low back pain. Med Hypotheses 1999; 53(3):246–252.
1. Takeyachi Y, Konno S, Otani K, et al. Correlation of low back pain with functional status, general health perception, social participation, subjective happiness and patient satisfaction. Spine 2003; 28(13):1461–1466.
31. Yong-Hing K, Kirkaldy-Willis WH. The pathophysiology of degenerative disease of the lumbar spine. Orthop Clin North Am 1983; 14(3):491–504.
2. Yelin E. Cost of musculoskeletal diseases: impact of work disability and functional decline. J Rheumatol (Suppl) 2003; 68:8–11.
32. Kirkaldy-Willis WH. The relationship of structural pathology to the nerve root. Spine 1984; 9(1):49–52.
3. Atlas SJ, Nardin RA. Evaluation and treatment of low back pain: an evidence-based approach to clinical care. Muscle Nerve 2003: 27(3):265–284.
33. Simpson EK, Parkinson IH, Manthey B, et al. Intervertebral disc disorganization is related to trabecular bone architecture in the lumbar spine. J Bone Miner Res 2001; 16(4):681–687.
4. Lee D. Low back pain intervention: conservative or surgical? J Surg Orthop Adv 2003; 12(4):200–202. 5. Long DM. Decision making in lumbar disease. Clin Neurosurg 1992; 39:36–51.
34. Ohnmeiss D, Vahharanta H, Ekholm J. Relation between pain location and disc pathology: a study of pain drawing and CT/discography. Clin J Pain 1999; 15(13):210–217.
6. Frymoyer JW, Cats-Baril WL. An overview of the incidences and costs of low back pain. Orthop Clin North Am 1991; 22(2):263–271.
35. Young S, Aprill C, Laslett M. Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3(6):460–465.
7. Hestbaek L, Leboeuf-Y de C, Engberg M, et al. The course of low back pain in a general population. Results from a 5-year prospective study. J Manipulative Physiol Ther 2003; 26(4):213–219.
36. Bernard TN Jr, Kirkaldy-Willis WH. Recognizing specific characteristics of nonspecific low back pain. Clin Orthop 1987; 217:266–280.
8. Salminen JJ, Erkintalo Mo, Pentti J, et al. Recurrent low back pain in early disc degeneration in the young. Spine 1999; 24(13):1316–1321. 9. Frymoyer, JW, Pope MH, Clements, JH, et al. Risk factors in low-back pain. J Bone Joint Surg [Am] 1983; 65(2):213–218. 10. Cady LD, Bischoff DP, O’Connell ER, et al. Strength and fitness and subsequent back injuries in firefighters. J Occup Med 1979; 21:269–272. 11. Frymoyer JW. Lumbar disk disease: epidemiology. Instr Course Lect 1992; 41: 217–223. 12. Biering-Sorensen F. A prospective study of low back pain in general population. ii Location, character, aggravating and relieving factors. Scand J Rehabil Med 1983; 15(2):81–88. 13. Borenstein DG. Epidemiology, etiology, diagnostic evaluation, and treatment of low back pain. Curr Opin Rheumatol 2000; 12(2):143–149. 14. Wasiak R, Verma S, Pransky G, et al. Risk factors for recurrent episodes of care and work disability: case of low back pain. J Occup Environ Med 2004; 46(1):68–76.
37. Dreyer SJ, Dreyfuss PH. Low back pain and the zygapophyseal joints. Arch Phys Med Rehab 1996; 77(3):290–300. 38. Gerbino PG, Micheli LJ. Low back injuries in the young athlete [review]. Sports Med Arthroscopy 1996; 4:122–131. 39. Young JL, Press JM, Herring SA. The disc at risk in athletes: perspectives on operative and nonoperative care. Med Sci Sports Exerc 1997; 29(S):222–232. 40. Kibler WB. A framework for sports medicine. PMR Clin N Am 1994; 5:1–8. 41. Revel M, Poiraudeau S, Auleley GR, et al. Capacity of the clinical picture to characterize low back pain relieved by facet joint anesthesia. Proposed criteria to identify patients with painful facet joints. Spine 1998; 23(18):1972–1976. 42. Bahshe R, Thumb N, Broll H, et al. Treatment of acute lumbosacral back pain with piroxicam: result of a double-blind placebo-controlled trial. Spine 1987; 12: 473–476. 43. Hosie GAC. The topical NSAID, felbinac versus oral ibuprofen: a comparison of efficacy in the treatment of acute lower back injury. Br. Clin Res 1993; 4:5–17.
15. Biering-Sorensen F. A prospective study of low back pain in a general population. ii Medical service-work consequence. Scand J Rehabil Med 1983; 15(2):89–96.
44. Spalski M, Hayez JP. Objective functional assessment of the efficacy of temoxican in the treatment of acute low back pain: a double-blind placebo-controlled study. Br J Rheumatol 1994; 33:74–78.
16. Hartvigsen J, Christensen K, Frederiksen H, et al. Genetic and environmental contributions to back pain in old age: a study of 2,108 Danish twins aged 70 and older. Spine 2004; 29(8):897–901.
45. Poslacchini F, Facchini M, Paleire P. Efficacy of various forms of conservative treatment in low back pain: comparative study. Neurol Orthop 1988; 6:28–35.
17. Simmons ED Jr, Guntupalli M, Kowalski JM, et al. Familial predisposition for degenerative disc disease. a case control study. Spine 1996; 21(13):1527–1529.
46. Dreiser RL, Marty M, Ionescu E, et al. Relief of acute low back pain with diclofenac-k 12.5 mg tablets: flexible dose, ibuprofen 200 mg and placebo-controlled clinical trial. Int J Clin Pharmacol Ther 2003; 41(9):375–385.
18. Livshits G, Cohen Z, Higla O, et al. Familial history, age and smoking are important risk factors for disc degeneration disease in Arabic pedigrees. Eur J Epidemiol 2001; 17(7):643–651.
47. Ruoff G, Lema M. Strategies in pain management: new and potential indications for COX-2-specific inhibitors. J Pain Symptom Manag 2003; 25(Suppl): 21–31
19. Pietila TA, Stendel R, Kombos T, et al. Lumbar disc herniation in patients up to 25 years of age. Neurol Med Chir 2001; 41(7):340–344.
48. Coats TL, Borenstein DG, Nangia NK, et al. Effects of valdecoxib in the treatment of chronic low back pain: results of a randomized, placebo controlled trial. Clin Ther 2004; 26(8):1249–1260.
20. Trainor TJ, Wiesel SW. Epidemiology of back pain in the athlete. Clin Sports Med 2002; 21(1):93–103. 21. Cooke PM, Lutz GE. Internal disc disruption and axial back pain in the athlete. Phys Med Rehabil Clin N Am 2000; 11(4):837–865. 22. Tong HC, Haig AJ, Nelson VS, et al. Low back pain in adult female caregivers of children with physical disabilities. Arch Pediatr Adolesc Med 2003; 157(11): 1128–1133. 23. Bogduk N. Anatomy and biomechanics. In: Cole A, Herring S, eds. Low back pain handbook: a guide for the practicing clinician. Philadelphia: Hanley & Belfus; 2003:9–26. 24. McGill S. Low back disorders: evidence-based prevention and rehabilitation. Champain (IL): Human Kinetics; 2002.
998
28. Rengachary SS, Balabhadra RS. Black disc disease: a commentary. Neurosurg Focus 2002; 13(2). Online Available: http://medscape.com/viewarticle/442455
49. Childers MK, Borenstein D, Brown RL, et al. Low-dose cyclobenzaprine versus combination therapy with ibuprofen for acute neck or back pain with muscle spasm: a randomized trial. Curr Med Res Opin 2005, 21(9):1485–1494. 50. Cosale R. Acute low back pain: symptomatic treatment with muscle relaxant drugs. Clin J Pain 1988; 4:81–88. 51. Arbus L, Fajadet B, Aurbet D, et al. Activity of tetrazepam in low back pain: a double-blind trial versus placebo. Clin Trials J 1990; 27:258–267. 52. Borenstein DG, Korn S. Efficacy of a low-dose regimen of cyclobenzaprine hydrochloride in acute skeletal muscle spasm: results of two placebo-controlled trials. Clin Ther 2003; 25(4):1056–1073.
25. Akuthota V, Nadler SF. Core strengthening. Arch Phys Med Rehabil 2004; 85(S): S86–S92.
53. Schnitzer TJ, Ferraro A, Hunsche E, et al. A comprehensive review of clinical trials on the efficacy and safety of drugs for the treatment of low back pain. J Pain Symptom Manage 2004; 28(1):72–95.
26. Bogduk N, Twomey LT. Clinical anatomy of the lumbar spine. Melbourne: Churchill Livingstone; 1997.
54. Nadler SF, Stitik TP, Malanga GA. Optimizing outcome in the injured worker with low back pain. Crit Rev Phys Med Rehabil 1999; 11:139–169.
Section 5: Biomechanical Disorders of the Lumbar Spine 55. Hagen KB, Hilde G, Jamtvedt G, et al. Bed rest for acute low-back pain and sciatica (Cochrane Review) The Cohrane Library 2004; Issue 2.
79. McGill SM. Low back exercises: evidence for improving exercise regimens. Phys Ther 1998; 78(7):754–765.
56. Hilde G, Hagen KB, Jamtvedt G, et al. Advice to stay active as a single treatment for low-back pain and sciatica (Cochrane Review) The Cochrane Library 2004; Issue 2.
80. Saal JA, Saal JS. Nonoperative treatment of herniated lumbar intervertebral disc with radiculopathy. An outcome study. Spine 1989; 14:431–437.
57. Feldman JB. The prevention of occupational low back pain disability: evidence based reviews point in a new direction. J Surg Orthop Adv 2004; 13(1):1–14. 58. Coste J, Lefrancois G, Guillemin F, et al. Prognosis and quality of life in patients with acute low back pain: Insights from a comprehensive inception cohort study. Arthritis Rheum 2004; 51(2):168–176. 59. Goubert L, Crombez G, De Bourdeaudhuij I. Low back pain, disability and back pain myths in a community sample: Prevalence and interrelationships. Eur J Pain 2004; 8(4):385–394. 60. Curkovic B, Vitulic Babic-Naglic D, Durrigh T. The influence of heat and cold on pain threshold in rheumatoid arthritis. Z Rheumatol 1993; 52:289–291. 61. Bleakley C, McDonough S, MacAuley D. The use of ice in the treatment of acute soft-tissue injury. Am J Sports Med 2004; 32(1):251–261. 62. Frost H, Lamb SE, Doll HA, et al. Randomised controlled trial of physiotherapy compared with advice for low back pain. Br Med J 2004; 329(7468):708. 63. van Tulder MW, Waddell G. Conservative treatment of acute and subacute low back pain. In: Nachemson A, Jonsson E, eds. Neck and back pain: the scientific evidence of causes, diagnosis, and treatment. Philadelphia: Lippincott Williams and Wilkins; 2000:241–269. 64. Han JS. Acupuncture and endorphins. Neurosci Lett 2004; 361(1–3):258–261. 65. Deyo RA, Walsh NE, Martin DC, et al. A controlled trial of transcutaneous electrical nerve stimulation (TENS) and exercises for chronic low back pain. N Engl J Med 1990; 322:1627–1634. 66. Marchand S, Charest J, Li J, et al. Is TENS purely a placebo effect? A controlled study on chronic low back pain. Pain 1993; 54:94–106. 67. Yueng C, Leung M, Chow D. The use of electro-acupuncture in conjunction with exercise for the treatment of chronic low back pain. J Altern Complement Med 2003; 9(4):479–490. 68. Gam AN, Johansen F. Ultrasound therapy in musculoskeletal disorders: a metaanalysis. Pain 1995; 63:85–91. 69. Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low back pain: A meta-analysis of effectiveness relative to other therapies. Ann Intern Med 2003; 138(8):871–881. 70. MacDonald RS, Bill CMJ. An open controlled assessment of osteopathic manipulation in non-specific low back pain. Spine 1990; 15:364–370 71. Sanders GE, Runert O, Tepe R, et al. Chiropractic adjustive manipulation on subjects with acute low back pain: visual analog pain scores and plasma beta-endorphines levels. J Manip Phys Ther 1990; 13:391–395.
81. Rashiq S, Koller M, Haykowsky M, et al. The effect of opioid analgesia on exercise test performance in chronic low back pain. Pain 2003; 106(1–2):119–125. 82. Curatolo M, Bogduk N. Pharmacologic pain treatment of musculoskeletal disorders: current perspectives and future prospects. Clin J Pain 2001; 17(1):25–32. 83. Lierz P, Gustorff B, Markow G, et al. Comparison between bupivacaine 0.125% and ropivacaine 0.2% for epidural administration to outpatients with chronic low back pain. Eur J Anaesthesiol 2004; 21(1):32–37. 84. Weiner DK, Ernst E. Complementary and alternative approaches to the treatment of persistent musculoskeletal pain. Clin J Pain 2004; 20(4):244–255. 85. Alaranta H, Rytohoski U, Ressannen A, et al. Intensive physical and psychological training program for patients with chronic low back pain: a controlled clinical trial. Spine 1994; 19:1339–1349. 86. Harhappa K, Mellin G, Jarvekaski A, et al. A controlled study on the outcome of inpatient and outpatient treatment of low back pain. Scand J Rehabil Med 1990; 22:181–188. 87. Hildebrandt J, Pfingsten M, Saur P, et al. Prediction of success from a multidisciplinary treatment program for chronic low back pain. Spine 1997; 22(9): 990–1001. 88. Rainville J, Sobel JB, Hartigan C, et al. The effect of compensation involvement on the reporting of pain and disability by patients referred for rehabilitation of chronic low back pain. Spine 1997; 22(17):2016–2024. 89. Cohen I, Rainville J. Aggressive exercise as treatment for chronic low back pain. Sports Med 2002; 32(1):75–82. 90. van Tulder MW, Jellema P, van Poppel MNM, et al. Lumbar supports for prevention and treatment of low-back pain. (Cochrane Review) From the Cochrane Library 2004; Issue 2. 91. Keller S, Ehrhardt-Schmelzer S, Herda C, et al. Multidisciplinary rehabilitation for chronic back pain in an outpatient setting: A controlled randomized trial. Eur J Pain 1997; 1(4):279–292. 92. Casso G, Cachin C, van Melle G, et al. Return to work status 1 year after muscle reconditioning in chronic low back pain patients. Joint Bone Spine 2004; 71(2):136–139. 93. Million R, Haavik-Nilsen K, Jayson M, et al. Evaluation of low back pain and assessment of lumbar corsets with and without back supports. Ann Rheum Dis 1981; 40:449–454. 94. Saal JA, Saal SS. Later stage management of lumbar spine problems. Phys Med Rehabil Clin North Am 1991; 2(1):221.
72. Senstad O, Leböeuf Y de C, Borchgrevink C. Frequency and characteristics of side effects of spinal manipulative therapy. Spine 1997; 22:435–441.
95. van Poppel MN, Koes BW, van der Ploeg T, et al. Lumbar supports and education for the prevention of low back pain in industry: a randomized controlled trial. JAMA 1998; 279:1789–1794.
73. Aina A, May S, Clare H. The centralization phenomenon of spinal symptoms: a systematic review. Man Ther 2004; 9(3):134–143.
96. McNair PJ, Heine PJ. Trunk proprioception: enhancement through lumbar bracing. Arch Phys Med Rehabil 1999; 80:96–99.
74. Donelson R. The McKenzie approach to evaluating and treating low back pain. Orthop Re. 1990; 19(8):681–686.
97. Buttermann GR. The effect of spinal steroid injections for degenerative disc disease. Spine J 2004; 4(5):495–505.
75. Kool J, De Bie R, Oesch P, et al. Exercise reduces sick leave in patients with nonacute non-specific low back pain: a meta-analysis. J Rehabil Med 2004; 36(2): 49–62.
98. Slipman CW, Bhat AL, Gilchrist RV, et al. A critical review of the evidence for the use of zygapophyseal injections and radiofrequency denervation in the treatment of low back pain. Spine J 2003; 3(4):310–316.
76. van Tulder MW, Goossens M, Waddell G, et al. Conservative treatment of chronic low back pain. In: Nachemson A, Jonsson E, eds. Neck and back pain: the scientific evidence of causes, diagnosis, and treatment. Philadelphia: Lippincott Williams and Wilkins; 2000:271–304.
99. Porta M, Maggioni G. Botulinum toxin (BoNT) and back pain. J Neurol 2004; 251(Suppl):5–8. 100. Difazio M, Jabbari B. A focused review of the use of botulinum toxins for low back pain. Clin J Pain 2002; 18(Suppl):155–162.
77. Rainville J, Hartigan C, Martinez E, et al. Exercise as a treatment for chronic low back pain. Spine J 2004; 4(1):106–115.
101. Yelland MJ, Del Mar C, Pirozzo S, et al. Prolotherapy injections for chronic low back pain: A systematic review. Spine 2004; 29(19):2126–2133.
78. Callghan JP, Gunning JL, McGill SM. The relationship between lumbar spine load and muscle activity during extensor exercises. Phys Ther 1998; 78(1):8–18.
102. Callaghan JP, McGill SM. Low back joint loading and kinematics during standing and unsupported sitting. Ergonomics 2001; 44(3):280–294.
999
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain
CHAPTER
Manipulation and Manual Methods
91
John J. Triano
INTRODUCTION Central axis pain is, perhaps, the core enigma of spine disorders. The diagnosis is one often made by exception and involving many forms of trial therapy before conclusion. Like all other sources of spine pain, the diagnosis may be confounded by the presence of other potential pain generators that have overlapping clinical and physical symptoms. Discogenic pain has variable presentation from primary, centralized aching spinal and paraspinal pain to bizarre sclerotomal pain of the lower extremities. Severity may wax and wane as patients undergo differing levels of weight-bearing load to their spine with episodes of overstrain to the disc material. Various forms of treatment from medication to spinal manipulation give relief that is temporary. Exercise may be relieving or aggravating. In a retrospective study, Smith and colleagues1 noted that 68% of patients with positive discography improved without surgery over a 4-year interval while 24% deteriorated. Some patients require more treatment to relieve their suffering than others. However, weight-bearing and activity intolerance is a consistent pattern among the various presentations of central axis pain. This section will discuss the foundation and application of spinal manipulation from a chiropractic perspective in the management of central axis spine pain. It is, perhaps, an axiom of today's healthcare environment that the approaches in spine care between chiropractors and allopathic physicians are perceived to somehow be diametrically opposed to each other. Such perceptions are the legacy of the sociopolitical conflicts of the twentieth century and its remnants that persist even today. This discussion contends that the facts of patient care make the approaches complementary and demands a greater need for integration of efforts by all providers to achieve the broadest benefit for patients. No more obvious a point of distinction is available than that of the treatment of discogenic, central axis pain syndromes. The key purposes for providing treatments (Fig. 91.1) are to relieve suffering, improve function, and maximize healing capacity. The nonoperative allopathic methods most often employ biochemical mediators to manage symptoms, followed by biomechanical interventions to modify loading of the spinal tissues to reduce local stress concentrations and strengthen core muscles while maximizing pain-free flexibility. The chiropractic methods seek to minimize or alter local physical tissue stress through the use of applied forces and moments, followed by interventions to modify behaviors that load the tissues, strengthen muscle and increase trunk stiffness, and improve painfree flexibility. Should either approach be insufficient, a surgical consultation can be considered. The practical difference, ignoring the debates over disciplinary jargon, is the relative emphasis on the best means to reduce tissue stress, inflammation, and pain. The allopathic view relies heavily on chemical intervention to block pain and suppress inflammation followed by efforts to reduce tissue stress. The
Allopathic methods
Chiropractic methods
Analgesics, anti-inflammatory, fomentation, injections
Manipulation, continuous passive motion, mobilization, neuromuscular therapy, herbal preparations, fomentation
Symptom control:
Patient activation: Assurance, resume activity to tolerance, patient education Rehabilitation: Flexibility exercise, muscular endurance & strengthening Maximum benefit Discharge to episodic management
Surgical consult, lifestyle modifications, chronic pain management
Fig. 91.1 Convergence of approach in the management of discogenic, central axis pain syndromes for chiropractic spinal manipulation versus allopathic disciplines.
chiropractic view prefers to alter the mechanical environment, allowing inflammation and pain to subside. Patients often consult both types of care simultaneously without disclosing to either. Increasing professional interactions between the groups suggest that a meaningful number of cases may benefit from both approaches. Only in recent years has there been quantitative evidence to understand the mechanical lesion treated by manipulation as well as the effects of the treatment itself. Moreover, the evidence suggests how the ‘subluxation lesion’ may contribute to symptom episodes in patients with discogenic pain. Spinal manipulation is a mechanically applied therapy used to relieve nociceptive pain and improve function. A number of clinical and physiological effects are known2–4 and their attributes require appropriate and skillful application to achieve safe and successful outcomes.5–9 The clinical benefit from use of these procedures has been studied10,11 in subacute and chronic back pain cases, a heterogeneous 1001
Part 3: Specific Disorders
population of patients including many with central axis pain. This chapter will discuss the theoretical underpinnings of spinal manipulation and its use in the management of central axis pain.
THE BASIS OF SPINAL MANIPULATION The lesion
Load step
Spinal manipulation is the use of controlled forces and moments applied to the spine or pelvis. Application of the loads may be manual or mechanically assisted. The intention of load application is to reduce local stress concentration within the intervertebral articulations and disc, improve function, and to reduce the associated local and, when present, remote symptoms. The mechanism of the manipulable spinal lesion is characterized biomechanically as a buckling event. These phenomena have been observed in orthopedics for some time among some patients with an unstable wrist carpus12,13 and are associated with multiarticular kinetic chain systems like the spine that rely on biarticular muscles for establishing local mechanical equilibrium and control. Detailed review of the biomechanics of these lesions can be found elsewhere.14–16 Briefly, buckling may involve single functional spinal units or an entire spinal region. They are caused by a mismatch in timing or amplitude of response between the local and regional muscular control systems (Fig. 91.2). A local shift of intersegmental joint configuration occurs within the bounds of normal range
that is disproportionate to the task at hand. Symptoms arise from the increase in local tissue strain. The clinical presentation of the patient and the exact symptoms depend on the identity of the tissues strained to injury threshold and the presence of comorbid conditions. The mismatch between the demand of spinal load and appropriate local intersegmental stiffness results in a sudden shift in relative joint configuration (Fig. 91.3). That is, there is a disproportionate repositioning of the joint within the bounds of its normal functional range. Instead of supporting the patient's posture and activity with minimum local tissue strain, the new configuration may result in a local stress concentration leading to symptoms of the involved tissue. Effectively, while the buckled equilibrium may be functional, it is with increased cost in terms of comfort. These types of buckling phenomena have now been observed under biomechanical testing conditions in vitro for isolated segments17–19 as well as the lumbar region20 and, by happenstance, during experimental studies of weight lifters when an unexpected injury occurred.16,21 The factors associated with development of local buckling are found in Table 91.1. Prior injury or degenerative disease potentiates buckling, allowing it to occur more easily, effectively lowering the critical load requirements and reducing the ultimate load capacity. Figure 91.4 describes the chain of events leading to symptoms.
0
0.5
1
1.5
2
2.5
3
Angular displacement (deg) Fig. 91.3 The mismatch between the demand of spinal load and appropriate local intersegmental stiffness results in a sudden shift in relative joint configuration.
Regional control muscles
Local control muscles
Table 91.1: Etiologic factors for local joint buckling events based on available biomechanical experiments in vitro and in vivo15,16
Fig. 91.2 Dual spinal stabilizing muscle systems. (Left) Regional stabilizers drive overall postural configurations to perform tasks. (Right) Local stabilizers coordinate intersegmental stiffnesses and movement to minimize joint structural stresses. Bergmark (1987) and McGill (2002). 1002
Causative
Facilitating
Sudden incremental load after prolonged static posture
Vibrating environments
Unexpected load
Disc damage
Rapid load events (500 lb/sec) Uncoordinated/fatigued effort
Section 5: Biomechanical Disorders of the Lumbar Spine
governing diagnostic interpretation is the partitioning of patient response to applied loads into categories of those that relieve or those that aggravate symptoms. Results that reduce symptoms and any referred or radicular pain components are the desired motions for directing the choice of procedure and the application of manipulative methods. Joint or nerve blocks may be helpful in identifying the pain generator (facet, sacroiliac, or nerve root) and quelling local inflammatory responses that may be interfering with patient recovery. Therapeutic trials provide an inexpensive and timely means to evaluate manipulation as a treatment option. Patients who are good candidates tend to show rather quick symptomatic response, resulting in noticeable improvement generally within a 2-week interval from onset of care.
Manipulable lesion (buckling)
Stress concentration
Neurogenic pain
Non-neurogenic pain
Inflammation
Neural sensitization
Local segmental/ central axis pain
Radicular/ pseudoradicular symptoms
Manipulation skill and control factors
Reduce response threshold
Sensitization to normal motions
Fig. 91.4 The chain of events leading to symptoms.
Diagnostic findings The determination of a manipulable lesion in isolation is relatively straightforward but is made more complicated by the presence of other pathology. Table 91.2 provides a review of findings warranting a trial of spinal manipulation. Unraveling symptoms that may respond to manipulative methods, however, is easily achieved through a trial therapy interval. Provocative testing can be used to identify the specific directions of loading that give comfort and relieve symptoms. Such maneuvers guide the selection of treatment procedures that match patient needs. These maneuvers apply controlled forces and moments, often involving postural positioning or tasks, to the suspected dysfunctional joint. Based on knowledge of any comorbid pathoanatomical diagnosis and associated findings (palpation sensitivity, flexibility, orthopedic/neurologic testing and imaging/laboratory test results), initial trials of provocation are performed in an effort to reduce local tissues stress. The principal
Table 91.2: Signs and symptoms of the isolated manipulable lesion Local back pain with or without limb pain absent progressive neural signs Focal sensitivity to manual pressure Local muscular hypertonicity with or without tender points Limited joint compliance in mid-range position and/or end-range limitations with pain on overpressure testing Reproduction of symptoms with joint compliance or end-range motion testing Local soft tissue edema Altered local skin turgor, temperature or color
Manipulation, like all other therapy, must be performed using sufficient skill and knowledge. Applications include the ability to use thrusting and nonthrusting techniques where appropriate, which requires an in-depth clinical assessment and differential diagnosis.22 Used in trained hands, these methods are remarkably safe.23–25 Evidence shows that minimally skilled individuals are ineffective in producing good outcomes6 with recovery from a symptomatic episode. Efforts to extend one's practice into the field of manipulation based on superficial weekend training programs may be pedagogically wrong and potentially dangerous.26,27 Effective treatment needs to be administered with sufficient threshold, dosage, and duration using appropriate procedures that account for patient stature and coincident pathology. Threshold is defined as the application of necessary and sufficient joint load to effect a change in its behavior and symptoms. Threshold levels are a function of patient joint stiffness, soft tissue viscoelastic properties, and muscular tension that may vary themselves, based on age, severity or acuteness of symptoms, and patient anxiety levels. Assessment of tissue condition to guide application of the procedures is a skill developed through supervised practice and experience. In cases where there are multiple tissue elements involved (e.g. reactive muscle tension, capsular swelling, adhesions, hemorrhage), sequential procedures may be necessary. Staged procedures can speed the removal of local fluid or breakdown interstitial adhesions without exceeding patient tolerance for more severely injured or sensitive tissues. Choice of treatment modality is dependent on the presence or absence of pain during the examination (provocation testing). Empirically, patients with localized pain seem to respond better to impulse loads as long as the preliminary joint positioning can be engaged without difficulty.22 Patients who are unable to be effectively positioned or have chronic or referred pain may initially benefit more rapidly using procedures without impulse. Effective dosage and duration of therapy varies with patient cooperation on reducing aggravating factors, performing recommended exercises to gain stability, the presence of other pathology or degenerative change, and condition severity. In general practice, initial treatment dosage is 2–3 sessions per week. Haas et al.28 have shown a direct relationship between treatment frequency and outcome scores for pain and disability for patients with chronic low back pain. A statistically significant linear relationship noted greater improvement for patients treated 3–4 times per week over a 3-week period. Across the literature, the average number of treatment sessions to maximum improvement for uncomplicated cases ranges from 8 to 18 with a range of approximately 1–40 treatments, depending on complexity and complications.29,30 1003
Part 3: Specific Disorders
TREATMENT METHODS Manual therapy concerns itself with the treatment of functional disturbances of muscle and joints including their local or remote symptoms. There are a number of ways in which manual therapy has been divided for discussion. Manipulation is a specific form of manual method that uses rapid impulse loads to the body structures. Manipulation can be quantitatively differentiated from other methods on the basis of speed of application14 and the differing response of the body tissues to rapid loading. While many systems of manual treatment methods exist, including manipulation, the common factor is the controlled application of loads (forces and moments) to the spine. The various approaches may be most easily understood when broken down into their biomechanical control parameters. Such classifications also help to align treatment objectives to therapeutic goals. That is, the body's biomechanical response to load application will depend on tissue properties and their reserve viscoelastic and stiffness characteristics. The various procedures span a spectrum of force and moment amplitude, speed, and direction of application that are designed to influence joint and disc strain and normalize mobility. The therapeutic loads can arise from two primary sources. They are generated either by action of the treating physician or from patient muscle action (stretching, relaxing, or contracting) under the guidance of the provider. Depending on the clinical discipline base (chiropractic, osteopathy, or manipulative medicine) of the provider administering these procedures, the specific name will vary (Table 91.3). Guided patient muscle action may be termed neuromuscular therapy, muscle energy, or counterstrain maneuvers. Provider-induced motions are typically characterized by repetition rate, speed, and amplitude and fall under the terms manipulation or adjustment and mobilization. Finally, various assistive devices that may be used to control the patient motion direction, rate, and amplitude are termed mechanically assisted procedures. These latter may be coupled with manipulation methods to provide motion assisted manipulation procedures.
Guided patient muscle activation Neuromuscular therapy (NMT) utilizes direct muscle action as well as associated neuromuscular reflex mechanisms to improve mobility and normalize muscle tone. Its action is based on the principle that inhibited or weakened agonists or competition of hypertonic antagonists may limit joint function. For example, spinal motion of rotation may be limited by inhibited contralateral transversospinal groups or by shortened ipsilateral transversospinal muscles. The pattern is determined by provoking local joint motion and determining its relative compliance in a direction and contrasting that with the presence of muscle tenderness and relative hypertonicity.22 There are three types of NMT, their use being dependent on whether the desired effect is to relax hypertonic agonists or strengthen them or to relax hypertonic antagonists as noted below. NMT1: Agonist muscle considered weakened or hypotonic. 1. Engage the functional motion barrier; 2. Select appropriate agonists; 3. Teach agonistic tension in the direction of movement to direction to increase the joint flexibility; a. Use passive motion to help position the patient; b. Use cutaneous stroking/tapping to facilitate muscle recruitment; 4. Homecare: 2–5-second repetitions.
1004
NMT2: Postisometric relaxation of shortened, tonic antagonists muscles 1. Passively stretch the shortened muscle limiting the motion; 2. Hold and have the patient isometrically contract the agonist muscle in a direction to increase the joint flexibility; 3. Gently stretch further during postisometric relaxation phase for 3–10 seconds; 4. Repeat steps 1–3 from the new position up to 4 cycles; 5. Homecare: muscle stretching for phasic and tonic muscles. NMT3: Mobilization using reciprocal inhibition of the antagonists 1. Identify the shortened muscles restricting motion; 2. Use NMT3 if contraction of the shortened muscle is painful (often when radicular pain is present); 3. Passively position at the functional barrier; 4. Contract in direction of motion restriction for 5–10 seconds; 5. Use manual mobilization (see below) in the same direction. Muscle energy techniques are essentially the same as NMT1. Counterstrain, on the other hand, is a different approach, based on the effort to shorten muscles that are tense in association with defined, painful trigger points that are palpated as tense nodular areas of soft tissue of reduced compliance. The painful point may reside in the muscle or be at a referred site typical for each muscle. The operator positions the joint to shorten the affected muscle and produce mild strain in its antagonist. The position continues to be refined until the local area of tenderness is reduced or disappears. The position is held for about a minute and a half to give time for proprioceptive adaptation within the muscle. When the tenderness has been resolved and position held for sufficient time, the limb is slowly returned to a neutral joint position so as not to introduce a rapid stretch to the previously sensitive stretch reflex receptors. These methods are often used for patients with acute strain injury and locally tissues to direct loading. They are also considered useful in older or frail patients. Whereas the action of NMT procedures is directed in altering joint mobility through muscle action (stretching, relaxation, and isometric tensing), the mechanism of muscle energy and counterstrain is believed to be more associated with the effects of direct alteration of muscle tone. As noted by Murphy31 the restoration of joint functional range and normal muscle tone arises from several hypothesized benefits. They include relaxing hypertonic muscle to decrease oxygen demand and local pain, increasing circulation to the area to wash out metabolic waste products, and promoting greater venous and lymphatic drainage to reduce edema.
Provider-induced loading Loads applied by the treating doctor to the patient's spine are controlled in terms of their speed, amplitude, displacement, frequency, duration, and direction. They may be induced manually, through use of instrumented treatment tables and devices, or a combination of both. The procedures fall into categories of continuous passive spinal motion (CPM); mobilization; high-velocity, low-amplitude (HVLA) thrusting techniques, and mechanically assisted procedures (see Table 91.3). Slow, externally applied procedures such as continuous passive motion (CPM), mobilization methods, and flexion distraction techniques result in decreasing internal disc pressures,32 as shown in Figure 91.5. Other benefits include the dispersion of local edema,15,33 prevention or disruption of joint adhesions and stimulation of connective tissue healing34–36 within functional limits. The slow, cycled motions influence time-dependent viscoelastic characteristics within the affected tissues, shifting fluid between various body compartments.
*
Manual + mechanical Manual + mechanical
CPM + HVLA Impulse hammers
Mechanically assisted HVLA
Manual
Manual
HVLA
Manual
Grades I–IV Manual
Manual
Flexion-distraction (F/D)
Flexion–distraction + auxiliary pressures
Mechanical
Continuous passive motion (CPM)
Agonist & Antagonist
Mobilization
Unloaded spinal motion
Counterstrain
Agonist muscle
Agonist muscle
NMT 3 (Analogous to NMT 1)
Antagonist muscle
Agonist muscle
NMT 1 NMT 2
Application
Subcategory
BW, patient body weight; ** BMI, patient body mass index.
Provider-induced loads
Neuromuscular therapy
Guided patient muscle action
Muscle energy
Category
Therapeutic loading source
Impulse
Periodic+high speed / impulse
High speed / impulse
Periodic / cyclic
Periodic / cyclic
Single, short duration impulse (LLar >LLur = MPur > HIur
Rotation
LLar = MPar > HIar
Lateral bending
HIur > MPur >LLur = HIar > MPar > LLar
Lateral shear
HIur > MPur = HIar >LLur > MPar > LLar
Axial compression
HIar > MPar > LLar
Anterior shear
MPar > MPur >LLur = LLar > HIar > HIur
Procedures: MP, mammillary push procedure; HI, hypothenar ischium; LL, long lever. Patient positioning: ar, axially rotated; ur, unrotated.
DIAGNOSTIC INDEPENDENCE OF MANIPULATION Significant cross-discipline confusion exists regarding the issue of pathoanatomical diagnosis. The disarray of thought revolves around two factors. First is the failure of the medical model to adequately predict treatment outcomes as a function of pathoanatomical diagnosis.38 The second is the continuing inability to quantitatively measure the manipulable lesion (buckling event) in a clinical setting. Spine dysfunction and disease is a continuum of interrelated severity and stages that may arrest with local healing or progress based on many
extrinsic and intrinsic variables. Despite the occasional clarion calls for a ‘specific diagnosis’ to drive selection of treatment for a predictable outcome, widespread evidence shows that only the extremes of some pathology reach that level of predictability. For the remainder, significant proportions of the population have abnormal structure on X-ray or advanced imaging that is clinically silent. Others with no identifiable abnormality suffer serious activity limitation because of pain. Likewise, patients with asymptomatic pathoanatomy may become symptomatic under given circumstances. These factors were discussed under the section on the evidence of buckling as the mechanism of the spinal lesion. Both those with pathoanatomy and those without are included among those patients who may benefit from use of manipulation methods in their care. Providers skilled in performing manipulation deal with biomechanical relationships among different tissue components. Pathoanatomical diagnosis, while unable to drive specific treatment successfully, remains an important part of treatment planning. Knowledge of existing pathology, along with information from the patient's examination, form a significant part of the treatment plan. The intent is to alter local tissue strains, particularly at the suspect pain generator, reducing pain and fostering normal healing as necessary. Thus, the tissue involved, local geometry, and pathomechanics form the starting point for procedure selection. The final procedure results from the feedback of provocation testing. The objective of altering local tissue strains, then, forces the doctor to view diagnosis differently. It is less from a classical perspective and more as a means of anticipating necessary modifications. For example, presence of degenerative spondylosis or a disc bulge narrowing the lateral recess will cause the provider to identify patient positioning for delivery of the treatment that will facilitate a maximum volume of the canal and recess. Similarly, patients with radicular syndrome must be positioned and treated using methods that decompress the offended
Table 91.6: Factors governing the development of load parameters during HVLA spinal manipulation Independent factors Postural configuration Phase
Dependent factors
Patient
Operator
Gravity
Muscular effort
Inertial load
Amplitudes**
−
+
+
+
−
Directions
+
+
−
+
−
−
−
+
+
−
−
−
−
+
−
Preload procedure setup ***
Magnitudes
*
Stability* Dynamic impulse Amplitudes**
−
−
+
+
+
Cycles
−
−
+
+
+
Directions
***
Durations Magnitudes Slopes
**
*
*
+
+
+
+
+
−
−
−
+
+
−
−
+
+
+
−
−
+
+
+
There are four magnitude quantities: 2 for loads (force & moment) & 2 for slopes, which are equivalent to the speed of force and moment development. ** Each factor has six components (3 forces & 3 moments). Only two of the three components are mathematically independent as they are mechanically coupled to the magnitudes by the equation M = (C12 + C22 + C32). *** There are six direction components (3 force & 3 moments) which may be defined as positive or negative with respect to a reference frame. From: Triano JJ, Rogers CM, Combs S, et al. Developing skilled performance of lumbar spine manipulation. J Manip Physiol Ther 2003; 26:539–548.
1008
Section 5: Biomechanical Disorders of the Lumbar Spine
A 500
400
Newtons
300
200
Review and best evidence synthesis of the English and Northern European literature on randomized trials by Bronfort and colleagues11 summarizes the information on utility of manipulation methods in contrast to sham and alternate treatments. For acute episodes, there is moderate evidence that HVLA provides more short-term pain relief than mobilization methods and detuned diathermy, and limited evidence of faster recovery than a commonly used physical therapy treatment strategy. For patients with more chronic pain, HVLA has an effect similar to11 or better than10 use of nonsteroidal antiinflammatory medication. It is effective in the short term when compared with placebo and general practitioner care, and in the long term compared to physical therapy. There is limited evidence that HVLA is superior to chemonucleolysis for disc herniation in the short term. Triano et al.,43 in a small sample of patients, showed evidence that painful internal disc derangement on CT discography will respond with symptom reduction using HVLA procedures. In a trial contrasting the effects of medication management versus manipulation, Giles and Muller10 showed that the highest proportion of early suppression of symptoms was found for manipulation at 27.3% with medication achieving 5%. In those not reaching asymptomatic status, manipulation achieved the best overall results as reported by pain scales, Oswestry scores, and range of motion. However, the data do not strongly support the use of only manipulation or only nonsteroidal antiinflammatory medication for the treatment of chronic spinal pain.10 As evidenced by patients who often elect to consult medical providers and chiropractors simultaneously without informing either, there appears to be a synergistic effect from both.
CASE EXAMPLES 100
0 −100 B Fig. 91.7 Measures of the summation effect of superimposing the momentum of CPM (lower trace) with the HVLA procedure (upper trace sums HVLA + CPM) at the lumbosacral junction.
nerve and are generally identified by those postures that are relieving rather than provoking of discomfort. Only those patients with distinct contraindications cannot undergo a trial of manipulation.
TREATMENT EFFECTIVENESS As in all other forms of treatment, the Hawthorne or placebo effect plays a role in treatment outcome. In numerous studies, chiropractic patients record greater satisfaction with their treatment experience than when they are attended by other providers,39,40 an observation often triggering the assumption of placebo as the sole operational mechanism. At least two controlled clinical trials have addressed the question of placebo effect directly.41,42 In both studies, all treatment groups showed improvement over time. However, the patients receiving thrusting procedures demonstrated significantly greater and more rapid rates of improvement from their symptoms and in their ability to function than in the control group. While physician attention, in any form, appears to benefit patients with back pain, the data also shows that, at least for thrusting techniques of manipulation, there is a treatment-specific advantage beyond the non-specific effects.
Figure 91.8 shows the discogram of a 36-year-old female patient with chronic low back pain onset following a heavy lifting incident 6 months earlier. Medical management and physical therapy procedures had failed. An intradiscal electrothermal therapy procedure was attempted following discography, yielding 2 months of pain relief. With renewed symptoms, she became increasingly weightbearing and activity intolerant with low back and pseudoradicular leg pain. Her range of motion, particularly in flexion, was limited to 30 degrees. The spinous processes of L4 and L5 were tender and there was significant muscle tone asymmetry in the paraspinal group and quadratus lumborum. Efforts to test midrange joint compliance reproduced pain when extension, right bending, or axial rotation provocation was attempted. The patient was initially treated with in-office prone CPM in flexion with left lateral bending (Fig. 91.9) followed by left lateral decubitus position using left lateral bending CPM coupled with flexion (Fig. 91.10). As CPM methods helped reduce immediate discomfort, motion-assisted HVLA was applied with the patient in left lateral decubitus posture with CPM in right lateral bending. Home exercise focused on flexibility in range of motion and spine stabilizing exercises. She experienced good relief of symptoms and a gradual return to normal activities of daily living over a period of 7 weeks. The patient remained sensitive to heavy lifting, push–pull tasks, and sudden or awkward trunk postures. Over a 3-year period, she has experienced decreasing frequency of episodes at 1–2 per year requiring 1–2 weeks of treatment.
SAFETY AND CONTRAINDICATIONS No discussion of the use of spinal manipulation would be complete without addressing the issue of safety. Rare reports of adverse effects from spinal manipulation to the lumbar spine have been recorded.24 Based on the rate of utilization for these procedures in 1009
Part 3: Specific Disorders
A
B
Fig. 91.8 Internal disc derangement at L4–5 by discogram showing a fissured disc from annular tears anteriorly and at the 3 o'clock position with extravasation.
Fig. 91.10 Left lateral bending with left lateral decubitus CPM. (From Bougie and Morganthal, with permission Triano J. 2001.) Fig. 91.9 Prone CPM in flexion with left lateral flexion coupling. (From Bougie and Morganthal, with permission Triano J. 2001).
CONCLUSIONS the reported literature, the incidence of serious complication is negligible (50% symptom reduction. They also reported more than 50% of the subjects improved standing and/or walking tolerance. The aforementioned literature strongly suggests that transforaminal ESI should be the standard of care index interventional spine procedure for patients with spinally mediated lumbar axial pain syndromes associated with radicular involvement due to HNP and/or spinal stenosis when more conservative measures have failed. Furthermore, in the case of the majority of HNPs, the known phagocytic immunologic response and consequent benign anatomic natural history assists in the relatively high rate and long-term success of transforaminal ESIs.34,35
CONCEPTUAL PATHOPHYSIOLOGIC MECHANISMS OF LUMBAR AXIAL PAIN SYNDROMES WITHOUT RADICULAR INVOLVEMENT DUE TO A DISCOGENICMEDIATED INFLAMMATORY RESPONSE Some important inferences from the aforementioned literature on the successful long-term treatment of HNP-associated lumbar axial pain syndromes with corroborative radicular involvement may be extracted that, when combined with known previously stated
basic science literature and lumbar spinal anatomy, suggest a possible utilization for transforaminal ESIs in the interventional treatment of discogenic-mediated lumbar axial pain without radicular involvement. The similarities in the basic ideologies by which the initial incorrect thought processes of compression as the sole mechanism of radicular pain due to HNP requiring discectomy as stated nearly a century ago by Mixter and Barr36 mirror recent theory that motion segment instability and/or structural disc pathology is the sole mechanism of discogenic-mediated lumbar axial pain without radicular involvement. In the decades subsequent to Mixter and Barr’s36 landmark article identifying HNP pathology as a key source of lumbar axial and radicular pain, there have been many attempts to identify the precise pathophysiologic mechanism of discogenicmediated lumbar axial pain without radicular involvement. As stated earlier in this chapter, over the years, there have been key pieces of literature to suggest that a tear in the outer one-third of the anulus of the intervertebral disc may be the most common etiology of acute spinally mediated lumbar axial pain.10,37 As with the painful sequelae of most degenerative spinal conditions, improvement and eventual remission within 6 weeks is the natural history. However, subacute symptoms can persist and the mechanism for this may be inflammatory in nature.38 The basic science literature discussed earlier in this chapter has repeatedly and clearly demonstrated the inflammagenic properties of the intervertebral disc, particularly the nucleus pulposus when it is exposed to the ventral epidural space.13–17,38 This literature lends credence to the mechanisms by which transforaminal ESI effectuate symptom relief on a molecular basis. Therefore, the possibility of a focally contained inflammatory response to a centrally or paracentrally contained herniated disc is entirely possible and may be instrumental in pain generation as well as inhibition of the natural healing processes known to exist. In fact, a contained HNP may chemically sensitize the posterior longitudinal ligament, resulting in axial pain in a fashion similar to that of inflammatory radicular pain due to an HNP sensitizing a nerve root. Furthermore, patients with internal disc disruption syndrome in which an annular fissure extends from the nucleus pulposus to the outer one-third of the anulus (which may or may not be associated with a HNP) and may pierce through the outer anulus and intermittently or consistently communicate microscopic amounts of nuclear material to the ventral epidural space ensuing in an intermittent and/or ongoing focal discogenicinduced inflammatory response (Fig. 92.2). This pathophysiologic model may explain why a randomized, prospective, double-blind clinical trial performed by Simmons et al.39 failed to demonstrate a statistically significant benefit to intradiscal corticosteroid infusions when compared to placebo. The aforementioned hypothesis suggests the inflammatory response occurs in the ventral portion of epidural space on the floor of the spinal canal juxtapositioned to the afflicted intervertebral disc(s) rather than within nuclear material encased by the anulus fibrosus.
EFFICACY OF TRANSFORAMINAL ESI FOR LUMBAR AXIAL PAIN SYNDROMES WITHOUT RADICULAR INVOLVEMENT To date, there have been only two nonrandomized, retrospective studies reporting on the outcome of transforaminal ESI on spinally mediated lumbar axial pain due to discogenic pathology without imaging evidence of nerve root involvement. One is a subgroup reported by Rosenberg et al.40 stating greater than 50% pain reduction after one year in 59% of patients. The other study reported by Manchikanti et al.41 on patients with spinally mediated lumbar axial pain treated by one of three interventions: (1) blind interlaminar 1015
Part 3: Specific Disorders Anterior (ventral)
Posterior (dorsal)
Route of infusion of transforaminal ESI Posterior longitudinal ligament
Location of discogenic-induced focal inflammatory response on spinal canal
Vertebral body
Inferior articular process Superior articular process
Spinal process
Nucleus pulposus Articular intervertebral disc
Neural foramen
Annulus fibrosis
Spinal process
Vertebral body Outer 1/3 of annulus containing a complex network of pain transmitting nerve fibers
Spinal canal
ESI, (2) fluoroscopically guided caudal ESI, and (3) fluoroscopically guided transforaminal ESI, states that superior short- and long-term pain relief is achieved via the transforaminal route. This conclusion makes anatomical sense as transforaminal ESIs likely distribute injectate more focally to the ventral epidural space when compared to interlaminar and caudal route and therefore are more target specific when attempting the deliver medication to a possible focal posterior discogenic-induced inflammatory response. We are in no way suggesting that transforaminal ESI should be utilized for low back pain in general. However, based on the previously described history of spinal disorders, spinal anatomy, basic science literature, inferences from the current class I evidence in the interventional treatment of HNP and ensuing inflammatory radicular pain, and some preliminary retrospective data, as well as our own anecdotal experience, transforaminal ESIs may be a possible spinal intervention in the treatment of discogenic-mediated lumbar axial pain. Certainly, further study is required in the form of randomized, double-blinded, placebo-controlled clinical trials to elucidate the role, if any, of transforaminal ESIs in the treatment of discogenic-mediated lumbar axial pain without radicular involvement. As previously implied, the best route for infusion of corticosteroids into the ventral epidural space in patients with a potential component of focal posterior discogenic inflammatory response is the transforaminal route. In many cases, the specific level of discogenic pathology has not yet been elucidated at the algorithmic point of consideration of ESIs for the treatment of lumbar axial pain thought to be potentially due to a discogenic inflammatory etiology. In fact, more than one segmental level may be contributing to inflammation in the ventral aspect of the lumbar epidural space. Therefore, unless imaging strongly suggests one segment, the S1 transforaminal ESI is recommended (Figs 92.3, 92.4). This route allows the clinician to mechanically drive the corticosteroid injectate, typically 12–18 mg of betamethasone, diffusely along the floor of the lumbar spinal canal via a pressure effect utilizing 3–5 cc of 1% lidocaine in an attempt to quell potential inflammation along the ventral epidural space incited by leakage of nuclear material. In those patients where one-level 1016
Fig. 92.2 Authors’ rendition of the pathophysiologic model by which an intermittent or continual posterior discogenic inflammatory response may occur in the ventral portion of the epidural space due to leakage of nuclear inflammogens.
Fig. 92.3 An AP view of a left S1 transforaminal ESI (note the outline of the left S1 root sleeve inferior and medial to the left S1 pedicle as well as the degree of dispersion of contrast dye upon cephalad flow into the inferior portion of the lumbar spinal canal with maintenance of ipsilateral flow cephalad to the L4 level).
disease is strongly suspected, a smaller volume of local anesthetic may be infused after the corticosteroid dose at the foraminal level below the suspected level to deliver the corticosteroids in the cephalad direction more focally on the ventral aspect of the spinal canal at the posterior aspect of the suspicious intervertebral segment. In cases where a nonhealing annular tear(s) exists communicating nuclear material to the ventral epidural space, mediation of the inflammatory response may create a more optimal environment for spontaneous healing of the annular tear.
Section 5: Biomechanical Disorders of the Lumbar Spine
Fig. 92.4 A lateral view of the S1 transforaminal ESI demonstrating relative ventral flow of contrast dye on the floor of the spinal canal flowing cephalad to the L4 level.
Technique of performing transforaminal ESI Transforaminal ESI absolutely requires fluoroscopic guidance in order for the site of pathology to be precisely targeted. The transforaminal route is the optimal access for delivering an injectate on the lumbar nerve sleeve and/or the ventral portion of the epidural space. Transforaminal ESIs are performed with the patient prone on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. Realtime fluoroscopy is utilized to identify the pedicle corresponding to the foramina through which injectate is to be delivered. In patients with a transitional segment, either a lumbarized S1 vertebral body or sacralized L5 vertebral body, the interventional spine specialist will need to count the vertebral bodies beginning with L1 after the most caudal rib (T12) to establish that the appropriate pedicle is identified. Once the targeted pedicle is correctly identified, the c-arm should be rotated ipsilaterally until the superior articular process of the juxtapositioned caudal vertebral body comes into view and advances to the medial portion of the targeted pedicle on the created oblique view. The targeted pedicle should now take on an ovoid shape once the correct degree of rotation is achieved as opposed to the circular shape on a true anteroposterior (AP) image with the lumbar spinous processes in the midline. Then, a skin wheal utilizing a combination of 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate42 is raised just inferior to the midline portion of the targeted pedicle on the oblique image. A long-handled sponge clamp is utilized to guide a 20-gauge, 3.5 inch spinal needle through the raised skin wheal in a bull’s-eye manner (the needle hub concentrically outlines the needle tip (Fig. 92.5) just inferior to the midline portion of the targeted pedicle until a change in tissue resistance is appreciated or until the spinal needle hub abuts the skin. If the needle abuts skin prior to a change in tissue resistance, the 3.5 inch spinal needle is then utilized as an introducer and is positioned to align its tip to the midline portion of the targeted pedicle and a 25-gauge, 6 inch needle is guided through the index needle until a change in tissue resistance is appreciated. In either instance, the needle tip should then feel stable or locked into position if it has entered the targeted foramen. Verification of needle tip placement is achieved by rotating the
Fig. 92.5 An oblique view of a right L5 transforaminal ESI demonstrating the bull’s-eye approach to needle advancement visualized as a black dot with a thin concentric ring circumscribing the needle tip just inferior to the mid portion of the right L5 pedicle.
c-arm in a manner that provides a true midline AP image. The needle tip is then slowly advanced to the six-o’clock position, proximated just inferior to the targeted pedicle. The lumbar spinal nerves exit the spinal canal just inferior and medial to the midposition of the corroborative pedicle on the AP image. Needle placement just superior to the spinal nerve and just inferior to the pedicle is confirmed by visualization of contrast medium centrally hugging the pedicle both inferiorly and medially as well as spreading cephalad along the ipsilateral ventral portion of the spinal canal, bathing the posterior aspect of the intervertebral discs as well as peripherally along the lumbar spinal nerve sleeve. Care must be taken and technique must be precise throughout needle advancement to maintain the bull’s-eye approach at all times via real-time fluoroscopy to prevent straying of the needle away from the targeted foramen. Inadvertent curvature of the needle outside the confines of the bull’s-eye approach may result in the needle tip hitting periosteum, such as the targeted pedicle if the needle tip strays superiorly, punctured viscus if the needle tip strays anteriorly towards the retroperitoneal and/or abdominal cavity, or punctured spinal nerve extraforaminally if the needle tip strays inferiorly. In some instances when performing a transforaminal ESI through the L5–S1 foramen, the targeted inferior aspect of the midline of the L5 pedicle may be accessible only by ipsilateral rotation due to one or a combination of a high-riding pelvis, significant loss of disc space height, large L5 transverse process, L5–S1 fusion, or a L5 on S1 spondylolisthesis. These obstacles can be overcome with a variable degree, depending on the severity of the aforementioned anatomical variations, of cranial to caudal tilt which will in effect move the pelvis inferiorly, creating direct access to the inferior portion of the targeted L5 pedicle. In cases of performing transforaminal ESI through the L5–S1 foramen in patients with a partially or completely sacralized L5 vertebral body, the approach is similar to that utilized when performing sacral transforaminal ESIs. When performing S1 transforaminal ESI, the skin wheal is raised superior and lateral to the targeted S1 pedicle. The needle is advanced through the skin wheal via a long-handled sponge clamp in the direction of the X-ray beam at a 45° angle to gently abut sacral periosteum just lateral to the S1 pedicle. Then, the needle is slightly withdrawn, reoriented inferiorly and medially, and slowly advanced, sliding to just inferior to the midline of 1017
Part 3: Specific Disorders
the S1 pedicle into the targeted foramen. A slight suction or vacuum phenomena may be felt as the needle tip enters the targeted sacral foramen. A similar approach is utilized for L5–S1 transforaminal ESI in patients with partial or complete sacralization of the L5 vertebral body; however, the skin wheal is raised lateral and inferior to the targeted L5 pedicle and the needle too is advanced superiorly and medially after depth is achieved by contacting periosteum.
Indications and efficacy of interlaminar ESI The interlaminar route most likely continues to be the most widely utilized approach to accessing the lumbar epidural space for ESI in the treatment of spinally mediated lumbar axial pain syndromes; however, there is little in the published randomized literature to suggest longterm efficacy.43–49 Carette et al.43 demonstrated short-term improvement in radicular complaints in patients with HNP but no difference between control and treated groups at 3 months in a prospective, randomized, double-blind, controlled trial. In a prior prospective, randomized, double-blind, controlled trial, Cuckler et al.44 demonstrated no significant improvement in both the short and long terms in patients with lumbar axial pain due to HNP and/or spinal stenosis. Ridley et al.48 reported statistically significant long-term benefit (6-month follow-up) to interlaminar ESIs in patients with lumbar axial and radicular pain in a randomized, placebo-controlled outcomes trial. Lending credence to the variables influencing such outcomes studies are the previously mentioned studies that report up to 40% of blind interlaminar ESI do not enter the epidural space even in experienced hands.18–21 Furthermore, an intrinsic problem with interlaminar ESI is that even when the physician is able to correctly place the needle tip into the epidural space, the dorsal aspect of the spinal canal is infused. Therefore, interlaminar ESIs are likely delivering injectate dorsal to the thecal sac and at a site relatively distal to the ventrally located pain-generating structures.
Technique of performing interlaminar ESI Interlaminar ESIs are performed under X-ray guidance with the patient prone or in the lateral decubitus position on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidoneiodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. Then, with fluoroscopic imaging, the inferior ipsilateral aspect of the lamina corresponding to the site of pathology is visually confirmed. A skin wheal utilizing a combination of 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate is raised.42 A 20- or 22-gauge, 3.5 inch spinal needle is carefully guided to abut the ligamentum flavum as resistance is felt. One of two techniques can be utilized for advancement into the dorsal epidural space. Firstly, the spinal needle can be slowly advanced using a loss of resistance technique. A ‘pop’ may be felt and/or heard when the ligamentum flavum is pierced and the needle tip has entered the epidural space. Otherwise, the stylet can be removed and a glass syringe filled with 5 cc of normal saline is attached to the needle hub. The spinal needle is slowly advanced with modest pressure being simultaneously applied to the plunger. Once a drop in resistance is encountered, the ligamentum flavum has been pierced and the dorsal epidural space has been infiltrated. The needle tip position is assessed on AP and lateral images and verified by the injection of contrast medium. Once needle confirmation is achieved, an injectate combination of 12–18 mg of betamethasone and 5–10 cc of lidocaine and/or normal saline is slowly infused. 1018
Indications and efficacy of caudal ESI The caudal ESI may be safer than other routes of ESI due to a substantially lower risk of inadvertent dural puncture and subsequent subarachnoid injection, as the dural sac rarely extends beyond the S1–2 level. The published randomized clinical outcomes literature as a whole provides a contradictory picture on both short- and longterm efficacy of caudal ESI in the treatment of lumbar axial pain with or without radicular involvement in patients both prior to and post surgical decompression.41,50–54
Technique of performing caudal ESI Caudal ESIs are performed with the patient prone on the fluoroscopy table. The skin overlying the sacrococcygeal area is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The clinician should then identify the right and left sacral cornu via palpation or fluoroscopic guidance, as the sacral hiatus is located between these two landmarks. A skin wheal utilizing a combination of 2–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate is raised.42 A 22-gauge, 3.5 inch spinal needle is carefully guided at a 45° angle through the sacrococcygeal ligament and into the sacral canal hiatus near the superior portion of the gluteal cleft and then advanced slightly into the sacral canal no further than the inferior edge of S2. The needle tip position is assessed on AP and lateral images and verified by the injection of contrast medium and observance of cephalad flow. Once needle confirmation is achieved, 12–18 mg of betamethasone is injected followed by an infusion of 5–15 cc of lidocaine and/or normal saline to assist in the cephalad spread of the corticosteroid to the lumbar epidural space via a direct mechanical pressure effect in the cephalad direction.
Timing of ESI The optimal timing for administration of ESIs has not yet been elucidated. It is standard practice for patients to undergo more conservative palliative measures (i.e. nonsteroidal antiinflammatory drugs (NSAIDs), lumbar spine stabilization physical therapy) prior to being considered for ESIs; however, the clinician must be wary not to delay ESIs when more conservative treatments do not seem to be helping. Delaying aggressive treatment may allow an ongoing inflammatory process to result in fibrosis and possibly cellular damage.13 It is unknown how often ESIs can be administered. Practitioners will often wait as long as 2 weeks prior to reassessing a patient for a response to an injection for possible re-injection. This practice became popular after Swerdlow and Sayle-Creer suggested that corticosteroids infused into the epidural space may remain in situ for up to 2 weeks.55
INTRADISCAL INJECTIONS OF BIOLOGICS FOR DISCOGENIC MEDIATED LUMBAR AXIAL PAIN SYNDROMES Patients with discogenic mediated lumbar axial pain have, at least a component of, a structural anatomic lesion within the outer annulus of the intervertebral disc. This lesion may or may not communicate with the nucleus pulposus and is conceptually regarded as the inciting pathologic event that progresses over time and results in degeneration of the disc and, potentially, discogenic mediated pain. Intradiscal infusions of active biologics may represent the future in the prevention of this progression and repair of structural lesions within the intervertebral disc. In vitro studies have demonstrated a cellular response of intervertebral disc cells to exogenous bone morphogenetic protein (BMP).
Section 5: Biomechanical Disorders of the Lumbar Spine
These studies have demonstrated improved disc height and signal changes on MRI suggestive of repair of the intervertebral disc following intradiscal administration of BMP to discs damaged via chemical and mechanical methods. In a rabbit model, Miyamoto et al.56 demonstrated that intradiscal infusion of osteogenic protein -1 (OP-1, BMP-7) restored the biomechanical properties of the degenerated intervertebral disc. Furthermore, An et al.57 demonstrated that infusion of OP-1 intradiscally resulted in increased disc height and proteoglycan content. In addition, Takegami et al.58 reported that intervertbral disc cells exposed to interleukin-1 alpha lost no intrinsic ability to upregulate proteoglycan synthesis in response to OP-1 stimulation. In fact, he went on to describe that the reformed matrix was actually richer in proteoglycans than that prior to interleukin-1 alpha exposure. Interestingly, Yoon et al.59 demonstrated that infusion of adenovirus carrying Lim Mineralization Protein – 1 increases disc production of proteoglycans as well as bone morphogenic proteins. In a rat model, Kawakami et al.60 demonstrated both enhancement of the extracellular matrix as well as inhibition of pain-related behavior with intradiscal OP-1 injection into painful degenerated discs. Based on these initial in vitro studies, it has been proposed that intradiscal infusion of BMP to a degenerated dessicated disc may initiate repair of the disc, manifested clinically as reduction in lumbar pain and concomitant improvement of physical function and potentially manifested structurally as a radiographic increase in disc height and/or an increase in MRI disc signal intensity. This author is a principal investigator in a multicenter phase 1 study evaluating infusion of a BMP into single level symptomatic degenerative disc disease in humans. Although transforaminal ESIs targeted on the floor of the spinal canal at a focal discogenic mediated inflammatory response holds promise for some patients episodic chemically induced discogenic pain as previously described (Fig. 92.2), randomized prospective double-blinded studies done by both Simmons et al.61 as well as Khot et al.62 have demonstrated no statistically significant benefit of intradiscal infusion of corticosteroids for discogenic pain diagnosed by provocative lumbar discography. Other biologics that have been reported upon but whose role has not yet been elucidated include infusions of hematopoietic precursor stem cells, methylene blue and ozone (O3). For example, Haufe et al.63 reported no reduction in discogenic pain at one year follow-up in patients who underwent intradiscal infusion of hematopoietic precursor stem cells harvested from the pelvic bone marrow. Peng et al.64 demonstrated that 87% of patient with chronic discogenic pain who met inclusion criteria for lumbar interbody fusion surgery but were instead treated with intradiscal injection of methylene blue were able to report marked improvement in pain and physical function. In 2004, Muto et al65 reported on 2200 patients treated with intradiscal oxygen-ozone injection reporting no side effects and a 75–80% success rate at 6 and 18 months. Buric et al66 conducted a prospective case series reporting on chemonucleolysis via ozone injections in 30 patients with non-contained disc herniations. They stated 90% of patients had a statistically significant improvement in pain and function as measured by VAS and Roland Morris Disability Questionnaires. Of course, further study is required before any of the aforementioned intradiscal infusions of various biologics can be regarded as a generally acceptable or standard of care intervention for discogenic lumbar axial pain syndromes.
PATHOPHYSIOLOGY OF Z-JOINTMEDIATED LUMBAR AXIAL PAIN SYNDROMES The lumbar Z-joint is the primary posterior element structure thought to be a potential etiology of spinally mediated lumbar axial
pain. The rationale is derived from conclusions drawn from the conceptual model of the lumbar spine degenerative cascade as initially described by Kirkaldy-Willis,10 as previously reported within this chapter, as well as properties intrinsic to the Z-joint. As outlined earlier in this chapter, the posterior elements take on more axial load in certain positions (standing) as well as with increasing age. Anatomically, the Z-joint is a true diarthrodial joint with articular and subchondral cartilage, a small meniscus, a capsule, and a fluidfilled synovium encased in synovial lining. The initiating event that is thought to implicate the Z-joint as an etiology of lumbar axial pain is synovitis and the resultant synovial reaction which occurs as a result of the shift in axial loading from the anterior elements to the posteriorly situated Z-joints due to the temporally related incompetence of the intervertebral disc. On the other hand, it is theorized that the aforementioned initiating pathology to the synovial capsule can result in a younger population when induced by sudden, unexpected flexion–extension moments as occurs commonly in motor vehicle trauma. The Z-joints are able to accommodate the increased load up to a critical maximum at which point synovial pathology ensues leading to eventual progressive destruction of the cartilaginous articular surface when facet joint weight bearing exceeds the critical maximum. Acute, recurrent, and/or chronic inflammation can result in these synovial joints filling with fluid and distending. This distention may result in pain perception because of mechanical and/or chemical stimulation of the richly innervated synovial capsule. Evidence suggests that the Z-joint’s synovial capsule has a complex innervation provided by small, C-type pain fibers.67 Furthermore, the majority of mechanosensitive somatosensory units found within the Z-joint were discovered to be group III high-threshold, slow-conduction units, which are thought to mediate nociception.68–70 Therefore, the Z-joint can result in nociception by osteochondral and/or capsular mechanisms similar to those found in other extensively studied degenerated joints, such as the hip or knee. Capsular laxity can result and the accompanying subluxation can stretch and/or tear the richly innervated capsule leading to one or a combination of inflammatory or structural lumbar axial pain syndromes emanating from the lumbar Z-joint. Another potential mechanism for nociception arising from lumbar Z-joint has not been recognized until recently. In most diarthrodial joints, prolonged immobilization can lead to a cascade of joint changes. These may include, among other things, capsular stiffness leading to contracture, decrease in synovial fluid production, and tightening of para-articular muscles, all leading to joint rigidity. In some cases, complete ankylosis may accompany extreme inactivity, immobilization, and inhibition of function. In such cases, mechanical loads applied to the rigid joints typically can produce pain, which may be related to capsular stretching/tearing, synovial irritation from cartilage fragmentation due to poor nutrition, and/or muscle spasm from sudden stretching of immobilized, debilitated muscle. In chronic lumbar axial pain conditions, patients often splint segments of the lumbar spine, and the chronic immobilization may lead to nociception. Stretching the involved joint–muscle complex is the obvious physiologic therapeutic modality. Unfortunately, pain and fear-avoidance may prevent some pain-sensitive patients from complying with such logical medical advice. Nevertheless, the Z-joint can be the source of pain associated with these mechanisms, particularly after chronic persistent or chronic episodic lumbar axial pain conditions have produced disability for longer than 6 months.71
Diagnosis of Z-joint-mediated lumbar axial pain syndromes Revel et al. suggested certain clinical features including age greater than 65 years, pain not exacerbated by coughing, hyperextension, 1019
Part 3: Specific Disorders
forward flexion, rising from forward flexion, or extension–rotation, or mitigated by recumbence, may be suggestive for a Z-joint etiology to lumbar axial pain.72,73 However, more recent studies demonstrate that no physical examination finding(s), including segmental rigidity, are specific for Z-joint-mediated lumbar axial pain.74,75 Although the aforementioned features on clinical presentation reported by Revel et al.72,73 may suggest the Z-joint as a possible etiology of lumbar axial pain and enter the Z-joint into the differential diagnosis, anesthetic blockade is currently the gold standard by which the diagnosis is ultimately made.76 Two methods are currently accepted: (1) a dual-block paradigm eliciting a positive response for the halflife duration of both a short- and long-acting local anesthetic performed on separate occasions, or (2) a single-block paradigm eliciting a positive response from a local anesthetic blockade with a negative response from a placebo control performed on separate occasions.
Efficacy of lumbar Z-joint injections in Z-jointmediated lumbar axial pain syndromes There has yet to be a study to determine the efficacy of intra-articular steroid injections of the lumbar Z-joints in patients diagnosed with Z-joint-mediated pain via a dual-block paradigm or placebo-controlled single-block paradigm. Carette et al.77 designed and implemented the best study to date assessing the efficacy of intra-articular corticosteroid injections of the lumbar Z-joints for Z-joint-mediated lumbar axial pain. They reported on 101 patients with lumbar axial pain diagnosed with Z-joint-mediated pain via a single intra-articular anesthetic blockade providing 50% pain reduction randomized into either a normal saline group and corticosteroid group. At 1 month, 42% of the corticosteroid group and 33% of the normal saline group reported significant pain relief (thus a one-third placebo response rate and requirement of a dual-block paradigm for diagnosis). There was a statistically significant difference in marked pain relief at 6-month follow-up between the corticosteroid group (46%) and normal saline group (15%). Carette et al.77 argued that intra-articular steroid Z-joint injections were not effective since the percentage of patients with long-term pain relief was low; however, one could retort that the inclusion criteria was detrimental to the study outcome because of the failure to exclude a placebo response. A more recent randomized, single-blind clinical trial by Mayer et al.75 found that fluoroscopically guided Z-joint injections with supervised stretching exercises when compared to exercise alone (control group) in patients with chronic disabling work-related lumbar spinal disorders demonstrated that incorporating Z-joint injections significantly increased lumbar range of motion (ROM) in all planes as well as lumbar mobility relative to the control group. However, Mayer et al.64 also observed that there was no increase in the improvement of pain and disability of the Z-joint injection group relative to the control group. The key point in this paradigm of segmental rigidity is that the purpose for the injection/exercise approach is to increase motion in spinal segments noted specifically to be rigid. The added goal of facilitating functional rehabilitation involving para-articular muscle strength, endurance, and coordination becomes possible only after joint mobility has been restored. This study demonstrated significant ROM gains were also present in the exercise-only control group, but that significantly greater improvements were noted when Z-joint injections were added to the standardized exercise program. It was also noted that only 17% of the patients meeting criteria for segmental rigidity also met criteria for Z-joint syndrome, as determined by the response to the Z-joint injections. As such, it appears that the entity of lumbar axial pain of Z-joint origin is noncongruent with the entity of segmental rigidity. More study of the relationships between these two phenomena is required, as comprehension will 1020
ultimately determine the prescription and efficacy of comprehensive treatment programs. The nonrandomized outcome studies offer varying short- and longterm results in the utilization of intra-articular Z-joint corticosteroid injections in the treatment of lumbar axial pain. For example, Lynch and Taylor78 reported total pain relief in nine of 27 patients receiving intra-articular Z-joint injections and partial relief in another 16 of those 27 patients. However, none of the 15 patients receiving extraarticular corticosteroid injections reported complete pain relief and only eight of the 15 reported partial pain relief. Destouet et al.79 reported significant pain relief for 1–3 months in 62% of their patient sample and 38% reported 3–6 months of pain relief. Murtagh80 reported that 54% of his patient sample claimed up to 6 months significant pain relief. Mironer and Somerville81 only reported 28% of patients in their study reporting significant long-term pain relief. Two separate retrospective outcome studies demonstrated approximately 50% of patients reporting short-term pain relief with much lower percentages of patients (approaching 8%) reporting long-term relief at 12 months.82,83
Technique of performing lumbar intra-articular Z-joint interventions Lumbar intra-articular Z-joint injections are performed with the patient prone on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. Real-time fluoroscopy is utilized to rotate the c-arm ipsilaterally until the medial and lateral edges of the targeted Z-joint are clearly visualized. Local anesthesia is achieved by infiltrating the skin, creating a skin wheal raised just medial to the midline or inferior aspect of the joint with a combination of approximately 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate.42 Real-time fluoroscopy is utilized to advance a 22-gauge, 3.5 inch spinal needle in a bull’s-eye fashion so that the needle tip abuts the lateral edge of the middle to inferior portion of the Z-joint. The spinal needle is then slightly withdrawn and directed just medially into the capsule of the targeted Z-joint. Approximately 0.1–0.3 cc of contrast can be utilized to verify needle placement, visualized by the presence of an hourglass-shaped arthrogram or portion thereof (Figs 92.6–92.8). Once needle tip confirmation is achieved, a combination of 0.5–0.8 cc of betamethasone and 0.2–0.5 cc of 1% lidocaine can be injected, dependent on the degree of compromise of the synovial capsule and the ensuing capacity to accommodate an infusion of volume.
Efficacy of medial branch injections in Z-joint-mediated lumbar axial pain syndromes Medial branch neural blockade is also performed in the treatment of lumbar axial pain of Z-joint etiology. Manchikanti et al.84 prospectively randomized 73 patients diagnosed with Z-joint mediated lumbar axial pain via a dual anesthetic block paradigm into one of two groups treated with therapeutic medial branch injections. One group received local anesthetic and sarapin whereas the other received a mixture local anesthetic, sarapin, and corticosteroid. Significant pain relief was achieved in both groups with a mean duration of relief greater than 6 months. In addition, physical, functional, psychological status, and return to work status were all improved. Of note, the efficacy of radiofrequency neurotomy of the medial branch of the corroborative spinal nerves has been
Section 5: Biomechanical Disorders of the Lumbar Spine
Fig. 92.6 An oblique view demonstrating a medial to lateral approach to the right L4–5 Z-joint. The needle tip is directed toward the inferior portion of the joint space. (Note that rotation must be adequate in order to clearly visualize the edges of the inferior articular process of L4 and superior articular process of L5.)
Fig. 92.8 An oblique view of a left L4–5 intra-articular Z-joint injection with visualization of a classic hourglass arthrogram pattern filling the superior and inferior capsules.
trial, North et al.86 demonstrated the short-term efficacy of medial branch blocks with a local anesthetic, but long-term improvement was infrequent.
Technique of performing medial branch injections
Fig. 92.7 An infusion of 0.2 cc of contrast dye demonstrates filling of the joint space and visualization of the right L4–5 Z-joint partial arthrogram.
demonstrated for patients diagnosed by a dual-block paradigm by Dreyfuss et al.76 In a nonrandomized study by Manchikanti et al,85 a retrospective analysis of 180 patients all diagnosed with Z-joint-mediated lumbar axial pain via a dual-anesthetic paradigm, three groups of 60 patients were evaluated, the groups receiving medial branch blocks with local anesthetic, local anesthetic and sarapin, or local anesthetic, sarapin, and corticosteroid. To summarize, the results of this retrospective study reported that diagnostic medial branch blocks alone had shortterm therapeutic effects which were enhanced by the addition or sarapin and/or corticosteroid. In another nonrandomized clinical
Medial branch neural blockade is performed with the patient in the prone position on the fluoroscopy table. The approximated area of skin overlying the level of the lumbar spine to be injected is cleaned thoroughly with povidone-iodine and the region is draped in a sterile fashion. The correct level, taking into account the possibility of a transitional segment, is verified by the process previously stated in the technique portion of the transforaminal ESI section. The c-arm is rotated until the eye of the ‘Scottie dog’ is clearly visualized on an oblique image. Local anesthesia is achieved by infiltrating the skin, creating a skin wheal raised over the eye of the ‘Scottie dog’ with a combination of approximately 1–3 cc of 1% lidocaine and 0.1–0.3 cc of sodium bicarbonate.42 A 22-gauge 3.5 inch spinal needle is advanced in a bull’s-eye manner to the eye of the ‘Scottie dog,’ representing the junction of the base of the corroborative transverse process and the superior articular process under fluoroscopic guidance. Injections must be performed at the level of the involved joint and the adjacent superior segmental level as both of these medial branches will contribute innervation to the targeted Z-joint. For example, the L4–5 Z-joint is innervated by the medial branches of the dorsal rami of both the L3 and L4 spinal nerves. Injectate consists of 0.5 cc of 1% or 2% lidocaine.
CONTRAINDICATIONS AND COMPLICATIONS OF INTERVENTIONAL SPINE PROCEDURES Contraindications to interventional spine procedures include possible pregnancy (secondary to the potential adverse effects of fluoroscopic radiation on the fetus), hypersensitivity to any component of the injectate, bacteremia, full anticoagulation, and bleeding diathesis. Other concerns are elevations of serum glucose levels in diabetics, elevations of blood pressure in hypertensive patients, and fluid 1021
Part 3: Specific Disorders
retention in congestive heart failure patients. The use of aspirin and other NSAIDs have not been demonstrated to predispose patients to any significant bleeding while receiving ESIs.87 Potential complications of fluoroscopically guided interventional spine procedures include increased pain, hypersensitivity reactions, dural puncture, subarachnoid injection, anaphylaxis, infection, unmasking of preexisting systemic infection, epidural abscess, increased pain, fever, epidural bleeding and/or hematoma, bladder dysfunction with urinary retention, weakness, permanent neural element damage via penetrating trauma, intravascular injection resulting in local anesthetic toxicity such as seizure, cardiac arrhythmia or arrest, and death. However, these events are quite rare. Botwin et al.88 reported no major complications and less than a 10% rate of minor complications, all of which resolved without hospitalization, in 207 patients undergoing 322 fluoroscopically guided lumbar transforaminal ESIs.
PHYSICAL REHABILITATION Physical rehabilitation is a key modality on the treatment of patients with spinally mediated lumbar axial pain. Physical therapy programs prescribed specifically to address the primary site of injury and secondary sites of dysfunction can provide a means of treatment with or without adjuvant medications and interventional spine procedures. Back schools and other training programs that are not job specific have not been shown to be statistically effective; however, programs that integrate the job requirements into the training program show statistical significant results.89 Relative rest, which restricts all occupational and avocational activities, for up to the first 2 days following an acute episode may be indicated to help calm down initial pain symptoms and relieve fatigue. Rest for longer periods of time has not been shown to be beneficial, and may be harmful, potentially causing deconditioning, loss of bone density, decreased intradiscal nutrition, loss of muscle strength and flexibility, and increased segmental stiffness.90 Passive modalities are valuable during the initial 48 hours of relative rest to aid in pain relief, but protracted courses of passive treatments become counter-productive as they place the patient in a dependent role instead of participating in an active, function maximizing rehabilitation program. One of the most important components of any back care program is education. Education should include an explanation of the natural history of an acute, subacute, and chronic disc injury. In addition, education should include training in proper body mechanics and lumber ergonomics during various functional, occupational, and avocational activities. The greatest successes in health education can be seen in two great medical problems, heart disease91 and cancer.92 Education has had a direct effect on decreasing the prevalence of smoking, from 40% of the population in 1965 to 29% in 1987.93 An education-based low back paradigm is inexpensive and begins with providing reassuring information to the patient. The seeds of the educational approach exist in back schools, functional restorative programs, and innovative prevention and rehabilitation strategies. LaCroix found that 94% of patients with a good understanding of their condition returned to work, whereas only 33% of patients with a poor understanding of their condition returned to employment.94 Reassurance that activity is helpful promotes return to function. Back school provides information on spine anatomy and function and was found to be one of only three interventions identified by the Quebec Task Force on Spinal Disorders as effective for patients in randomized, controlled trials.95 Myofascial manual techniques may be employed to increase soft tissue pliability when secondary myofascial tightness is present. If the aforementioned measures are appropriate and completed, then an active, dynamic, outpatient lumbar spine stabilization rehabilitation program should be prescribed. In addition, rehabilitation of other associated components of the functional kinetic chain may be appropriate, as these 1022
structures may also be affected. A dynamic lumbar spine stabilization rehabilitation program is aimed at maintaining a neutral spine position throughout various daily activities. An extension bias is commonly employed to help reduce intradiscal pressure. This position allows for a balanced segmental force distribution between the intervertebral disc and Z-joints, provides functional stability with axial loading to help minimize the chance for acute dynamic overload upon the discs, minimizes tension on ligaments and fascia planes, and alleviates symptoms. Repetition is key in increasing flexibility, building endurance, and developing the required muscle motor programs that activate a series of key multimuscular contractions subconsciously that maintain the lumbar spine in a neutral position throughout static and dynamic activities. For athletes, the aforementioned program can be combined progressively with sport-specific polymetrics to help the lumbar spine maintain a neutral position during high-intensity, unpredictable, reaction-intensive sports. Another method for rehabilitation of athletes is to train them in maintaining a neutral spine position in the individual motions of their sport, then subsequently grouping these component motions into a new, safe, stable spine movement. Cardiovascular fitness training is an important component to a comprehensive rehabilitation program as it assists in providing the endurance necessary to prevent fatigue of the spine-stabilizing musculature.
CASE STUDIES Case study 1 S.G. is a 36-year-old male with a history of occasional spontaneously resolving short-term (less than 1 week duration) low back pain episodes who presents to a spine specialist complaining of 12 weeks of worsening low lumbar axial pain initiated while lifting a heavy television set helping a friend move into a house. The patient states his symptoms are located across the width of the low back without lower extremity radiation. He qualifies his pain as a constant, deep, dull ache worsened with prolonged sitting, especially riding in his car, as well as with twisting motions when bent forward. The patient reports lumbar extension and staying active seem to provide some symptom mitigation. Physical examination reveals some tenderness and spasm to palpation over the bilateral low lumbar paraspinal musculature. Lumbar flexion is significantly limited due to worsening of the patient’s lumbar pain; however, lumbar extension alleviates the patient’s lumbar pain. In addition, the patient reported increasing lumbar pain with decreasing angle acuity during sustained hip flexion. Sacroiliac joint stress maneuvers and provocative maneuvers were not pain provoking. The lumbosacral spinal neurologic examination was normal. Plain films of the lumbar spine ordered by the patient’s primary care physician revealed moderate loss of disc height posteriorly at the L5–S1 segment. Physical therapy had been initiated 10 weeks previously with minimal improvement. The patient reports that mostly passive modalities had been employed in therapy for pain and spasm control, as several attempts at advancement to an active extension-biased McKenzie stabilization program proved too difficult due to pain provocation. An MRI of the lumbar spine was ordered, revealing focal degenerative disc desiccation at the L5–S1 segment with reactive endplate edema and a highintensity zone lesion posteriorly (Figs 92.9, 92.10). A diagnosis of discogenic lumbar axial pain was made and the patient underwent two therapeutic bilateral S1 transforaminal ESIs. After the second procedure, the patient reported greater than 90% alleviation of his lumbar pain. Physical therapy was reinitiated, resulting in nearcomplete symptom resolution. The patient understood the key to obtaining long-term success with management of his disc disease included compliance with his home exercise program and proper
Section 5: Biomechanical Disorders of the Lumbar Spine
lumbar spine mechanics during all activities. Although the patient continues to have occasional lumbar pain episodes, he reports that these episodes resolve within a few days with rest, activity modification and/or mild analgesics.
Case study 2
Fig. 92.9 T-weighted sagittal and axial images of a high-intensity zone lesion located within the posterior rim of the L4–5 intervertebral disc. Note the high signal intensity of the lesion easily visualized due to the backdrop of a dark, desiccated intervertebral disc.
A.D. is a 61-year-old female who presents to an interventional spine specialist with a 1-year history of slowly worsening left-sided lumbar axial pain of spontaneous onset. The patient reports focal lumbar pain just to the left of midline of the low lumbar spine without lower extremity radiation and qualifies the symptoms as a dull ache which worsens with prolonged standing and becomes sharp with left-sided lumbar extension. Physical examination reveals tenderness upon deep palpation over the left side of the low lumbar spine and limitation of lumbar extension by 50%, eliciting sharp left-sided lumbar pain. The patient had a normal lumbosacral spine neurologic examination. Imaging of the lumbar spine revealed varying degrees of degenerative changes throughout the lumbar spine. Z-joint arthropathy was found at all segmental levels with the left side affected worse than the right. In addition, asymmetric levels of fluid were noted in the left L4–5 and L5–S1 Z-joints. A presumptive diagnosis of left lumbar Z-joint syndrome was made and the patient underwent successive diagnostic intra-articular injections of the left lumbar Z-joints. The diagnostic left L5–S1 was negative but the left L4–5 level proved positive. Subsequent therapeutic left intra-articular L4–5 Z-joint injections resulted only in short-term pain improvement. The presumptive diagnosis of left L4–5 Z-joint syndrome was verified via medial branch blocks of the L3 and L4 spinal nerves via a dual-block paradigm. This test proved positive and subsequent radiofrequency ablation of the medial branches of the dorsal rami of the left L3 and L4 spinal nerves provided 75% relief of the patient’s left-sided lumbar pain. Physical rehabilitation focusing on lumbar spine stabilization exercises and core strengthening was stressed to the patient as an important adjunct in optimizing spinal health in the future.
References 1. Anderson GBJ. Epidemiologic aspects of low back pain in industry. Spine 1981; 6:53. 2. Dixon ASJ. Diagnosis of low back pain – sorting the complainers. In: Jayson M, ed. The lumbar spine and back pain. New York: Grune & Stratton; 1976. 3. Fry J. Back pain and soft tissue rheumatism: advisory services colloquium proceedings. London; 1972. 4. White AWM. Low back pain in men receiving workmen’s compensation. Can Med Assoc J 1966; 95:50. 5. Deyo RA, Tsui-Wu Y-T. Descriptive epidemiology of low back pain and its related medical care in the United States. Spine 1987; 12:264–268. 6. Troup JDB, Martin JW, Lloyd DCEF. Back pain in industry: A prospective survey. Spine 1981; 6:61–69. 7. Valkenburg HA, Haanen HCM. The epidemiology of low back pain. In: White AA III, Gordon SL, eds. American Academy of Orthopaedic Surgeons Symposium on Idiopathic Low Back Pain. St. Louis: Mosby; 1982. 8. Von Korff M, Deyo RA, Cherkin D, et al. Back pain in primary care: outcomes at one year. Spine 1993; 18:855–862. 9. Wiltse LL. The History of spinal disorders. In: Frymoyer JW, ed. The adult spine: principles and practice. Philadelphia: Lippincott-Raven; 1997:3–40. 10. Kirkaldy-Willis WH. The pathology and pathogenesis of low back pain. In: KirkaldyWillis WH, ed. Managing low back pain. New York: Churchill Livingstone; 1988:49. 11. McCarron RF, Wimpee MW, Hudkins PG, et al. The inflammatory effect on nucleus pulposus: a possible element in the pathogenesis of low back pain. Spine 1987; 12:760–764.
Fig. 92.10 T-weighted sagittal and axial images of a high-intensity zone lesion located within the posterior rim of the L4–5 intervertebral disc. Note the high signal intensity of the lesion easily visualized due to the backdrop of a dark, desiccated intervertebral disc.
12. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15(7):674–678. 13. Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated disc of the lumbar spine. Spine 1996; 21(2):218–224.
1023
Part 3: Specific Disorders 14. Kang JD, Georgescu HI, McIntyre-Larkin L, et al. Herniated lumbar intervertebral discs spontaneously produce matrix metalloproteinases, nitric oxide, interleukin-6 and prostaglandin E2. Spine 1996; 21(3):271–277.
42. Nakayama M, Munemura Y, Kanaya N, et al. Efficacy of alkalinized lidocaine for reducing pain on intravenous and epidural catheterization. J Anesth 2001; 15(4):201–203.
15. Verbout AJ. The development of the vertebral column. Adv Anat Embryol Cell Biol 1985; 90:1–122.
43. Carette S, Lecaire R, Marcoux S, et al. Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus. N Engl J Med 1997; 336:1634–1640.
16. Viner N. Intractable sciatica – the sacral injections – an effective method of giving relief. Can Med Assoc J 1925; 15:630–634.
44. Cuckler JM, Bernini PA, Wiesel SW, et al. The use of epidural steroid in the treatment of radicular pain. J Bone Surg Joint 1985; 67:63–66.
17. Robecchi A, Capra R. L’idrocortisone (composto F): prime esperienze cliniche in campo reumatologico. Minerva Med 1952; 98:1259–1263.
45. Snoek W, Weber H, Jorgensen B, et al. Double-blind evaluation of extradural methylprednisolone for herniated lumbar disc. Acta Orthop Scand 1977; 48:635–641.
18. Fredman B, Nun MB, Zohar E, et al. Epidural steroids for treating ‘failed back surgery syndrome’: is fluoroscopy really necessary? Anesth Analg 1999; 88(2): 367–372.
46. Dilke TFW, Burry HC, Grahame R. Extradural corticosteroid injection in the management of lumbar nerve root compression. Br Med J 1973; 2:635–637.
19. Watanabe AT, Nishimura E, Garris J. Image-guided epidural steroids injections. Tech Vasc Interv Radiol 2002; 5(4):186–193. 20. Renfrew DL, Moore TE, Kathol MH, et al. Correct placement of epidural steroid injections: fluoroscopic guidance and contrast administration. Am J Neuroradiol 1991; 12(5):1003–1007. 21. Johnson BA. Image-guided epidural injections. Neuroimaging Clin N Am 2000; 10(3):479–491. 22. Winnie AP, Hartman JT, Meyers HL Jr, et al. Pain clinic II: intradural and extradural corticosteroids for sciatica. Anesth Analg 1972; 1:990–1003. 23. Riew KD, Yin Y, Gilula L, et al. The effect of nerve-root injections on the need for operative treatment of lumbar radicular pain. J Bone Joint Surg [Am] 2000; 82:1589–1593. 24. Kraemer J, Ludwig J, Bickert U, et al. Lumbar epidural perineural injections: a new technique. Eur Spine J 1999; 8(1):81–82. 25. Karppinen J, Malmivaara A, Kurunlahti M, et al. Periradicular infiltration for sciatica. Spine 2001; 26:1059–1067. 26. Karppinen J, Ohinimaa A, Malmivaara A, et al. Cost effectiveness of periradicular infiltration for sciatica. Spine 2001; 26:2587–2595. 27. Thomas E, Cyteval C, Abiad L, et al. Efficacy of transforaminal versus interspinous corticosteroid injection in distal radiculalgia – a prospective, randomized, doubleblind study. Clin Rheumatol 2003; 22(4–5):299–304. 28. Butterman GR. Treatment of lumbar disc herniation: epidural steroid injection compared with discectomy. A prospective, randomized study. J Bone Joint Surg [Am] 2004;86(4):670–679. 29. Weiner BK, Fraser RD. Foraminal injection for lateral lumbar disc herniation. J Bone Joint Surg [Br] 1997; 79:804–807. 30. Lutz GE, Vad VB, Wisneski RJ. Fluoroscopic transforaminal lumbar epidural steroids: An outcome study. Arch Phys Med Rehab 1998; 76:1362–1366. 31. Wang JC, Lin E, Brodke DS, et al. Epidural injections for the treatment of symptomatic lumbar herniated discs. J Spinal Disorders & Tech 2002; 15:269–272. 32. Delport EG, Cucuzzella AR, Marley JK, et al. Treatment of lumbar spinal stenosis with epidural steroid injections: a retrospective outcome study. Arch Phys Med Rehabil 2004; 85(3):479–484. 33. Botwin KP, Gruber RD, Bouchlas CG, et al. Fluoroscopically guided lumbar transforaminal epidural steroid injections in degenerative lumbar stenosis: an outcome study. Am J Phys Med Rehabil 2002; 8(12):898–905. 34. Burke JG, Watson RW, McCormack D, et al. Spontaneous production of monocyte chemoattractant protein-1 and interleukin-8 by the human intervertebral disc. Spine 2002; 27(13):1402–1407. 35. Saal JA, Saal JS, Herzog RJ. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine 1990; 15(7):683–686. 36. Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal canal. N Engl J Med 1934; 211:210–215. 37. Osti OL, Vernon-Roberts B, Fraser RD. 1990 Volvo Award in Experimental Studies. Annulus tears and intervertebral disc degeneration: an experimental study using an animal model. Spine 1990; 15:762–767. 38. Burke JG, Watson RW, McCormack D, et al. Intervertebral discs which cause low back pain secrete high levels of proinflammatory mediators. J Bone Surg Joint 2002; 84(2):196–201. 39. Simmons JW, McMillin JN, Emery SF, et al. Intradiscal steroids: a prospective, double-blind clinical trial. Spine 1992; 17(6 Suppl):172–175. 40. Rosenberg SK, Grabinsky A, Kooser C, et al. Effectiveness of transforaminal epidural steroid injections in low back pain: A one year experience. Pain Physician 2002; 5:266–270. 41. Manchikanti L, Pampati V, Rivera JJ, et al. Caudal epidural injections with sarapin steroids in chronic low back pain. Pain Physician 2001; 4:322–335.
1024
47. Klenerman L, Greenwood R, Davenport HT, et al. Lumbar epidural injection in the treatment of sciatica. Br J Rheumatol 1984; 23:35–38. 48. Ridley MG, Kingsley GH, Gibson T, et al. Outpatient lumbar epidural corticosteroid injection in the management of sciatica. Br J Rheum 1988; 27:1003–1007. 49. Rogers P, Nash T, Schiller D, et al. Epidural steroids for sciatica. Pain Clinic 1992; 5:67–72. 50. Revel M, Auleley GR, Alaoui S, et al. Forceful epidural injections for the treatment of lumbosciatic pain with postoperative lumbar spinal fibrosis. Rev Rheum Engl Ed 1996; 63:270–277. 51. Helsa PE, Breivik H. Epidural analgesia and epidural steroid injection for treatment of chronic low back pain and sciatica. Tidsskr Nor Laegeforen 1979; 99:936–939. 52. Meadeb J, Rozenberg S, Duquesnoy B, et al. Forceful sacrococcygeal injections in the treatment of postdiscectomy sciatica. A controlled study versus glucocorticoid injections. Joint Bone Spine 2001; 68:43–49. 53. Breivik H, Hesla PE, Molnar I, et al. Treatment of chronic low back pain and sciatica. Comparison of caudal epidural injections of bupivacaine and methylprednisolone with bupivacaine followed by saline. In: Bonica JJ, Albe-Fesard D, eds. Advances in pain research and therapy. New York: Raven Press; 1976:(1)927–932. 54. Southern D, Lutz GE, Cooper G, et al. Are fluoroscopic caudal epidural steroid injections effective for managing chronic low back pain? Pain Physician 2003; 6:167–172. 55. Swerdlow M, Sayle-Creer W. A study of extradural medication in the relief of the lumbosciatic syndrome. Anesthesia 1970; 25:341–345. 56. Miyomoto K, Masuda K, Kim JG. Intradiscal injections of osteogenic protein-1 restore the viscoelastic properties of degenerated intervertebral discs. Spine J. 2006; 6(6):692-703. 57. An HS, Takegami K, Kamada H. et al. Intradiscal administration of osteogenic protein-1 increases intervertebral disc height and proteoglycan content in the nucleus pulposus in normal adolescent rabbits. Spine. 2005; 30(1):25–31 58. Takegami K, Thonar EJ, An HS. Osteogenic protein-1 enhances matrix replenishment by intervertebral disc cells previously exposed to interleukin-1. Spine. 2002; 27(12):1318–1325. 59. Yoon ST, Park JS, Kim KS, et al. ISSLS prize winner: LMP-1 upregulates intervertebral disc cell production of proteoglycans and BMPs in vito and in vivo. Spine. 2004; 29(23):2603–2611. 60. Kawakami M, Matsumoto T, Hashizume H, et al. Osteogenic protein-1 (osteogenic protein-1/bone morphogenetic protein-7) inhibits degeneration and pain-related behavior induced by chronically compressed nucleus pulposus in the rat. Spine. 2005; 30(17):1933–1939. 61. Simmons JW, McMillin JN, Emery SF, et al. Intradiscal Steroids. A Prospective Double-Blind Clinical Trial. Spine. 1992; 17(6 suppl): s172–175. 62. Khot A, Bowditch M, powell J, et al. The use of intradiscal steroid therapy for lumbar spinal discogenic pain: a randomized controlled trial. Spine. 2004; 29(8): 833–836. 63. Haufe SM, Mork AR. Intradiscal injectin of hematopoietic stem cells in an attempt to rejuvenate the intervertebral discs. Stem Cells Dev. 2006; 15(1):136–137. 64. Peng B, Zhang Y, Hou S, et al. Intradiscal Methylene blue injection for the treatment of chronic discogneic low back pain. Eur Spine J. 2006. 65. Muto M, Andreula C, Leonardi M. Treatment of herniated lumbar disc by intradiscal and intraforaminal oxygen-ozone (O2-O3) injection. j Neuroradiol. 2004; 31(3):183–189. 66. Buric J, Molino, LR. Ozone chemonucleolysis in non-contained lumbar disc herniations: a pilot study with 12 months follow-up. Acta Neurochir Suppl. 2005; 92:93–97. 67. Marks RC, Houston T, Thulbourne T. Facet joint injection and facet nerve block: a randomized comparison in 86 patients with chronic low back pain. Pain 1992; 49:325–328.
Section 5: Biomechanical Disorders of the Lumbar Spine 68. Ashtar IK, Aston BA, Gibson SJ, et al. Morphological basis for back pain: The demonstration of nerve fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum. J Orthop Res 1992; 10:72–78. 69. Yamashita T, Cavanaugh JM, El-Boly AA, et al. Mechanosensitive afferent units in the lumbar facet joint. J Bone Joint Surg [Am] 1990; 72:865–870. 70. Yamashita T, Cavanaugh JM, Ozaktay AC, et al. Effect of substance P on mechanosensitive units of tissues around the facet joint. J Orthop Res 1993; 11:205–214. 71. Mayer T, Robinson R, Pegues P, et al. Lumbar segmental rigidity: can its identification with facet injections and stretching exercises be useful? Arch Phys Med Rehabil 2000; 81:1143–1150. 72. Revel ME, Listrat VM, Chevalier XJ, et al. Facet joint block for low back pain: identifying predictors of a good response. Arch Phys Med Rehabil 1992; 73(9):824–828. 73. Revel M, Poiraudeau S, et al. Capacity of the clinical picture to characterize low back pain relieved by facet joint anesthesia. Proposed criteria to identify patients with painful facet joints. Spine 1998; 23(18):1972–1976.
82. Lau LS, Littlejohn GO, Miller MH. Clinical evaluation of intra-articular injections for lumbar facet joint pain. Med J Aust 1985; 143:563–565. 83. Lippitt AB. The facet joint and its role in spine pain. Management with facet joint injections. Spine 1984; 9:746–750. 84. Manchikanti L, Pampati V, Bakhit CE, et al. Effectiveness of lumbar facet nerve blocks in chronic low back pain: a randomized clinical trial. Pain Physician 2001; 4:101–117. 85. Manchikanti L, Pampati V, Fellows B, et al. Prevalence of lumbar facet joint pain in chronic low back pain. Pain Physician 1999; 2:59–64. 86. North RB, Han M, Zahurak M, et al. Radiofrequency lumbar facet denervation: analysis of prognostic factors. Pain 1994; 57:77–83. 87. Horlocker TT, Wedel DJ, Offord KP. Does preoperative antiplatelet therapy increase the risk of hemorrhagic complications associated with regional anesthesia? Anesth Analg 1990, 70:631–634. 88. Botwin KP, Gruber RD, et al. Complications of fluoroscopically guided transforaminal lumbar epidural injections. Arch Phys Med Rehabil 2000; 81(8):1045–1050.
74. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19(10):1132–1137.
89. Shulenberger CC. Ergonomic intervention for the prevention and treatment of spinal disorders. In: White AH, Schofferman JH, eds. Spine care: diagnosis and conservative management. St. Louis: Mosby; 1995:472–485.
75. Mayer TG, Gatchel RJ, Keeley J, et al. A randomized clinical trial of treatment of lumbar segmental rigidity. Spine 2004; 29(20):2199–2205.
90. Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med 1986; 315:1064–1070.
76. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal pain. Spine 2000; 25:1270–1277.
91. National Center for Health Statistics: Vital statistics of the United States. Washington, DC: Government Printing Office; 1968–1988.
77. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections into facet joints for chronic low back pain. N Engl J Med 1991; 325:1002–1007.
92. Department of Health and Human Services: Reducing the health consequences of smoking. 25 years of progress: a report of the Surgeon General. Washington, DC: Government Printing Office (DHHS pub. No. (CDC) 89-8411); 1989.
78. Lynch MC, Taylor JF. Facet joint injection for low back pain. A clinical study. J Bone Joint Surg [Br] 1986; 68:138–141. 79. Destouet JM, Gilula LA, Murphy WA, et al. Lumbar facet joint injection: Indication, technique, clinical correlation, and preliminary results. Radiology 1982; 145: 321–325. 80. Murtagh FR. Computed tomography and fluoroscopy guided anesthesia and steroid injection in facet syndrome. Spine 1988; 13:686–689. 81. Mironer YE, Somerville JJ. Protocol for diagnosis and treatment of facet joint pain syndrome. A modified three-step approach. Pain Digest 1999; 9:188–190.
93. Manson J, Tosteson H, Ridker P, et al. The primary prevention of myocardial infarction. N Engl J Med 1992; 326:1406. 94. LaCroix J, Powell J, Lloyd G. Low back pain, factors of value in predicting outcome. Spine 1990; 15:495. 95. Spitzer W, LeBlanc F, Dupuis M. Scientific approach to the assessment and management of activity related spinal disorders: report of the Quebec Task Force on Spinal Disorders. Spine 1987; 12:51.
1025
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain
CHAPTER
Radiofrequency Denervation
93
Atul L. Bhat
INTRODUCTION Low back pain is ubiquitous to mankind by virtue of our upright posture. Traditionally, it has been believed that most episodes of spinal pain are short lived and that at least 90% of patients with low back pain recover in about 6 weeks with or without treatment.1–3 Contrary to this prior assumption of only 10–20% patients experiencing recurrent or chronic symptoms after an initial episode of low back pain, recent literature puts that number as high as 35–79%.4–7 The challenge lies, in this subgroup of subjects, to identify the specific pain generator so that appropriate interventional therapy may be initiated as and when indicated. The study by Kuslich et al.8 identified along with intervertebral disc, dura, ligaments, fascia, and muscles, zygapophyseal or facet joints as capable of transmitting pain in the low back region. Even prior to this anatomical study, Goldthwait9 in 1911 first recognized lumbar zygapophyseal joints as potential source of low back pain. He believed that joint asymmetry could result in pain secondary from nerve root pressure. Subsequently, in 1933, Ghormley10 first coined the term ‘facet syndrome’ as lumbosacral pain with or without sciatic pain, occurring after a twisting or rotary strain of the lumbosacral region. Badgley11 in 1941 suggested that facet joints by themselves could be a primary source of low back pain separate from the nerve compression component. However, it was not until 1963 when Hirsch et al.12 demonstrated that the low back pain distributed along the sacroiliac and gluteal areas with referral to the greater trochanter could be induced by injecting hypertonic saline in the region of the lumbar facet joints. In 1976, Mooney and Robertson,13 and three years later McCall et al.14 used fluoroscopy to confirm the location of intra-articular lumbar facet joint injections in asymptomatic individuals, demonstrating reproduction of back and leg pain after injection of hypertonic saline. Eventually, Marks15 in 1989, followed by Fukui et al.16 in 1997, described the distribution of pain patterns after stimulating the lumbar facet joints. Recent literature17 indicates that the prevalence of chronic lumbar zygapophyseal joint-mediated pain has a wide range that varies from 15% in the relatively younger patients, with confidence limits of 10–20%. This prevalence can be as high as 40% among the elderly population with confidence limits of 27–53%.18
ANATOMY The lumbar facet or zygapophyseal joints are paired, true synovial, diarthrodial joints that form the posterior aspect of the respective intervertebral foramina. The joint consists of hyaline cartilage, a synovial membrane, a fibrous capsule, and nociceptive fibers transmitted via the medial branches of the dorsal rami.19,20 These facet joints are innervated by the medial branches of the dorsal rami (posterior
primary rami) that exit the intervertebral foramina. The posterior primary rami travel posteriorly over the base of the transverse process. The dorsal ramus divides into a medial, an intermediate, and a lateral branch. The lateral branch ascends from the dorsal ramus just before it reaches the transverse process. The medial branch passes under the mammilloaccessory ligament and sends branches to the adjacent facet joint, the facet joint below, and the more medial erector spinae muscles. Thus, the joint is typically innervated from a branch at the same level and a branch originating from the foramen above. In contrast, the dorsal ramus at the fifth lumbar vertebral level (L5) travels between the ala of the sacrum and its superior articular process, which divides into the medial and lateral branches at the caudal edge of the process, the medial branch continuing medially, where it innervates the lumbosacral joint.21–23 Neuroanatomical studies12,24–26 indicate that the facet joint capsule is richly innervated, containing both free and encapsulated endings, and can undergo extensive stretch under physiological loading.27 It has been reported that protein gene product (PGP) 9.5, substance P (SP), calcitonin gene-related peptide (CGRP), dopamine β-hydroxylase (DBH), vasoactive intestinal polypeptide (VIP), neural peptide Y (NPY), and choline acetyl transferase (chAT) immunoreactive (IR) fibers are present within the human facet joint capsule.21,26,28–30 Ashton et al.31 confirmed immunoreactivity for SP, CGRP, and VIP in surgically removed human facet joint capsule. A subsequent anatomical study confirmed higher concentration of inflammatory cytokines in facet joint tissue from patients with lumbar spinal stenosis than in lumbar disc herniations, suggesting that these cytokines may have some contribution to the etiology of symptoms in degenerative spinal stenosis.32
PATHOPHYSIOLOGY With aging, the changes that occur in the zygapophyseal joints are the same as those seen in any diarthrodial joint. The earliest change is synovitis, which may persist with the formation of a synovial fold which projects into the joint space itself. Later, degenerative changes set in gradually, and eventually become more marked. Eventually, the capsular laxity allows for subluxation of the joint surfaces. Continued degeneration mainly due to repeated torsional strains results in the formation of subperiosteal osteophytes, and possibly subchondral synovial cysts. The end result is that of gross articular degeneration, with almost complete loss of articular cartilage, and formation of bulbous zygapophyseal joints and marked periarticular fibrosis. The pathogenesis of a degenerative cascade in the context of a threejoint complex involving the intervertebral disc and the adjacent zygapophyseal joint also leads to the assumption that the degenerative changes within the disc are also believed to lead to associated facet degeneration.33–35 1027
Part 3: Specific Disorders
PAIN PATTERNS The clinical presentation of lumbar zygapophyseal joint-mediated low back pain appears to overlap considerably with the presentation of low back pain due to various other etiologies. Lumbar facet joints have been shown to be capable of producing pain in the low back and referred pain in the lower extremity in normal volunteers.13–16 McCall et al.14 concluded that pain referral patterns overlap between the upper and lower lumbar spine. Marks15 also studied patterns of pain induced from lumbar facet joints, from the posterior primary rami of L5, and from the medial articular branches of the posterior primary rami from T11 to L4. He observed no consistent segmental or somatic referral pattern. Marks also concluded that pain referred to the buttocks or trochanteric region occurred mostly from the L4 and L5 levels, while inguinal or groin pain was produced from L2 to L5. This latter finding led to the conclusion that the nerves innervating the joints gave rise to distal referral of pain more commonly than the facet joint itself. Fukui et al.16 concluded that the major site of referral pain from the L1–2 to L4–5 joints was the lumbar region itself. However, stimulation of the L5–S1 joint caused referred spinal pain as well as gluteal pain. Referred pain into the lower extremities was not observed by Fukui et al.16 as was reported by Mooney and Robertson.13 However, it must not be overlooked that in the study by Mooney and Robertson, the relatively large volume of the injectate (3 cc) used may very well have inadvertently anesthetized structures other than the facet joint intended. In essence, these studies indicate that there is no clear dermatomal or somatic pattern that is diagnostic of lumbar facet joint-mediated pain and an overlap with a varied pattern is the norm.
DIAGNOSIS All this being said, there is no identified correlation between a clinical picture or any imaging study used, such as the magnetic resonance imaging (MRI), computed tomography (CT) scan, single photon emission computed tomography (SPECT), or radionuclide bone scan in diagnosing pain mediated via the lumbar zygapophyseal joint.36–40 Simple static radiographs of the lumbar spine, and also dynamic images including standing flexion–extension films, may reveal evidence of arthritis involving the lumbar zygapophyseal joint as commonly in asymptomatic individuals as in patients with axial low back pain. What remains contentious is how lumbar zygapophyseal joint-mediated pain should be diagnosed. Another point not to be overlooked is the fact that psychological factors can be involved in cases of chronic low back pain. Long before the monumental work of Freud, it was recognized that emotional states could be associated with physical symptoms in the absence of an organic pathology. Consequently, it behooves the primary spine care provider to learn how to identify these patients, how to diagnose their conditions, how to treat them, and how, when, and from whom to seek consultation. Unless chronic spinal pain is simultaneously understood and treated from a musculoskeletal and psychological perspective, treatment failure will be the norm. Treatment modalities directed only at a physical or mechanical problem will not be sufficient or helpful if there is an associated unrecognized or ignored psychological problem. Diagnosis is the cornerstone of a rational treatment approach to any kind of illness. Spine physicians confronted with a patient describing chronic or ongoing back pain are pressed to establish a diagnosis. Appropriately, any clues derived from the history and from the physical examination are pursued toward that end. Schemata describing the great classifications of disease illustrate the breadth and scope of physical pathologic conditions that can be associated with low back pain. Thus, the differential diagnosis in a patient presenting with chronic low back encompasses 1028
numerous entities. Clinical problems tend to become complex when there is difficulty in establishing a diagnosis or when then the treatment options are unclear or difficult to implement. In approximately a quarter of the patient population there is a coexisting lesion responsible for the patient’s symptoms. Up-to-date laboratory and imaging techniques notwithstanding, nothing supplants and nothing exceeds the diagnostic accuracy of a thorough history and a careful physical examination. Because the causes of back pain are legion and involve virtually every organ system as well as the psyche, a truncated history, focused only on the spine should be avoided. A tunnel vision, essentially blinding oneself, will only lead to diagnostic followed by therapeutic pitfalls.
Diagnostic injections The only available means of establishing a diagnosis of lumbosacral zygapophyseal joint-mediated pain is to utilize diagnostic injections. Diagnostic blockade of a structure with a nerve supply with ability to generate pain can be performed to test the hypothesis that the target structure is the source of symptoms. If pain is relieved by blocking the medial branch or the zygapophyseal joint itself, the joint may be considered prima facie to be the source of pain.41 Pain relief is considered as the essential criterion, rather than provocation of pain from stimulating the target area. The choice lies with the spine interventionist whether to pursue an intra-articular zygapophyseal joint injection or anesthetize the medial branches of the dorsal rami that innervate the target joint. Debate continues regarding the appropriateness of intra-articular injections or medial branch blocks. For diagnostic intra-articular injection only a small volume (0.5–0.8 cc) of the local anesthetic agent is to be injected. Using small aliquots of local anesthetic will minimize extravasation of the anesthetic agent and necessarily diminish the frequency of a false-positive response. In essence the specificity of the diagnostic injection is enhanced. A small amount (0.2 cc) of contrast medium should be instilled to ensure an intra-articular spread. A partial arthrogram ensures appropriate needle placement and protects against false appreciation of joint entry and venous infiltration.42 Similarly, when a medial branch block is performed, contrast should be instilled prior to the actual injection of the anesthetic agent to ensure against venous uptake. Theoretically, medial branch injections may be more specific because there is a less likelihood of anesthetizing the epidural space or the neural foramina as long as the anesthetic volume is limited to 0.5 cc. The author prefers to peruse an intraarticular injection in the younger patient population where the joint is not affected by significant arthritis. A medial branch block is preferred in the elderly where it may be technically difficult to access the severely arthritic zygapophyseal joint or when lack of adequate joint space is suspected. Kaplan et al.43 did find that medial branch blocks can fail to anesthetize the target joint in a minority of cases, ostensibly in 11% but possibly in as many as 31%, based on 95% confidence interval intervals. These authors have postulated that an aberrant or additional innervation of the targeted joint may provide for a pathway for persistent nociception. While not refuting the ability of the medial branch blocks to positively diagnose zygapophyseal joint pain, they warn that facet joint pain may be underdiagnosed by such diagnostic blocks. Based on the response to a single diagnostic injection, the prevalence of the lumbar zygapophyseal joint pain in patients with chronic low back pain demonstrates a wide range of 7.7–75%.42,44–50 This wide range in numbers may represent a selection bias, variable population subsets, or even placebo responders. Similarly, a diagnosis cannot be made reliably on the basis of a single diagnostic injection, and falsepositive rates as high as 38% have been demonstrated.51 To increase the sensitivity of these diagnostic injections it has been suggested
Section 5: Biomechanical Disorders of the Lumbar Spine
that controlled diagnostic injection should include placebo injections utilizing normal saline.41 This may be accurate theoretically but is not practically viable, logistical, or ethical to use placebo injections in all patients presenting with low back pain presumably of lumbar facet origin. An attractive, reasonable alternative is the use of comparative local anesthetic blocks using two local agents with different duration of actions on two separate occasions.52–55 A double-block diagnostic injection involves the use of two different anesthetic injections, each with a different duration of action. A true-positive response to comparative local anesthetic injections is one in which the patient experiences pain relief for a shorter duration when a short-acting agent is used and for a longer duration when a long-acting agent is utilized. A triple-block paradigm requires three injections. The first uses a short-acting anesthetic agent. If a positive response is obtained, the patient is subjected to a series of two blinded injections. One injection uses intraparticular anesthetic agent, whereas the second is an extraparticular injection with saline. However, again it may not be logistically possible or ethically sound to use such regimens in a conventional practice on every patient. Once a diagnosis of lumbar zygapophyseal joint-mediated pain is established, therapeutic intra-articular zygapophyseal joint injection utilizing a steroid preparation or medial branch block can be utilized. These procedures have been described elsewhere in this textbook. The efficacy of such interventions may not be long lived and repeat injections may need to be performed on an individual basis. Most interventionist spine physicians limit the frequency of intra-articular steroid injections to 2–4 per year. However, there are no data to support or refute this number. From anatomical studies of the innervation of the facet joint it is clear that the medial branch of the dorsal ramus supplies sensory innervation to the joint. Radiofrequency neurotomy of medial branch of the dorsal ramus eliminates this sensory input for a considerably longer duration of time as compared with simple medial branch block and may be used in patients with the goal of achieving long-lasting pain relief.56 In the classic conception of pain, afferent nerves that are exposed to noxious stimuli transmit ascending pain signals through the dorsal horn to the brain where sensory perception is processed. This simplistic conception of pain has now been superseded and augmented by new evidence of pain signaling through many additional pathways. In addition to the psychological component of the perception of pain mediated by cultural, behavioral, and experimental influences, pain signaling can be modified within both the periphery and central nervous system to produce a self-sustaining, vicious cycle of pain syndromes. In the periphery, the imbalance of small and large fibers transmitting pain signals at the dorsal horn have been implicated in sustaining pain impulses even after the stimulation of the afferent nerve has been eliminated. Centrally, chronic pain may be mediated by changes in neuronal function in the dorsal horn or in biochemical mediators involved in descending signals of pain perception. This being said, it is rather naïve or too simplistic to assume almost complete resolution of lumbar pain will occur after attacking the medial branches of the presumably affected zygapophyseal joints.
REVIEW OF LITERATURE SUPPORTING CLINICAL EFFECTIVENESS OF LUMBAR RADIOFREQUENCY Historically, interventional management of lumbar zygapophyseal joint pain started with the use of a knife-cut in the region of the lumbar facet joint for denervation. Rees57 reported immediate relief of pain in 998 of 1000 patients suffering from ‘intervertebral disc syndrome’ using this technique. Shealy58,59 introduced the procedure
in North America but, after a large number of operations, changed to a radiofrequency coagulation lesion through a probe placed in the region of the nerve supply of the facet joint. Many investigators have studied the effectiveness of radiofrequency denervation of medial branches of the lumbar zygapophyseal joint, of which only four are prospective studies. These include two randomized, controlled trials by van Kleef et al.60 and Leclaire et al.,61 one double-blind, controlled study by Gallagher et al.,62 and a case series by Dreyfuss et al.55 In each of these studies, patients were included when they had failed to respond to traditional conservative treatment, such as a trial of bed rest, medications, and physical therapy. However, the inclusion or exclusion criteria were inconsistent across the studies. Gallagher et al.62 included patients with low back pain for at least 3 months and used diagnostic injections of 0.5 cc of 0.5% bupivacaine in and around the lumbar zygapophyseal joint. Patients with good or equivocal response to this injection within 12 hours were randomized to undergo either a lumbar facet joint denervation or placebo treatment. Radiofrequency lesions were performed for 90 seconds at a temperature of 80°C. McGill pain questionnaire63 and the visual analog scale (VAS)64 were used at 1 month but only the VAS at 6 months. Statistical comparison of pain scores was conducted using the Kruskal-Wallis and Mann Whitney U tests. Reduction in pain scores was approximately 50% at 1 month and was sustained at 6 months. The only difference in pain scores were seen when comparing people, all of whom met the inclusion criteria of a good response to an initial injection using 0.5 cc of 0.5% bupivacaine. The only statistical differences in pain scores in the post-treatment group occurred during comparing patients with a good initial response to local anesthetic injection but proceeding to a sham procedure. The randomized, controlled trial of van Kleef et al.60 included 31 patients with low back pain of at least 12 months. These were injected with 0.75 cc of 1% lidocaine about the two medial branches innervating a particular zygapophyseal joint. Patients were evaluated 30 minutes after this injection. Those with at least a 50% relief on a four-point Likert scale (0–30% pain relief was considered as no relief; 30–50% was defined as moderate; 50–80% pain relief was good, and 80% or more was considered as pain free) were randomized. Radiofrequency probes were placed in both groups but only one group underwent the actual radiofrequency lesioning for 60 seconds. Patients were followed for at least 12 months and the outcome measures included the VAS instrument, Oswestry disability index, and global perceived effect. At 8 weeks, a higher rate of success in the treatment group compared to the control group was noted. Subsequent log rank test showed a statistically significant difference ( p=0.02) at 3, 6, and 12 months. Leclaire et al.61 performed a diagnostic intra-articular facet joint block with 0.5 cc of lidocaine 2% and 0.5 cc of 40 mg of triamcinolone acetonide. Significant relief of low back pain for at least 24 hours in the week after this injection was considered as positive. For each nerve, radiofrequency neurotomy was performed at two locations, one at the proximal portion and another at the distal portion of the dorsal ramus with the temperature controlled at 80°C for 90 seconds. For patients in the control group the temperature of the probe was maintained at 37°C. Follow-up assessments were undertaken at 4 and 12 weeks when the disability questionnaire, the visual analog scale, the triaxial dynamometry, and the return to work assessment was repeated. The primary analysis was based on the intention to treat principle. At the end of 4 weeks, there was an improvement in the Roland-Morris score65 by 8.4% and 2.2% in the radiofrequency and control groups, respectively. However, at 12 weeks there was no significant difference in the Roland-Morris,65 Oswestry disability,66 VAS,64 strength/mobility, and return-to-work status in both groups. 1029
Part 3: Specific Disorders
Dreyfuss et al.55 used 0.5 cc of lidocaine 2% for the initial zygapophyseal joint injection. A positive response was defined as at least 80% relief of pain lasting longer than 1 hour. At the end of 1 week, this group of patients underwent another diagnostic injection using bupivacaine 0.5%. Subjects experiencing greater than 80% relief, lasting longer than 2 hours, were included in the study. The technique used by Dreyfuss et al.55 was different in that the radiofrequency ablation was performed for 8–10 mm along the length of the target nerve with the temperature being maintained at 85°C. The outcome measures included VAS,64 Roland-Morris questionnaire,65 prescription analgesic medication, McGill pain questionnaire,63 ShortForm (SF)-36 general health questionnaire,67,68 North American Spine Society (NASS)69 treatment expectations, isometric push and pull, dynamic floor-to-waist lift, and isometric above-shoulder lifting tasks. In addition, a needle electromyography of the L2–L5 bands of the multifidus muscle was performed before and at 8 weeks after the radiofrequency denervation. Patients were evaluated with at least a 12 month follow-up. Statistical analysis was performed using median scores and interquartile ranges of all outcome measures, Friedman two-way analysis of variance, Wilcoxon paired test, and Spearman correlation coefficients. Sixty percent of patients experienced at least a 90% pain reduction, whereas 87% of patients experienced at least a 60% reduction in pain. This effect lasted for 12 months. Fortyseven percent of patients obtained absolute reduction of at least 5 in the VAS,64 and 60% obtained relative reduction of at least 3. They noted that, even for patients who experienced pain for more than 5 years, radiofrequency denervation of the medial branch was helpful, cost effective, and less time consuming than other interventions such as exercise-based physical therapy or manipulative care. The results of needle electromyography warrants a special mention, with 11 of 15 patients sustaining 100% denervation, whereas 4 achieved partial denervation. A critical review of each of these studies is of prime importance if one is to derive a deep understanding of this therapeutic intervention for the treatment of lumbar zygapophyseal joint mediated pain. Each study used a small sample size, with van Kleef et al.60 and Dreyfuss et al.55 using only 15 subjects each in the treatment group. Gallagher et al.62 and Leclaire et al.61 did not specify how a successful outcome to the diagnostic injections was objectively rated. Dreyfuss et al.55 and Leclaire et al.61 were the only two sets of authors who followed their patients for at least 12 months. There were also discrepancies noted in reporting the diagnostic injection. Gallagher et al.,62 in their abstract, mention that the solution used was a combination of local anesthetic agent with steroid, whereas the main text of the paper states that the solution used was only local anesthetic. Van Kleef et al.60 used a double-blind, placebo-controlled injection paradigm. Unfortunately, patients were selected on the basis of a single positive diagnostic injection which, as discussed previously, is known to have a false-positive rate of approximately 38%.51 The technique used by van Kleef et al.61 was different, such that the electrodes were placed at an angle to the target nerve. Laboratory studies have shown that the electrode must lie parallel to the nerve if the nerve is to be optimally and maximally coagulated.56 This may explain why van Kleef et al.60 obtained only modest results. Similarly, van Kleef et al.60 and Dreyfuss et al.55 included subjects with low initial VAS scores. Although Dreyfuss et al.55 used the strictest inclusion criteria in their prospective audit, they unfortunately treated only a small sample size. By performing two different diagnostic injections with two anesthetic agents, each with a different duration of action, they tried to eliminate the false-positive responders. Also, during the radiofrequency denervation, the electrodes were placed meticulously to optimize coagulation of the nerve. As previously stated, these authors conducted a needle electromyography of L2–L5 bands of multifidus 1030
before and at 8 weeks after the denervation. Although electromyographic evidence of denervation indicates that the radiofrequency ablation successfully coagulated the assessed medial branch, such an outcome did not correlate with symptom improvement. However, this study did not include a control group. In the Leclaire et al.61 study, the inclusion criteria was significant relief of low back pain for more than 24 hours after the facet injection. Roland-Morris score65 was used as an important outcome measure, which is a measurement of functional limitation and not of pain relief. A more in-depth questionnaire on pain, such as the McGill Pain Questionnaire,63 possibly could better identify the therapeutic response in these patients. These conflicting trials, discussing the use of radiofrequency denervation in the management of lumbar zygapophyseal joint-mediated pain, highlight the use of varied inclusion criteria, varied treatment, lack of uniform outcome measures, use of concurrent interventions, and lack of a sufficient follow-up. A detailed review of these deficiencies and critical analysis of the relevant peer-reviewed publications can be found elsewhere.70,71 A more recent anatomical study undertaken by Lau et al.72 validates the prime importance of placement of electrodes parallel to the target nerve. This underscores the fact that a meticulous technique will lead to superior results. Because of the insufficient quantity of high-quality studies, it is evident that prospective, randomized, controlled trials with uniform inclusion and exclusion criteria and assessing an appropriate number of subjects in each are necessary, as dictated by a power analysis. Additionally, such studies should use a standardized treatment, uniform outcome measures, and have an adequate follow-up duration of at least 12 months. The Agency for Health Care and Policy Research describes evidence rating for management of low back pain in adults.73 For the development of these guidelines, a rating schema was used to assess the strength or efficacy of a treatment or procedure. They offered five levels of strength: level I (conclusive): research-based evidence with multiple relevant and high-quality scientific studies; level II (strong): research-based evidence from at least one properly designed randomized, controlled trial of appropriate size (with at least 60 patients in each arm) and high-quality or multiple adequate scientific studies; level III (moderate): evidence from well-designed trials without randomization, single group pre-post cohort, time series, or matched case-controlled studies; level IV (limited): evidence from well-designed nonexperimental studies from more than one center or research group; and level V (intermediate): opinions of respected authorities, based on clinical evidence, descriptive studies, or reports of expert committees. Critical review of the literature reveals that the type and strength of efficacy evidence for radiofrequency neurotomy in managing lumbar zygapophyseal joint-mediated pain is level III evidence.
CONCLUSION In summary, the process of establishing a diagnosis of lumbar zygapophyseal joint-mediated pain, the techniques used to make this diagnosis and implementing an effective treatment algorithm has evolved extensively over the past three decades since Mooney and Robertson proposed the posterior joints of the lumbar spine as a potential source of low back pain (Fig. 93.1). The question is not whether the syndrome of lumbar zygapophyseal joint pain exists but how to come to an accurate diagnosis and how to treat it effectively. The challenge lies in the accurate diagnosis of this entity so that appropriate interventional therapy may be instituted. Regardless of the approach used, the diagnosis can only be affirmed using, at a minimum, a double-block paradigm due to the low positive predictive value of a single diagnostic injection. If attractive, compelling results
Section 5: Biomechanical Disorders of the Lumbar Spine Axial pain on extension/rotation single stance extension facet arthrosis on imaging studies
5. Cassidy D, Carroll L, Cote P. The Saskatchewan health and back pain survey. Spine 1998; 6. Carey TS, Garrett JM, Jackman A, et al. Recurrence and care seeking after acute low back pain. Results of a long-term follow-up study. Med Care 1999; 37:157–164. 7. Van Den Hoogen HJM, Koes BW, Deville W, et al. The prognosis of low back pain in general practice. Spine 1997; 22:1515–1521.
Conservative care (therapy/medications)
8. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica: A report of pain response to tissue stimulation during operation on the lumbar spine using local anesthesia. Orthop Clin North Am 1991; 22:181–187.
No relief
Consider interventional therapy
9. Goldthwait JE. The lumbosacral articulation: An explanation of many cases of lumbago, sciatica, and paraplegia. Boston Med and Surg J 1911; 164:365–372. 10. Ghormley RK. Low back pain. With special reference to the articular facets, with presentation of an operative procedure. JAMA 1933; 101:1773–1777. 11. Badgley CE. The articular facets in relation to low back pain and sciatic radiation. J Bone Joint Surg 1941; 23:481.
Diagnostic intra-articular block with 2% lidocaine or medial branch block
12. Hirsch D, Inglemark B, Miller M. The anatomical basis for low back pain. Acta Orthop Scand 1963; 33:1. 13. Mooney V, Robertson J, The facet syndrome. Clin Orthop 1976; 115:149–156. 14. McCall IW, Park WM, O’Brien JP. Induced pain referral from posterior elements in normal subjects. Spine 1979; 4:441–446.
Negative: think of lumbar myofascial pain, enthesopathy
Positive
15. Marks R. Distribution of pain provoked from lumbar facet joints and related structures during diagnostic spinal infiltration. Pain 1989; 39:37–40. 16. Fukui S, Ohseto K, Shiotani M, et al. Distribution of referral pain from the lumbar zygapophyseal joints and dorsal rami. Clin J Pain 1997; 12:303–307.
Two sets of diagnostic blocks with lidocaine and bupivacaine at different times
17. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints: Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137. 18. Schwarzer AC, Wang S, Bogduk N, et al. Prevalence and clinical features of lumbar zygapophyseal joint pain. Ann Rhem Dis 1995; 54:100–106.
Positive
Negative: exclude facet pain
19. Bogduk N, Engel R. The menisci of the lumbar zygapophyseal joints. A review of their anatomy and clinical significance. Spine 1984; 9:454–460. 20. Bogduk N, Twomey LT. Clinical anatomy of the lumbar spine, 2nd edn. London: Churchill Livingstone; 1991. 21. Pedersen HE, Blunck CFJ, Gardner E. The anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves (sinu-vertebral nerves). J Bone Joint Surg [Am] 1956; 38A;377–391.
Therapeutic block with steroid and lidocaine
22. Bogduk N, Wilson AS, Tynan W. The human lumbar dorsal rami. J Anat 1982; 134:383–397. 23. Bogduk N. The innervation of the lumbar spine. Spine 1983; 8(3):286–293.
Recurrence
24. Jackson HC, Winkelmann RK, Bickel WH. Nerve endings in the human spinal column and related structures. J Bone Joint Surg [Am] 1966; 48A:1272
Medial branch blocks
Repeat therapeutic block
25. Bogduk N. Nerves of the lumbar spine. In: Clinical anatomy of the lumbar spine and sacrum, 3rd edn. New York: Churchill Livingstone; 1997:127–143. 26. Suseki K, Takahashi Y, Takahashi K, et al. Innervation of the lumbar facet joints. Spine 1997; 22:477–485.
Radiofrequency denervation Fig. 93.1 Effective treatment algorithm.
are to be achieved following a lumbar radiofrequency denervation, the clinician needs to follow two basic but often overlooked steps: establish an accurate diagnosis of lumbar facet syndrome and then, during treatment, adhere to a meticulous placement of electrodes.
References
27. El-Bohy AA, Goldberg SJ, King AI. Measurement of facet capsular stretch. Biomechanics symposium, Annual conference of the American Society of Mechanical Engineers, Cincinnati, OH. AMD 1987; 84:161. 28. Edgar MA, Ghadially JA. Innervation of the lumbar spine. Clin Orthop Rel Res 1976; 115:35–41. 29. Brink EE, Pfaff DW. Vertebral muscles of back and tail of albino rat (Rattus norvegicus albinus). Brain Behab Evol 1980; 17:1–47. 30. Cavanaugh JM, El-Bohy A, Hardy WN, et al. Sensory innervation of soft tissues of the lumbar spine in the rats. J Orthop Res 1989; 7:378–388. 31. Ashton KI, Ashton BA, Gibson SJ, et al. Morphological basis for low back pain. Demonstration of fibers and neuropeptides in the lumbar facet joint capsule but not in ligamentum flavum. J Orthop Res 1992; 10:72.
1. Anderson GBJ, Svensson HO. The intensity of work recovery in low back pain. Spine 1983; 8:880–887.
32. Igarashi A, Kikuchi S, Konno S, et al. Inflammatory cytokines released from the facet joint tissue in degenerative lumbar spinal disorders. Spine 2004; 29:2091–2095.
2. Spitzer WO, Leblanc FE, Dupuis M, eds. Quebec Task Force on Spinal Disorders. Scientific approach to the assessment and management of activity-related spinal disorders: A monogram for clinicians. Spine 1987; S12:1–59.
33. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, et al. Pathology and pathogenesis of lumbar spondylolysis and stenosis. Spine 1978; 3:319–327.
3. Manchikanti L, Singh V, Kloth D, et al. Interventional techniques in the management of chronic pain: Part 2.0. Pain Phys 2001; 4:24–96.
34. Fujiwara A, Tamai K, Yamato M, et al. The relationship between the facet joint osteoarthritis and disc degeneration of the lumbar spine: An MRI study. Eur J Spine 1999; 8:396–401.
4. Lawrence RC, Helmick CG, Arnett FC. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 1998; 41:778–799.
35. Fujiwara A, Tamai K, An HS. The relationship between disc degeneration, facet joint osteoarthritism, and stability of the degenerative lumbar spine. J Spinal Disord 2000; 13:444–450.
1031
Part 3: Specific Disorders 36. Wiesel SW, Tsourmas N, Feffer HL. A study of computer assisted tomography I: The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1981; 9:549–551. 37. Jensen M, Brant-Zwawadzki M, Obuchowski N. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994; 2:69–73. 38. Schwarzer AC, Wang S, O’Driscoll D, et al. The ability of computed tomography to identify a painful zygapophyseal joint in patients with chronic low back pain. Spine 1995; 20:907–912. 39. Ryan PJ, Di Vadi L, Gibson T, et al. Facet joint injection with low back pain and increased facetal activity on bone scintigraphy with SPECT: A pilot study. Nucl Med Commun 1992; 13:401. 40. Schwarzer AC, Scott AM, Wang S, et al. The role of bone scintigraphy in chronic low back pain: Comparison of SPECT and planar images and zygapophyseal joint injection. Aust NZ J Med 1992; 22:185. 41. Bogduk N. International Spinal Injection Society guidelines for the performance of spinal injection procedures: Part 1: Zygapophyseal joint blocks. Clin J Pain 1997; 13:292–297. 42. Dreyfuss PH, Dryer SJ, Herring SA. Contemporary concepts in spine care: Lumbar zygapophyseal (facet) joint injections. Spine 1995; 20(18):2040–2047. 43. Kaplan M, Dreyfuss P, Halbrook B, et al. The ability of lumbar medial branch blocks to anesthetize the zygapophyseal joint: A physiologic challenge. Spine 1998; 23(17):1847–1852. 44. Carette S, Marcoux S, Truchon R, et al. A controlled trial of corticosteroid injections in the facet joints for chronic low back pain. N Engl J Med 1991; 325:1002–1007. 45. Carrera GF. Lumbar facet joint injection in low back pain and sciatica: Preliminary results. Radiology 1980; 137:665–667. 46. Carrera GF, Williams AL. Current concepts in evaluation of the lumbar facet joints. Crit Rev Diagn Imaging 1984; 21:85–104. 47. Destouet JM, Gilula LA, Murphy WA, et al. Lumbar facet joint injection: Indication, technique, clinical correlation, and preliminary results. Radiology 1982; 145:321–325. 48. Destouet JM, Murphy WA. Lumbar facet block: indication and technique. Orthop Rev 1985; 14:57–65. 49. Helbig T, Lee CK. The lumbar facet syndrome. Spine 1988; 13:61–64. 50. Raymond J, Dumas JM. Intra-articular facet block: diagnostic test or therapeutic procedure? Radiology 1989; 151:333–336. 51. Schwarzer AC, Aprill CN, Derby, et al. The false-positive rate of uncontrolled diagnostic blocks of the lumbar zygapophyseal joints. Pain 1994; 58:195–200. 52. Bonica JJ. Local anesthesia and regional blcoks. In: Wall PD, Melzack R, eds. Textbook of pain, 2nd edn. Edinburgh: Churchill Livingstone; 1989:724–743. 53. Bonica JJ, Buckley FP. Regional analgesia with local anesthetics. In: Bonica JJ, ed. The management of pain. Philadelphia: Lea & Fibeger; 1990:1883–1966. 54. Boas RA. Nerve blocks in the diagnosis of low back pain. Neurosurg Clin North Am 1991; 2:806–816. 55. Dreyfuss P, Halbrrok B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25(10):1270–1277.
1032
56. Bogduk N, Macintosh J, Marshland A. Technical limitations to the efficacy of radiofrequency neurotomy for spinal pain. Neurosurgery 1987; 20:529–535. 57. Rees WES. Multiple bilateral subcutaneous rhizolysis of segmental nerves in the treatment of the intervertebral disc syndrome. Ann Gen Pract 1971; 16:126–127. 58. Shealy CN. The role of spinal facets in back and sciatic pain. Headache 1974; 14:101. 59. Shealy CN. Facet denervation in the management of back and sciatic pain. Clin Orthop 1976; 115:157–164. 60. Van Kleef M, Barendse GAM, Kessels A, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999; 24(18):1937–1942. 61. Leclaire R, Fortin L, Lambert T, et al. Radiofrequency facet joint denervation in the treatment of low back pain: a placebo-controlled clinical trial to assess efficacy. Spine 2001; 26(13):1411–1417. 62. Gallagher J, Petriccione di Vadi PL, Wedley JR, et al. Radiofrequency facet joint denervation in the treatment of low back pain: a prospective controlled double-blind study to assess its efficacy. Pain Clin 1994; 7(3):193–198. 63. Melzack R. The McGill pain questionnaire: Major properties and scoring methods. Pain 1975; 1:277–299. 64. Huskisson EC. Visual analog scales. In: Melzack R, ed. Pain measurement and assessment. New York: Raven Press; 1983:33–37. 65. Roland M, Morris R. A study of the natural history of back pain. Part I: Development of a reliable and sensitive measure of disability in low-back pain. Spine 1983; 8:141–144. 66. Fairbank JC, Couper J, Davies JB, et al. The Oswestry low back pain disability questionnaire. Physiotherapy 1980; 66(8):271–273. 67. McHorney CA, Ware JE, Raczek AE. The MOS 36-item short-form health survey (SF-36): II. Psychometric and clinical tests of validity in measuring physical and mental health constructs. Med Care 1993; 31:247–263. 68. Ware JE, Sherbourne CD. The MOS 36-item short-form health survey (SF-36): I. Conceptual framework and item selection. Med Care 1992; 30:473–483. 69. Daltroy LH, Cats-Beril WL, Katz JN, et al. The North American Spine Society lumbar spine outcome assessment instrument: reliability and validity tests. Spine 1996; 21:741–749. 70. Niemisto L, Kalso E, Malmivaara A, et al. Radiofrequency denervation for neck and back pain: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2003; 28:1877–1888. 71. Slipman CW, Bhat AL, Gilchrist RV, et al. A critical review of the evidence for the use of zygapophyseal injections and radiofrequency denervation in the treatment of low back pain. Spine J 2003; 3:310–316. 72. Lau P, Mercer S, Govind J, et al. The surgical anatomy of lumbar medial branch neurotomy (facet denervation). Pain Med 2004; 5:289–298. 73. Bigos SJ, Boyer OR, Braen GR, et al. Clinical practice guideline number 4: Acute low back problems in adults. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services, December 1994. AHCPR Publication 95-0642.
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disk Disorders ■ iii: Lumbar Axial Pain
CHAPTER
94
Lumbar Provocation Discography: Clinical Relevance, Sensitivity, Specificity, and Controversies Michael B. Furman, William A. Ante, and Ryan S. Reeves
INTRODUCTION Lumbar provocation discography is a commonly used diagnostic procedure utilized to determine the presence or absence of discogenic pain at a specific spinal segment. Although discography has been proposed as the criterion standard for identifying discogenic pain [NASS statement], the test is controversial. Skeptics argue that newer diagnostic tests such as MRI scans make discography obsolete and the test should be discontinued unless its utility can be validated.1 This chapter will discuss the clinical relevance of lumbar provocation discography by correlating discography findings with the standard clinical work-up, and by its ability to help guide treatment. Additionally, we will describe controversies in technique and interpretation.
CORRELATION OF LUMBAR PROVOCATION DISCOGRAPHY WITH HISTORY AND PHYSICAL EXAMINATION FINDINGS Various studies have attempted to correlate history and physical examination findings with the diagnosis of discogenic pain by discography and to compare these findings with respect to treatment outcome (Fig. 94.1). Simmons and Segil2 reported a diagnostic accuracy of 44% for clinical examination and 82% for discography based on ability to predict symptomatic level as confirmed by successful clinical result after surgery. They did not specify any particular tests used preoperatively, but used the following in follow-up examinations: straight leg raise, neurologic examination including reflexes, sensory or motor, range of motion, and tenderness. Although they correlated discogram results with these physical examination techniques, no other outcome instruments were correlated. Schwarzer et al.3 found that no historical or clinical examination finding that they studied in 92 patients could accurately identify patients with internal disc disruption as diagnosed by provocation discography. Historical findings sought were pain increased or was relieved by sitting, standing, or walking. Pain referral patterns studied were pain into the buttock, groin, thigh, calf, or foot and whether the pain was unilateral, bilateral, or midline. Physical examination findings performed included provocation of pain with forward flexion, extension, rotation, combined rotation with extension, or straight leg raising making either back or leg pain worse.3 There was a trend (lowest p values obtained) with historical finding of pain increased with sitting ( p=0.13), pain increased with standing ( p=0.13), but also pain relieved with sitting ( p=0.16) and physical examination finding of pain increased with forward flexion ( p = 0.16). There was a negative trend (highest p values obtained) with a historical finding of pain increased with walking ( p=0.89) or physical examination finding of pain increased with extension.
Young et al.4 prospectively examined 81 patients with clinical examination and various diagnostic injections and found a weak but statistically significant correlation of discogenic pain as diagnosed by discography with centralization of pain with repeated end-range movements ( p=0.025, Phi=0.5). Although localization of a specific symptomatic level was not studied, 47% of those with positive discograms had ‘retreat of referred symptoms from the periphery toward the midline of the spine’ (centralization) during the standard McKenzie evaluation. Centralization was not seen with zygapophyseal joint pain as diagnosed by single intra-articular injection. Furthermore, all patients with a positive discogram (15 of 24 total discograms) reported pain when rising from sitting. A positive correlation ( p=0.02) was, however, also noted in patients with sacroiliac joint pain. Donelson et al.5 also prospectively studied 63 patients with chronic low back pain to evaluate the ability of the McKenzie mechanical lumbar assessment to diagnose discogenic pain and assess annular competence as determined by provocation discography. Seventyfour percent of centralizers and 69% of peripheralizers had a positive discogram as defined as exact pain reproduction accompanied by an abnormal image (nucleogram/CT), provided no pain was reproduced at an adjacent control level. The disc was interpreted as having a complete annular disruption or noncontained pathology if there was poor resistance to injection and contrast spread through the anulus to the epidural/perineural or peridiscal space. The disc was interpreted as having an intact outer anulus or contained pathology if there was firm resistance to injection even if contrast leaked from the disc at peak injection pressure. Of the centralizers, 91% had a competent anulus. Of the peripheralizers, 54% had a competent anulus. Of the patients whose symptoms did not change with repeated end-range movement, only 12.5% had a positive discogram. These differences were significant. The localization of a specific symptomatic level was not addressed and, therefore, these maneuvers could only be used for screening but not for identifying specific symptomatic disc levels for targeted interventional treatment. A ‘bony vibration stimulation test’ or ‘vibration pain provocation’ was described by Yrjama and Vanharanta and the results of bony vibration were compared to the results of provocation discography.6 The studies assumed provocation discography as the reference standard and compared the bony vibration stimulation test by itself or in combination with either ultrasound or MRI. The bony vibration stimulation test described utilized a Braun 3-D electric toothbrush as a modified vibrator device with a frequency of vibration of 42–50 Hz. The patient was laid on the more symptomatic side. The lumbar spinous processes were sequentially compressed with the vibrator's head in either the on or off position. If there was more pain with vibration than without vibration and this pain was described as concordant, the test was classified as ‘painful.’ 1033
Part 3: Specific Disorders
Left
Left
Right
Right
Right
B
A
Fig. 94.1 Pain drawings can be an important clinical tool in the prescreening evaluation. By having a patient diagram the location of their pain, a more streamlined approach to the patient can be pursued. (A) is an ideal discography candidate with axial back pain. (B and C) could potentially be screened out since patients with major components of radicular and whole body pain are suboptimal discography candidates.
Left
Right
Right
C
Thirty-eight patients were studied with the bony vibration stimulation test, ultrasound, and provocation discography.7 Discs were graded by ultrasonographic findings. Grade 0 was a normal disc. Grade 1 discs showed a hyperechoic lesion in the inner anulus. Grade 2 discs demonstrated a hyperechoic lesion in the outer anulus. Grade 3 discs showed a hyperechoic area extending outside the disc. When used alone, the bony vibration stimulation test yielded a sensitivity of 65% and a specificity of 58%. In the patients with a grade 1 or grade 2 disc, the sensitivity was 90% and specificity 75%. In the patients who had a grade 3 disc and pain on bony vibration the sensitivity and specificity were 50%. The authors also studied 33 patients with low back pain, correlating the results of bony vibration stimulation test and MRI with
1034
the results of provocation discography.8 When used alone, the bony vibration stimulation test yielded a sensitivity of 63% and specificity of 44%. If patients with history of previous lumbar surgery were excluded, the sensitivity was 61% and specificity 67%. In patients with or without previous history of surgery who had MRI findings of ‘partial annular rupture’ (as defined as irregular or absent intranuclear cleft images or bright-signal nuclear material into the outer anulus on T2-weighting), the sensitivity was 88% and specificity 50%. If the patients with previous surgery were excluded from this group, the sensitivity was 88% and the specificity 75%. The only false-positive finding in this group was a patient who was ‘hypersensitive’ and felt pain at all levels tested. If a ‘total annular rupture’ (defined as
Section 5: Biomechanical Disorders of the Lumbar Spine
T2-weighted or proton density images showing discontinuity of the low-signal band representing the outer rim of the anulus) was seen, the sensitivity decreased to 47% and specificity to 50%. These studies were, however, limited by their small sample sizes. Provocation discography was regarded as the reference standard for determining a symptomatic level without comparison to postprocedural outcome. Additionally, the findings of both bony vibration stimulation test and provocation discography were not recorded according to a specific spinal level. Finally, the protocol for discographic examination and interpretation was not fully elaborated.
UTILITY OF POSTDISCOGRAM COMPUTED TOMOGRAPHY Discography was originally used as an adjunctive to myleography to visualize lateral herniations (Fig. 94.2). There are, however, fundamental limitations to using discograms exclusively as an imaging tool. The classic nucleogram patterns viewed with anteroposterior (AP) and lateral
Fig. 94.2 Discography showing a far lateral herniation.
A The above normal nucleogram is described as a cottonball pattern where the contrast is a centralized mass within the nucleus
B The above normal nucleogram is described as a lobular pattern where the contrast is also centralized with two distinct arcs juxtaposed to the superior and inferior end plates
radiographs have been described as both normal and degenerative. Quinnell is credited with the original description of interpreting radiographic images of discography although he never proposed a classification scheme.9 He discussed the importance of monitoring contrast flow and volume to help improve the interpretation of the nucleograms. In 1986, Adams et al. initially classified nucleogram patterns into five categories; cottonball, lobular, irregular, fissured, and ruptured (Fig. 94.3).10 Cottonball and lobular patterns are thought to be normal variations, while fissured and ruptured are pathological. An irregular pattern is considered intermediate between these normal and pathological presentations. Adams et al. hypothesized the pathological patterns were due to disc degeneration. Cottonball nuclear patterns show the contrast central to the disc with an ovoid appearance (Fig. 94.3A). Lobular nuclear patterns also show the contrast centralized within the disc; however, there are two distinct arcs that may or may not be contiguous (Fig. 94.3B). An irregular pattern shows some tracking of the contrast outside the central nucleus without extension to the outer anulus (Fig. 94.3C). Although the contrast is intranuclear with irregular nucleograms, the small crevices and clefts exhibit early evidence of degeneration. Fissured nucleograms extend to the posterior annular margin, while ruptured nucleograms demonstrate complete radial tears and show contrast spread into the epidural space (Figs 94.3D, 94.3E).10 Adams speculated that by viewing the first four types of nucleograms, a natural progression of disc degeneration can be seen. Postdiscogram CT scans provided a more comprehensive view of the disrupted anulus (Figs 94.4–94.6). Axial views allowed a more detailed view of pathological contrast patterns than the AP and lateral radiographs (see Figs. 94.3C, 94.3D, 94.3E). The disorganized patterns seen on radiographs now coalesced into structured images, demonstrating organized annular tears with circumferential spreading. In 1989, Thomas Bernard published a case series of 250 patients who underwent both discography and postdiscography CT.11 He showed that computed tomography scanning after discography was not only able to define the type of herniation and disc architecture (protrusion, extrusion, sequestration, or internal disc disruption), but it could also be used to rationalize false-positive levels in the setting of non-nuclear injections (annular injections) (Fig. 94.4). In 1987, Sachs et al. organized the previously inexactly described axial contrast patterns into the Dallas discogram scale (Fig. 94.5).12
C The above nucleogram is described as irregular. This pattern is considered an intermediate between normal and pathological. The pattern contains tracking outside the central nucleus without annular extension
D The fissured nucleogram is pathological. Characteristically, it displays extension of contrast into the outer margins of the anulus
E The above pathological nucleogram is ruptured. There is a complete tear in the anulus with contrast extension into the epidural space
Fig. 94.3 Illustrated examples of Adams's nucleogram classifications. 1035
Part 3: Specific Disorders
A
Fig. 94.4 Postdiscography CT with left-sided inner annular injection: (A) axial and (B) coronal views.
B
A Grade 1 spread into the inner 1/3 of the annulus
B Grade 2 spread into the outer 1/3 of the annulus
C Grade 3 extension of contrast beyond the outer annulus
D
E
F
Category 1: Spread of contrast in < 10% of the annulus
Category 2: Spread of contrast through < 50% of the annulus
Category 3: Contrast extending into > 50% of the annulus
Fig. 94.5 Illustrated is the annular description for the radial tear findings and circumferential degenerative findings for the original Dallas discogram scale described by BL Sachs et al. In (A), the radial extension of contrast moving away from the inner nucleus is shown. Grading of 1–3 is based upon the radial spread of the contrast towards the anulus (A–C). (D–F) The percentage quadrant distribution of circumferential spread displays the amount of degeneration within each disc. In addition to radial extension, grade 1–3 is also used to describe circumferential extension (D–F). Addition modifiers are meant to be employed to specify the areas of annular leakage as anterior, posterior, lateral, posterolateral, anterior, and posterior.
Sachs's original description was based on the appearance of the anulus. This allowed objective categorization of the anulus, classifying both degeneration and annular disruption separately. Sachs's grading 1036
of the Dallas discogram scale is based on a four-point scale of 0 to 3, with zero defined as normal. Annular disruption defined as ‘leaking/protrusion/annular fissuring’ is based on the radial spread of the contrast away from the center of the nucleus to the periphery (Fig. 94.5A–C). Grade 1 is defined as spread within the inner third of the anulus; grade 2 is into the outer third of the anulus, while a grade 3 is defined as moving beyond the outer anulus.12 Degeneration findings were based on the circumferential distribution of contrast contained in quadrants of the anulus (Fig. 94.5D–94.5F). Grade 1 was defined as local spread in less than 10% of the anulus. Grade 2 was defined as partial spread or less than 50%, while grade 3 was defined as greater than 50% spread of contrast across the anulus. The development of the Dallas discogram scale not only allowed a new perspective to classify annular degeneration and disruption, but it also increased the inter-rater reliability when interpreting these findings. Sachs et al. were able to show 91% reproducibility and 88% repeatability when using the Pearson correlation test.12 Furthermore, they showed how standard AP and lateral discogram radiographs may appear normal until viewed axially. This reproducibility helped validate the Dallas discogram scale. Aprill and Bogduk soon added a grade 4 to the disruption scale.13 Approximately 10 years after its original description, Schellhas et al. expanded upon the three-grade disruption classification system to propose the modified Dallas discogram scale. The modified Dallas discogram scale incorporates both aspects of degeneration described as circumferential involvement as well as annular disruption depicted as radial contrast extension. The definitions of grades 0–2 remained the same. Grade 3 was expanded slightly to include either focal or radial extension of contrast into the outer third of the anulus, with a limitation of circumferential spread less than 30 degrees. Grade 4 was defined the same as grade 3, but with greater than 30 degrees of circumferential spread into the outer anulus. Grade 5 is a full-thickness tear, either focal or circumferential, with extension of contrast outside the anulus (Fig. 94.6).14
CORRELATION OF LUMBAR PROVOCATION DISCOGRAPHY WITH LUMBAR MRI Lumbar MRI is a sensitive means to investigate anatomic abnormalities of the low back. However, even asymptomatic subjects have been noted to have significant spinal pathology on imaging, including disc protrusion or
Section 5: Biomechanical Disorders of the Lumbar Spine
extrusion with or without neural compromise.15–17 Therefore, although MRI demonstrates pathology, it does not necessarily reveal whether the abnormality is causing a patient's symptoms. The correlation between MRI findings and provocative discography results has been investigated. The common goal of these studies was to determine whether imaging findings could predict the presence of concordant discogenic pain. If imaging studies could reliably predict discography findings, discography was unnecessary. The accuracy of MRI findings such as the high-intensity zone (HIZ) and endplate changes in determining symptomatic levels have been compared to the results of discography.18
High-intensity zone A
B
C
The high-intensity zone in the lumbar spine was first described by Aprill and Bogduk (Fig. 94.7)13 as a high-intensity zone (HIZ) seen on T2-weighted, sagittal images and defined by the authors as a highintensity signal (bright white) located in the substance of the posterior anulus fibrosus. The HIZ must be clearly dissociated from the signal of the nucleus pulposus because it is surrounded superiorly, inferiorly, posteriorly, and anteriorly by the low-intensity (black) signal of the anulus fibrosus and because the HIZ has an appreciably brighter signal than the nucleus pulposus. Aprill and Bogduk investigated a subset of 41 patients who had both MRI and discography with postdiscography CT scan. The HIZ was identified in 28% of patients with low back pain sent for lumbar MRI. All discs with HIZ had abnormal imaging on postdiscography CT with either a modified Dallas discogram scale grade 3 or grade 4 annular tear, specifically a radial tear extending into the outer third of the anulus without (grade 3) or with (grade 4) circumferential contrast encompassing an arc of greater than 30 degrees. When compared to reproduction of pain by disc stimulation, the HIZ had a high correlation with exact or similar pain with a sensitivity of 63%, specificity of 97%, and positive predictive value of 95%. For exact pain reproduction, the sensitivity was 82% and specificity 89%. Schellhas et al.14 sought to reproduce Aprill and Bogduk's findings with a similar study. In their retrospective analysis of 100 HIZs in 63 symptomatic patients, all discs with HIZ were internally deranged with annular disruption, 87 of 100 HIZ discs were concordantly
HIZ
D
E
Fig. 94.6 Illustrated is the annular description for combination of radial tears and degenerative findings in the Modified Dallas discogram scale ultimately proposed by K.P. Schellhas et al. (A) Grade 1 of 5, unchanged from the original description, demonstrates extension within the inner third of the annulus. (B) Grade 2 of 5, also unchanged from the original description, illustrates extension into the outer third of the annulus. (C) Grade 3 of 5 reveals radial extension of contrast into the outer third of the annulus, with a limitation of circumferential spread less than 30 degrees. (D) Grade 4 of 5 demonstrates extension of contrast into the outer annulus with greater than 30 degrees of circumferential spread into the outer annulus. (E) Grade 5 of 5 illustrates a full thickness tear (focal in this example, although it may be circumferential) with extension of contrast freely into the epidural space.
Fig. 94.7 T2-weighted image shows a highintensity zone (HIZ) at L4–5. As originally described by Aprill and Bogduk in the British Journal of Radiology in 1992, an HIZ is an area of brightness or high signal intensity located in the posterior anulus fibrosus, distinctly separate from the nucleus pulposus and brighter than the nucleus on T2weighted images. 1037
Part 3: Specific Disorders
painful at discography, and all 87 of these concordantly painful HIZcontaining discs had grade 3 to grade 5 annular tears on their modified Dallas discogram scale. Their schema is identical to Aprill and Bogduk's; however, they further stratified the Dallas discogram and added grade 5 to identify those discs which had a ‘full-thickness tear, either focal or circumferential, with extra-anular leakage of contrast.’ Individual discs could be classified into two categories, such as grade3/grade 5 or grade 4/grade 5.14 After the symptomatic group was analyzed, 17 asymptomatic volunteers underwent MRI without discography in an attempt to determine the prevalence of HIZ in patients not exhibiting low back pain (LBP). Only 1 of 17 (5.9%) of lifelong asymptomatic volunteers had a lumbar MRI with an HIZ. Those volunteers who never had prior LBP had a younger average age as compared to the symptomatic group (29.6 years old versus 37.5 years old). Other similar studies correlating HIZ with positive provocation discography have shown poor sensitivity of 26%, high specificity of 90–95.2%, positive predictive values of 40–88.9%, and negative predictive value of 47–83%.19 The interobserver reliability of HIZ also varies. Aprill and Bogduk found that out of 67 images, the two observers agreed on the presence of HIZ in all but one (1.5%). Though both observers noted the abnormality, the two disagreed on its meeting the criterion of brightness due to poor-quality film. However, Smith et al.19 only found fair to good interobserver reliability with a kappa value of 0.57 with 95% confidence interval 0.44–0.70. The original description by Aprill and Bogduk13 only included HIZ located in the posterior anulus and had a prevalence of 28%. The clinical significance of the HIZ was further studied by Rankine et al.20 in a patient population without neural compression. When including HIZs in any aspect of the anulus, the prevalence in a specialty spine surgery clinic was 45.5%. Most of these were posterior (77%) followed by posterolateral (22%). The HIZ was associated with moderate disc degeneration as assessed by signal reduction on T2-weighted sagittal images. There was no correlation of presence of HIZ with clinical features such as age, duration of symptoms, Oswestry score, or Schober's extension–flexion range of motion testing. There was also no correlation with patient history of employment, pain above or below the knee, or the positions or activities worsening pain. No physical examination findings studied predicted the presence of HIZ. The examination findings tested were paraspinal muscle spasm, spinal tenderness, straight leg raise, neurologic testing with reflexes, myotomal and dermatomal testing, and Waddell's testing. Correlation of HIZ presence with positive provocative maneuvers producing concordant axial pain with forward bending or extension/quadrant loading was not measured.
Endplate degeneration on MRI Magnetic resonance signal intensity changes adjacent to vertebral endplates have been described and are associated with degenerative disc disease.21 Modic classified these endplate changes into two types, while others have expanded their classification to three.22 Type 1 endplate changes have decreased signal on T1-weighted images and increased signal intensity on T2-weighted images. Type 2 endplate changes have increased signal on T1-weighted images and isointense or slightly increased T2-weighted image signal intensity. Type 3 endplate changes have a decreased signal intensity on both T1-weighted and T2weighted images. Kokkonen et al.18 compared endplate degeneration to pain provocation on discography and to the original Dallas discogram description which included three grades of annular disruption. Modictype endplate degeneration was found to have a strong correlation with disc (anular) degeneration. There was no correlation between endplate degeneration and ‘disc rupture’(annular rupture) and no correlation between endplate degeneration and pain provocation by discography. 1038
Based on these data, provocation discography would not necessarily be positive for those who have pain associated with endplate changes.
LUMBAR PROVOCATION DISCOGRAPHY AND ITS PREDICTIVE VALUE FOR TREATMENT AND PROGNOSIS Discography is a presurgical technique used to identify concordantly painful disc(s) and to verify that adjacent discs are negative for concordant pain prior to a therapeutic interventional procedure. Together with imaging studies, the provocation of concordant back pain during disc pressurization is used to confirm one's clinical impression that a specific disc is a source of pain. The procedure is usually performed in patients with predominately axial pain who have failed conservative management and are considering more invasive treatments such as percutaneous intradiscal or open discal procedures based on the results of discography. Because the results of discography are used to justify interventional treatments, the results should have predictive value for treatment success or prognosis. Although several studies compare the results of discography to decision formulation and outcome, most of the studies have methodological shortcomings such as the use of nonvalidated and/or subjective outcome scales. Additionally, many early studies were done before the routine use of MRI and CT and used discography to identify a disc herniation while today discography is used to ‘prove’ a disrupted disc is the source of the patient's axial pain. The studies which correlate discography with clinical outcome after procedures assume that (1) the treatment chosen is appropriate for the given lesion, and (2) the procedure accomplished its intended goal (i.e. successful fusion, adequate decompression, etc.). This may have valid grounds and gives valuable information if there is a strong correlation of a discographically proven lesion with successful clinical outcome. If poor results are obtained from the surgical procedure, either the test (discography) or the treatment (specific procedure) is suspect. In 1975, Simmons and Segil retrospectively reported the value of discography for the cervical, thoracic, and lumbar spine by accurately localizing a symptomatic spinal level based on postoperative results.2 Lumbar discograms were performed at 995 levels in 393 patients. Discogram results were assessed by patient pain response, amount and resistance to injection, and discographic appearance by Collis criteria, which describes discs as normal, degenerate, or protruded. Various clinical examinations were compared to the results of surgery on a scale with poor, fair, good, or excellent categories based on patient rating, complaints, occupation, activities, examination findings, and radiographic findings. It was assumed that if the patient was relieved of preoperative symptoms or was significantly improved after surgery, that the level of surgery selected by a certain test was accurate. Specific diagnoses and numbers for each were not reported but lumbar surgeries performed were ‘discotomy,’ ‘discotomy and fusion’ (usually posterolateral and intertransverse), and fusion alone without laminectomy. Overall, 94% of these lumbar surgery patients had satisfactory (fair to excellent) results. Diagnostic accuracy for these surgical outcomes was 44% for clinical examination, 71.5% for routine radiography, 45.6% for myelography, and 82% for discography. Specificity, sensitivity, falsepositive, and false-negative rates were not addressed. In 1979, Brodsky and Binder23 performed a retrospective study of patients who underwent discography. The authors performed discography only if the myelogram was negative but the patient was clinically thought to have discogenic pain. Specific indications included complaints which were atypical or without localizing neurologic signs, a myelogram which was equivocal or indeterminate, and a myelogram which was positive at one level while symptoms were suggestive of another. Discography was also performed to evaluate discs adjacent
Section 5: Biomechanical Disorders of the Lumbar Spine
to a herniated disc. Decision-making was ‘significantly influenced’ by the discogram in 77.9% of cases. Decision-making would have been the same without discogram in 22.1%. Positive discography was confirmed with surgery in 55.8% of the cases. In 1988, Calhoun et al. prospectively studied the predictive value of symptom reproduction during provocation discography as a guide to planning spine surgery for symptomatic intervertebral discs in the absence of nerve root compression.24 All 195 patients had lumbar provocation discography at L4–5 and L5–S1, most at L3–4, and some at L2–3 and all underwent lumbar surgery including anterior or posterior fusion and/or laminectomy. With at least 2-year followup, surgical success was based on whether the surgical objective was achieved radiographically (successful fusion, etc.) and clinical result was based on complete or significant relief of symptoms, resumption of work and/or normal activities, and no intake of analgesics. Failure to achieve these results was ‘clinical failure.’ There were 137 patients who had a painful injection of a morphologically diseased disc in which 89% had significant clinical relief. There were 25 patients who had technically successful surgery for a morphologically abnormal disc but without symptom production on disc injection, and in these patients only 52% had significant symptomatic relief while most of the remaining 48% had no clinical benefit. Additionally, morphologically abnormal discs that did not cause symptoms during disc injection that were adjacent to symptomatic discs were found in 43 patients. These levels were not included in levels of surgical intervention and significant clinical benefit was 95% (41 of 43) in these patients. Of six patients who were surgically treated despite normal discography, only 50% had clinical benefit. Overall, comparing lumbar provocation discography to clinical outcome after technically successful surgery yielded an 82% accuracy rate, 90% sensitivity, and 9.7% false-negative rate. ‘Accuracy’ was defined by combining the 137 patients who had a positive discogram and did well with surgery (true positive) and the 25 patients who had morphologic abnormal discs but no symptoms on discogram. Also in 1988, Blumenthal et al.25 used provocation discography to diagnose internal disc disruption (IDD) with the main purpose of the study being to evaluate the efficacy of anterior lumbar fusion as a treatment for IDD. All 34 patients underwent provocation discography and anterior fusion with average follow-up of 29 months. The diagnosis of IDD required radiographic signs of degeneration and discography with concordant pain reproduction with ‘instillation of small amounts of contrast.’ Successful treatment was defined as return to work or normal activities and either no medications or use of NSAIDs only. Fusion success was judged by radiographs only. The successful fusion rate was 73 %, but successful clinical treatment rate was 74%. Four cases were indeterminate for fusion. Of those with healed grafts, 73% had clinical success while only 62.5% of those with nonunion had clinical success. Of those patients with a successful clinical result, 81% had evidence of fusion while only 56% of the clinical failures had evidence of fusion. The authors cite higher previous fusion rates of 91–96%.Wetzel et al. performed a retrospective review of 48 patients, with a minimum follow-up of 2 years, who had lumbar arthrodesis based on provocation discography results.26 All were symptomatic for a mean time of 34.4 months prior to discography. Pain reproduction was graded as concordant or nonconcordant. The discography protocol did not, however, include a negative control disc. Fifty-four percent were single-level discographies, presumably without a control level. Two- and three-level discographies accounted for 31% and 14.5%, respectively. Sixty three-levels were graded as positive based on a concordant pain response. Seventy-five percent of patients had a single-level positive discogram, but 72% of these ‘single-level positive’ patients only had a single level studied. Two-level and three-level positive results were obtained in 18.9% and 6.2%, respectively. However, of the two-level positive discs, 77.8% only had a two-level discogram. None of the previously operated levels was included in discography. Fusion was
performed to include all symptomatic levels determined by discography. Previously operated discs were included in fusion if they were adjacent to symptomatic discs. Anterior and posterior fusion techniques with and without varying instrumentation were performed. The clinical outcome was evaluated on the criteria of Zucherman which includes subjective symptom improvement, functional limitations, and amount of analgesic use. Categories were poor, fair, good, and excellent. Success of fusion was also assessed radiographically. At mean 35-month (range 24–65 months) final follow-up, there was a 46% (n=22) satisfactory clinical outcome with solid arthrodesis in 47.9% (n=23). All patients who had satisfactory clinical outcome had a solid fusion. Conversely, 95.7% of patients who had a solid fusion had a satisfactory clinical outcome. None of the patients who had nonfusion had a satisfactory outcome. Therefore, if the surgical goal of fusion of the symptomatic levels as determined by provocation discography was obtained, the clinical success rate was 95.7%. This study was limited by its retrospective nature, small sample size, discography technique as judged by today's standards, and varying operative techniques. Derby et al. retrospectively evaluated pressure-controlled discography for its ability to predict surgical outcomes for interbody fusion, intertransverse fusion, combination fusion, or nonsurgical treatment.27 The study's premise is that pressure-controlled manometric discography may allow improved and more specific diagnosis and categorization of discogenic pain and may have the potential to predict outcome of surgery (Fig. 94.8). The positive discs found on provocation discography of 90 patients were classified as ‘chemically sensitive,’ ‘mechanically sensitive,’ or ‘indeterminate’ based on pain provocation at specific values above ‘static opening pressure.’ ‘Opening pressure’ is the manometric reading taken when injected contrast is first visualized entering the disc on fluoroscopy. Derby et al. classified a chemically sensitive disc as one which has positive concordant pain provocation of (1) immediate onset when less than 1 mL of contrast is visualized reaching the outer anulus, or (2) at less than 15 psi above opening pressure. These discs were considered the ‘most positive’ since the lowest pressures resulted in significant concordant pain. A disc was classified as ‘mechanically sensitive’ when concordant pain was noted between 15 psi and 50 psi above opening pressure. A disc was categorized as ‘indeterminate’ when concordant pain occurred between 51 and 90 psi above opening pressure. A disc was classified as normal if no pain occurred at pressures up to 90 psi above opening pressure. Thirty-six patients with chemically sensitive discs were identified. Clinical out-
Fig. 94.8 Manometry has become an invaluable tool in the interrogation of painful discs. Several brands are currently available, with slight differences in the manometry meter and the ways to dispense the contrast while pressurizing the disc. 1039
Part 3: Specific Disorders
comes were based on the Patient Satisfaction Index adapted from the NASS low back pain outcome instrument, numerical rating scale for pain, and a modified ADL scale. ‘Favorable outcome’ was defined as at least two favorable outcomes of the three scales. There was no significant difference in patient outcome between those who underwent interbody/combined fusion versus those who had intertransverse fusion if pressure-controlled discographic classification was not considered. However, those patients who had chemically sensitive discs were found to have an 89% rate of favorable outcome with interbody/combined fusion, 20% favorable outcome with intertransverse fusion, and only 12% favorable outcome with nonoperative treatment. Although this study was limited by its small sample size and retrospective, nonrandomized nature, it demonstrates that lowpressure-sensitive discs may have a different pathobiology and respond differently to treatment than discs that are concordantly painful at higher pressures.28 Derby et al. went on to perform a pilot study in which 32 patients were prospectively followed before and after undergoing IDET.29 Percutaneous treatment was based on chronic low back pain for more than 6 months, axial pain comprising at least 60% of pain symptoms, negative neurologic and neural tension testing, and failure of conservative management. All had at least one positive disc (mean 2.04 symptomatic discs) on provocation discography as defined as provocation of at least 6/10 concordant pain accompanied by an abnormal nucleogram. The discs were classified as low-pressure discs if there was pain produced at minimal pressure less than 15 psi above opening pressure or high-pressure discs if pain was produced at more than 15 psi above opening pressure. Low-pressure discs comprised 37.5% of the discs and high-pressure discs were more common and comprised 62.5% of the discs. If there were more than two positive discs, a ‘clinical decision was made as to which discs were likely to be most symptomatic, and … included’ in the treatment levels. Outcome was assessed using Roland-Morris Disability Questionnaire and Visual Analogue Scale, NASS Low Back Pain Outcome Assessment Instrument Patient Satisfaction Index, and a general activity questionnaire. Favorable outcome was defined as improvement of three or four of the tools while nonfavorable outcome was defined as worsening of three or four of the tools. No change was recorded for all other results. Overall, 62.5% had a favorable outcome, 25% had no change, and 12.5% had a nonfavorable outcome. Among the low-pressure-sensitive discs, 75% had a favorable outcome while 55% of the high-pressuresensitive discs had a favorable outcome. Thus, patients who had lowpressure-sensitive discs tended to do better that those patients whose discographic pain was reproduced at higher pressures. This study was only a pilot study and was limited by small numbers of patients as well as the fact that the study population included patients with multilevel disc disease. There were also no data reported that compared pretreatment pain and disability scores between the low- and high-pressure disc groups. The heating protocol had been changed during the course of the study. Rhyne et al.30 retrospectively reviewed 25 cases in which patients who had single-level positive provocation discography did not undergo surgical treatment. The patients had been offered posterolateral fusion but refused due to fear of complications, insurance denial, knowledge of acquaintances who worsened after surgery, or desire to change lifestyle and live with the pain. The patients had a mean follow-up of 4.9 years and completed clinical evaluation including Roland-Morris disability scale and pain scale of Million et al. These scales were filled out twice, one representing their current status and the second to represent the recall of their status at the time of discography. Based on this assessment, 68% of patients improved, 8% had no perceived change in status, and 24% worsened. No patient was pain-free or free of disability. Of those who improved, pain improved an average of 39% and 1040
disability decreased an average of 42%. Patients who reported improvement had a shorter history of low back pain (3.5 years versus 11 years) and were older (45 years old versus 33 years old). Psychiatric disease was present in 66.7% of those who worsened. This study is certainly flawed in that not only is it a retrospective study, but the subjects were asked to retrospectively enter data to reflect their status an average of 5 years prior to the time of the study. However, it does demonstrate that 68% perceived an improvement. In summary, these studies suggest that provocation discography is useful in the preoperative planning and prognostication for certain procedures. Discs that have been found to cause concordant pain on disc stimulation may also improve spontaneously. However, due to methodological insufficiencies and differences in these studies, more research is needed in the form of prospective, randomized trials with adequate sample size and validated outcome measures. The use of manometry may decrease the false-positive rate of provocation discography.
VALIDITY AND FALSE-POSITIVE RATES OF PROVOCATION DISCOGRAPHY AS A DIAGNOSTIC TOOL Holt's classic study questioned discography's value, concluding that the false-positive rate of discography in asymptomatic volunteers was 36% based on the ratio of abnormal discographic images to the number of satisfactory disc injections.31 Holt's work has been widely criticized. Simmons et al. ‘acknowledge[d] that Holt's study was appropriate for its time,’ but noted subsequent advances in nonirritating contrast dye and radiologic equipment.32–34 In their reassessment they noted Holt's high failure rate for proper needle placement, which was 30% for the lower two disc levels (site of most disc pathology), 37% for L5–S1, and 23% for L4–5. The selection process for asymptomatic volunteers (who were prison inmates) was not clearly defined and there were discrepancies within the text. Additionally, only disc morphology, and not pain provocation, was considered in calculation of false positives. If pain response and disc morphology were considered, then reanalysis demonstrates that the true negative rate would be 74%. If only patients with successful injections were considered, then the accuracy rate of discography would be 81.9% despite the use of highly irritating contrast material (Hypaque). ‘Major advances in the techniques of discography’ occurring after Holt's 1968 study prompted Walsh et al.33 to perform a similar study in 1990, reevaluating discography's value and specificity using ‘current techniques’ and more precise methodology. They used the much less irritating contrast, iopamidol, instead of diatrizole. More importantly, they included pain provocation evaluation. They rated the pain reproduction according to intensity, presence of pain-related behavior, and pain similarity (concordancy) for symptomatic patients. A ‘positive pain-related response’ to disc injection was recorded if the subject exhibited two or more types of pain behavior and rated the pain intensity a 3 or more (‘bad’ on a scale 0 to 5). Pain behaviors considered were guarding/bracing/withdrawing, rubbing, grimacing, sighing, or verbalizing. (Inter-rater reliability for these was 92.6%.) Because asymptomatic subjects could not report ‘concordant’ pain, they were termed ‘positive’ if there was an abnormal disc morphology with positive ratings for pain intensity and pain behavior. Symptomatic control patients required a typical rating for pain similarity to be called ‘positive.’ They included two groups: an asymptomatic group of young men and a symptomatic control group determining interobserver reliability for pain response evaluation and semiblinding the raters as to which participants were asymptomatic. The asymptomatic test subjects demonstrated an abnormal discographic disc morphology in 17% but a false-positive rate of 0% based on pain response. Even if more liberal criteria were used such as only minimal pain (at least
Section 5: Biomechanical Disorders of the Lumbar Spine
1 on a scale of 5) or presence of only one pain behavior, the falsepositive rate would have been 3% and 7%, respectively. Because the false-positive rate was lower than that of the Holt study (0% as compared to 36%), Walsh et al. concluded that the ‘single most important way to improve the specificity of discography is to incorporate assessment of pain into the definition of a positive discogram.’ Carragee and colleagues have extensively studied the possibility of false-positive results obtained from provocation discography in clinical practice (Table 94.1). Tanner and Carragee35 suggest that ‘the reproduction of concordant pain has less diagnostic utility that [sic] often assumed, particularly if there is pathology in a similar sclerotomal region.’ Initially, Carragee et al. presented case studies in which patients with positive lumbar discography were later found to have other painful processes such as sacroiliac joint abnormalities and posterior element neoplasm.36 With these in mind, they appropriately sought to test the validity of provocation discography and determine its false-positive rates among various subjects by replicating and extending Walsh et al.'s study. They reasoned that in order to check the validity of any clinical test, it is essential to know how many subjects
without a given disease will test positive with a particular test for that disease. Also, the relative risk of certain subsets of subjects will affect the meaning of the test. Therefore, they took as their starting point the use of asymptomatic control subjects.35 Their first study applied ‘experimental disc injections’ to subjects with no previous history of low back pain to evaluate the pain responses and pain-related behaviors in the experimental setting. Its aim was to test the ‘first assumption in discography’ that ‘stimulation of a disc in an asymptomatic individual will not cause a significant sensation of pain.’37 Twenty-six volunteers with an mean age of 43 years were selected from three sources: patients being followed after cervical surgery with best results and pain free (n=10), patients from the same cervical surgery cohort but with the worst results and with cervical-related chronic pain(n=10), and finally patients meeting the DSM-IV criteria for somatization disorder (initial n=10). All were asymptomatic for low back pain. Provocation discography was performed according to the protocol of Walsh et al.33 with a ‘positive’ result scored if the pain response was greater than or equal to 3 out of 5, but only if accompanied by two or more pain behaviors (inter-rater agreement was 97.4%).37
Table 94.1: Summary of studies from Eugene J. Carragee, M.D., et al. Publication
Objective
Conclusion
Positive provocation discography as misleading finding in the evaluation of low back pain. Chicago, IL: North American Spine Society; 1997.
To compare results and outcomes with Walsh's 1990 discography results.
Patients with positive lumbar discography were later found to have other painful processes such as sacroiliac joint abnormalities and posterior element neoplasm. The reproduction of concordant pain has less diagnostic utility than assumed, particularly if there is pathology in a similar sclerotomal region.
False-positive findings on lumbar discography: Reliability of subjective concordance assessment during provocative disc injection. Spine 1999; 24(23):2542–2547.
To determine if patients subjective interpretation of pain concordancy during provocative discal injections is reliable.
In patients without a history of low back pain, lumbar discography is able to concordantly produce pain from a posterior iliac crest bone graft harvest site, questioning the reliability of concordant pain production originating from discal pathology.
The rates of false-positive lumbar discography in select patients without low back pain symptoms. Spine 2000; 25:1373–1381.
To test the null hypothesis of discography; ‘the first assumption in discography’ that ‘stimulation of a disc in an asymptomatic individual will not cause a significant sensation of pain.’
When performing discography according to Walsh's criteria (IASP criteria was NOT used) the rate of false-positive findings may be low in patients without chronic pain conditions and normal psychometric profiles. However, when performing discography in patients with annular disruption, chronic pain, or abnormal psychometric testing, concordant injections are very common.
Lumbar high-intensity zone and discography in subjects without low back problems. Spine 2000; 25(23):2987–2992.
To investigate the prevalence and significance of HIZ in symptomatic and asymptomatic patients and compare discography results between the two groups.
The presence of a HIZ does not represent a diagnosis of internal disc disruption, while the same percentages of discs with HIZs were found to be painful during discography in both symptomatic and asymptomatic populations.
Provocative discography in patients after limited lumbar discectomy: a controlled, randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2000; 25(23):3065–3071.
To investigate the intensity of pain after lumbar discectomy in both symptomatic and asymptomatic patients.
When performing discography according to Walsh's criteria (IASP criteria was NOT used) the rate of false-positive findings were reported to be 40% in the asymptomatic group. In the symptomatic postsurgical group, 70% of patients experienced provoked pain during discography.
Prospective controlled study of the development of lower back pain in previously asymptomatic subjects undergoing experimental discography. Spine 2004; 29:1112–1117.
To determine if asymptomatic patients who underwent discography with positive findings would proceed to develop back pain after discography and up to 4 years later.
Independently, a positive discogram can be a poor indicator of developing low back pain.
1041
Part 3: Specific Disorders
They found that disc stimulation was ‘false positive’ in at least one disc in 10% of subjects in the pain-free group and 40% of those with chronic pain (cervical-related chronic pain). Of the somatization group, 40% (n=4) dropped out before discographic injection and two others stopped the procedure after only one or two disc levels were injected. Of those remaining in the somatization group who completed all disc injections, 75% (3 of 4 subjects) had a least one-level positive discogram. If the somatization subjects who had at least one disc injected were considered, then there was an 83% rate of subjects with false-positive pain provocation. When correlating radiologic (MRI and discogram) findings with pain provocation in subjects who completed at least 3 disc injections, there were no positive injections in the 31 radiologically normal discs, 11% (2 of 18) positive disc injections in the intermediate disruption discs (abnormal MRI and discographic nucleogram but no extension of dye to the outer anulus), and 37% (10 of 26) positive disc injections in the annular disruption discs (discogram with dye extension to or through the anulus). Patients on disability who completed three disc injections (4 of 5) had an 80% false-positive rate. Subjects with active worker's compensation or personal injury claims had an 89% rate (8 of 9) of false-positive injections. All subjects in the somatization group had some type of ongoing compensation claim which confounded separation of those two variables. A positive discogram correlated with an elevated modified Zung Depression Test and Modified Somatic Pain Questionnaire. This study has been criticized on the basis that ‘concordant pain,’ paramount in provocation discography, cannot, by definition, be tested in asymptomatic individuals.34 In response, Tanner and Carragee point out that all clinical tests must be evaluated in part by the results obtained in asymptomatic or disease-free persons.35 Bogduk re-analyzed Carragee's data in this study using IASP criteria (Table 94.2): that is, concordant pain with an intensity of 6/10, abnormal morphology, and at least one painless control level.38 Specifically, he imposed the criteria that the suspect disc(s) be surrounded by at least one painless adjacent disc. He also applied the manometric criteria for pressure of injection. When at least one adjacent disc was required to be painless in order to call a given level positive, the false positives in the chronic pain group fell from 40% to 20%. But the rate remained stable for the no-pain group (10%) and somatization group (75%). Bogduk then used two different manometric parameters to analyze Carragee's data. Under the criterion that the pressure of disc injection be less than 50 psi, the false-positive rates of both the chronic pain and somatization groups fell. The false-positive rates for the chronic pain group decreased to 10% (original 40%) while the somatization group had a resultant 50% false-positive rate (original 75%). If the stricter criterion of disc injection pressure less than 15 psi (called the ‘chemically sensitive disc’ by some) is used, then the false-positive rates fall to 0% in the pain-free group, 0% in the chronic pain group, and 25% in the somatization group. Additionally, Bogduk stated that because of the small sample size, confidence intervals should be used, and with these adjustments found that the false-positive rates either became zero or the confidence intervals overlapped zero even in the somatiza-
Table 94.2: IASP criteria for positive discography P0 control level Concordant locational pain Pain intensity ≥ 6/10 Morphological disc changes
1042
tion group. Based on this reanalysis of Carragee et al.'s data, Bogduk suggested using the criterion of 50 psi in general clinical practice to restore sensitivity but 15 psi in patients with suspected or known somatization. In order to evaluate false-positive rates of ‘concordant’ back and buttock pain, Carragee et al. devised a study in which patients who had never had low back pain prior to posterior iliac crest bone grafting for nonlumbar spinal reasons were evaluated with provocation discography for concordant bone graft donor site pain.39 Eighty-five percent of subjects (7 of 8) experienced similar or exact pain. Sixty-four percent of discs caused similar or exact pain. Of the discs with annular tears, 70% (7 of 10) caused similar or exact pain reproduction of the patient's usual iliac crest bone graft harvest site. In this small sample of 8 patients and 24 discs, 50% of subjects had false-positive concordant donor site pain on disc stimulation if pain magnitude, concordancy, and demonstration of pain behavior are all considered. Carragee et al., again, did not use the IASP criteria. If these data are reanalyzed with IASP criteria, 25% of subjects would have false-positive findings if disc injection pressure was less than 50 psi, or a 12.5% false-positive rate for less than 15 psi. Still, these results call into question whether a patient can reliably distinguish pain from discogenic versus nondiscogenic sources. After the rates of false positives in subjects without previous history of low back and/or buttock pain due to spinal pathology were evaluated, Carragee et al. next sought to determine the rate of positive disc injection in patients who had a previous history of lumbar-related complaints.40 They no longer called these ‘false positive,’ presumably to eliminate the association with concordancy of pain response. They performed provocative discography on 20 patients from a cohort who had a previous history of symptomatic single-level lumbar pathology, underwent subsequent limited posterior discectomy 2–10 years prior to the study, but were now asymptomatic. They compared the rates of positive injection in this group to a control group of 27 subjects who were symptomatic with persistent or recurrent lumbar or lower limb symptoms after similar surgery 14 months to 6 years prior to the study. Twenty-six percent of these symptomatic patients had normal psychometric scores. In the asymptomatic group, 40% of subjects had positive provocation disc injection at the level of previous surgery while only 10% (2 of 20) of asymptomatic subjects had a positive provocation if only the nonsurgically treated discs were considered. In total, 45% of the asymptomatic group had at least one positive provocation injection. All previously surgically treated discs that had significant pain on injection had discographic grade 2 to 3 tears with dye penetrating to or through the outer anulus. Sixty-three percent of symptomatic subjects had a positive pain response at the level of previous surgery. If the symptomatic group was subdivided according to psychometric scores, those with normal psychometrics had a 43% rate of positive provocation (all concordant) while those with abnormal psychometrics had a 70% rate of positive provocation (86% of which were concordant). The intensity of pain was significantly rated as higher in the symptomatic group with abnormal psychometrics (3.4 of 5) versus those in both the asymptomatic group and the symptomatic group with normal psychometrics (both 2.1 of 5). In reanalyzing this asymptomatic group data with IASP criteria for manometric injection, the positive provocation rate in previously surgically treated discs would decrease to 35% if pressure on injection was less than 50 psi or to 25% if pressure on injection was less than 15 psi. Of unoperated discs, the positive rate would fall to 5% if either the less than 50 psi or less than 15 psi criteria was used. If the requirement for a pain-free adjacent control disc is also required, then the positive rate falls to 25% if less than 50 psi is used, or 15% if less than 15 psi is used. Still, previously operated discs may be more likely to be painful on injection than discs which have never been operated on.
Section 5: Biomechanical Disorders of the Lumbar Spine
In summary, the Carragee et al.40 studies point out the fact that false-positive results can occur in discography as with any clinical test. These false positives are more likely in those with abnormal psychometric scores, specifically somatization disorder, and in previously operated discs. Bogduk has pointed out that adherence to the IASP criteria can decrease the false-positive results to an acceptable level. O'Neill and Kurgansky published a retrospective study of 253 patients in an attempt to further delineate false-positive rates and offer suggestions to increase specificity.41 Particularly, they wanted to determine if the distribution of disc pain thresholds would organize into subgroups to help identify false positives. To accomplish this, they incorporated pressure-controlled discography through manometry. By correlating the manometry information with false-positive findings from Carragee's asymptomatic populations,36,37,39,40,42 they were able to select out for false positives. They concluded that there was a 100% chance of false positives above 50 psi. Pressures ranging 10–25 psi had a 50% chance of being a false positive. However, discs with pain responses at 0–10 psi were most likely true positives. Based on these data, there appears to be a bimodal distribution of true positives. One population of true positive were those who had positive pain responses with cut-off values above 25 psi and below 50 psi ; the other population of patients were those who had pain responses at less than 10 psi. However, it was difficult to confirm that the latter are true positive due to testing limitations..
DISCOGRAPHY COMPLICATIONS Passing a needle into the disc has risks that should be recognized and anticipated before they occur. Perhaps the most common reaction or complication to any procedure is a vasovagal episode. This involuntary reaction of the parasympathetic nervous system causes reflex bradycardia and vasodilatation. Patients should be monitored with pulse oximetry, pulse rate, and blood pressure. A vagal episode is recognized by an audible slowing of the pulse rate and is usually accompanied by perfuse sweating and nausea. Increasing the intravenous fluids and raising the legs will usually restore cerebral perfusion, but 0.5–1 mg of intravenous atropine can be administered and incremental intravenous doses of 5–10 mg of ephedrine may be required in more severe reactions Other common reactions include paravertebral muscle pain and potential contusions from local punctures. Less common complications include nerve injury, dural puncture, bowel perforation, epidural abscess, local cellulitis, and allergic reactions to contrast agents, topical iodine and prophylactic antibiotics. These risks can usually be avoided by using proper techniques and due diligence. The ventral ramus crosses the posterolateral quadrant of the target disc and is vulnerable to direct trauma, but the risk is minimized by slowly advancing the needle medial and under the root in the safe triangle and redirecting the needle when the patient complains of buttock or leg pain. Dural puncture and bowel perforation is possible but should not occur if one uses proper technique and carefully monitors the advancing needle with both AP and lateral imaging. An individual with a pendulous abdomen may have an increased risk of bowl perforation and subsequent disc space infection because the retroperoteneum is pushed posteriorly. Placing these patients in a lateral decubitus position may help avoid this potential complication. Local cellulitis can be avoided with strict adherence to sterile techniques, but if it occurs it is treated with cold compresses and empiric coverage for group A streptococci and Staphylococcus aureus. Allergic reactions to drugs utilized can potentially be avoided with through histories. Patients with a serous allergic reaction to iodine and shell-
fish can be pretreated with prednisone 50 mg p.o. 24 hours before the procedure, prednisone 50 mg p.o. 12 hours before the procedure, and benadryl 50 mg p.o. 1 hour before the procedure or i.v. at the time of the procedure. The most serious potential complication is disc space infection. Before antibiotic prophylaxis became routine, the reported rate of discitis ranged from 2.3% per patient and 1.3% per disc to 0.1% per patient and 0.05% per disc.43 The most common causative organisms are S. aureus and S. epidermidis. The reported incidence of discitis may be reduced by using a double-needle techniques and preprocedural antibiotics.44 In 1990, Osti et al.45 designed an experimental discography model using sheep. They added cefalozin to the intradiscal suspension or administered it intravenously 30 minutes prior to intradiscal inoculation of bacteria. The prophylactic treatment prevented any radiographic, macroscopic, or histological signs of discitis. In a follow-up study of 127 patients this protocol also prevented disc space infection following discography and became the basis of the routine use of intravenous antibiotics (e.g. 1 g of cefalozin) prior to discography, adding antibiotics to the injected contrast, or the use of both intravenous and intradiscal antibiotics.
CONTROVERSIES Although the issue of discography itself remains controversial, there are subjects within the procedure itself which should be addressed in order to further increase its diagnostic utility.
False-negative results False-negative results could occur because there is a rupture through the outer anulus or endplate and one is not able to pressurize the disc. Rapid injection of contrast will raise the dynamic pressure to over 50 psi, but whether this technique reduces false-negative results or increases false-positive results is unknown. Other potential causes of false-negative results include oversedation or injected local anesthetics.
Sources for false-positive results Potential anatomic sources of false-positive findings are adjacent structures which are mechanically or chemically irritated. Possibilities include distension of the zygapophyseal joints or the posterior longitudinal ligament. Some have even advocated performing medial branch blocks prior to lumbar discography. Commonly, initial pressurization will provoke significant concordant pain, but repressurization will be significantly less painful and not meet the criteria for a positive response. Although one could argue that this is not a positive response, interpretation is not standardized. Pressurizing an adjacent symptomatic disc is also a potential cause of false-positive results. There is an assumption that when injecting an intervertebral disc (IVD) and checking its pain response, adjacent intervertebral discs are not pressurized. Therefore, any pain response is believed to be solely attributed to the IVD level injected. Some practitioners have anecdotally observed that pressurizing IVDs with normal anatomy occasionally results in significant pain when there is an immediately adjacent nonruptured pathologic IVD. These practitioners believe that if this adjacent pathologic IVD is later anesthetized, the original normal-appearing IVD will no longer be painful with IVD injection. If validated, such a response supports the theory that a positive pain response may be caused by pressurizing an adjacent pathologic IVD and not from the injected IVD. On the other hand, preliminary data suggest that pressurizing an intact lumbar disc to pressures exceeding 100 psi will not result in any measurable pressure changes in the adjacent discs.45a 1043
Part 3: Specific Disorders
Is analgesic response validated? Instead of, or in addition to, the provocative response, some discographers use pain relief following intra-discal injection of local anesthetic to help determine whether the disc is symptomatic. An invalidated emerging technology call functional analgesic discography by Kyphon Inc, evaluates a dynamic analgesic response post procedurally. Intra-discal analgesic is injected via a catheter into the suspected pain generator. The patient is then asked to perform various functional activities that typically cause their pain. Although this may help validate single level positive discs, multilevel functional pathology is more challenging unless near 100% relief of symptoms can be obtained after single level disc anesthesia is performed. Certain interpretative challenges remain given multilevel interpretations. Currently there are no published studies correlating clinical outcome to results of analgesic lumbar discography.
Does needle insertion site affect discography results? Discogenic pain often lateralizes to one side. Some discographers, therefore, advocate approaching the target disc contralateral to the patient's more painful side to theoretically differentiate index pain from needle insertion pain on nondiscal structures.46 For example, a patient with predominantly right-sided back pain (index pain) would be investigated with needle entry left of midline. Needle insertion ipsilateral to the patient's index pain has been speculated to increase the false-positive rate. False-positive pain reproduction could occur by stimulation of the adjacent spinal nerve, soft tissue, or osseous structures. Stimulation of a nerve root usually causes a characteristic lancinating pain that is different than the dull, aching pain provoked by contrast injection. However, residual pain after needle repositioning may still cause interpretive challenge to the patient and physician. Cohen et al.47 attempted to determine if needle insertion affected discography results. Retrospective analysis of 127 discography patients who all had a right-sided approach due to limitations of their fluoroscopic unit revealed no significant difference in the rate of positive results among patients with midline, left-sided, or right-sided pain. Unfortunately, one limitation of the study was the lack of any correlation to radiological findings. There was no analysis of left- or right-sided MRI findings and how those results may have factored in on the outcome of discography. The authors concluded that the side from which discography is performed had no effect on results of provocation discography. No ‘gold standard’ or postdiscography treatment outcomes were correlated. Instead, they based their conclusion on the assumption that their population should theoretically have an anticipated equal incidence of rightand left-sided pain source. Slipman et al.48 investigated the commonly held notion that the site of pain reproduced during discography should correspond to the side of their annular tear in one-level positive discography. In their retrospective study, they found a random correlation between the side of a concordantly painful, CT visualized annular tear and the lateralization of one's perceived pain. Slipman et al. postulated that there are two possible theories to describe this finding. There may be a misperception of the origin of the somatic referred signal to the brain occurring via a convergent sensory pathway or possibly a remote pain source independent from the stimulated disc. Until more conclusive studies are completed, we recommend consideration of performing discography with needle entry contralateral to the patient's more painful side unless the physician faces tactical problems imposed by c-arm or procedure suite limitations. 1044
Does needle insertion into a normal or abnormal morphological disc result in damage? One of the more elusive topics concerns the potential for transitory or permanent iatrogenic disc injury secondary to disc puncture or disc pressurization. Carragee et al.42 published a prospective, controlled study to determine whether asymptomatic subjects develop low back pain after discography. They performed discography on 50 asymptomatic patients. The attempt of the study was to determine if asymptomatic patients with positive LBP on discography were not actually false positives but possible true positives predicting ‘near-term future chronic LBP.’ All 50 patients were followed for up to 4 years. There was no conclusive evidence that a painful injection was an independent predictor of developing low back pain in patients without any abnormal psychometric scores. They also determined whether the presence of high-intensity zones (HIZs) or annular fissures seen on MRI and discographic nucleograms were predictive factors for developing LBP. They compared their findings to the previous studies that demonstrated that an area of HIZ in the outer anulus is an independent finding and not necessarily directly related to LBP.14 Caragee et al. found a weak association with late-onset LBP episodes with HIZ and annular fissured nucleograms subsequent to discography. These two studies suggest that the late onset of permanent disc injury in previously asymptomatic patients is purely coincidental or, at best, a subclinical finding. Studies performed in the 1940s evaluated the potential of disc punctures to cause a disc herniation.49 Hirsch could not alter a normal disc to any structural pathology from needle penetration. In 1984, Kahanovitz et al. looked at the histological effect of discography in dogs.50 They injected the L1 through L6 discs. The first intervertebral disc was used as a control without any needle perforation or intradiscal substance introduction. The next level was punctured without any infusion of an injectate. The third level underwent injection of saline, while the fourth and fifth discs underwent injection of Hypaque and metrizamide contrast agents. All 10 dogs were eventually sacrificed at 2, 4, 6, 8, and 10 weeks postdiscography. The discs underwent gross examination as well as saffranin-O mucopolysaccharide staining during histological examination. There was no discernable histological difference in any dog at any level, nor was there evidence of any inflammatory response or annular necrosis. In 1989, Robert Johnson published results from 34 patients who underwent a second discogram.51 The purpose of the study was to determine whether previously normal nucleograms became abnormal within a 2–28-month period of time. He hypothesized that discography does not cause disc herniation or other types of disc damage. Unfortunately, the methodology was flawed. Discography was not performed according to prescribed IASP and ISIS standards (Tables 94.2, 94.3). Furthermore, limited information could be gathered from the outcome because of inadequate statistical analysis of data, the limited number of discs reported, and the constrained means of data collection. Despite these shortcomings, this study demonstrates that within the 42 discs that were initially normal, eight of the discs were fissured on follow-up discograms. The pain was reported as similar or concordant within seven discs, while one disc did not provoke pain. Within all 42 discs with normal nucleograms, there was no evidence of herniation of nuclear material. Three of eight patients with abnormal discs underwent fusions subsequent to the primary discogram. The initially normal discs, now adjacent to the level of fusion, developed abnormal nucleograms. However, the mechanism for these segment changes are not necessarily from the initial discogram, but could be caused by altered biomechanics, surgical trauma, or another unknown cause.
Does antibiotic use mitigate complication rates? Before antibiotic prophylaxis became a routine component of disc stimulation, reported rates of discitis varied. Preprocedural antibiotics are
Section 5: Biomechanical Disorders of the Lumbar Spine
Table 94.3: ISIS scoring sheet for provocative pain responses Variable
Segments studied
Concordant levels
Points
Concordant pain Pain > 5/10 Pain > 7/10 Pressure < 50 psi Pressure < 15 psi
30 5 5 10 10
Sum of rows
L2–3
L3–4
L4–5
L5–S1
L2–3
L3–4
L4–5
L5–S1
Subtotal Divide subtotal by number of concordant discs. Enter result in this row. Control levels
Points
No pain Pain at < 50 psi Pain at < 15 psi Total of sums of rows below the double line Interpretation: > 70 points = POSITIVE 40–60 points = INDETERMINATE < 40 points = NEGATIVE
30 −10 −10
1. For each disc studied (see columns), enter the appropriate score for each of the variables indicated (rows). For discs with CONCORDANT PAIN, Enter 30 if the concordant pain is produced Enter 5 if the pain produced is greater than 5/10 Enter another 5 if the pain produced is also greater than 7/10 Enter 10 if the pressure at which pain occurred is anything less than 50 psi Enter another 10 if the pressure is also less than 15 psi For discs at CONTROL LEVELS, i.e. not concordant pain, Enter +30 if the disc was painless Enter −10 if pain occurred at a pressure less than 50 psi Enter another −10 if pain occurred at a pressure also less than 15 psi 2. For the CONCORDANT DISCS, add up the scores in each row, and record the sum of each row in the column labeled Sum of rows. 3. Add up the sums of the rows for all concordant discs, i.e. all scores above the double line. Divide this total by the number of concordant discs, and record the quotient in the cell indicated, immediately below the double line, in the column labeled Sum of rows. 4. For the NON-COCORDANT DISCS, add up the scores in the rows, taking heed of any negative numbers, and record the sum of each row in the column labeled Sum of rows. 5. Add up the total of the Sums column below the double line, taking care to heed negative numbers. 6. Interpret the result.
now the standard of care. Osti et al.'s landmark 1990 publication presented the most compelling evidence to date supporting the use of prophylactic antibiotics.45 We are unaware of any recent studies that have compared infection rates with and without prophylactic antibiotics.
Should psychometrics be routinely performed prior to discography? Caragee demonstated that individuals with primary somatization disorders are likely to have positive discograms regardless of disc architecture.37 In addition, Block et al. previously showed that patients with elevation of select scales in the Minnesota Mutiphasic Personality Inventory were more likely to over-report pain during discography.52 Both studies suggest that psychometrics should be performed prior to discography. If psychometrics demonstrate concomitant anxiety or depression, the results of discography should be more strictly evaluated.
Can discographic data guide treatment? Elaborate descriptions are available for fluoroscopic AP and lateral and postdiscography CT axial contrast patterns that try to classify stages of radial and concentric spread of contrast. In addition, some discographers record manometry data to help determine whether the discogram meets the criteria of a positive response, and most require
the provocation of 6/10 or greater concordant pain provocation at less than 50 psi above opening pressure. Treatments for internal disc disruption are still evolving and range from the most conservative (rest, therapy, bracing) to the maximally invasive 360 fusions, or disc replacements. Newer, evolving treatments include biological treatments and gene therapy. Currently, however, an ideal treatment for internal disc disruption. There is currently work in progress retrospectively comparing outcome data with the information obtained during discography. Perhaps we can eventually establish specific criteria based on imaging and pressure data to direct treatment.
Are the current standards reliable? When is a disc ‘positive?’ Determining whether a disc is a source of pain is more an art than a science. For example, performing a ‘sham injection’ may help one uncover over-reactive or deceitful responses. One may fake an injection by going through all the motions such as holding the syringe, clicking the fluoroscopy pedal, and asking the patient if they are experiencing any of their typical pain. If the patient responds inappropriately to this sham injection, the quality of information obtained from the rest of the procedure is dubious. 1045
Part 3: Specific Disorders
Likewise, any unexpected behavioral responses should be recorded. Examples include concordant pain response during local skin anesthetic injection and hysterical reactions during the procedure. Although difficult to interpret accurately, many discographers perform a repeat ‘confirmatory’ pressurization following initial concordant pain provocation and most will require equal or similar pain provocation on the repeat pressurization before calling the disc ‘positive.’ There are, however, no generally accepted standards, and whether the initial or succeeding response is the most accurate assessment could be argued either way. Current IASP and ISIS discography criteria are outlined in Tables 94.2 and 94.3. IASP standards are concrete. ISIS standards further objectify the results by including manometry and attempt to interpret a questionably positive disc through an elaborate scoring system. To their credit, they attempt to objectify factors which are measurable. However, neither criterion takes into account factors which would compromise data interpretation, such as awareness of a pain response to sham injections or reproducibility of pain with repeat pressurization of a specific disc. Unlike bimodal test outcomes which fall into groups of positive or negative, such as stool guaiac or pregnancy testing, discography requires interpretation. One's judgment must be based on a combination of many sources of information, including clinical, radiological, psychological, and pain provocation data. Discogram findings should be reproducible and there should be a negative response to a ‘sham’ injection. An inaccurate interpretation may lead to a failed surgery. Judging the reliability of the data will always remain an art.
CONCLUSIONS Lumbar discography is a diagnostic test that helps one determine whether a particular intervertebral disc is a source of pain. Properly performed and interpreted, discography is an invaluable tool. Together with the history, physical examination, and radiological studies, discography will identify asymptomatic discs and provide confirmatory evidence that a particular disc is the source of the patient's pain. Because this information is often used to determine at which levels to perform a percutaneous or open surgical procedure, accurate and precise interpretation of the results is vital.
10. Adams MA, Dolan P, Hutton WC. The stages of disc degeneration as revealed by discograms. J Bone Joint Surg [Br] 1986; 68:36–41. 11. Bernard TN. Lumbar discography followed by computed tomography: refining the diagnosis of low-back pain. Spine 1990; 15:690–707. 12. Sachs BL, Vanharanta H, Spivey MA, et al. Dallas discogram description: a new classification of CT/discography in low-back disorders. Spine 1987; 12:287–298. 13. Aprill C, Bogduk N. High-intensity zone: a diagnostic sign of painful lumbar disc on magnetic resonance imaging. Br J Radiol 1992; 65(773):361–369. 14. Schellhas KP, Pollei SR, Gundry CR, et al. Lumbar disc high-intensity zone: correlation of magnetic resonance imaging and discography. Spine 1996; 21:79–86. 15. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg [Am] 1990; 72: 403–408. 16. Boos N, et al. Volvo Award in Clinical Science: the diagnostic accuracy of MRI. Spine 1995; 20(24):2613–2625. 17. Weishaupt D, et al. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology 1998; 209:661–666. 18. Kokkonen S, et al. Endplate degeneration observed on magnetic resonance imaging of the lumbar spine: correlation with pain provocation and disc changes observed on computed tomography discography. Spine 2002; 27:2274–2278. 19. Smith BM, Hurwitz EL, Solsberg D, et al. Interobserver reliability of detecting lumbar intervertebral disc high-intensity zone on magnetic resonance imaging and association of high-intensity zone with pain and annular disruption. Spine 1998; 23:2074–2080. 20. Rankine JJ, et al. The clinical importance of the high-intensity zone on lumbar magnetic resonance imaging. Spine 1999; 24(18):1913–1920. 21. Modic MT, et al. Degenerative disc disease: assessment of changes in vertebral body marrow with MR imaging. Radiology; 1988; 166:193–199. 22. Miller G. The spine. In: Berquist T. MRI of the musculoskeletal system, 2nd edn. New York: Raven Press; 1990. 23. Brodsky AE, Binder WF. Lumbar discography: its value in diagnosis and treatment of lumbar disc lesions. Spine 1979; 4(2):110–120. 24. Calhoun E, et al. Provocation discography as a guide to planning operations on the spine. J Bone Joint Surg [Br] 1988; 70(2):267–271. 25. Blumenthal SL, et al. The role of anterior lumbar fusion for internal disc disruption. Spine 1988; 13(5):566–569. 26. Wetzel FT, et al. The treatment of lumbar spinal pain syndromes diagnosed by discography: lumbar arthrodesis. Spine 1994; 19(7):792–800. 27. Derby R, et al. The ability of pressure-controlled discography to predict surgical and non-surgical outcomes. Spine 1999; 24(4):364–372. 28. Carragee EJ. Point of view. Spine 1999; 24(4):371–372.
References 1. Nachemson A. Lumbar discography – Where are we today? [Editorial comment]. Spine 1989; 14(6):555–557. 2. Simmons EH, Segil CM. An evaluation of discography in the localization of symptomatic levels in discogenic disease of the spine. Clin Orthopaed Rel Res 1975; 108:57–69.
30. Rhyne AL III, et al. Outcome of unoperated discogram-positive low back pain. Spine 1995; 20(18):1997–2001. 31. Holt EP. The question of lumbar discography. J Bone Joint Surgery [Am] 1968; 50:720.
3. Schwarzer AC, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20(17):1878–1883.
32. Simmons JW, et al. A reassessment of Holt's data on ‘The question of lumbar discography.’ Clin Orthopaed Rel Res 1988; 237:120–123.
4. Young S, Aprill C, Laslett M. Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3:460–465.
33. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects: a controlled, prospective study. J Bone Joint Surg [Am] 1990; 72(7):1081–1088.
5. Donelson R, et al. A prospective study of centralization of lumbar and referred pain: a predictor of symptomatic discs and annular competence. Spine 1997; 22(10):1115–1122.
34. Wetzel FT. Point of view. Spine 2000; 1381. 35. Tanner C, Carragee EJ. Letter to editor in response. Spine 2001; 26(8):995–996.
6. Yrjama M, Vanharanta H. Bony vibration stimulation: a new, non-invasive method for examining intradiscal pain. Eur Spine J 1994; 3:233–234.
36. Carragee E, Tanner C, Vittum D, et al. Positive provocation discography as a misleading finding in the evaluation of low back pain. Chicago, IL: North American Spine Society; 1997.
7. Yrjama M, Tervonen O, Vanharanta H. Ultrasonic imaging of lumbar discs combined with vibration pain provocation compared with discography in the diagnosis of internal annular fissures of the lumbar spine. Spine 1996; 21(5):571–574.
37. Carragee EJ, Tanner CM, Khurana S, et al. The rates of false-positive lumbar discography in select patients without low back pain symptoms. Spine 2000; 25:1373–1381.
8. Yrjama M, Tervonen O, Kurunlahti M, et al. Bony vibration stimulation test combined with magnetic resonance imaging: Can discography be replaced ? Spine 1997; 22(7):808–813.
38. Bogduk N. An analysis of the Carragee data on false-positive discography. International Spinal Injection Society Scientific Newsletter Summer 2001; 4 (2):3–10.
9. Quinnell RC. Pressure standardized lumbar discography. Br J Radiol 1980; 53(635):1031–1036.
1046
29. Derby R, Eek B, Chen Y, et al. Intradiscal electrothermal annuloplasty (IDET): a novel approach for treating chronic discogenic back pain. Neuromodulation 2000; 3(2):82–88.
39. Carragee EJ, Tanner CM, Yang B, et al. False-positive findings on lumbar discography: reliability of subjective concordance assessment during provocative disc injection. Spine 1999; 24(23):2542–2547.
Section 5: Biomechanical Disorders of the Lumbar Spine 40. Carragee EJ, Chen Y, Tanner CM, et al. Provocative discography in patients after limited lumbar discectomy: a controlled, randomized study of pain response in symptomatic and asymptomatic subjects. Spine 2000; 25(23):3065–3071. 41. O'Neill C, Kurgansky M. Subgroups of positive discs on discography. Spine 2004; 29(19):2134–2139. 42. Carragee EJ, et al. Prospective controlled study of the development of lower back pain in previously asymptomatic subjects undergoing experimental discography. Spine 2004; 29:1112–1117.
46. Endres S, Bogduk N. Practice guidelines and protocols: lumbar disc stimulation. ISIS 9th Annual Scientific Meeting Syllabus. Sep 2001; 1456–1475. 47. Cohen SP, Larkin T, Fant GV, et al. Does needle insertion site affect discography results? A retrospective analysis. Spine 2002; 27(20):2279–2283. 48. Slipman CW, Patel RK, Zhang L, et al. Side of symptomatic annular tear and site of low back pain: is there a correlation ? Spine 2001; 26(8):E165–E169. 49. Hirsch C. An attempt to diagnose the level of disc lesion clinically by disc puncture. Acta Orthop Scand 1948; 18:131–140.
43. Bogduk N, Aprill C, Derby R. Discography. In: White AH, ed. Spine care, vol. 1. St Louis: Mosby; 1995:219–238.
50. Kahanovitz N, et al. The effect of discography on the canine intervertebral disc. Spine 1986; 11:26–27.
44. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg [Br] 1987; 69:26–35.
51. Johnson RG. Does discography injure normal discs? An analysis of repeat discograms. Spine 1989; 14:424–426.
45. Osti OL, Fraser Rd, Vernon-Robers B. Discitis after discography: the role of prophylactic agents. J Bone Joint Surg [Br] 1990; 72:271–274.
52. Block AR, Vanharanta H, Ohnmeiss DD, et al. Discographic pain report: influence of psychological factors. Spine 1996; 21:334–338.
45a. Furman MB, Lee TS, Puttlitz KM et al. Lumbar provocative discography: evaluation of possible disc pressurization. Proceedings of the North American Spine Society Mid Year Meeting – Meeting of the Americas II, 2002 [abstract].
1047
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ i: Intervertebral Disc Disorders ■ iii: Lumbar Axial Pain
CHAPTER
95
Intradiscal Steroids and Prolotherapy: Clinical Relevance, Outcomes and Efficacy Michael B. Furman, Ryan S. Reeves and William A. Ante
Internal disc disruption treatments are evolving. This chapter focuses on alternative intradiscal treatments distinct from the well-recognized ones (i.e. electrothermal annuloplasty, nucleoplasty, chemonucleolysis) discussed elsewhere in this book. In particular, this chapter focuses on intradiscal steroid injections and intradiscal prolotherapy. We discuss the rationale, efficacy, and potential therapeutic effects of these interventions based on a comprehensive literature review.
RATIONALE FOR INTRADISCAL STEROID INJECTIONS Inflammatory processes theoretically contribute to discogenic pain. Nucleus pulposus material leaks along radial tears into or through the annular fibers causing a local inflammatory response with associated pain. Studies have shown the presence of both inflammatory mediators1 and inflammatory cells2–4 within herniated nuclear material. The high-intensity zone, often seen in symptomatic individuals, may represent inflamed grade 3 to 5 annular fissures with neovascularization.5–7 Corticosteroid administration has been used since the 1950s to treat symptomatic degenerative intervertebral discs. However, its efficacy and mechanism of action remained controversial. Feffer8 first described using intradiscal hydrocortisone injections for its antiinflammatory properties, attempting to reverse the degenerative process. He also suggested that it had a polymerizing effect and could thus heal annular tears and restore the disc's biomechanical load-bearing properties. He proposed this hypothesis after observing that rheumatoid arthritis patients' synovial fluid viscosity increased after intra-articular hydrocortisone injections. This was attributed to polymerization of the hyaluronic acid's polysaccharide component. The synovial fluid's depolymerized hyaluronic acid is replaced by fluid with normal viscosity within 4 days.9 Leao stated that in degenerative processes, the interfibrillar substance's mucopolysaccharide can have an abnormal sulfuric chondroitin cleavage. The polymerization caused by hydrocortisone could repair the connection.10 Based on findings of accelerated disc degeneration following intradiscal Depo-Medrol administration, some11 have proposed that this agent may exert its therapeutic effect by reduction of disc bulging or protrusion.
INTRADISCAL STEROID INJECTION TECHNIQUE The intradiscal steroid injection's disc access and technique is essentially the same as that used for provocation discography.12–15 When indicated, the steroids are administered into the symptomatic level immediately after positive diagnostic disc stimulation using the same spinal needles. However, the discography's contrast volume and the
disc's capacity may limit this technique. Intranuclear injection should distribute medication into contiguous radial fissures and annular tears.
INTRADISCAL STEROID INJECTION EFFICACY Table 95.1 summarizes this section’s studies. In 1956, Feffer described using intradiscal steroids for low back and sciatic pain.16 He injected a hydrocortisone and iodopyracet solution during a single-level discography procedure using a modified Erlacher technique. The injected solution included 3 cc of 35% iodopyracet and 1 cc of 50 mg hydrocortisone. The total injectate volume varied with the patient’s intradiscal capacity The two lowest lumbar discs were routinely injected with a few days between injections. Occasionally, he injected more cephalad levels, depending on the patient's clinical scenario. If the first injection provided adequate relief, another level was not injected. Sixty patients were studied. None of the five patients with normal nucleograms had any symptom improvement. At a maximum 8-month follow-up, 37 patients (67%) of those with abnormal nucleograms had symptom improvement, with ‘permanent’ remission in 33 patients. Symptoms improved but then recurred in four patients at 2 weeks (one of four patients), 2 months (one of four), and 3 months (two of four). There was no improvement in 18 patients (33%) of those patients with abnormal nucleograms. This study did not detail its patient inclusion criteria, patient demographics, or outcome measurement method. In 1969, Feffer published a retrospective review in which he evaluated 244 patients who had undergone therapeutic intradiscal hydrocortisone injection.8 Discography was performed using a posterolateral approach with an injectate composed of 25 mg hydrocortisone per 1.5 cc contrast dye. Initially, the contrast agent Diodrast was used but was subsequently replaced with Hypaque due to the ‘better contrast’ obtained on radiographic imaging. Feffer stated that, ‘In most cases, two interspaces were injected, although a conscientious effort was made to correlate the levels treated with the clinical picture.’ At an average follow-up of 7.3 years (range 4–10 years), 46.7% had ‘permanent remission’ while 53.3 % had response failure defined as either no initial response to injection or relapse of symptoms. They reported complications on both their study population as well as all other discograms performed in their center over the previous 4 years. These included postprocedural spinal headaches, one case of disc infection requiring interbody fusion and a missed intrathecal meningioma which was previously misdiagnosed for lack of a prediscography myelogram. Radiographs obtained routinely 2 years after discography did not reveal accelerated disc degeneration.
1049
1050 Steroid Hydrocortisone (50 mg)
Hydrocortisone (25 mg)
Depo-Medrol (40–80 mg)
Triamcinolone hexacetonide (2 ml with no dose given) Depo-Medrol (80 mg)
Depomedrone or lederspan Depo-Medrone (40 mg)
Sample size
60
244
42
30
25
105
98
Author
Feffer 1956
Feffer 1969
Wilkinson and Schuman
Bertin
Simmons
Bull
Khot
Table 95.1: Intradiscal injection efficacy studies
No significant change vs. saline control
24% better
43% improvement on VAS; 36% functional improvement (Per Oswestry)
36.6% good results, 36.6% moderate results, 26.7% poor results
Lumbar: 31% good results for > 3 months. Cervical: 25% good results
46.7% permanent remission
55% (33) patients with complete resolution; 62% (37) with improvement
Improvement
1 year VAS and Oswestry
8 weeks
10–14 days VAS and Oswestry
1–3 months
2.4 year (average)
4–10 years
8 months
Follow-up
Validated Outcome measures, double blinded RCT, large sample size. No intermittent shortterm outcomes prior to 1 year.
Comparison of Modic changes and response rates. Retrospective abstract publication, no dose given.
Small sample sized, short follow up.
Limited methodology, nonvalidated outcome scale.
Prospective-non randomized trial; Nonvalidated outcome scale, no blinding, variable steroid dose. See Table 95.2.
Retrospective review; multiple discs injected at once, no true statistical analysis, no validated outcome measures.
No outcome measures or inclusion/ exclusion criteria or patient demographics.
Comments
Part 3: Specific Disorders
Section 5: Biomechanical Disorders of the Lumbar Spine
Older patients or those with primarily back symptoms responded better to intradiscal steroids while gender and neurologic deficit did not affect results. Disc characteristics in patients with positive results were analyzed. Patients with ‘posterior degeneration only’ also had more favorable responses. This was defined by discographic results demonstrating an intact anulus anteriorly and laterally, without hypertrophic or bony changes. The degree or direction of the disc protrusion did not affect prognosis. This study was limited by its retrospective nature, lack of validated outcome measures, nonstandard discography technique and reporting as compared to today's methods. The discography protocol did not include a control level or emphasize obtaining concordant pain responses. Also, the data tables presented were not easily decipherable, nor was the data statistically analyzed. In 1980, Wilkinson and Schuman15 performed a prospective, nonrandomized intradiscal Depo-Medrol study investigating degeneratively mediated lumbar and cervical axial pain. Inclusion criteria required greater than 6 months' symptom duration despite aggressive noninvasive therapy which was not defined. No patient was considered an ideal surgical candidate since they lacked any neurologic deficits. The study included 29 lumbar and 13 cervical patients. Myelography was reportedly normal in almost all patients except for degenerative changes. ‘Contrast and/or anesthesia discography’ was performed prior to the initial therapeutic intradiscal injection. Nearly all patients had pathology, most having a single-level abnormal disc. The study protocol changed after the first eight lumbar injections: Depo-Medrol increased from 30–40 mg to a dose of 60–80 mg into one or two discs. Each subject in the cervical group received 40–80 mg of Depo-Medrol. Average follow-up was 2.4 years with a 1-year minimum. This assessment was either a clinical examination or simply a referring orthopedist report. Outcomes were documented using a three-point Likert scale. ‘Good’ was defined as significant pain improvement for at least 3 months, ‘limited’ results denoted significant pain relief from 10 days to 3 months, and ‘none’ referred to no improvement or improvement lasting less than 10 days (Tables 95.2 and 95.3) For the 45 intradiscal injections in the 29 patients with lumbar disc disease, including those with previous lumbar surgery, and mainly axial low back pain with little or no lower limb radicular pain, 31% had good results lasting more than 3 months, 15% had limited relief, and 54% responded poorly (see Table 95.2). In patients with predominantly radicular pain, 37% had good results, 31% had limited relief, while 42% responded poorly. If patients with previously surgically treated lumbar discs were considered alone (8 patients), 23% had good results, 15% had limited relief, and 62% did poorly. In the patients who only received 40 mg or less of Depo-Medrol, 12% had good results, 26% had only limited relief, and 62% did poorly. If only the injections in patients with axial low back pain who had never had surgery and received ‘full dose steroid therapy’ of 80 mg are considered (n=13 injections), then 54% responded with good results, 15% had limited relief, and 31% had poor results. If only the injections in patients with lumbar radicular pain who never had surgery and received full-dose steroid therapy were considered (n=10 injections), then 40% gave good results, 30% limited results, and 30% poor results. Eighteen patients subsequently underwent lumbar surgery. Twelve of these were from the group that did not receive any clinical benefit from intradiscal injection and similarly only 2 (17%) of these received good results, 4 (33%) limited results, and 6 (50%) poor results from surgery. Eighteen injections in 13 patients with cervical disc disease were also studied (see Table 95.3). None had previous cervical surgery and all received 60–80 mg of Depo-Medrol (80 mg/mL). For those with mainly axial neck pain, 25% had good results, 50% had limited relief, and 25% did poorly. For those with predominantly cervical radicular
symptoms, 20% had good results, 30% had limited relief, and 50% did poorly. Nine cervical patients subsequently underwent anterior interbody surgery with 5 (56%) having good results from surgery. None of the patients who had good results from cervical intradiscal injection underwent surgery. The only complications reported were occasional spinal headaches and minor menstrual irregularity. No disc infections or increased disc degeneration were encountered. Based on these data, the authors conclude that intradiscal steroid injections may be beneficial for those with discogenic pain but may have more efficacy for axial pain than radicular pain. The study included only patients who had symptoms for longer than 6 months without improvement despite conservative care. Theoretically, this reduces the possibility that improvement in patients' symptoms after intradiscal steroid treatment was due merely to the natural course of the disease process. Unfortunately, this study was limited by small sample size, lack of validated outcome measures, the nonrandomized and nonblinded nature, and heterogeneity of dosages of steroid used. The data were not subjected to formal statistical analysis and the discography technique was not fully elaborated In 1990, Bertin et al.17 studied the effect of triamcinolone hexacetonide for acute, subacute, and chronic sciatica with a prospective, nonrandomized study. Each patient had sciatica with evidence of ‘disc protrusion,’ ‘discal hernia,’ or ‘epidural fibrosis’ by CT scan or ‘saccoradiculography’ (myelography). Operational definitions for disc protrusion, discal hernia, and sciatica were not given. The presenting sciatica symptoms were resistant to conservative care including rest, nonsteroidal antiinflammatory drugs, and, occasionally, epidural steroid injections. Each patient underwent discography followed by intradiscal injection of local anesthetic combined with 2 mL of triamcinolone hexacetonide. The exact dosage was not given. Followup occurred at 1 and 3 months following injection. There were 30 patients who had a mean age of 46 years (range 25–63 years) and mean duration of symptoms of 36 months (range 1 month to 10 years). Outcomes were categorized according to the authors' idiosyncratic criteria. Good results were defined as return to work or normal activity, discontinuation of analgesics and/or antiinflammatory drugs, and absence of clinical signs of radiculopathy. Moderate results were defined as commencement of restricted occupational or recreational activity, ‘improvement but insufficient’ reduction of axial or appendicular pain, and continued use of antiinflammatories or analgesics. Poor results yielded no change in pain and no return to work. The only two complications reported were one case of transient urinary retention and one case of foot dorsiflexion weakness that persisted at 1 year. Due to the small number of patients (n=30), Woolf's G test was utilized. There was no significant difference between the results at 1 versus 3 months although there was a trend for diminished number of good results and an increase in poor results with the number of moderate results remaining relatively unchanged. After 3 months, 36.6% had good results, 36.6% had moderate results, and 26.7% had poor results. Essentially, one-third of patients had a good, moderate, or poor result. Duration of symptoms of less than 6 months and CT-scan appearance of disc herniation ( p 15 or L4–5 > 20 or L5–S1 > 25
1114
Fig. 101.7 Measurement of sagittal plane rotation of L4–5 functional spinal unit on dynamic (flexion–extension) lateral radiographs. (Adapted from White AA III, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: JB Lippincott; 1990.)
To date, no diagnostic gold standard for segmental instability has been identified. Historically, patients complain of chronic and recurrent pain localized to the low back or radiating into the lower extremities and associated with high levels of functional disability.58 Because the condition is mechanically based, the pain typically worsens with greater loads on the spine such as general activity, lifting, standing, sitting, and motions such as bending or twisting. Kirkaldy-Willis and Farfan suggested that segmental instability is a condition in which ‘minor perturbations produce acute pain.’14 Conversely, the pain is relieved by lying supine, the position that places the least mechanical load on the lumbar spine.75 Patients most commonly describe their back pain as recurrent, constant, catching, locking, giving way, or associated with a feeling of instability.76 Several researchers have reported similar physical examination findings that are consistent with a movement–control problem within the neutral zone:14,56,77 (1) active spinal movement with good ranges of spinal mobility but with ‘through-range’ pain or a painful arc rather than end-of-range limitation of motion, and (2) the inability to return to erect standing from forward bending without the use of the hands to assist in this motion. Segmental shifts or hinging were frequently associated with the painful movement. Deep abdominal muscle activation during the provocative movement often reduced or eliminated pain. Neurological examination and neural tissue provocation tests were generally normal.78
by which patients can be evaluated and movement dysfunction analyzed in a segment-specific and individual manner. Common to all the microinstability syndromes are the patient's subjective feeling of instability and an objectively observed lack of movement control and related symptoms within the neutral zone, all of which are associated with an inability to initiate co-contraction of the local muscle system within this zone. The local muscle system consists of muscles that attach directly to the lumbar vertebrae and are responsible for providing segmental stability and directly controlling the lumbar segments. The lumbar multifidus, psoas major, quadratus lumborum, the lumbar parts of the lumbar iliocostalis and longissimus, transverses abdominis, the diaphragm, and posterior fibers of the oblique abdominis internus form part of this local muscle system. Patients may develop compensatory movement strategies that ‘stabilize’ the motion segment out of the neutral zone and towards an end-range position (such as flexion, lateral shift, or extension). This is achieved by the recruitment of global system muscles and by generating high levels of intra-abdominal pressure during low-load tasks. The global muscle system consists of large torque-producing muscles that act on the trunk and spine without directly attaching to it. These muscles include the rectus abdominus, obliquus abdominus externus, and the thoracic part of the lumbar iliocostals; they provide general trunk stabilization but are not capable of exerting a direct segmental influence on the spine.76,78
Clinical syndromes of microinstability
Flexion pattern of microinstability
The directional nature of instability based upon the mechanism of injury, resultant site of tissue damage, and clinical presentation is well understood in the knee and shoulder but poorly understood in the lumbar spine. Based on experimental and radiological data, Dupuis et al.64 concluded that the location of the dominant lesion in the motion segment determines the pattern of instability manifested. Because the motion within the lumbar spine is three-dimensional and involves coupled movements, tissue damage is likely to cause movement dysfunction in more than one direction.76 The descriptions of microinstability syndromes have been developed from clinical observation and are based on the mechanism of spinal injury, the resultant tissue damage, the reported and observed aggravating activities, and movement problems relating to a specific movement quadrant or quadrants. These descriptions provide a basis
Patients with flexion pattern microinstability, the most common type, complain of central back pain and relate their injury to either a single flexion–rotation injury or to repetitive strains relating to flexion–rotation activities. Symptoms and ‘vulnerability’ are aggravated by flexion–rotation movements and patients are unable to sustain semiflexed postures (Fig. 101.8). A loss of segmental lumbar lordosis at the level of the ‘unstable motion segment’ often is noticeable when the patient is standing and is accentuated in sitting postures because patients tend to hold the pelvis in a degree of posterior pelvic tilt. Lower lumbar segmental lordosis is further decreased in flexed postures and usually is associated with increased tone in the upper lumbar and lower thoracic erector spinae muscles, with an associated increase in lordosis in this region. During forward bending, patients have a tendency to flex more at the symptomatic level
Section 5: Biomechanical Disorders of the Lumbar Spine ‘Unstable’ movement zone Flexion
Left side bending
Neutral zone
‘Unstable’ movement zone Flexion
‘Stable’ movement zone
Right side bending
Extension
Left side bending
Neutral zone
‘Stable’ movement zone
Right side bending
Extension
Fig. 101.8 Unstable movement zone: flexion pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)
Fig. 101.9 Unstable movement zone: extension pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)
than at the adjacent levels, usually producing an arc of pain and an inability to return from flexion to neutral without use of the hands to assist the movement. During backward bending, extension often is less in the affected segment than in the more proximal segments. Specific movement testing reveals an inability to differentiate anterior pelvic tilt and low lumbar spine extension independent of upper lumbar and thoracic spine extension. Movement tests such as squatting, sitting with knee extension or hip flexion, ‘sit to stand,’ and forward-loaded postures reveal an inability to control a neutral segmental lordosis, with a tendency to segmentally flex at the unstable motion segment, posteriorly tilt the pelvis, and extend the upper lumbar and thoracic spine. Specific muscle tests reveal an inability to activate the lumbar multifidus in co-contraction with the deep abdominal muscles at the ‘unstable’ muscle segment within a neutral lordosis. Many patients are unable to assume a neutral lordotic lumbar spine posture, particularly in four-point kneeling and sitting. Attempts to activate these muscles commonly are associated with bracing of the abdominal muscles with a loss of breathing control and excessive coactivation of the thoracolumbar erector spinae muscles and external oblique. This is associated with a further flattening of the segmental lordosis at the unstable motion segment, often resulting in pain. Palpation reveals a segmental increase in flexion and rotation mobility at the symptomatic motion segment.
During forward bending, these patients tend to hold the lumbar spine in lordosis (particularly at the level of the unstable motion segment), with a sudden loss of lordosis at the midrange of flexion that usually is associated with an arc of pain. During return-to-neutral, they tend to hyperlordose the spine segmentally before the upright position is achieved, with pain on returning to the erect posture and the necessity to assist the movement with the use of the hands. Specific movement tests reveal an inability to initiate posterior pelvic tilt independent of hip flexion and activation of the gluteals, rectus abdominis, and external obliques. Specific muscles tests also reveal an inability to co-contract the segmental lumbar multifidus with the deep abdominal muscles in a neutral lumbar posture, with a tendency to ‘lock’ the lumbar spine into extension and brace the abdominal muscles. Attempts to isolate deep abdominal muscle activation commonly are associated with excessive activation of the lumbar erector spinae, external oblique, and rectus abdominis and an inability to control diaphragmatic breathing. Palpation reveals a segmental increase in extension and rotation mobility at the symptomatic motion segment.
Extension pattern of microinstability Patients with extension pattern microinstability relate their injury to an extension–rotation incident or repetitive trauma usually associated with sporting activities involving extension–rotation. Their symptoms are aggravated by extension and extension–rotation movements and activities such as standing, fast walking, running, swimming, and overhead activities such as throwing (Fig. 101.9). When the patient is standing, segmental lordosis at the unstable motion segment usually is increased, sometimes with an increased level of segmental muscle activity at this level and anterior pelvic tilt. Extension activities reveal segmental hinging at the affected segment with a loss of segmental lordosis above this level and associated postural ‘sway.’ With the patient prone, hip extension and knee flexion movement tests reveal a loss of co-contraction of the deep abdominal muscles and dominant patterns of activation of the lumbar erector spinae that cause excessive segmental extension–rotation at the unstable level.
Lateral shift pattern of microinstability The recurrent lateral shift pattern of microinstability usually is unidirectional and is associated with unilateral low back pain, usually reported to occur during reaching or rotating in one direction with the spine flexed (Fig. 101.10). This is the same movement direction that patients report as ‘injuring’ their back. Their standing posture is similar to that of patients with flexion pattern microinstability, with a loss of lumbar segmental lordosis at the affected level, but with an associated lateral shift at the same level. Palpation of the lumbar multifidus muscles with the patient standing commonly reveals resting muscle tone on the side of the shift, and atrophy and low tone on the contralateral side. The lateral shift is accentuated when the patient stands on the foot ipsilateral to the shift. When walking, the patient has a tendency to transfer weight through the trunk and upper body rather than through the pelvis. Sagittal spinal movements cause a further lateral shift at the midrange of flexion, usually associated with an arc of pain. With the patient supine, rotary and lateral trunk control is lost in the direction of the shift, with asymmetrical leg loading and unilateral bridging, and during four-point kneeling trunk control is lost when one arm is flexed. Sitting-to-standing and squatting movements usually 1115
Part 3: Specific Disorders ‘Unstable’ movement zone Flexion
Left side bending
Neutral zone
‘Stable’ movement zone
Right side bending
REHABILITATION OF INSTABILITY
Extension Fig. 101.10 Unstable movement zone: lateral shift pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)
reveal a tendency towards lateral trunk shift with increased weightbearing on the side of the shift. Specific muscle testing reveals an inability to bilaterally activate segmental lumbar multifidus in co-contraction with the deep abdominal muscles, with dominance of activation of the quadratus lumborum, lumbar erector spinae, and superficial lumbar multifidus on the side ipsilateral to the shift and an inability to activate the segmental lumbar multifidus on the contralateral side.
Multidirectional pattern of microinstability The most serious and debilitating of the clinical presentations, multidirectional microinstability frequently is associated with a traumatic injury and high levels of pain and functional disability. Provocative movements are described as multidirectional (Fig. 101.11), all weight-bearing postures are painful, and pain-relieving positions during weight-bearing are difficult to obtain. Locking of the spine commonly is reported after sustained flexion, rotation, and extension postures, and patients may assume a flexed, extended, or laterally shifted spinal posture. Excessive segmental shifting and hinging patterns may be present in all movement directions, with ‘jabbing’ pain and associated back muscle spasm. Assuming neutral lordotic spinal positions is very difficult, and attempts to facilitate lumbar
‘Unstable’ movement zone
Flexion
Left side bending
Neutral zone
Right side bending
Extension Fig. 101.11 Unstable movement zone: multidirectional pattern. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.) 1116
multifidus and transverses abdominis co-contraction (especially during weight bearing) usually are associated with a tendency to flex, extend, or laterally shift the spine segmentally, with associated global muscle substitution, bracing of the abdominal wall, and pain. Palpation reveals multidirectional increased intersegmental motion at the symptomatic level. High levels of irritability and an inability to tolerate compression loading in any position indicate a poor prognosis for conservative exercise management.
A recent focus in the rehabilitation of patients with chronic low back pain has been the training of specific muscles, such as the transverses abdominis, diaphragm, and lumbar multifidus, involved in the dynamic stability and segmental control of the spine based on the identification of specific motor control deficits in these muscles.79–81 Once the faulty movement pattern or patterns are identified, the individual components of the movement are isolated and the muscles are retrained for functional tasks specific to the patient's needs. O'Sullivan et al. have reported reductions in pain and functional disability with this exercise training approach in patients with chronic low back pain and a diagnosis of lumbar segmental instability.76,80,82 In its simplest form, this exercise program represents the process of motor learning; three stages have been described in the learning of a new motor skill (Fig. 101.12).76,83
First stage of rehabilitation The first stage of rehabilitation is cognitive and requires a high level of patient awareness so that they can isolate the co-contraction of the local muscle system without global muscle substitution. The goal of the first stage is to train the specific isometric co-contraction of the transversus abdominis with the lumbar multifidus at low levels of maximal voluntary contraction and with controlled respiration during weight-bearing with neutral lordosis. This is accomplished by training independence of the pelvis and lower lumbar spine from the thoracic spine and hips to achieve a neutral lordosis without global muscle substitution and by training central and lateral costal diaphragm breathing control. The patient learns to maintain neutral lordosis and facilitate the ‘drawing up and in’ contraction of the pelvic floor and lower and middle fibers of the transverses abdominis with gentle controlled lateral costal diaphragm breathing and without global muscle substitution. If accurate co-contraction cannot be obtained in weight-bearing postures such as sitting or standing, non-weight-bearing postures, such as four-point kneeling, prone, or supine, can be used. The goal is to teach the patient to achieve bilateral activation of segmental lumbar multifidus (at the unstable level) in co-contraction with the transverses abdominis and controlled lateral costal diaphragm breathing while maintaining a neutral lordosis. This should be done with the patient sitting and standing, with correction to posture as needed. If global muscle substitution occurs (i.e. breathing control is lost, muscle fatigue occurs, or resting pain is increased), the patient is instructed to stop the co-contraction. The inhibition of global muscle substitution is mandatory if appropriate co-contraction is to be obtained. The actions of the obliquus externus abdominis and rectus abdominis muscles can be inhibited by having the patient focus on the pelvic floor contraction and on optimal postural alignment during weight-bearing; ensuring upper lumbar lordosis and lateral costal diaphragm breathing also are beneficial to open the sternal angle. The thoracolumbar erector spinae muscles can be inhibited by having the patient avoid thoracic spine extension and excessive lumbar spine lordosis, focus on independence of pelvic
Section 5: Biomechanical Disorders of the Lumbar Spine
Isolate LMS
Train LMS control
Train LMS functionally
and low lumbar spine movement from thoracic spine and hip movement, and continue lateral costal diaphragm breathing. Palpatory and electromyogram (EMG) biofeedback and muscle release techniques also are helpful. Training is done for 10–15 minutes at least once a day in a quiet environment. Once a pattern of muscle activation has been isolated, the contractions must be done with postural correction while sitting and standing and with the ‘holding’ time of the contraction increased from 10 to 60 seconds before it can be integrated into functional tasks and aerobic activities such as walking. At this stage, a degree of pain control is expected in these postures, which provides a powerful biofeedback for the patient. Three to 6 weeks may be required to achieve this stage.
Second stage of rehabilitation The second stage of rehabilitation is associative, where the focus in on refining a particular movement pattern. The aim of this stage is to identify two or three faulty and pain-producing movement patterns based on the examination and break them down into component movements with high repetitions (50–60). The patient is taken through these steps while isolating the co-contraction of the local muscle system. This is done first with the spine in a neutral lordotic position, then with normal spinal movement, always maintaining segmental control and pain control. This can be done for such movements as sit-to-stand, walking, lifting, bending, twisting, and extending. Patients practice the movement components every day and gradually increase the speed and complexity of the movement pattern until
Fig. 101.12 Stages of rehabilitation based on a motor learning model (LMS, local muscle system). (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)
they can move smoothly and freely. They are encouraged to carry out regular aerobic exercise such as walking while maintaining correct postural alignment, low-level local muscle system co-contraction, and controlled respiration. This helps increase the muscle tone and aids in making the pattern automatic. Patients also are encouraged to perform the co-contractions in situations where they experience or anticipate pain or feel ‘unstable.’ This is essential to having the patterns of co-contraction become automatic. This stage can last from 8 weeks to 4 months, depending on the patient, the degree and nature of the pathology, and the intensity of practice. Once the motor pattern is learned and becomes automatic, patients often report the ability to carry out previously aggravating activities without pain. Although they now no longer require the formal specific exercise program, they are instructed to maintain local muscle system control functionally with postural awareness, while maintaining regular levels of general exercise.
Third stage of rehabilitation The third stage of rehabilitation is the autonomous stage, in which correct performance of motor tasks requires only a low degree of attention.83 At this stage, patients can automatically stabilize their spine during functional demands of daily living. The success of specific exercise intervention in achieving automatic patterns of muscle recruitment has been validated by surface EMG data and reports of long-term good outcomes in patients who completed the protocol.80,82,84 1117
Part 3: Specific Disorders Identify the symptomatic motion segment and correlate this with radiological findings if present
2. Nachemson A. Instability of the lumbar spine. Neurosurg Clin North Am 1991; 2:785–790. 3. Pope M, Frymoyer J, Krag M. Diagnosing instability. Clin Orthop 1992; 296:606–667. 4. Friberg D. Functional radiography of the lumbar spine. Ann Med 1939; 21:341–346.
Identify direction specificity of the instability problem
Determine the neuromuscular strategy of dynamic stabilization
5. Mimura M. Rotational instability of the lumbar spine; a three-dimensional motion study using biplane X-ray analysis system. Nippon Seikeigeka Gakkai Zasshi 1990; 64:546–559. 6. Montgomery D, Fischgrund J. Passive reduction of spondylolisthesis on the operating room table: a retrospective study. J Spinal Disord 1994; 7:167–172. 7. Wood K, Popp C, Transfeldt E, et al. Radiographic evaluation of instability in spondylolisthesis. Spine 1994; 19:1697–1703. 8. Long D, BenDebba M, Torgenson W. Persistent back pain and sciatica in the United States: patient characteristics. J Spinal Disord 1996; 9:40–58. 9. Sihvonen T, Partanen J. Segmental hypermobility in lumbar spine and entrapment of dorsal rami. Electromyogr Clin Neurophysiol 1990; 30:175–180.
Observe for loss of dynamic trunk stabilization during functional movement and limb loading
Identify local muscle dysfunction and faulty patterns of global muscle substitution
Determine the relationship between symptoms and local muscle system control Fig. 101.13 Recommended flow diagram for physical examination assessment to determine spinal instability. (Adapted from O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12.)
10. Gertzbein S. Segmental instability of the lumbar spine. Semin Spinal Surg 1991; 3:130–135. 11. Lindgren K, Sihvonen T, Leino E, et al. Exercise therapy effects on functional radiographic findings and segmental electromyographic activity in lumbar spine instability. Arch Physical Med Rehab 1993; 74:933–939. 12. Gertzbein SD, Seligman J, Holtby R, et al. Centrode patterns and segmental instability in degenerative disc disease. Spine 1985; 10:257–261. 13. Kirkaldy-Willis WH. Presidential symposium on instability of the lumbar spine. Introduction. Spine 1985; 10:254. 14. Kirkaldy-Willis WH, Farfan HF. Instability of the lumbar spine. Clin Orthop 1982; 165:110–123. 15. Panjabi MM, Thibodeau LL, Crisco JJ, et al. What constitutes spinal instability? Clin Neurosurg 1988; 34:313–339. 16. Pope MH, Panjabi M. Biomechanical definition of spinal instability. Spine 1985; 10:255–256. 17. Boden SD, Wiesel SA. Lumbosacral segmental motion in normal individuals. Have we been measuring instability properly? Spine 1989; 15:571–576.
SUMMARY Lumbar segmental instability continues to be a diagnostic challenge. Correlating clinical instability and radiographic instability has been difficult because of the overlap of symptomatic and asymptomatic motion patterns. Additionally, conventional radiography often is insensitive and unreliable in detecting abnormal or excessive intersegmental motion. As the pathomechanics of the lumbar spine have become better understood, however, defining instability in terms of quality of motion throughout the range of motion rather than relying solely on the traditional total range of motion values for diagnosis has been useful in providing a basis by which patients can be evaluated in a segment-specific and individual manner (Fig. 101.13). Lumbar segmental instability can be viewed as a purely movement syndrome: microinstability (without osseous injury) in which directional patterns of motion produce an observed lack of movement control and relative symptoms within the neutral zone or may be associated with other conditions. With increasing understanding of the relative involvement of different muscle groups contributing to lumbar stability, diagnosis-specific rehabilitation protocols are being developed to assist in the assessment and treatment of patients with lumbar instability. Good results have been reported with such an approach using a motor learning model in which the faulty movement pattern or patterns are identified and the components of the movement are isolated and retrained into functional tasks specific to the patient's individual needs. Scientific trials comparing this approach to other treatment methods are required to validate its efficacy.
References 1. Eisenstein SM. Instability and low back pain. A way out of the semantic maze. In: Szpalski M, Gunzburg R, Pope MH, eds. Lumbar segmental instability. Philadelphia: Lippincott Williams & Wilkins; 1999:39–44.
1118
18. Dvorak J, Panjabi MM, Novotny JE, et al. Clinical validation of functional flexion–extension roentgenograms of the lumbar spine. Spine 1991; 16:943–950. 19. Pope M, Frymoyer J, Krag M. Diagnosing instability. Clin Orthop 1992; 296:60–67. 20. Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord 1992; 5:383–389. 21. Fritz JM, Erhard RE, Hagen BF. Segmental instability of the lumbar spine. Phys Ther 1998; 78:889–896. 22. Panjabi MM. The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. J Spinal Disord 1992; 5:390–396. 23. Panjabi MM. Clinical spinal instability and low back pain. J Electromyogr Kinesiol 2003; 13:371–379. 24. Indahl A, Kaigle AM, Reikeras O, et al. Interaction between the porcine lumbar intervertebral disc, zygapophyseal joints, and paraspinal muscles. Spine 1997; 22:2834–2842. 25. Haher TR, O'Brien M, Dryer JW, et al. The role of the lumbar facet joints in spinal stability: identification of a alternative paths of loading. Spine 1994; 19:2667–2670. 26. Panjabi MM, Goel VK, Takata K. Physiologic strains in the lumbar spinal segments: an in vitro biomechanical study. Spine 1982; 7:192–203. 27. Sharma M, Langrana NA, Rodriguea J. Role of ligaments and facets in lumbar spinal instability. Spine 1995; 20:887–900. 28. McGill SM. Estimation of force and extensor moment contributions of the disc and ligaments at L4–L5. Spine 1988; 13:1395–1402. 29. Adams MA, Hutton MC, Stott JRR. The resistance to flexion of the lumbar intervertebral joint. Spine 1980; 5:245–253. 30. Farfan HF, Cossette JW, Robertson GW, et al. The effects of torsion on the lumbar intervertebral joints: the role of torsion in the production of disc degeneration. J Bone Joint Surg [Am] 1970; 52:468–497. 31. Jiang H, Russell G, Raso J, et al. The nature and distribution of human supraspinal and interspinal ligaments. Spine 1995; 20:869–876. 32. Panjabi MM, Abumi K, Durancaeu J, et al. Spinal stability and intersegmental muscle forces: a biomechanical model. Spine 1989; 14:194–199. 33. Nachemson A, Evans J. Some mechanical properties of the third lumbar interlaminar ligament (ligamentum flavum). J Biomech 1968; 1:211–220. 34. Crisco JJ III, Panjabi MM. The intersegmental and multisegmental muscles of the lumbar spine: a biomechanical model comparing lateral stabilizing potential. Spine 1991; 16:793–799.
Section 5: Biomechanical Disorders of the Lumbar Spine 35. Macintosh JE, Pearcy MJ, Bogduk N. The axial torque of the lumbar back muscles: torsion strength of the back muscles. Aust NZ J Surg 1993; 63:205–212.
61. Macnab I. The traction spur: an indicator of segmental instability. J Bone Joint Surg [Am] 1971; 53:663–670.
36. Gracovetsky S, Farfan HF, Helleur C. The abdominal mechanism. Spine 1985; 10:317–324.
62. Knutsson F. The instability associated with disk degeneration in the lumbar spine. Acta Radiol 1944; 25:593–609.
37. Tesh KM, Dunn JS, Evans JH. The abdominal muscles and vertebral stability. Spine 1987; 12:507–508.
63. Arkin AM. The mechanism of rotation in combination with lateral deviation in the normal spine. J Bone Joint Surg [Am] 1950; 32:180–188.
38. Hodges PW, Richardson A. Inefficient muscular stabilization of the lumbar spine associated with low back pain. Spine 1996; 21:2640–2650.
64. Dupuis P, Yong-Ming K, Cassidy D, et al. Radiological diagnosis of degenerative spinal instability. Spine 1985; 10:262–276.
39. Bogduk N. Clinical anatomy of the lumbar spine and sacrum, 3rd edn. New York: Churchill Livingstone; 1997:67–69.
65. Frymoyer JW, Hanley EN Jr, Howe J, et al. A comparison of radiographic findings in fusion and nonfusion patients, ten or more years following lumbar disc surgery. Spine 1979; 4:435–440.
40. Peck D, Buxton DF, Nitz A. A comparison of spindle concentrations in large and small muscles acting in parallel combinations. J Morphol 1984; 180:243–252. 41. Bogduk N, Macintosh JE, Pearcy MJ. A universal model of the lumbar back muscles in the upright position. Spine 1992; 17:897–913.
66. Lindahl O. Determination of the sagittal mobility of the lumbar spine. Acta Orthop Scand 1966; 37:241–254.
42. Macintosh JE, Bogduk N. The biomechanics of the lumbar multifidus. Clin Biomech 1986; 1:205–213.
67. Bernhardt M, White AA III, Panjabi MM, et al. Biomechanical considerations of spinal stability. In: Rothman RH, Simeone FA, eds. The spine. Philadelphia: WB Saunders; 1992:1167–1196.
43. McGill SM, Juker D, Kropf P. Quantitative intramuscular myoelectric activity of quadratus lumborum during a wide variety of tasks. Clin Biomech 1996; 11:170–172.
68. Rutkow IM. Orthopaedic operations in the United States, 1979 through 1983. J Bone Joint Surg [Am] 1986; 68:716–719.
44. Bartelink DL. The role of abdominal pressure in relieving the pressure on the lumbar intervertebral discs. J Bone Joint Surg [Br] 1957; 39:718–725.
69. Hayes MA, Howard TC, Gruel CR, et al. Roentgenographic evaluation of lumbar spine flexion–extension in asymptomatic individuals. Spine 1989; 14:327–381.
45. McGill SM, Norman RW. Potential of lumbodorsal fascia forces to generate back extension moments during squat lifts. J Biomed Eng 1988; 10:312–318.
70. Spratt KF, Weinstein JN, Lehmann TR, et al. Efficacy of flexion and extension treatments incorporating braces for low back pain patients with retrodisplacement, spondylolisthesis, or normal sagittal translation. Spine 1993; 18:1839–1849.
46. Gardner-Morse MG, Stokes IAF. The effects of abdominal muscle coactivation on lumbar spine stability. Spine 1998; 23:86–91. 47. Cresswell AG, Gundstrom H, Thorstensson A. Observations on intra-abdominal pressure and patterns of abdominal intramuscular activity in man. Acta Physiol Scand 1992; 144:409–481.
71. Shaffer WD, Weinstein J. Segmental spinal instability. A survey of measurement techniques. Semin Spine Surg 1991; 3:124–149. 72. Newman PH, Stone KM. The etiology of spondylolisthesis. J Bone Joint Surg [Br] 1963; 45:39–59.
48. Gardner-Morse MG, Stokes IAF, Laible JP. Role of muscles in lumbar spine stability in maximum extensor efforts. J Orthop Res 1995; 13:802–808.
73. Grubb SA, Lipscomb MJ, Conrad RW. Degenerative adult-onset scoliosis. Spine 1988; 13:241–245.
49. Luoto S, Taimela S, Hurri H, et al. Psychomotor speed and postural control in chronic low back pain patients: a controlled follow-up study. Spine 1996; 21:2621–2627.
74. Hayes MA, Tompkins SF, Herndon WA, et al. Clinical and radiological evaluation of lumbosacral motion below fusion levels in idiopathic scoliosis. Spine 1988; 13:1161–1167.
50. Luoto S, Hurri H, Alaranta H. Reaction times in patients with chronic low-back pain. Eur J Phys Med Rehabil 1995; 5:47–50.
75. Nachemson AL. The lumbar spine: an orthopaedic challenge. Spine 1976; 1:59–71.
51. Nies N, Sinnott PL. Variations in balance and body sway in middle-aged adults: subjects with healthy backs compared with subjects with low-back dysfunction. Spine 1991; 16:325–330.
76. O'Sullivan PB. The efficacy of specific stabilizing exercise in the management of chronic low back pain with radiological diagnosis of lumbar segmental instability. PhD thesis, Curtin University of Technology, Western Australia, 1997.
52. Hodges PW, Richardson CA. Contraction of the abdominal muscles associated with movement of the lower limb. Phys Ther 1997; 77:132–142.
77. Paris S. Physical signs of instability. Spine 1985; 10:277–278.
53. Olerud S, Sjostrom L, Karlstrom G, et al. Spontaneous effect of increased stability of the lower lumbar spine in cases of severe chronic back pain. The answer of an external transpeduncular fixation text. Clin Orthop 1986; 203:67–74. 54. Panjabi MM, Lydon C, Vasavada A, et al. On the understanding of clinical instability. Spine 1994; 19:2643–2650. 55. Hazlett JW, Kinnard P. Lumbar apophyseal process excisions and spinal instability. Spine 1982; 7:171–176. 56. White AA, Panjabi MM. Clinical biomechanics of the spine, 2nd edn. Philadelphia: JB Lippincott; 1990. 57. Boden SD, Weisel SW, Laws E Jr, et al. The aging spine. Philadelphia: WB Saunders; 1991. 58. Boden SD, Frymoyer JW. Segmental instability: overview and classification. In: Frymoyer JW, ed. The adult spine: principles and practices, 2nd edn. New York: Raven Press; 1997. 59. Mirkovic S, Garfin SR. ‘Segmental’ instability as related to the degenerative disc. Semin Spine Surg 1991; 3:119–123. 60. Vo P, MacMillan M. The aging spine: clinical instability. South Med J 1994; 1987: S26–S35.
78. O'Sullivan PB. Lumbar segmental instability: clinical presentation and specific stabilizing exercise management. Manual Therapy 2000; 5:2–12. 79. O'Sullivan P, Twomey L, Allison G. Dynamic stabilization of the lumbar spine. Crit Rev Phys Rehab Med 1997; 9:315–330. 80. O'Sullivan P, Twomey L, Allison G. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiological diagnosis of spondylolysis and spondylolisthesis. Spine 1997; 15:2959–2967. 81. Richardson C, Jull G. Muscle control – pain control. What exercise would you prescribe? Manual Therapy 1995; 1:2–10. 82. O'Sullivan P, Twomey L, Allison G, et al. Specific stabilizing exercise in the treatment of chronic low back pain with clinical and radiological diagnosis of lumbar segmental instability. Third Interdisciplinary World Congress on Low Back Pain and Pelvic Pain, Vienna, Austria, 1998. 83. Shumway-Cook A, Woollacott M. Motor control – theory and practical applications. Baltimore: Williams & Wilkins; 1995. 84. O'Sullivan P, Twomey L, Allison G. Altered abdominal muscle recruitment in back patients following specific exercise intervention. J Orthop Sports Phys Ther 1998; 27:1–11.
1119
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iii: Instability
CHAPTER
102
Fusion Surgery Andrew Perry, Choll W. Kim and Steven R. Garfin
INTRODUCTION Fusion has been used for decades to manage a variety of spinal disorders. However, the incidence of spinal fusion surgery varies among countries and among regions within a country. During its infancy, spinal fusion surgery typically involved extensive muscle dissection, copious amounts of autogenous bone graft, bracing, and prolonged bed rest. The introduction of spinal instrumentation provided an opportunity to increase the rate of successful fusion, decrease the recovery period, minimize the cardiopulmonary and musculoskeletal deconditioning resulting from immobility, and allow surgeons to perform more complex spinal reconstructive surgeries. Initial fusion techniques were primarily posterior, but anterior column support was subsequently developed to minimize the failure rates associated with the use of posterior instrumentation. Anterior column fusion can be achieved with bone graft material secured within the disc space from either an anterior or posterior approach. Anterior column fusion has inherent advantages as it occurs along the weight bearing portion of the lumbar spine (80% anterior versus 20% posterior), has superior blood supply, and a superior ability to maintain sagittal alignment. At present, controversy still exists concerning the indications for spinal fusion, the type of procedure to perform, the choice of graft material, and the use of instrumentation. The most widely accepted indication for spinal fusion is instability, which may arise from trauma, tumor, infection, and degenerative disease. Instability may also arise iatrogenically from the surgical treatment of these aforementioned conditions. With the improvement of surgical techniques, along with the development and marketing of spinal instrumentation, there has been a noticeable trend toward the increasing use of spinal instrumentation.1 In general, the goal of surgical fusion is to produce a solid arthrodesis through the segments considered unstable. This is true regardless of the surgical technique used or the approach taken. The end result should be a well-aligned and stable spine that is capable of protecting the neural elements and alleviating pain.
INDICATIONS The indications for surgical fusion of the lumbar spine for instability are not clearly defined. Much of the rationale for fusion has been based on expert opinion and retrospective studies. Over the last decade, there has been increased interest in designing objective studies that use validated outcome measures of success. This is evidenced by the development of a plethora of outcome assessments tools. This differing opinion of surgeons concerning the precise indications for fusion has led to a wide discrepancy in the rate of fusion surgery in various parts of the world. Although there is agreement regarding instability as an indication for fusion, there is a lack of consensus on the precise definition of
instability. The clinical manifestations and assessment of instability of the spinal column are discussed in detail in the previous chapter. In general, the various methods for determining spinal instability are either for trauma, degenerative conditions, or tumor. The White and Panjabi ‘checklist approach’ and the Denis classification system remain the most recognized methods of determining instability in the setting of trauma.2 Recently, Gertzbein and coworkers have developed a detailed description of thoracolumbar fracture patterns that can also be helpful in determining instability.3,4 Gaines and coworkers utilize a ‘load-sharing’ system to determine the stability of the anterior column in the setting of burst fractures.5,6 This system is useful for determining when anterior reconstruction is necessary or when short-segment posterior instrumented fusion may be helpful to treat burst fractures. Whichever system is used, instability due to trauma must take into consideration the mechanism of injury, the degree of deformity, and the location of injured ligamentous and bony structures. Instability due to degenerative conditions is typically described as relative instability. Relative instability due to these conditions is thought to lead to abnormal intervertebral motion which in turn causes pain. It is uncertain whether excessive sagittal translation on flexion–extension radiographs along with high-intensity zones seen on T2-weighted magnetic resonance imaging (MRI) images, endplate irregularities, and Modic changes on MRI, result from relative instability. This type of instability can insidiously develop into spondylolisthesis, degenerative scoliosis, and/or painful disc degeneration. As well, the surgical treatment of these disorders can lead to iatrogenic instability. For destructive lesions, particularly tumors, the degree of vertebral body and/or pedicle involvement and the degree of deformity enter into in the determination of instability.5–7 At present, no method of systematically assessing impending instability exists for infectious processes. Other forms of instability, such as inflammatory, congenital, degenerative, and postoperative instability, are not well assessed with grading systems such as those described by Gaines and coworkers. Once instability is determined, surgical treatment generally requires adequate correction of deformity, reconstruction of bony defects, and fusion of the affected segments. The choice of method by which surgical correction is performed remains a challenging task.
TECHNIQUE The method by which surgery is performed depends on the cause and character of the instability. The available methods of treatment include anterior, posterior, or combined anterior–posterior surgical approaches. General guidelines have some degree of support either in the literature or by consensus (Fig. 102.1). 1121
Part 3: Specific Disorders Trauma
Tumor
Infection
Iatrogenic
Instability
Anterior-only lesion
Anterior column intact
Posterior-only lesion
Anterior column deficient
No canal compromise Normal bone
Osteoporotic bone
Posterior instrumented fusion
Anterior and posterior lesion
Anterior column intact
Posterior fusion
Pseudoarthrosis risk
Anterior column deficient
Posterior fusion
Posterior fusion + anterior interbody fusion
Significant deformity
Canal compromise
Anterior strut + posterior fusion
Anterior strut + posterior fusion Anterior strut + anterior instrumentation
Anterior strut + anterior instrumentation
Fig. 102.1 Algorithm for the surgical treatment of instability via fusion. Instability due to trauma, tumor, infection, as well as iatrogenic induced instability are discussed. Instability due to degenerative conditions such as spondylolisthesis, scoliosis, and disc disease are discussed in previous chapters.
Anterior lesions When instability is due to a lesion that is primarily anterior, surgical stabilization can be performed from an anterior approach. This anterior approach generally involves discectomy, perhaps corpectomy, structural grafting and anterior instrumentation. Anterior surgery is indicated if there is canal compromise due to the anterior lesion, if anterior column stability is deficient, or a previous posterior procedure has failed to stabilize the segment(s). The load-sharing classification system of Gaines and coworkers is one method of determining the integrity of the anterior column.5,6 The load-sharing classification system describes the integrity of the anterior column in the setting of trauma. However, this concept can be applied to other lesions of the anterior column. If there is no significant osteoporosis or deformity that requires correction, then anterior strut grafting with anterior instrumentation will provide sufficient stabilization (Fig. 102.2). However, certain conditions warrant posterior surgery, either together with the anterior surgery or posterior surgery alone. Posterior surgery alone can be used to treat lesions that are otherwise anterior if the anterior column has sufficient stability and there is no need for decompression. In some cases, such as when there is no neurologic deficit, posterior-only surgery can be used to indi1122
rectly reduce retropulsed fragments of bone. Posterior surgery may be further entertained if there are anteriorly exposure risks, such as previous abdominal surgery or severe obesity. Posterior fusion may also be necessary if there is significant osteoporosis. In the setting of osteoporosis, anterior surgery alone may be inadequate in achieving spinal stability (Fig. 102.3).
Posterior lesions When instability stems from a posterior lesion, posterior surgery via instrumented fusion is usually the best option (Fig. 102.4). Unfortunately, instability due to a purely posterior lesion is relatively uncommon. The most common such lesion is the Chance fracture involving a flexion–distraction injury. If there is severe osteoporosis, additional levels may be added to the construct. The length of posterior instrumentation can be extended as necessary to achieve stability without much added difficulty. If necessary, pedicle screws can also be reinforced with bone cement to achieve better fixation in osteoporotic bone. Interbody fusion can be performed posteriorly via transforaminal lumbar interbody fusion (TLIF) or posterior lumbar interbody fusion (PLIF) to improve fusion rates, especially in long fusions or in fusions to the sacrum.
Section 5: Biomechanical Disorders of the Lumbar Spine
C
A A
B
C
Fig. 102.2 L2 pathologic fracture due to metastatic adenocarcinoma. (A) T2-weighted sagittal MRI showing pathologic fracture of L2. (B) T1 axial image with contrast showing canal stenosis. (C) Postoperative radiographs after L2 corpectomy, anterior cage strut, and anterior instrumentation.
Combined anterior–posterior lesions In combined lesions of both the anterior and posterior columns, the surgical approach is dictated by several factors. The first issue is whether anterior surgery is necessary. Anterior surgery is nec-
B
D
Fig. 102.4 Metastatic erosion of posterior elements. (A) Lateral radiograph showing posterior element bony destruction. (B) Sagittal MRI showing canal compromise. (C) Axial CT image showing bone erosion of facets, right pedicles, lamina, and spinous process. (D) Lateral radiograph after resection, decompression, and posterior instrumented fusion.
essary if there is isolated or predominantly anterior canal compromise requiring decompression or if anterior column stability is compromised. Anterior surgery is usually in the form of strut or structural grafting. If there is good bone stock and no significant deformity, then anterior instrumentation may be all that is needed. If there is no canal compromise and the anterior column is stable, posterior instrumented fusion alone is sufficient to obtain stability. If there is osteoporosis, the levels of posterior fusion can be increased for improved fixation. When the anterior column is deficient and it is combined with severe deformity, osteoporosis, or infection, then anterior strut graft fusion combined with posterior instrumentation is necessary (Fig. 102.5).
FACTORS AFFECTING THE OUTCOME OF FUSION SURGERY A
B
Fig. 102.3 Construct failure after anterior-only treatment of a osteoporotic burst fracture. (A) Lateral radiograph immediately after vertebral corpectomy, allograft strut fusion, and anterior instrumentation. Black dotted lines highlight endplates above and below the fusion site. (B) Lateral radiograph 4 weeks after surgery. Black dotted lines highlighting the endplates show interim kyphosis above the construct. The vertebral body above has collapsed into the superior screws.
Achieving arthrodesis and determining when this occurs are still problems that confront the spine surgeon. In general, spinal fusion is a nonphysiological operation that attempts to achieve bone formation in a site where this does not normally occur. In addition to the local and systemic factors that influence typical fracture healing, mechanical factors also influence the healing process during spinal fusion. These mechanical factors include the distance to be bridged by the fusion mass, the magnitude and planes of motion, and the structural properties of the graft. For convenience, the factors that affect successful spinal arthrodesis can be grouped into local, biologic, and surgical factors. 1123
Part 3: Specific Disorders
the graft material is to be placed also plays an important role in determining the outcome of fusion. Decortication allows vascularization of the fusion bed. In addition, it is important to remove avascular tissue such as scar tissue during surgery since a fusion bed with excessive scar tissue is less likely to achieve successful fusion.
Biologic factors Nutrition C
A
Malnutrition is associated with reduced cognitive function, poor wound healing, impaired muscle function, decreased bone mass, immune dysfunction, anemia, delayed recovery from surgery, and ultimately increased morbidity and mortality.7 Nutritional deficiencies can be confirmed using various studies such as total white blood cell count, serum albumin and total protein, transferrin levels, nitrogen balance, and anthropometric measurements.
Hormones
B
D
Fig. 102.5 Spinal osteomyelitis and epidural abscess. (A) Contrastenhanced sagittal MRI showing osteomyelitis of L5 and S1 along with anterior and posterior epidural abscesses. (B) Contrast-enhanced axial MRI showing circumferential infection. There are also abscesses in the right paraspinal muscles. (C) Lateral radiograph after surgical treatment. Treatment involved L5 and partial S1 laminectomies and right L5–S1 facetectomy. (D) Second stage partial L5–S1 corpectomies with cage strut graft were followed by third stage posterior instrumented fusion.
Smoking
The physiologic and biomechanical forces acting on the healing of anterior interbody and posterolateral fusions are quite different. Anterior interbody fusions are revascularized through the vertebral bodies themselves and the graft material used in the interspace is under compressive loading. Bone healing is favored under conditions of axial loading and stability. As such, interbody fusion tends to occur more readily than posterolateral spinal fusion. In a posterolateral fusion, revascularization is primarily derived from the bony surface of the transverse process and surrounding muscle tissue. In this region, there are few or no compressive forces acting on the graft material. Consequently, the posterolateral spinal fusion environment generally does not tolerate the use of purely osteoconductive materials as stand-alone substitutes. At this site, osteoinductive substitutes are more likely to be successful as extenders or enhancers for spinal fusion. In the anterior spine, purely osteoconductive substitutes may be suitable when they are rigidly immobilized.
The pathophysiological effects of smoking are multidimensional and include arteriolar vasoconstriction, cellular hypoxia, demineralization of bone, and delayed revascularization. Cigarette smoking also inhibits osteoblastic activity resulting in decreased rate of successful unions, with slowed bone healing and prolonged treatment.12,13 It appears that cigarette smoke has a greater impact upon cancellous bone than cortical bone, and causes decreased bone healing around implants. The constituents of cigarette smoke, and not only nicotine, seem to be more important.14,15 Complication rates after surgery and the rate of nonunion in smokers has been shown to be consistently higher than in nonsmokers.16,17 In a recent prospective clinical study designed to determine the effects of smoking on the healing of tibial deformities, half of the smokers and only one-fifth of nonsmokers developed complications.18 Smokers required an average of 16 days more treatment. Delayed healing and pseudoarthroses were more common in smokers than nonsmokers. The risk ratio for smokers to develop complications as compared to nonsmokers was 2.5.18 For spinal fusion, an increased rate of pseudoarthrosis has been observed following posterolateral lumbar spine grafting or anterior cervical interbody fusion in smokers.19 Smoking had a significant negative impact on healing and clinical recovery after these procedures.
Fusion site
Drugs
Arthrodesis depends on ingress of osteoprogenitor and inflammatory cells from the fusion bed and from the surviving bone cells located in the bone graft. Bone healing is greatly affected by the local blood supply along with the availability of osteoprogenitor cells. The fusion bed vascular supply is a source of supportive nutrients, a vehicle for endocrine signals, and a pathway for the recruitment of osteoprogenitor and inflammatory cells. The preparation of the bony surfaces where
Many drugs such as methotrexate and Adriamycin can inhibit bone formation if administered in the early postoperative period. Nonsteroidal antiinflammatory drugs (NSAIDs) act by inhibiting action of cyclooxygenase (COX) enzymes and decreasing production of prostaglandins (PGs). This can result in diminished bone formation, healing, and remodeling. These effects seem to be greater with nonselective COX inhibitors, such as ketorolac, than with selective COX-2 inhibitors
Local factors Location
1124
Thyroid hormones have a direct stimulatory effect on cartilage growth and maturation, and promote bone healing.8 These hormones are required for the synthesis of somatomedins by the liver.9 Growth hormone promotes bone healing by increasing calcium absorption from the intestine, and promoting bone formation and mineralization.8 Androgens and estrogens are considered important for skeletal development and preventing age-related bone loss. Estrogens may increase bone mineralization through their effect on increasing serum parathyroid hormone (PTH).10 Excess corticosteroids can negatively affect bone healing by decreasing synthesis of the major components of the bone matrix. These steroids have also been shown to inhibit the differentiation of osteoblasts from mesenchymal cells.11
Section 5: Biomechanical Disorders of the Lumbar Spine
at therapeutic levels.20 Ketorolac also decreases bone mineralization and endochondral ossification in a dose-dependent manner.21 Other NSAIDs, such as diclofenac, can also significantly delay fracture healing.22 The timing of administration of NSAIDs also appears important. In animal studies, the earlier indometacin was resumed postoperatively, the greater was its negative effect on intertransverse process arthrodesis.23 Recombinant bone morphogenetic protein-2 (BMP-2), however, seems to show promise for combating the inhibitory effect of ketorolac on bone formation during spinal arthrodesis.24 It has been observed that longer duration of administration of selective COX inhibitors decreases the rate of successful fusion.25 In a recent study, however, it was found that the perioperative (shortterm) administration of celecoxib had no apparent effect on the rate of nonunuion at 1 year following surgery. In this study, patients had elective decompressive lumbar laminectomy and instrumented spinal fusion. In addition, the use of the selective COX-2-specific NSAID resulted in a significant reduction in postoperative pain and opioid use following surgery.26 As such, short-term administration of selective COX inhibitors for perioperative pain, unlike long-term use, appears to be a reasonable therapeutic option. AGE The effects of aging on spinal fusion are multifactorial. With the elderly there is often a decrease in food intake secondary to reduction in appetite. If prolonged, this can lead to a decline in nutritional status. Bone healing, including spinal fusion is affected by the nutritional status of the individual.7 Common medical conditions, such as renal and cardiac insufficiency, may exist in the elderly and can affect bone healing. The clinical observation that incisional wounds also heal less well in the aged may be secondary to these coexisting pathologies.27 The number of osteogenic stem cells may be more deficient in the elderly than in younger individuals. In animal studies, the numbers of osteoprogenitor cells present in the bone marrow from aged rats were 65% lower than the amount found in young adults. These cells were also 10 times less likely to differentiate in vitro and to form bone in vivo.28 However, bone-stimulating growth factors may have a role in increasing the bone-forming capacity of aged bone in the future.29,30 During aging, bone mass loss, structural continuity, and strength gradually diminish. Osteoporotic bone is weak and difficult to stabilize with spinal instrumentation. Although gradual bone loss starts at 30 years of age, an accelerated rate of loss occurs after menopause in women. Men also experience bone loss, but in a more insidious fashion. The rate of successful fusion in elderly individuals of both sexes with osteoporotic bone tends to be lower.31
Surgical factors Approaches The surgical approach can affect the outcome of lumbar fusion. Fritzell et al. studied the outcomes of fusion surgery using three different, well-accepted techniques of lumbar fusion.32 In their randomized prospective study, they show that posterolateral fusion without instrumentation achieves arthrodesis in 72% of patients. With the addition of posterior instrumentation, the fusion rate increased to 87%. For patients treated with combined posterior instrumented fusion and interbody fusion (i.e. circumferential fusion) the fusion rate was 91%. Overall, the fusion rates for grafts used in circumferential, posterior interbody, anterior interbody, and posterolateral fusions methods are about 91% , 89%, 86%, and 85%, respectively.1
Instrumentation It is well established that spinal instrumentation increases the likelihood of successful fusion. Fischgrund et al. demonstrated that the fusion rate with instrumentation was twice that obtained without
instrumentation for patients with degenerative spondylolisthesis.33 Zdeblick observed statistically greater fusion rates in patients with rigid instrumentation than those without. In his study, the fusion success with semirigid instrumentation (plate/screw system) was not different from that obtained without instrumentation.34 In contrast, Thomsen et al. found that the fusion rates were not significantly different between instrumented (supplementary pedicle screw fixation) and noninstrumented groups for patients undergoing posterolateral lumbar spinal fusion.35 Perhaps the best perspective regarding the impact of instrumentation on the fusion rate was revealed in a meta-analysis of the outcomes of lumbar fusion surgeries that were reported in the literature from 1970 to 2000.1 In this study, the average instrumented fusion rate (89%) was significantly higher than the noninstrumented fusion rate (84%). The fusion rates with semirigid instrumentation and rigid instrumentation were not significantly different (91% and 88%, respectively). In addition, both semi-rigid and rigid stabilization resulted in significantly higher fusion rates than no instrumentation (p=0.019, p=0.022, respectively).
Number of levels fused The number of levels fused is an important factor that can dramatically affect the outcome of spinal fusion. In a retrospective study, the length of hospital stay, operative time, amount of intraoperative blood loss, and transfusion requirements were closely related to the number of levels fused for patients having revision posterior lumbar spine decompression, fusion, and segmental instrumentation. The arthrodesis rate also decreased with number of levels fused.36 Exact figures of fusion rates with number of levels fused vary according to the disease or condition in question, the approach, and whether the fusion was augmented with bone growth enhancers. In a meta-analysis study which assessed data obtained from fusions done over the past 20 years, the mean fusion rates were 89% in one-level operations, 69% in two-level operations, and 71% when three or more levels were fused.1
Graft source The choice of graft material can influence the outcome of a spinal fusion. During spinal arthrodesis, graft material may not only provide structural support but may also possess osteogenic, osteoconductive, and/or osteoinductive properties. The osteogenic potential of a graft is determined by the number of viable cells that can form bone or differentiate into bone-forming cells. Osteogenic grafts are usually obtained from fresh autologous bone and bone marrow cells. Osteoconduction is the physical property of a graft that allows vascular ingrowth and infiltration of osteogenic precursor cells. Osteoconductive grafts act as nonviable scaffolds that support the healing response. Examples are autologous and allograft bone, bone matrix, collagen, and calcium phosphate ceramics. Osteoinduction is the ability of a substance or factor to stimulate an undetermined osteoprogenitor cell to differentiate into an osteogenic precursor. The most common source of graft material is autogenous bone from the iliac crest. This is still considered the gold standard. However, due to the morbidity of autograft harvesting along with its limited supply, allograft bone and synthetic bone substitutes are being used with increasing frequency. Autograft cancellous bone has all three ideal transplant properties: osteogenicity, osteoconductivity, and osteoinductivity. It possesses a large trabecular surface area for new bone formation and contains viable bone cells. Cortical autologous bone grafts have less capacity for new bone formation but are ideal when structural support is needed. Allograft bone can be procured in greater quantities than autografts. Allografts are incorporated more slowly and to a lesser 1125
Part 3: Specific Disorders
degree than autografts. Fresh-frozen grafts are stronger, more immunogenic, and more completely incorporated than freezedried grafts. In most studies, fusion using autograft bone leads to higher fusion rates than fusion, using allograft or synthetic bone substitutes alone. In a selected comparison, uninstrumented interbody fusion using autograft was compared with uninstrumented interbody fusion using autograft/allograft mixtures. The fusion rates were 88% and 82%, respectively, and were not statistically different.37 If used anteriorly, allografts are well suited for reconstructive procedures and have good fusion rates, especially if combined with posterior fusions. When used with BMP-2, the effectiveness of an allograft can be increased. In one study, patients undergoing anterior lumbar fusion surgery with structural threaded cortical allograft bone dowels showed higher rates of fusion, improved neurologic status, and lower back and leg pain when compared with the autologous control group.38 Considering the possible complications associated with harvesting iliac crest bone, the use of allogenic bone appears justified.39,40 Xenografts have been used in orthopedic surgery and have included cow horn and bovine bone. Due to the immune response evoked by the host to these materials, xenografts are not commonly used in spine surgery.
Graft morphology The size of a structural bone graft, its positioning, and elasticity should be considered when used for lumbar fusions. A larger graft with low stiffness should be favored from a mechanical point of view. Stiff bone grafts increase stresses on adjacent endplates.41 Placement of a bone graft in a more anterior location can better resist flexion moments and decreases the tensile forces acting on the posterior ligaments. Bone grafts placed at a posterior site are better in resisting torsional moments and decreasing contact force of the facet joint in the fused segment.42 The degree to which these aforementioned observations may influence the long-term clinical outcome of spinal fusion is unclear.
Bone morphogenic proteins The osteoinductive potentials of bone morphogenic proteins have been well described. Recombinant human BMP-2 has been approved by the FDA for single-level interbody fusions of the lumbar spine. In the first prospective, multicenter study involving 279 patients with degenerative lumbar disc, the fusion rate at 24 months was higher for the BMP-treated group compared with those who received autogenous iliac-crest bone graft (94.5% versus 88.7%).43 Clinical trials have shown that rhBMP-2-filled fusion cages can eliminate the need for harvesting iliac crest graft.44,45 The benefits of BMPs in other applications of spinal fusion are currently under study.
Interbody cages Intervertebral cages or spacers were developed to prevent the collapse and pseudoarthrosis seen with bone-only interbody fusions. Initially, the early types consisted of vertically placed titanium mesh cylinders and rectangular carbon fiber cages. Later, this was followed by the development of stand-alone threaded Bagby and Kuslich (BAK) intervertebral cages. Threaded intervertebral cages usually stabilize a segment through distraction and tensioning of the annular and ligamentous structures. By partially reaming the endplates, one may expose cancellous bone for arthrodesis, increasing the likelihood for successful fusion.46 Anteriorly placed threaded cages significantly stabilize the motion segment in all directions except extension. With posteriorly placed cages, there is less stability as a result of the facetectomy required for placement of the device. Interbody cages may 1126
be implanted via a variety of surgical approaches to the disc space, with or without supplemental posterior fixation. For single-level degenerative disc disease, anteriorly placed intervertebral threaded cages have shown a high degree of clinical success.47 Both patient selection and technical expertise seem equally important in determining patient outcome.47 Patients with multilevel disease, normal (tall) looking disc on radiographs, or with osteoporotic bone, have a higher incidence of complication and failure. Posteriorly or transforaminally placed cages which are supplemented by pedicle screws seem successful for the treatment of spondylolisthesis.47 For the management of pure discogenic pain without collapse, multilevel disc disease, or disc degeneration in elderly patients, the use of cages is less certain.47
Electrical stimulation During the last 20 years, electrical stimulation has shown promise for improving the success rate of spinal fusion. The maximum benefit, in terms of an increased successful fusion rate, is estimated to be approximately 10%. At present, the types of electrical stimulation used as adjuncts to spinal fusion includes direct current electrical stimulation (DCES), pulsed electromagnetic fields (PEMF), combined magnetic fields (CMF), and capacitive coupling. These devises are usually implanted close to the fusion mass intraoperatively or worn externally. Internal devices utilize DCES. Their mechanism of action is thought to involve the attraction of charged proteins, growth factors, and bone-forming cells to the fusion site. They may also alter the function of voltage-gated channels with activation of cyclic AMP and triggering of a second messenger cascade. Other proposed mechanisms include Faradic reactions at the cathode–bone graft interface with formation of OH and H2O2. This reduces the local oxygen tension (PO2) and slightly increases the pH. The end result of both the electric field effects and the Faradic products is a stimulation of calcium uptake.48–50 Increased pH stimulates osteoblastic bone formation and mineralization but inhibits osteoclastic bone resorption. The end result is an increased rate of new bone formation.51 In contrast to DCES, PEMF devices generate an electromagnetic field across the spinal fusion area and are worn externally, usually 3–8 hours per day for 3–6 months. As these braces can be removed by patients, noncompliance can potentially hinder treatment.52 Successful arthrodesis can also be obtained with shorter application times. In a prospective study by Linovitz and coworkers, successful outcomes for one-level or two-level fusions (between L3 and S1) without instrumentation, either with autograft alone or in combination with allograft, were obtained when the combined magnetic field device was worn for 30 minutes per day for 9 months.53 Such devices with shorter wearing times may have better patient acceptance. The mechanism of action of PEMF is not well understood, but is thought to involve alterations in cell membrane potentials and parahormone receptors of bone cells. An increase in calcium influx into bone cells, promotion of calcification, and vascularization also occurs with PEMF. PEMF may also be capable of altering the production of cytokines, and increasing the expression of bone morphogenic protein (BMP)-2 and BMP-4 mRNA by cells. In ovariectomized rats, PEMF stimulation can decrease local production of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6) and inhibit osteoclastogenesis.54 A possible effect on prostaglandin E2 (PGE2) levels is also suggested.55 PEMF seems to enhance cellular differentiation and does increase the number of bone-forming cells. This stimulatory effect is greatest during the early stages of bone healing.56 However, there may be some place for PEMF stimulation in the later stages of treatment in cases of nonunion. For example, in
Section 5: Biomechanical Disorders of the Lumbar Spine
patients with symptomatic pseudoarthrosis after lumbar spinal fusion, pulsed electromagnetic field stimulation has been shown to be an effective nonoperative salvage approach to achieving fusion.57 In one study, 67% of patients who were treated with a pulsed electromagnetic field device worn consistently 2 hours a day for at least 90 days achieved fusion. Treatment was equally effective for posterolateral fusions (66%) as with interbody fusions (69%).57 Since 1985 when the first report of the clinical efficacy of PEMF on spinal fusion was published, numerous studies have demonstrated the benefits of electrical stimulation for improving the success rate of spinal fusion surgery.58,59 Not all modes of electrical stimulation are equally effective in promoting successful spinal arthrodesis. Clinical data reveal superiority of DCES to PEMF, particularly when used to enhance posterior spinal fusions. Capacitive coupling seems superior to PEMF, and perhaps DCES as an adjunct to posterior spinal fusion.60
Demineralized bone matrix Demineralized bone matrix (DBM) is prepared by decalcification of cortical bone. It is less immunogenic than allograft bone graft. The active components consists of several glycoproteins including BMPs. Preclinical investigations on the use of DBM in the spine have shown promising results. However, clinical studies on the effects on DBM on spinal fusion are lacking. In one study, titanium mesh cages and coralline hydroxyapatite combined with DBM were effective for anterior interbody fusion of the lumbar spine when used as part of a rigidly instrumented circumferential fusion.61 DBM was also effective in reducing the amount of autologous bone graft required for successful lumbar spinal fusion.62 Further clinical studies are needed to clearly establish the usefulness of DBM in spinal fusion.
SUMMARY Spinal fusion for the treatment of lumbar instability remains a complex topic. Accurate determination of lumbar instability requires evaluation of multiple factors, including patient disease, cause/mechanism of injury, location of injury, and anticipated demands of the patient. The decision for surgery requires a careful appraisal of all of these factors if high success rates are to be achieved. Determining the method by which the surgery is performed, whether to use instrumentation, along with choosing the proper graft type and deciding upon the appropriateness of including adjunctive materials is equally complex. When these key decisions are correctly instituted, the ultimate goal of fusion – achieving spinal function by protecting the neural elements, restoring spinal alignment, and alleviating pain and disability associated with instability – will be achieved.
References 1. Bono CM, Lee CK. Critical analysis of trends in fusion for degenerative disc disease over the past 20 years: influence of technique on fusion rate and clinical outcome. Spine 2004; 29(4):455–463; discussion Z5.
7. Einhorn TA, Bonnarens F, Burstein AH. The contributions of dietary protein and minerals to the healing of experimental fractures. A biomechanical study. J Bone Joint Surg [Am] 1986; 68(9):1389–1395. 8. Udupa KN, Gupta LP. The effect of growth hormone and thyroxine in healing of fractures. Indian J Med Res 1965; 53(7):623–628. 9. Schalch DS, Heinrich UE, Draznin B, et al. Role of the liver in regulating somatomedin activity: hormonal effects on the synthesis and release of insulin-like growth factor and its carrier protein by the isolated perfused rat liver. Endocrinology 1979; 104(4):1143–1151. 10. Gallagher JC, Riggs BL, DeLuca HF. Effect of estrogen on calcium absorption and serum vitamin D metabolites in postmenopausal osteoporosis. J Clin Endocrinol Metab 1980; 51(6):1359–1364. 11. Pereira RM, Delany AM, Canalis E. Cortisol inhibits the differentiation and apoptosis of osteoblasts in culture. Bone 2001; 28(5):484–490. 12. Hoogendoorn JM, Simmermacher RK, Schellekens PP, et al. [Adverse effects of smoking on healing of bones and soft tissues]. Unfallchirurg 2002; 105(1):76–81. 13. Harvey EJ, Agel J, Selznick HS, et al. Deleterious effect of smoking on healing of open tibia-shaft fractures. Am J Orthop 2002; 31(9):518–521. 14. Cesar-Neto JB, Duarte PM, Sallum EA, et al. A comparative study on the effect of nicotine administration and cigarette smoke inhalation on bone healing around titanium implants. J Periodontol 2003; 74(10):1454–1459. 15. Nociti FH Jr, Cesar NJ, Carvalho MD, et al. Bone density around titanium implants may be influenced by intermittent cigarette smoke inhalation: a histometric study in rats. Int J Oral Maxillofac Implants 2002; 17(3):347–352. 16. Ishikawa SN, Murphy GA, Richardson EG. The effect of cigarette smoking on hindfoot fusions. Foot Ankle Int 2002; 23(11):996–998. 17. Adams CI, Keating JF, Court-Brown CM. Cigarette smoking and open tibial fractures. Injury 2001; 32(1):61–65. 18. Toksvig-Larsen S. Cigarette smoking delays bone healing: a prospective study of 200 patients operated on by the hemicallotasis technique. Acta Orthop Scand 2004; 75(3):347–351. 19. Hilibrand AS, Fye MA, Emery SE, et al. Impact of smoking on the outcome of anterior cervical arthrodesis with interbody or strut-grafting. J Bone Joint Surg [Am] 2001; 83A(5):668–673. 20. Gerstenfeld LC, Thiede M, Seibert K, et al. Differential inhibition of fracture healing by non-selective and cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs. J Orthop Res 2003; 21(4):670–675. 21. Ho ML, Chang JK, Wang GJ. Effects of ketorolac on bone repair: A radiographic study in modeled demineralized bone matrix grafted rabbits. Pharmacology 1998; 57(3):148–159. 22. Beck A, Krischak G, Sorg T, et al. Influence of diclofenac (group of nonsteroidal anti-inflammatory drugs) on fracture healing. Arch Orthop Trauma Surg 2003; 123(7):327–332. 23. Riew KD, Long J, Rhee J, et al. Time-dependent inhibitory effects of indomethacin on spinal fusion. J Bone Joint Surg [Am] 2003; 85A(4):632–634. 24. Martin GJ Jr, Boden SD, Titus L. Recombinant human bone morphogenetic protein2 overcomes the inhibitory effect of ketorolac, a nonsteroidal anti-inflammatory drug (NSAID), on posterolateral lumbar intertransverse process spinal fusion. Spine 1999; 24(21):2188–2193; discussion 2193–2194. 25. Gerstenfeld LC, Einhorn TA. COX inhibitors and their effects on bone healing. Expert Opin Drug Saf 2004; 3(2):131–136. 26. Reuben SS, Ekman EF. The effect of cyclooxygenase-2 inhibition on analgesia and spinal fusion. J Bone Joint Surg [Am] 2005; 87A(3):536–542. 27. Viidik A, Mosekilde L, Quirinia A. [Research on aging: biological perspectives]. Ugeskr Laeger 1992; 154(42):2884–2889. 28. Quarto R, Thomas D, Liang CT. Bone progenitor cell deficits and the age-associated decline in bone repair capacity. Calcif Tissue Int 1995; 56(2):123–129.
2. White AA, Panjabi M. Clinical biomechanics of the spine. Philadelphia: Lippincott; 1990.
29. Blumenfeld I, Srouji S, Lanir Y, et al. Enhancement of bone defect healing in old rats by TGF-beta and IGF-1. Exp Gerontol 2002; 37(4):553–565.
3. Gertzbein SD, Seligman J, Holtby R, et al. Centrode patterns and segmental instability in degenerative disc disease. Spine 1985; 10(3):257–261.
30. Sumner DR, Turner TM, Cohen M, et al. Aging does not lessen the effectiveness of TGFbeta2-enhanced bone regeneration. J Bone Miner Res 2003; 18(4):730–736.
4. Gertzbein SD, Seligman J, Holtby R, et al. Centrode characteristics of the lumbar spine as a function of segmental instability. Clin Orthop 1986; 208:48–51.
31. Tunturi T, Kataja M, Keski-Nisula L, et al. Posterior fusion of the lumbosacral spine. Evaluation of the operative results and the factors influencing them. Acta Orthop Scand 1979; 50(4):415–425.
5. McCormack T, Karaikovic E, Gaines RW. The load sharing classification of spine fractures. Spine 1994; 19(15):1741–1744. 6. Parker JW, Lane JR, Karaikovic EE, Gaines RW. Successful short-segment instrumentation and fusion for thoracolumbar spine fractures: a consecutive 4½-year series. Spine 2000; 25(9):1157–1170.
32. Fritzell P, Hagg O, Wessberg P, et al. 2001 Volvo Award Winner in clinical studies: Lumbar fusion versus nonsurgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine 2001; 26(23):2521–2532; discussion 2532–2534.
1127
Part 3: Specific Disorders 33. Fischgrund JS, Mackay M, Herkowitz HN, et al. 1997 Volvo Award winner in clinical studies. Degenerative lumbar spondylolisthesis with spinal stenosis: a prospective, randomized study comparing decompressive laminectomy and arthrodesis with and without spinal instrumentation. Spine 1997; 22(24):2807–2812.
47. Zdeblick TA, Phillips FM. Interbody cage devices. Spine 2003; 28(15 Suppl): S2–S7.
34. Zdeblick TA. A prospective, randomized study of lumbar fusion. Preliminary results. Spine 1993; 18(8):983–991.
49. Brighton CT, Friedenberg ZB, Black J, et al. Electrically induced osteogenesis: relationship between charge, current density, and the amount of bone formed: introduction of a new cathode concept. Clin Orthop 1981; 161:122–132.
35. Thomsen K, Christensen FB, Eiskjaer SP, et al. 1997 Volvo Award winner in clinical studies. The effect of pedicle screw instrumentation on functional outcome and fusion rates in posterolateral lumbar spinal fusion: a prospective, randomized clinical study. Spine 1997; 22(24):2813–2822. 36. Zheng F, Cammisa FP Jr, Sandhu HS, et al. Factors predicting hospital stay, operative time, blood loss, and transfusion in patients undergoing revision posterior lumbar spine decompression, fusion, and segmental instrumentation. Spine 2002; 27(8):818–824. 37. Urist MR, Dawson E. Intertransverse process fusion with the aid of chemosterilized autolyzed antigen-extracted allogeneic (AAA) bone. Clin Orthop 1981; 154: 97–113. 38. Burkus JK, Transfeldt EE, Kitchel SH, et al. Clinical and radiographic outcomes of anterior lumbar interbody fusion using recombinant human bone morphogenetic protein-2. Spine 2002; 27(21):2396–2408. 39. Ehrler DM, Vaccaro AR. The use of allograft bone in lumbar spine surgery. Clin Orthop 2000; 371:38–45. 40. Wimmer C, Krismer M, Gluch H, et al. Autogenic versus allogenic bone grafts in anterior lumbar interbody fusion. Clin Orthop 1999; 360:122–126. 41. Cheng CK, Chen CS, Liu CL. Biomechanical analysis of the lumbar spine with anterior interbody fusion on the different locations of the bone grafts. Biomed Mater Eng 2002; 12(4):367–674.
50. Brighton CT, Friedenberg ZB. Electrical stimulation and oxygen tension. Ann NY Acad Sci 1974; 238:314–320. 51. Oishi M, Onesti ST. Electrical bone graft stimulation for spinal fusion: a review. Neurosurgery 2000; 47(5):1041–1055; discussion 1055–1056. 52. Mooney ML, Carlson P, Szentpetery S, et al. A prospective study of the clinical utility of lymphocyte monitoring in the cardiac transplant recipient. Transplantation 1990; 50(6):951–954. 53. Linovitz RJ, Pathria M, Bernhardt M, et al. Combined magnetic fields accelerate and increase spinal fusion: a double-blind, randomized, placebo controlled study. Spine 2002; 27(13):1383–1389; discussion 1389. 54. Chang K, Hong-Shong Chang W, Yu YH, et al. Pulsed electromagnetic field stimulation of bone marrow cells derived from ovariectomized rats affects osteoclast formation and local factor production. Bioelectromagnetics 2004; 25(2):134–141. 55. Chang K, Chang WH. Pulsed electromagnetic fields prevent osteoporosis in an ovariectomized female rat model: a prostaglandin E2-associated process. Bioelectromagnetics 2003; 24(3):189–198. 56. Diniz P, Shomura K, Soejima K, et al. Effects of pulsed electromagnetic field (PEMF) stimulation on bone tissue-like formation are dependent on the maturation stages of the osteoblasts. Bioelectromagnetics 2002; 23(5):398–405.
42. Zander T, Rohlmann A, Klockner C, et al. Effect of bone graft characteristics on the mechanical behavior of the lumbar spine. J Biomech 2002; 35(4):491–497.
57. Simmons JW Jr, Mooney V, Thacker I. Pseudoarthrosis after lumbar spine fusion: nonoperative salvage with pulsed electromagnetic fields. Am J Orthop 2004; 33(1):27–30.
43. Burkus JK, Gornet MF, Dickman CA, et al. Anterior lumbar interbody fusion using rhBMP-2 with tapered interbody cages. J Spinal Disord Tech 2002; 15(5): 337–349.
58. Mooney V. A randomized double-blind prospective study of the efficacy of pulsed electromagnetic fields for interbody lumbar fusions. Spine 1990; 15(7):708–712.
44. Haid RW Jr, Branch CL Jr, Alexander JT, et al. Posterior lumbar interbody fusion using recombinant human bone morphogenetic protein type 2 with cylindrical interbody cages. Spine J 2004; 4(5):527–538; discussion 538–539. 45. Mummaneni PV, Pan J, Haid RW, et al. Contribution of recombinant human bone morphogenetic protein-2 to the rapid creation of interbody fusion when used in transforaminal lumbar interbody fusion: a preliminary report. Invited submission from the Joint Section Meeting on Disorders of the Spine and Peripheral Nerves, March 2004. J Neurosurg Spine 2004; 1(1):19–23. 46. Sasso RC, Kitchel SH, Dawson EG. A prospective, randomized controlled clinical trial of anterior lumbar interbody fusion using a titanium cylindrical threaded fusion device. Spine 2004; 29(2):113–122; discussion 121–122.
1128
48. Baranowski TJ Jr, Black J, Brighton CT, Friedenberg ZB. Electrical osteogenesis by low direct current. J Orthop Res 1983; 1(2):120–128.
59. Mooney V, McDermott KL, Song J. Effects of smoking and maturation on longterm maintenance of lumbar spinal fusion success. J Spinal Disord 1999; 12(5): 380–385. 60. Kahanovitz N. Electrical stimulation of spinal fusion: a scientific and clinical update. Spine J 2002; 2(2):145–150. 61. Thalgott JS, Giuffre JM, Klezl Z, et al. Anterior lumbar interbody fusion with titanium mesh cages, coralline hydroxyapatite, and demineralized bone matrix as part of a circumferential fusion. Spine J 2002; 2(1):63–69. 62. Girardi FP, Cammisa FP Jr. The effect of bone graft extenders to enhance the performance of iliac crest bone grafts in instrumented lumbar spine fusion. Orthopedics 2003; 26(5 Suppl):s545–s548.
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar
CHAPTER
103
Failed Back Surgery Jerome Schofferman
Failed back surgery syndrome (FBSS) is a non-specific term that implies the final outcome of surgery did not meet the expectations of both the patient and the surgeon that were established before surgery.1 It should not and does not suggest that the patient failed to get total pain relief or did not return to full function. The surgeon’s expectations for the results in a specific surgical patient should be based on published medical evidence, the type of structural problem, the number and types of prior surgeries the patient has had, the psychological health of the patient, and the skills and experience of the surgeon. For example, expectations after discectomy in a patient with radiculopathy due to a single disc herniation, no prior back surgeries, good psychological health, ability to work, and with private health insurance should be high. Conversely, expectations for a multilevel salvage surgery for pseudoarthrosis and spinal stenosis despite two prior surgeries in an injured worker who also has two painful discs will be far lower. It is the responsibility of the surgeon to convey realistic expectations to the patient. The patient must also have realistic expectations, and must rely to some degree on the surgeon’s input. In patients with chronic pain, an improvement in 0–10 numerical rating scale (NRS) or visual analog score (VAS) of 1.8 units is equivalent to a change in pain of about 30%, which will be considered by most patients as a ‘somewhat satisfactory result.’2 An improvement in NRS or VAS of 3 units or more is equivalent to a change in pain of about 50%, which most patients will consider an ‘extremely satisfactory result.’ Interventional spine specialists have many options to treat patients with FBSS. It appears that the best outcomes occur when the treatment is matched to the patient’s particular pathology. The pain specialist must understand the nature of FBSS to accurately diagnose the structural disorder and thereby render the most specific treatment.
In 1981, Burton et al. reported an analysis of several hundred patients with FBSS.3 They found that about 58% had lateral canal stenosis (foraminal stenosis), 7–14% had central canal stenosis, 12–16% had recurrent (or residual) disc herniations, 6–16% had arachnoiditis, and 6–8% had epidural fibrosis. Other less common causes in their series included neuropathic pain, chronic mechanical pain, painful segment (disc) above a fusion, pseudoarthrosis, foreign body, and surgery performed at the wrong level. They were unable to establish a definitive diagnosis in less than 5% of their patients despite the fact that their study was done early in the computed tomography (CT) scan era and well before magnetic resonance imaging (MRI) scans. They did use discography. There have been major advances in diagnostic testing since the Burton paper. In 2002, Waguespack et al.4 and Slipman et al.5 each independently reported their results of evaluations of patients with FBSS (Table 103.1). Waguespack et al. performed a retrospective review of 187 patients who presented to a tertiary care spine center. They established a predominant diagnosis in 95% of their patients. Slipman et al. performed a similar study in which they reached a diagnosis in more than 90% of patients as well. In these two recent studies the most common structural causes of FBSS were foraminal stenosis (25–29%), painful disc (20–22%), pseudoarthrosis (14%), neuropathic pain (10%), recurrent disc herniation (7–12%), instability, facet pain (3%), and sacroiliac joint pain (2%), among some others (Table 103.2). Several authors have presented their unquantified impressions and experiences regarding the causes of FBSS. Fritsch et al.6 reviewed 136 patients who had revision surgeries after clinical failure of an initial laminectomy and discectomy, and found a high prevalence of recurrent disc herniations and instability. Kostuik7 reviewed the potential causes of failure of decompression, but provided no quantitative data.
STRUCTURAL ETIOLOGIES OF FAILED BACK SURGERY In this section, the author will briefly review the most common structural causes of FBSS based on published data.3–5 These are lateral canal stenosis (foraminal stenosis), recurrent or residual disc herniation, one or more painful discs, neuropathic pain, facet joint pain, and sacroiliac joint pain. It is interesting to note that the causes of FBSS and the causes of chronic low back pain (LBP) are quite similar. By combining a careful history, physical examination, and specialized testing, the structural cause of FBSS can be delineated in more than 90% of patients.4,5 In some patients, the structural cause of the FBSS was present prior to surgery and was not adequately addressed (e.g. painful disc, lateral canal stenosis, facet or sacroiliac joint [SIJ] pain). In others the problem occurred after surgery, either as a direct consequence of the surgery (e.g. SIJ pain after fusion, pseudoarthrosis, etc.) or as new and unrelated pathology.
Table 103.1: Most Common Causes of Failed Back Surgery in Three Reported Studies Diagnosis
Burton (1981) (3)
Waguespack (2002) (4)
Slipman (2002) (5)
Lateral stenosis
58%
29%
25%
HNP
12–16
7
12
Painful discs
N/A
20
22
Neuropathic pain
6–16
10
10
Total %
76–90%
66
69
All numbers are % HNP = herniated disc
1129
Part 3: Specific Disorders
Table 103.2: Differential Diagnosis of Common Causes of FBS by Symptoms, Signs, Radiology, and Injections Diagnosis
Symptoms
Signs
Radiology
Injections
Lateral canal stenosis
Leg pain > LBP Relief with sitting
Loss of lumbar lordosis
MRI: foraminal stenosis
Relief with transforaminal epidural
Painful disc
LBP; ? worse with sitting
Restricted flexion in standing MRI: degenerated disc(s)
No sustained relief
Neuropathic pain
Leg pain Burning Dysesthesia
Hypoalgesia Allodynia
No alternative diagnosis
No sustained relief
Facet joint pain
Left or right LBP
?Facet tenderness
Not specific
Medial branch block relieves pain
Recurrent HNP
Vary with location. Leg pain > LBP
Variable
HNP on MRI
Epidural may provide temporary relief
SI joint pain
Gluteal pain with referral to leg and groin
May have + provocative testing
Not helpful
SI joint injection relieves pain
LBP = Low Back Pain HNP = disc herniation +/– May be helpful DDD = degenerative disc disease SIJ = sacroiliac joint CT = computed axial tomography MRI = magnetic resonance imaging
In this chapter, the author has used functional definitions which are a composite of those proposed by the North American Spine Society8 and the International Association for the Study of Pain,9 modified by personal clinical experiences.
Lateral canal stenosis Lateral canal stenosis was found in 25–29% of FBSS patients in the more recent studies, but was twice that 25 years ago.3–5 The lower prevalence in later studies may be due to better preoperative recognition of the condition and more meticulous decompression. Lateral canal stenosis usually presents with pain that is predominantly in one leg or buttock region (see Table 103.2). The leg and gluteal pains are usually worsened by standing and walking and improved by sitting. MRI or CT scan must show narrowing of the nerve root lateral canal at the index level or an adjacent segment. Lateral canal stenosis may be characterized as ‘up-down stenosis’ due to loss of disc space height or ‘front-back stenosis’ due to facet hypertrophy and osteophyte formation. There is usually at least temporary relief of leg pain after transforaminal epidural blockade of the suspected nerve root.10,11 It is important to differentiate lateral canal stenosis from neuropathic pain and from mixed pain syndrome because the treatments are different. Stenosis is treated with flexion-biased body mechanics, transforaminal corticosteroid injections, and/or surgical decompression. Neuropathic pain is better treated with medications (anticonvulsants, tricyclic antidepressants, opioids) or spinal cord stimulation. Mixed pain syndromes may require both types of treatment.
Painful discs One or more painful discs were the cause of FBSS in about 21% of patients.3–5 Painful discs may occur at the index level, adjacent level, and occasionally at the level of a prior posterolateral fusion.11 In the Waguespack study,4 painful discs were responsible for FBSS in 31 (17%) patients who did not have prior fusion and 5 (3%) additional 1130
patients had a painful disc at a level contained within a prior solid fusion. It is clear that discs have the substrate to become painful. They are richly innervated with nerve endings that have the potential to be nociceptive.12,13 In the normal disc, nerve endings are limited to the outer third of the anulus. In the degenerated disc, there is proliferation of nerve endings, and in 40% of severely degenerated discs, the nociceptors have grown inward to reach the nucleus.12 Discogenic pain presents with LBP with or without referred buttock or leg pain (see Table 103.2). Painful discs usually appear desiccated and may be narrowed on MRI scan. Schwarzer et al. found no symptoms or signs that are specific for discogenic pain,14 but there may be a few clues.15 Discogenic pain is usually worsened by sitting and by transition from sitting to standing.15 Pain may be improved somewhat by standing or walking. During examination, pain is usually worsened by flexion during standing, which is also decreased due to pain. There may be tenderness over the spinous processes, but not over the facet joints. Discography is often used to confirm the clinical impression of discogenic pain. It is controversial in chronic LBP and even more so in patients with FBSS.16–18 In every instance, discography must be interpreted very carefully and only in conjunction with the history, examination, imaging studies, and psychological status of the patient.19 The value of discography at a disc that has had prior surgery is not totally clear, but may be useful when carefully interpreted.13 When the diagnosis of discogenic pain is suggested by history and examination, MRI shows only the one bad disc, and other potential causes of LBP are excluded, there is probably no need to perform discography. If discography is used in the setting of FBSS and probable discogenic pain, it is probably most useful to prove other discs are not involved. Discogenic pain is difficult to treat. Intensive 4–6 week interdisciplinary functional rehabilitation programs may be helpful. Medications, particularly opioids and tricyclic antidepressants, can reduce pain. Surgery can be useful for patients with severe pain. There are no published reports to justify minimally invasive intradiscal procedures in the setting of FBSS.
Section 5: Biomechanical Disorders of the Lumbar Spine
Disc herniation Recurrent or residual disc herniation occurred 7–12% of patients with FBSS.3–5 In the presence of epidural or perineural fibrosis and a nerve root that is surrounded by scar, a disc herniation may cause more leg pain than expected if there were no fibrosis. The symptoms of recurrent or residual disc herniation (HNP) depend on its location (see Table 103.2). A midline HNP presents as discogenic LBP. Posterolateral HNP will usually present with a predominance of leg pain in the distribution of a single dermatome, but if the disc is sufficiently damaged internally, there can be a significant amount of low back pain as well. There will be MRI evidence of the disc herniation. Treatment depends upon the pain. Leg pain can be treated by physical therapy, epidural corticosteroids, and other medications. If these fail, discectomy may help. However, LBP rarely responds to discectomy alone, and requires fusion surgery.
Neuropathic pain Neuropathic pain was the predominant problem in 9% of the author’s patients.4 Burton et al. observed neuropathic pain in less than 5% of their patients.3 It is not clear if there has been an increase in nerve root injury or an increased recognition of neuropathic pain. Nerve roots can be damaged during surgery, but damage is more likely due to prolonged unrelieved compression by spinal stenosis or disc herniation. The incidence of arachnoiditis may be decreasing, perhaps because oil-based myelography is no longer performed. Neuropathic pain implies that pain arises from nerve injury or dysfunction. There is a predominance of leg pain, which is usually present in one or two adjacent dermatomes. In classic presentations, the pain is described as burning or dysesthetic, but in neuropathic disorders and FBSS this may not be the case (see Table 103.2). Pain is usually constant but it may be worsened by activity because the damaged nerve is sensitized and minor biomechanical changes may worsen pain. In pure neuropathic pain, there is no evidence of nerve root compression on MRI or CT scan. Neuropathic pain must be distinguished from neurogenic pain, a phrase the author uses to imply that a nerve is being compressed or irritated by structural pathology such as residual foraminal stenosis or HNP described above. Again there are also patients with mixed pain syndromes who have compressive lesions on scan (stenosis, HNP) but who also have irreversible nerve damage from the longstanding compression.
Facet syndrome Pain that arises from the facet joint is responsible for the pain in about 3% of patients with FBSS and 15–30% of patients with chronic LBP.5,20 The facet joint is susceptible to inflammation, damage during surgery, or the mechanical stresses of fusion at a segment below. There are no data that specifically address the symptoms or signs of facet syndrome in patients with FBSS, but several papers have addressed the problem in chronic LBP.15,20–24 Schwartzer et al. felt there were no symptoms typical for facet joint pain, although the presence of midline LBP was not likely in facet syndrome.21 Others feel there are symptoms that are suggestive (see Table 103.2).22,24 Pain is more likely to be experienced just lateral to the midline and is frequently referred to one or both gluteal regions. Pain is better when the patient is lying supine.22 It is less severe sitting than standing or walking, and pain is not worsened during transition from sitting to standing.25 Examination findings are not specific, but there may be tenderness with palpation directly over the joints but not over the spinous processes, and more pain with extension than flexion while standing. As discussed elsewhere in this text, the diagnosis of facet joint pain is made by intra-articular infusion of local anesthetic or block-
ade of the medial branches of the primary dorsal rami that serve the putative painful joint. The preferred treatment is radiofrequency neurotomy (RFN), which is successful in a high percentage of wellselected patients.26–29 RFN generally relieves pain for 9–12 months and then it can be repeated, and Schofferman and Kine have shown that repeated RFN remains effective.29
Sacroiliac joint pain The sacroiliac joint (SIJ) is responsible for the pain in about 2% of patients with FBSS5 and 15–30% of patients with chronic LBP.30 There are many potential inciting events that may lead to the development of SI joint pain. The joint may become painful after acute or cumulative trauma, but the cause is often not known.31 The SIJ is vulnerable to the mechanical stresses of fusion to the sacrum32 and can be injured during bone graft harvesting for fusion.33 There are no data that have specifically examined the symptoms or signs of sacroiliac joint syndrome in patients with prior surgery, but several papers have addressed the problem in the chronic LBP population.15,30 Schwartzer et al. reported that there were no typical symptoms for SIJ pain.30 Others believe there is a pattern with pain experienced in the gluteal regions distal to the posterior superior iliac crest just off the midline. The patient may point directly over the joint when asked to show where the pain is the worst. Pain is worsened during transition from sitting to standing15 and appears to increase with single leg weight bearing. Examination findings are not specific, but there may be tenderness with palpation directly over the SIJ, and when there are three or four other signs, diagnosis is probable.34 As discussed elsewhere, the diagnosis is made by local anesthetic blockade of the SIJ under fluoroscopic guidance. Treatment is multidimensional. It requires strengthening the gluteal muscles, teaching the patient to self-mobilize the joint, and increasing the flexibility of the gluteal and hamstring muscles. This may be supplemented by spinal manipulative therapy. Therapeutic SIJ injection utilizing glucocorticoid can be helpful.35 Very rarely SIJ fusion is necessary.
Epidural fibrosis Epidural fibrosis occurs after most, if not all, posterior lumbar decompressive surgeries. Scar forms in patients with good and bad outcomes alike. There is controversy whether fibrosis can cause pain after lumbar surgery in the absence of other structural disorders or neuropathic pain. Some interventional spine specialists believe fibrosis alone can cause pain, but most spine specialists do not. Although it has been established that fibrosis occurs, that fibrosis may alter neural sensitivity, and that fibrosis may make re-operation more difficult, there is no good evidence that perineural fibrosis itself can cause pain or that treatment directed toward only the fibrosis can improve the pain. There is no proven method to determine whether fibrosis might be a cause of pain, only a somewhat circuitous theoretical construct.36 Finally, even if fibrosis were pathological rather than an innocuous bystander, it would be more likely to cause leg pain rather than LBP. The author believes fibrosis can make other structural problems worse. It traps nerve roots, which are then more susceptible to compression from small disc herniations, foraminal stenosis, or other more primary structural problems.
TECHNICAL FAILURE AND COMPLICATIONS Pseudoarthrosis Pseudoarthrosis is a failure of fusion (nonunion), and was the predominant problem in 15% of the patients of Waguespack et al. with 1131
Part 3: Specific Disorders
FBSS who had prior attempted fusion.4 They did not collect sufficient data to establish the number of patients who had undergone an attempted fusion, and therefore it is not possible to know the clinical relevance of this percentage. Some patients with nonunions have pain, but others do not. Therefore, one cannot assume that the nonunion is the cause of the pain. The author likes this summary poem: If there’s pain and a pseudoarthrosis, It’s usually a disc or spinal stenosis; But think of facet joints or SI – they’re closest. Nerves can be damaged and lose their gliosis And pains can be worsened by depression or neurosis. Rarely an infection can spread by osmosis, But a careful work-up will lead to gnosis. A definitive diagnosis of pseudoarthrosis requires surgical exploration, but radiological findings can be suggestive. Plain radiographs are not reliable to prove fusion is solid, but certainly can be suggestive of nonunion.37 Standing films with sagittal views taken in flexion and extension are useful if there is motion. CT scans that include reformatted curved coronal as well as sagittal and axial images are the most useful test.38 They can visualize the anterior column when there has been attempted interbody fusion (bone or cages), and curved coronal sections extended out to the spinous processes are the best test to visualize the integrity of posterolateral fusions. After interbody fusion with threaded metal cages, a nonunion may be particularly difficult to diagnose.39 There may be no lucency on plain X-rays, no motion with standing X-rays in flexion versus extension, and no lucency on CT scan, and still pseudoarthrosis may be present. The author has noted that patients who are not significantly improved by 6 months after fusion with threaded interbody cages often benefit from a salvage posterolateral fusion.
Instability Some patients who undergo surgery develop instability due to the amount of posterior elements that have been removed. This is referred to as postlaminectomy instability, and implies there is more than 4 mm translation on standing flexion versus extension X-rays or neutral X-ray versus supine cross-table lateral view. The author frequently sees patients who had very slight spondylolisthesis before surgery for disc herniation or spinal stenosis in whom no fusion was done because the slip was so slight. Then some months after surgery, the back pain worsens, and plain X-rays reveal progression of the slip.
Pedicle screw or cage misplacement New leg pain immediately after a lumbar fusion using pedicle screws may be caused by a screw breaching the medial cortex of the pedicle. CT scan may show this, but surgical exploration may be needed. Threaded interbody fusion cages have been used much more frequently recently. At times, one or both cages may either be placed too far laterally and compress or displace a nerve root. This too should be seen on CT scan, particularly on the curved coronal images.
PSYCHOLOGICAL FACTORS IN FAILED BACK SURGERY Psychological disorders are often invoked when evaluating patients with FBSS. Pure psychogenic pain (pain disorder, psychological type) is rare in patients with FBSS.40 It is more likely that if psychological factors are present they make pain worse rather than cause it. More importantly, if psychological problems are present in a patient with FBSS, it is most likely they were present before surgery and did not 1132
just appear afterwards. Psychological issues should always be considered and diagnosed preoperatively. In the author’s opinion, it is not appropriate for a surgeon to invoke a psychological cause of FBSS and, in a sense, ‘blame the patient’ after the surgery. A pain syndrome due to psychological disorders might be defined as LBP with or without leg pain, not attributable to any pathological structural cause or far out of proportion to pain usually produced by that structural abnormality present in the presence of a diagnosable psychological illness by DSM-IV criteria that has been shown to cause or exacerbate pain. Most patients with refractory LBP have symptoms of at least one major psychiatric disorder, most commonly depression, substance abuse disorder, or anxiety disorder. The question is whether a psychological disorder is in fact the primary cause of the FBSS. There are psychological conditions that probably do not impact on surgical outcome as long as one treats them psychiatrically first – major depression, mania, severe anxiety disorder, or active addiction. There are other people who are never going to be good surgical patients, such as borderline personality disorder, antisocial personality, and the addict or alcoholic who is not in recovery.
RADIOLOGICAL EVALUATION OF FAILED BACK SURGERY Herzog discussed the requirements for imaging patients with FBSS and much of the following section is a summary of his presentation.1,38,41 Radiological examination usually includes X-rays and either MRI or CT scan. Standard radiographs with standing flexion and extension lateral views are used to assess alignment, extent of disc space narrowing, instability, and, when fusion has been attempted, perhaps pseudoarthrosis.36 MRI is the optimal examination for most FBSS patients unless the issue is pseudoarthrosis, in which case CT with multiplanar reformations (CT/MPR) is much better.1,37 MRI should be done using a high-field strength (1.0–1.5 Tesla) scanner for maximum information. With MRI, it is necessary that the study be done to visualize left and right extraforaminal zones so as to avoid missing foraminal or extraforaminal pathology. At least one axial sequence should have contiguous stacked images. Angled T2-weighted sections from T12– L1 to L5–S1 through the disc spaces are done to evaluate the crosssectional area of the thecal sac, to evaluate the central canal, and to define the exact relationship of the structural changes to all the neural elements. A coronal sequence is useful to see foraminal and extraforaminal herniations.1,40 In evaluating patients who had surgery for disc herniation, contrast-enhanced MRI became the standard, but with newer equipment and imaging sequences, nonenhanced MRI is frequently adequate if the radiologist monitors the study and administers contrast only if the routine sequences are not adequate. MRI is excellent for spinal stenosis, and can detect hypertrophy of facet joints and ligamenta flava, synovial cysts, or prominence of epidural fat. It will show if decompression was adequate to decompress the nerve root. Arachnoiditis can easily be detected with MRI. In patients with spinal instrumentation using titanium alloys, there should be no significant distortion with a high field-strength MRI if the sequences are optimized for the presence of metal using fast spin echo T2-weighted sequences without fat saturation to reduce artifacts. Short tau inversion recovery (STIR) sequences should be employed if fat saturation is needed. The central canal and neural foramina can be adequately assessed even with the presence of pedicle screws. The artifacts generated by ferromagnetic metal alloys may completely obscure the spinal anatomy and this is one of the few instances that CT myelography may be needed.
Section 5: Biomechanical Disorders of the Lumbar Spine
High-resolution CT/MPR is the optimal study when the integrity of a fusion or the placement of pedicle screws needs assessment.38 It is helpful in a CT examination to perform stacked 1 mm thick sections through the segment containing the cage to detect early loosening or the presence of bridging bone. CT/MPR should employ stacked 2–3 mm sections with sagittal and coronal reformations, and cover several segments proximal and distal to the surgery. There are only rare indications for nuclear imaging studies (e.g. infection, missed malignancy), myelography (pseudomeningocele), or CT myelography in the setting of FBSS.
ROLE OF THE HISTORY The history is the most important part of the evaluation of FBSS. It establishes the differential diagnosis, suggests the emphasis for the physical examination, and provides guidelines for selecting the most appropriate imaging studies and diagnostic injections. With a careful history, the examiner may also be able to discern why things went wrong.
Establishing the structural diagnosis Most often, the history can narrow the potential structural causes of FBSS to a few likely probabilities. The most important elements to this aspect of the history include the location and quality of the pain, and the effects of mechanical changes.
Location of pain It is useful to divide patients into those with predominance of LBP versus those with a predominance of leg pain. In general terms, if LBP is greater than leg pain, the most common causes of FBSS are discogenic pain at the level of prior surgery or adjacent levels, facet pain, SIJ pain, and instability; and if fusion was attempted, pseudoarthrosis. If leg pain predominates, the common causes include foraminal stenosis, recurrent or residual disc herniation, and neuropathic pain. There may be more than one diagnosis present. Pain generally flows down hill. LBP in the midline is often discogenic. Pain 1 or 2 cm off the either side of the midline is often of facet origin. Facet pain is not usually limited to the midline.21 Pain in the gluteal regions is not specific, as the buttocks is a watershed area for pain emanating from most structures in the lumbar spine. Pain directly over the sacral sulcus may indicate the SIJ is the source of the pain. SIJ pain often is referred to the ipsilateral groin. Leg pain is not specific unless it follows a dermatomal pattern.
Quality of pain The words the patient uses to describe the pain is occasionally helpful. Burning pain is often of neurologic origin, particularly neuropathic. Exquisite tenderness to light touch (allodynia) also suggests neuropathic pain. A complaint of numbness in the absence of sensory loss on examination suggests referred pain. Paresthesias and dysesthesia suggest neurologic problems but does not help separate neurogenic from neuropathic pain.
Response to mechanical changes (see Table 103.2) SITTING: LBP or leg pain that increases with sitting and with flexion while standing is more likely due to one or more painful discs or instability (spondylolisthesis). Leg pain that improves with sitting is usually due to spinal stenosis. TRANSITION FROM SITTING TO STANDING: LBP that worsens during the transition from sit to stand suggests disc pain or SIJ and speaks against facet joint pain.15
STANDING: LBP that increases with standing suggests posterior element pathology such as facet joint pain. Leg pain that increases with standing or walking suggests spinal stenosis.
Establishing what went wrong In the author’s experience, it is more likely that FBSS is due to an error in surgical judgment or an incomplete evaluation rather than a technical failure or complication of the surgery itself. Establishing the reason for the failure by the history does simplify the evaluation and may markedly change the treatment. If a patient had the wrong surgery for the preoperative condition, then recommending the patient undergo the correct surgery may be the most conservative and definitive treatment. The history is the key to this aspect of the evaluation of FBSS. It is necessary to compare the current symptoms with the preoperative symptoms and to see if the surgery performed was appropriate for the preoperative symptoms. If the pain before and after surgery share essentially the same location, quality, and response to mechanical maneuvers, this suggests an error in selecting the correct surgery (e.g. laminectomy for LBP) or incomplete surgery (e.g. inadequate foraminal decompression, one-level fusion when there were two degenerated discs). On the other hand, if the symptoms have changed, this suggests new pathology, either as a result of the surgery (e.g. SIJ pain distal to a fusion, disc space collapse after extensive discectomy) or progression of the underlying disease (new disc degeneration).
Mismatch of the surgery performed to the surgery required The judgment error may be straightforward, but requires a baseline understanding of the appropriate surgery for the underlying symptoms and pathology. This underlying premise is that there are surgeries for leg pain (decompression, discectomy) and surgeries for LBP (fusion). If the patient had predominantly LBP but had a leg pain operation, it would not be expected to work. For example, when patients with LBP, even if they have a disc herniation or spinal stenosis, undergo simple depression it is not likely to succeed. In other words, they had a ‘leg pain operation’ when the major problem was low back pain.
Technically inadequate surgery If the surgery was appropriate for the symptoms and pathology, determine whether the technical goals of surgery were accomplished. This usually requires good-quality imaging studies. As described above, residual foraminal stenosis remains a very common problem. There may be three reasons for this: (1) the surgeon did not recognize the degree of the lateral canal stenosis before surgery, often because there is also central stenosis, (2) the surgeon thinks the canal was adequately decompressed, but it remains stenotic in the mid or exit zones, and (3) the surgeon may feel that in order to adequately decompress there would be instability and did not want to fuse.
Technical failure Technical failures that are common include pseudoarthrosis and misplaced instrumentation. At times pseudoarthrosis is obvious, but at other times it is a challenge. There are two common types of fusion: interbody and posterolateral. Interbody fusion can be done via an anterior or posterior approach and can be done with bone or cages. Posterolateral fusions are done with or without instrumentation. Finally there may be combinations. It is reasonably straightforward to diagnose pseudoarthrosis when there is an interbody fusion with bone. It is very useful, but often 1133
Part 3: Specific Disorders
overlooked, to get a Furgeson (angled) view of the L5–S1 interspace to look for lucency. CT scan will often reveal the lucency if plain X-rays are not diagnostic. Posterolateral fusion without instrumentation will usually be seen on CT if there are adequate curved coronal sections taken out to the tips of the transverse processes. If there is instrumentation, nonunion may be difficult to see. Occasionally, oblique radiographs are helpful. The diagnosis of pseudoarthrosis in the presence of interbody fusion with cages presents a real challenge. Plain X-rays and even CT scan may not disclose the nonunion. If one of the author’s patients does well initially after interbody fusion with cages, but then deteriorates, the suspicion is of occult nonunion. However, occasionally the cages can subside into the vertebral bodies and this can be identified by comparing serial X-rays. If the patient is not better by 6 months after surgery, the author will look for other causes, but frequently find none. The author will then offer the patient a salvage posterolateral fusion with instrumentation, and has been gratified with the results (unpublished observation).
Complication If pedicle screws are misplaced medially through the cortex, there can be leg pain in a single dermatome that corresponds to the breach in the pedicle. CT often will suggest this. Complications such as infection usually occur early in the postoperative period but rarely can occur later.41,42
Incomplete evaluation Incomplete evaluation implies that the most obvious structural pathology was addressed surgically, but there may have been additional problems as well. However, a scenario often seen is that there were two or more abnormal discs before surgery but only one was fused. This is an error in judgment due to an incomplete evaluation. The surgeon must determine if any disc that looks abnormal on MRI before surgery is a cause of part or all of the patient’s pain. Some discs that look abnormal cause pain, but others do not. The surgeon can infer from the history if the patient is likely to have discogenic pain, but not which disc is responsible. Discography, although somewhat controversial, is a useful in making this decision when taken in context of the history, examination, and other tests. Discography nihilists can opine that it is not a useful test, but they offer no better alternative to determine whether a disc is a source of pain or not.
CONCLUSIONS Interventional pain specialists evaluate and treat many patients with FBSS. Treatments are most effective when they are matched to the specific cause of the pain. In order to efficiently evaluate the patient, it is very helpful to know and understand the causes of FBSS. In this chapter, the author reviewed the common causes of FBSS and provided the important elements of the history, examination, radiographic studies, and most briefly outlined the roles of injections. Armed with this information, the cause of FBSS should be uncovered in an overwhelming number of patients, and FBSS will no longer be a non-specific and pejorative mystery.
References
1134
3. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, et al. Causes of failure of surgery on the lumbar spine. Clin Orthop 1981; 157:191–199. 4. Waguespack A, Schofferman J, Slosar P, et al. Etiology of long-term failures of lumbar spine surgery. Pain Med 2002; 3:18–22. 5. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Med 2002; 3:200–214. 6. Fritsch EW, Heisel J, Rupp S. The failed back surgery syndrome. Reasons, intraoperative findings, and long-term results: a report of 182 operative treatments. Spine 1996; 21:626–633. 7. Kostuik JP. The surgical treatment of failures of laminectomy. Spine: state of the art reviews 1997; 11:509–538. 8. Fardon DF, Herzog RJ, Mink JH, et al. Contemporary concepts in spine Care. Nomenclature of lumbar disc disorders. North American Spine Society. May, 1995. 9. Merskey H, Bogduk N. Classification of chronic pain. 2nd edn. Seattle: IASP Press; 1994. 10. Slosar PJ, White AH, Wetzel FT. The use of selective nerve root blocks: diagnostic, therapeutic, or placebo? Spine 1998; 20:2253–2256. 11. van Akkerveeken P. The diagnostic value of nerve root sheath infiltration. Acta Orthop Scand 1993; 64:61–63. 12. Freemont A, Peacock T, Goupille P, et al. Nerve ingrowth into diseased intervertebral discs in chronic low back pain. Lancet 1997; 350:178–181. 13. Coppes M, Marani E, Thomeer R, et al. Innervation of ‘painful’ lumbar discs. Spine 1997; 22:2342–2350. 14. Schwarzer A, Aprill C, Derby R, et al. The prevalence and clinical features of internal disc disruption in patients with chronic low back pain. Spine 1995; 20: 1878–1883. 15. Young S, Aprill C, Laslett M. Correlation of clinical examination characteristics with three sources of chronic low back pain. Spine J 2003; 3:460–465 16. Walsh TR, Weinstein JN, Spratt KF, et al. Lumbar discography in normal subjects. J Bone Joint Surg 1990; 72A:1081–1088. 17. Derby R, Howard MW, Grant JM, et al. The ability of pressure-controlled discography to predict surgical and nonsurgical outcomes. Spine 1999; 24:364–372. 18. Wetzel FT, LaRocca H, Lowery GL, et al. The treatment of lumbar spinal pain syndromes diagnosed by discography. Lumbar arthrodesis. Spine 1994; 19:792–800. 19. Carragee EJ, Alamin TF. Discography: a review. Spine J 2001; 1:364–372. 20. Barrick W, Schofferman J, Reynolds J, et al. Anterior fusion improves discogenic pain at levels of posterolateral fusion. Spine 2000; 25:853–857. 21. Schwarzer A, Wang S, Bogduk N, et al. Prevalence and clinical features of lumbar zygapophyseal joint pain: A study in an Australian population with chronic low pack pain. Ann Rheum Dis 1995; 54:100–106 22. Schwarzer AC, Aprill CN, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137 23. Revel M, et al. Capacity of the clinical picture to characterize facet joint pain. Spine 1998; 23:1972–1977. 24. Jackson RP. The facet syndrome: myth or reality? Clin Orthop 1992; 279: 110–121. 25. Helbig T, Lee CK. The lumbar facet syndrome. Spine 1988; 13:61–64. 26. Dreyfuss P, Halbrook B, Pauza K, et al. Efficacy and validity of radiofrequency neurotomy for chronic lumbar zygapophyseal joint pain. Spine 2000; 25:1270–1277. 27. van Kleef M, Barendse GA, Kessels A, et al. Randomized trial of radiofrequency lumbar facet denervation for chronic low back pain. Spine 1999; 24:1937–1942. 28. Leclaire R, Fortin L, Lambert R, et al. Radiofrequency facet joint denervation in the treatment of low back pain. Spine 2001; 26:1411–1417. 29. Schofferman J, Kine G. The effectiveness of repeated radiofrequency neurotomy for lumbar facet pain. Spine 2004; 29:2471–2473. 30. Schwarzer A, Aprill C, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37. 31. Chou L, Slipman CW, Bhagia SM, et al. Inciting events initiating injection-proven sacroiliac joint syndrome. Pain Med 2004; 5:26–32.
1. Schofferman J, Reynolds J, Dreyfuss P, et al. Failed back surgery. Spine J 2003; 3:400–403.
32. Katz V, Schofferman J, Reynolds J. The sacroiliac joint: a potential cause of pain after lumbar fusion. J Spinal Disord Tech 2003; 16:96–99.
2. Farrar JT, Young JP, LaMoreaux L, et al. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain 2001; 94:149–158.
33. Ebraheim NA, Elgafy H, Semaan HB. Computed tomographic findings in patients with persistent sacroiliac pain after posterior iliac graft harvesting. Spine 2000; 25:2047–2051.
Section 5: Biomechanical Disorders of the Lumbar Spine 34. Slipman C, Sterenfeld E, Chou L, et al. The predictive value of provocative sacroiliac joint stress maneuvers in the diagnosis of sacroiliac joint syndrome. Arch Phys Med Rehab 1998; 79:288–292. 35. Slipman CW, Lipetz JS, Vresilovic EJ, et al. Fluoroscopically guided therapeutic sacroiliac joint injections for sacroiliac joint syndrome. Am J Phys Med Rehab 2001; 80(6):425–432. 36. Schofferman J. Failed back surgery. Response to letter to the editor. Spine J. In press. 37. McAfee P, Boden S, Brantigan J, et al. Symposium: a critical discrepancy – a criteria of successful arthrodesis following interbody spinal fusions. Spine 2001; 26: 320–324.
38. Herzog RJ, Marcotte PJ. Imaging corner. Assessment of spinal fusion. Critical evaluation of imaging techniques. Spine 1996; 21:1114–1118. 39. Heithoff K, Mullin W, Holte D, et al. The failure of radiographic detection of pseudoarthrosis in patients with titanium lumbar interbody fusion cages. Presented at the 14th annual meeting, North American Spine Society. Chicago, IL; 1999. 40. Polatin PB, Kinney RK, Gatchel RJ, et al. Psychiatric illness and chronic low-back pain. The mind and the spine – which goes first? Spine 1993; 18:66–71. 41. Herzog R. Radiological studies in failed back surgery. Presented at the 18th annual meeting, North American Spine Society. Montreal, Canada. October; 2002. 42. Schofferman L, Schofferman J, Zucherman J, et al. Occult infections as a cause of low-back pain and failed back surgery. Spine 1989; 14:417–419.
1135
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar
CHAPTER
104
Neural Scarring David W. Chow
INTRODUCTION Of the myriad causes of failed back surgery syndrome (FBSS), neural scarring has been reported to be the cause of failed back surgery syndrome in 6–24% of patients.1–7 In 1996, Ross et al., using a prospective, controlled, randomized, blinded, multicenter methodology, demonstrated a significant association between the gross amount of peridural scar and the occurrence of recurrent radicular pain; those with extensive epidural scarring were 3.2 times more likely to experience recurrent radicular pain than those with less scarring.7 The degree of postoperative scarring relates to the extent and magnitude of the surgery. It is undeniable that the presence of postoperative scar tissue is not solely due to the operative trauma, but is also generated as a reparative response to the herniated disc material as not all patients with scarring are symptomatic.8 Although epidural adhesions are most commonly present following spine surgery, leakage of disc material from a herniated nucleus pulposus or annular disc tear can cause an inflammatory response with fibrocyte deposition and resultant epidural adhesions in the absence of surgery.9,10 There are those who believe that neural scarring such as epidural and/or intraneural fibrosis do not ever cause symptoms. This school of thought is based upon the fact that neural scarring is a normal bodily response to injury and that all postoperative patients will have some degree of scarring, the majority of which are asymptomatic.8 However, just as there are symptomatic and asymptomatic disc protrusions, the same tenet holds true for epidural fibrosis and neural scarring. The fact that not all focal disc protrusions or epidural fibrosis, as demonstrated by magnetic resonance imaging (MRI), are clinically symptomatic does not prove that focal disc protrusions or epidural fibrosis are not pain generators and have no relationship to low back or lower limb pain preoperatively or postoperatively. Such a view is simplistic and is more a function of the lack of an effective clinical pathway in the diagnosis of symptomatic neural scarring. Historically, epidural fibrosis or arachnoiditis was an uncommon clinical entity prior to the introduction of lumbar spine surgery for the treatment of degenerative spine conditions.11 A large number of reports of epidural fibrosis found on repeat surgery led to the association of recurrent symptomatology with perineural scarring.11–13 This chapter will offer a diagnostic algorithmic approach to determine an accurate diagnosis of symptomatic neural scarring. A review of the clinical anatomy of the nerve root and its anatomic relationships is critical to understanding the basis and pathophysiology of symptomatic neural scarring.
Endoneurial sheath
Nerve axon
Perineurial sheath
Axon Finniculus
Finniculus
ANATOMY Sunderland14 described the connective tissue coverings of the nerve fiber. Each axon is surrounded by an endoneurial sheath in which multiple axons or nerve fibers form a funiculi. The endoneurial sheath resists elongation under tension. Each funiculi is invested by perineurial connective tissue. Multiple funiculi are surrounded by the epineurium which consists of alveolar connective tissue. The outer perinerium and epineurium provide some degree of protection from tensile and compressive forces (Fig. 104.1). The portions of the nerve
Epineurial sheath Nerve fiber
Fig. 104.1 Cross-section of nerve fiber and its connective tissue coverings. 1137
Part 3: Specific Disorders
roots which lack this outer sheath are more vulnerable to traction or compression. When there is nerve injury, fibrotic tissue may form perineurally/epidurally or intraneurally. It is important to understand the relationship between the nerve roots and the intervertebral foramen (IVF). Each intervertebral foramen is in the shape of an inverted pear that is bounded laterally by the pedicle, posteriorly by the articular facets and ligamentum flavum, and anteriorly by the intervertebral disc and vertebral bodies.15 The radicular complex of ganglia, nerve roots, spinal nerve, and surrounding sheath accounts for 20–35% of the cross-sectional area of the IVF (Fig. 104.2).15 The remainder of the IVF is occupied by loose areolar or adipose tissue, a radicular artery, and numerous venous channels that often encircle the nerve roots. The depth of the foramen varies from 4 to 9 mm.15 The lumbar nerve root complex is situated toward the upper pole of the foramen. At and beyond the ganglion, the dura loses its identity and forms the outer connective tissue sheath which represents the epineurium and perineurium of the ganglion, anterior nerve root, and the newly formed spinal nerve. The Hofmann ligaments, initially described in 1898, are fine filamentous bands of connective tissue that connect the ventral surface of the dural sac and the exiting nerve roots to the posterior longitudinal ligament and posterior vertebral periosteum (Fig. 104.3).16 The ventral ligamentous attachments within the spinal canal reduce the ability of a nerve root to be dorsally displaced by a disc herniation. The nerve root complex is mobile, but does not have unlimited motion. The lumbar
Fissure in annulus fibrosus
roots undergo an excursion of 0.5–5 mm, depending on the anatomic level.17 There is an average excursion of 3 mm for the intrathecal portion of the L5 nerve root, while for the S1 nerve root this value ranges between 4 and 5 mm.17 Movement is induced by straight leg raising in the lumbosacral roots, nerves, and plexus, and in the intrapelvic section of the sciatic nerve.17 Since the nerve root and its dural sheath are relatively fixed within the spinal canal and the radicular foramen, they cannot easily slip away from a disc protrusion. Fibrosis and adhesions may impair the gliding capacity of the lumbar nerve roots within the radicular canals and increase the vulnerability of the extrathecal intraspinal nerve root to compression. Consequently, the nerve root is stretched and compressed, resulting in edema, ischemia, and radicular symptoms. Postoperative scar tissue formation in the spine can occur within the dura (arachnoiditis) or outside the dura (epidural fibrosis).
ADHESIVE ARACHNOIDITIS Arachnoiditis is inflammation of the pia–arachnoid membrane that covers the spinal cord, cauda equina, nerve roots, or a combination. The extent of scarring varies from mild membrane thickening to severe scarring that can obliterate the subarachnoid space and obstruct cerebrospinal fluid (CSF) flow. The etiology of arachnoiditis is unclear, but typically the intrathecal contents are exposed to an inciting agent such as lumbar spine surgery, intraoperative dural tears, postoperative
Nucleus pulposus Phospholipase A2 Prostaglandins Nitric oxide Metalloproteinases ? Unidentified inflammatory agents
Neovascularization of disc
Inflammatory cell infiltrate (chemical signal for revascularization)
Intervertebral disc Sinuvertebral nerve Nociceptors in annulus fibrosus Pedicle
Ventral rumus
Chemicals may reach nociceptors via fissure to lower threshold for firing. Pain caused by mechanical forces superimposed on chemically activated nociceptors
Intervertebral foramen
Transverse process
Dorsal root ganglion Dorsal ramus
Superior articular process
Spinal nerve root Radicular veins Hoffman’s ligaments
Nerve root–dura interface may be involved by inflammatory process. Chemical factors and compression both contribute to lumbar pain Radicular arteries
Fig. 104.2 Nerve root complex with dorsal root ganglion, nerve root, and its arterial and venous blood supply. 1138
Section 5: Biomechanical Disorders of the Lumbar Spine
Intervertebral disc Posterior longitudinal ligament Sinuvertebral nerve Pedicle Ventral ramus
Dorsal root ganglion Dorsal ramus Spinal nerve root Hoffman’s ligaments and their attachments to the ventral dural sac Thecal sac
infections, intrathecal pharmacologic medications, and injection of oil-based contrast agents. Arachnoiditis is more common in patients who undergo extensive or bilateral surgical procedures, and repeat surgeries.
Pathophysiology Adhesive arachnoiditis causes proliferation of soft tissue leading to filmy adhesions and later to a dense fibrotic matrix. Inflammatory changes are seen microscopically. It is thought that the severity and duration of arachnoiditis is directly correlated to the degree of inflammation and tissue remodeling associated with wound healing. A vascular etiology has also been proposed whereby venous obstruction and dilatation leads to endothelial damage, fibrin deposition, intravascular thromboses, and ultimately fibrosis of the neural elements.18 In the subarachnoid space, the nutritional support of nerve roots is dependent upon its limited vascular supply and the circulation of CSF. The tenuous blood supply and nutrition to the nerve roots within the subarachnoid space can easily be interrupted by neural scarring with subsequent ischemia possible. The exact mechanism of adhesive arachnoiditis is still unknown.
BATTERED NERVE ROOT SYNDROME This entity is frequently discussed in relation to epidural fibrosis as a cause of severe radicular pain postoperatively after a benign immediate postoperative course with incomplete resolution of radicular limb pain. It involves frank nerve root injury, as opposed to reversible nerve root swelling, with worsening of limb pain and associated sensory or motor deficits. Symptoms generally occur over a course of 3–6 months after surgery.
EPIDURAL AND INTRANEURAL FIBROSIS Epidural fibrosis refers to scar tissue formation outside the dura, on the cauda equina or directly on the nerve roots. Epidural fibrosis develops when epidural fat is replaced by the hematoma that typically forms in the path of surgical dissection. The hematoma is gradually absorbed and simultaneously replaced by granulation tissue
Fig. 104.3 Hoffman ligaments connect the ventral surface of the dural sac and the exiting nerve roots to the posterior longitudinal ligament and posterior vertebral periosteum.
that matures into fibrotic connective tissue. Scar tissue development in postoperative patients is not solely due to the operative trauma, but is also a physiologic and reparative response to a herniated disc.8 Epidural scar tissue may constrict the neural elements and cause postoperative pain. Intraneural fibrosis is the formation of scar tissue within the nerve root as opposed to epidural fibrosis, which refers to scar tissue formation outside the nerve root or directly on the nerve root. Intraneural fibrosis cannot be detected by any imaging study and can only be confirmed by pathologic examination under microscopy.
Pathophysiology The pathophysiology of radicular pain caused by epidural or intraneural fibrosis may be the result of inflammation, mechanical compression, or vascular compromise of the spinal nerve roots.
Mechanical compression Nerve fibers encased in collagenous scar tissue suffer an increase in neural tension, impairment of axoplasmic transport, and restriction of arterial supply and venous return. Spinal nerve roots and dorsal root ganglia are particularly sensitive to mechanical deformation due to intraspinal disorders.19 The importance of axonal stretching and deformation in response to a mechanical force and the consequent morphological changes within the nervi nervorum were first described by Horsley et al. in 1883.20 A chronic compressive force decreases blood perfusion causing ischemia and limits CSF circulation which leads to endoneural hyperemia21 and further intraneural damage.22 Since a nerve root lacks a perineurium and has a poorly developed epineurium, it may be more susceptible to compression from intraspinal disorders such as epidural fibrosis or a disc herniation. It has been shown that compression of a peripheral nerve will induce direct mechanical effects on the nerve tissue such as deformation of nerve fibers, displacement of nodes of Ranvier, decreased intraneural microcirculation, and neurophysiologic changes of conduction block. Olmarker et al.19 reported increased permeability of the endoneurial capillaries of the nerve roots resulting in edema from mechanical compression. Intraneural edema may impair capillary blood flow and compromise 1139
Part 3: Specific Disorders
Intervertebral disc Ventral ramus
Dorsal root ganglion Spinal nerve root Thecal sac Facet joint
Clumping of nerve roots Spinous process
nutritional transport, causing ischemia. Compression and edema may lead to intraneural fibrosis. These processes have important implications as intraneural damage causes inflammation and eventual fibrotic tissue formation after healing leading to intraneural fibrosis. Similarly, perineural or epidural fibrotic tissue in response to surgical trauma or part of the normal reparative process, in response to inflammation or vascular compromise, may mechanically compress the nerve roots and initiate the above cascade, leading to intraneural fibrosis. Tension or stretching of nerve segments may lead to similar anatomic alterations. This may occur if a segment of the spinal nerve root is fixed (e.g. intervertebral foramen) or tethered by fibrotic epidural scar tissue (Fig. 104.4.) Ebeling et al.2,23 demonstrated nerve root immobilization as a result of epidural fibrosis causing nerve root impingement from small recurrent disc fragments embedded in fibrotic tissue. This finding occurred in 23% of cases during second operation following lumbar disc surgery in 92 patients.
Inflammatory etiology Marshall24 suggested that leakage of breakdown products from degenerating nucleus pulposus may induce a chemical radiculitis. In animal studies, Bobechko and Hirsch25 demonstrated an autoimmune response to the nucleus pulposus of rabbits. This was confirmed by Gertzbein et al.26 in 1975. Using human nucleus pulposus tested with rabbit sera, they demonstrated the presence of a cellular immune response in 73% of patients whose discs were found to be sequestered at the time of surgery and 26% in those patients whose discs were herniated. McCarron et al.9 showed that there was an inflammatory response to nucleus pulposus injectate in the epidural fat and dura. Saal et al.27 demonstrated that high concentrations of phospholipase A2, the ratelimiting enzyme for the inflammatory cascade of prostaglandins and leukotrienes, were present in human lumbar herniated nucleus pulposus and degenerative discs. Franson et al.28 reported that extracted PLA2 form human lumbar disc has powerful inflammatory activity in vivo. Byrod et al.29 reported that epidural application of substances can have a direct transport route to the axons of the spinal nerve 1140
Fig. 104.4 Lumbar spinal nerve root and dorsal root ganglion tethered by epidural fibrotic adhesions and postsurgical scarring. Thecal sac displaced to the right from postsurgical scar. Left hemi-laminectomy defect.
roots. PLA2 may act to excite nociceptors within the anulus or within the epidural space. Direct contact with a nerve root may cause neural injury either by enzymatic activity on the membrane phospholipids or by production of inflammatory mediators. Human disc PLA2 has been shown to cause perineural inflammation, conduction block, and axonal injury by extrathecal application to animal nerve.30 Leakage of PLA2 or another neurotoxic chemical within the disc may irritate small unmyelinated nerve fibers in the anulus or nearby structures such as spinal nerve roots. It has been suggested that radicular pain results from the ectopic firing within sensory fibers injured by the inflammatory chemical mediators released from degenerated disc tissue.31,32 Perineural inflammation or demyelination induced by phospholipase A2 may be responsible for the hypersensitivity of a nerve root to mechanical stimulation.33 Herniated intervertebral disc material can cause inflammatory changes which may lead to epidural or intraneural fibrosis. It has also been suggested that ventrally located epidural scar tissue that adheres to the dorsal aspect of the disc can create injury via mechanical tension followed leakage of inflammatory enzymes.34
Vascular etiology Disc degeneration has been known to be closely associated with abnormalities in the anatomy and physiology of the adjacent nerve roots. Holt and Yates35 correlated the histology of cervical disc degeneration with adjacent spinal nerve root fibrosis in their cadaver study. Lindahl and Rexed36 demonstrated intraneural fibrosis in 78% of dorsal nerve root biopsies taken at the time of surgery in patients operated on for herniated intervertebral discs. Jayson37 found that there is a statistically significant relationship between the extent of disc degeneration and prolapse with evidence of epidural venous obstruction, perineural/intraneural fibrosis, focal demyelination and neuronal atrophy. A fibrinolytic defect was found in patients with back pain, suggesting that a decreased ability to clear fibrin may be responsible for chronic tissue damage.38 Epidural fibrotic tissue may induce vascular compromise and ischemia with resultant intraneural fibrosis (Fig. 104.5).
Section 5: Biomechanical Disorders of the Lumbar Spine
Intervertebral disc Hoffman’s ligaments Fibrotic adhesions Ventral ramus
Dorsal root ganglion Dorsal ramus
Thecal sac
Post-surgical scarring Fig. 104.5 Nerve root, ventral ramus, dorsal root ganglion, and its vascular supply mechanically compressed by epidural fibrosis.
DIAGNOSIS Imaging Gadolinium-enhanced MRI is the imaging study of choice when evaluating for epidural fibrosis.7,34 Epidural fibrosis can only be seen on MRI performed with gadolinium dye. Gadolinium enhances vascularized fibrotic scar tissue and distinguishes epidural fibrosis from a recurrent disc protrusion in a postoperative spine patient. MRI is the imaging study of choice in diagnosing arachnoiditis and differentiating other causes of FBSS such as epidural fibrosis, retained or recurrent disc protrusion, lateral recess stenosis, and infection.7,34 MRI has demonstrated excellent correlation with CT-myelography
in the diagnosis of adhesive arachnoiditis without the additional risks of an intrathecal injection.39 The characteristic central clumping or clustering of nerve roots within the thecal sac is best seen on axial T2-weighted images (Fig. 104.6).40,41 Peripheral adhesions or severe thecal sac distortion can also be seen. These findings are due to the adhesive nature of the inflamed pia–arachnoid membranes. There is still an occasional role for CT-myelography in a patient with clinically suspected adhesive arachnoiditis and a normal MRI. The ability of CT-myelography to delineate the intrathecal nerve root anatomy may be useful in those patients with limited, localized areas of arachnoiditis involvement.42 It is important to note that findings consistent with arachnoiditis on an imaging study may be clinically asymptomatic.
Intervertebral disc Hoffman’s ligaments Epidural fibrosis and scarring Ventral ramus Radicular artery Dorsal root ganglion
Radicular vein Dorsal ramus Thecal sac Post-surgical scarring Spinal process
Fig. 104.6 Clumping of nerve roots in the thecal sac characteristic of arachnoiditis. 1141
Part 3: Specific Disorders
Clinical assessment The diagnosis of postoperative low back and limb pain due to neural scarring is a diagnosis of exclusion. Any possible cause for the radicular symptoms other than scar formation has to be excluded.43 The common etiologies of FBSS must be algorithmically eliminated. This concept has been discussed by Jerome Schofferman in the preceding chapter. The clinical presentation of radicular pain due to neural scarring is variable. The classically described arachnoiditis patient typically includes a history of postoperative leg pain with or without back pain 1–6 months after a brief pain-free interval. Pain is the consistent complaint. However, the location, character, and frequency of pain complaints vary in each patient. Physical examination may demonstrate sensory and/or motor deficits. Nerve root tension signs such as straight leg raising are typically positive. It is not uncommon for the initial preoperative history and physical examination findings to be unchanged postoperatively. As always, other more treatable conditions such as a recurrent disc protrusion, small lateral disc protrusion, neuroforaminal stenosis, lateral recess stenosis, or spinal stenosis need to be ruled out.
NONSURGICAL TREATMENT Medical rehabilitation and interventional physiatric treatment of FBSS for those patients with recurrent radicular leg pain greater than back pain and with radiologic abnormalities limited to the presence of epidural fibrosis have not shown long-term success.6,44 The majority of the current literature examining FBSS secondary to epidural/intraneural fibrosis has investigated surgical outcomes.6,45–48 Treatment is multidisciplinary. This may include a combination of physical therapy and modalities, pharmacologic agents of various classes, fluoroscopically guided selective nerve root blocks, activity modifications, education, and pain counseling.
Physical therapy Bed rest is not indicated and the patient is encouraged to be as active as possible. Postoperative rehabilitation and physical therapy is necessary to treat the deconditioned lumbar spine stabilizers, pelvic girdle musculature, and lower limb muscles. Although there are no randomized, controlled studies investigating the effectiveness of physical therapy and modalities such as transcutaneous electrical nerve stimulation (TENS) in the treatment of symptomatic neural scarring, current studies to date do show that these patients may show improvement in their overall functional ability and even in their subjective complaints of pain.49 Nerve root glide maneuvers may also be helpful to slacken the tethered nerve roots from fibrotic tissue.
Pharmacologic agents Medications including nonsteroidal antiinflammatory drugs (NSAIDs), neuropathic agents such as tricyclic antidepressants (TCAs) or anticonvulsants, muscle relaxants, and opioid pain medications can be tried. These medications should be given in a step-wise fashion with NSAIDs as first-line treatment. Neuropathic agents are membrane stabilizers and should be initiated if there is a significant component of limb pain with neurogenic symptoms such as dysesthesias, paresthesias, and burning or lancinating pain. Gabapentin, one of the most commonly used agents for neuropathic pain, has been reported to be effective in the management of symptomatic limb pain due to epidural fibrosis.50 Muscle relaxers, as a pharmacologic class, are not consistently effective for the treatment of muscle spasms but may be initiated if the spasms are a primary complaint. Most muscle relaxers are also sedatives and should be best taken in 1142
the evenings. Medications to restore normal sleep cycle are important for those patients with impaired sleep. Opioid pain medications are primarily used for analgesia but do have secondary effects of membrane stabilization. Anxiolytics and antidepressants are indicated for treatment of mood disorders, which are frequent in this population.
Selective nerve root block There are few studies that have examined the nonsurgical outcomes of FBSS secondary to epidural/intraneural fibrosis treated with selective nerve root blocks (SNRB). Devulder51 demonstrated good pain relief in 12 out of 20 patients with FBSS treated with SNRB consisting of local anesthetic diluted in 1500 U hyaluronidase and 40 mg of methylprednisolone. However, this retrospective pilot study lacked stringent inclusion criteria, used only verbal pain scores, and had a follow-up period of only 3 months. Devulder and colleagues52 found no statistical difference between three patient groups treated with SNRB using a combination of either bupivacaine, hyaluronidase, methylprednisolone, or saline in 60 patients with documented fibrosis and a follow-up period of 6 months. Unfortunately, this study also lacked stringent inclusion criteria and used verbal pain scales as the sole outcome measure. A preliminary study by Slipman et al.53 reported epidemiologic data and outcomes of patients with FBSS secondary to epidural or intraneural fibrosis treated nonsurgically with fluoroscopic guided therapeutic selective nerve root blocks using stringent inclusion criteria and multiple outcome measures. The preliminary study reported successful outcomes from the selective nerve root blocks; however, the frequency of a successful outcome was less than 25% in the small sample size of subjects. One of the most effective methods the authors use, and similarly employed at The Penn Spine Center, is the institution of a membrane stabilizer. Typically, the authors use neurontin as a first-line agent. If that is not tolerated then they move on to zonegran, trileptal, keppra and so forth. If symptom reduction is achieved, even only 20% or so, then a therapeutic selective nerve root block is added. These two measures seem to be symbiotic and allow for continued relief that will be maintained provided the patient continues the membrane stabilizing agent. When the side effect of an agent exceeds the benefit obtained then there is a switch to another medication. A therapeutic block is not performed until some symptom reduction is achieved with an oral agent. This approach requires a vigorous scientific trial, which has not yet been conducted. In contrast, several studies have demonstrated the efficacy of fluoroscopically guided transforaminal selective nerve root blocks in the treatment of painful radiculopathy due to a focal disc protrusion. Although selective nerve root blocks may provide reduction of painful lower limb symptoms in the presence of epidural or intraneural fibrosis, the outcomes are much poorer. The injection approach and technique are critical for the successful performance of the selective nerve root block. A fluoroscopically guided SNRB or transforaminal injection is preferably employed instead of an interlaminar or translaminar injection because this facilitates ventral epidural flow to the involved nerve root complex or the posterior surface of the intervertebral discs. The therapeutic agents injected with the posterior translaminar injection approach may remain in the dorsal epidural space without spreading to the affected nerve root or intervertebral disc in the ventral epidural space.54 Furthermore, it is inappropriate to use an interlaminar or translaminar injection technique in patients who have had prior lumbar spine surgery. Surgery alters the normal spinal anatomy with postoperative scar tissue obliterating the normal posterior epidural space and obstructing the flow of contrast dye or medication to the target structures. A transforaminal injection
Section 5: Biomechanical Disorders of the Lumbar Spine Spinal nerve
Intervertebral disc
Pedicle
Ventral ramus
Intervertebral foramen
Spinal needle
circumvents this problem by placing the needle just inside the neural foramen at the disc–nerve root interface in the ventral epidural space (Fig. 104.7). In addition, the needle track of a transforaminal injection, as opposed to an interlaminar injection, will not be impeded by postoperative scar tissue. Confirmation of proper needle position during a fluoroscopically guided diagnostic SNRB occurs when contrast outlines the targeted nerve root and extends extraforaminally without evidence of epidural flow. The rationale for employing an SNRB is that both corticosteroids and local anesthetic agents have been shown to stabilize neural membranes.55–58 Local anesthetic agents also improve intraradicular blood flow.55 These effects may reduce intraneural or epidural fibrosis and/or the endoneurial edema, compression, or ischemia of the nerve roots. Glucocorticoids suppress inflammatory cytokines and inhibit inflammatory cells.59,60 By modulating cytokines controlling proteolytic enzymes such as collagenase, corticosteroids may affect collagen formation and the organization of the epidural or intraneural fibrotic tissue. The combination of an oral membrane stabilizer, a selective nerve root block with corticosteroids, and physical therapy with nerve root gliding techniques may help to reorganize dense fibrotic scar toward looser connective tissue. If such a process occurs, nerve root excursion within the neural foramen may be restored to a more normal state. Due to the sparse literature, no definitive judgment can currently be made regarding the efficacy of therapeutic SNRB for the treatment of radicular pain caused by epidural or intraneural fibrosis. Based upon personal observation and communications with experienced colleagues, these injections typically do not cure the painful symptoms but may relieve these symptoms for varying periods when they are used in isolation.
Minimally invasive procedures Percutaneous lysis of epidural adhesions has been described to be an effective treatment for chronic low back and/or leg pain secondary to epidural fibrosis.10,61–66 Racz initially described the technique involving epidurography, adhesiolysis, and injection of local anesthetic agents, corticosteroids, and hyaluronidase followed by injection of hypertonic saline.10,64,65,67,68 One-year outcome studies reported 25–47% good outcomes.62,64,65 However, there are devastating consequences such as cauda equina syndrome, spinal cord compression, paraplegia, myelopathy, and arachnoiditis if not performed properly.10,69–71 Retinal hemorrhages due to increased intracranial pressure
Fig. 104.7 Position of needle during a selective nerve root block in a postoperative patient. Note Post-surgical scarring the postsurgical scarring that would obstruct (in a post-operative patient) an interlaminar or translaminar epidural steroid Spinal process injection. Superior articular process
from rapid high-volume injections72–76 and catheter shearing with retention in the epidural space have also been reported.10,77 Gabor Racz addresses these issues in much greater detail in Chapter 106. Implantable intrathecal morphine pumps are an option if a patient responds to oral opioid treatment but requires high dosages due to tolerance. The major advantage of a morphine pump is that a small dosage intrathecally can provide the same or better clinical analgesia when compared to oral opioid treatment.78 A drawback to the morphine pump is that the intrathecal agent may act as another insult to the neural elements and worsen arachnoiditis or neural scarring. A detailed discussion of implantable pain pumps including indication, contraindications, and outcomes is covered by Joshua Prager in Chapter 108. The use of TENS units can sometimes reduce painful neurogenic symptoms. Implantable dorsal column stimulators are a more invasive form of TENS, but may provide significant reduction of painful neurogenic lower limb symptoms in carefully selected patients. A more detailed review of this treatment modality is provided by Robert Windsor in Chapter 107.
Education and counseling Concurrent treatment with a psychologist who is adept at addressing the variety of issues confronting the patient with chronic pain is helpful. This will enable a reduction in the subjective component of the patient’s pain threshold. This includes counseling for coping skills, biofeedback, goal setting, reinforcement of activity modifications, and the subjective reduction of pain behavior. Social support from family and friends is important for successful treatment of this difficult entity. Initiating their participation in the overall treatment plan of the patient is important so that they understand the challenging nature of this clinical diagnosis. It should emphasized that psychological counseling is not a categorical requirement. Some patients will respond quite well to the aforementioned therapy, medication and injection cocktail, thereby dramatically diminishing their distress.
ALGORITHMIC APPROACH When approaching a postoperative patient with persistent lower limb pain who has failed a reasonable trial of conservative treatment consisting of physical therapy and medications, one must first determine the location of the lower limb pain and its time course in relation 1143
Part 3: Specific Disorders
to the surgery. The time course characteristically involves onset of radicular symptoms within 1 year of postoperative pain relief. Nerve root pain due to epidural or intraneural fibrosis classically follows a radicular pattern of the involved nerve root and is within all or part of the radicular symptom distribution prior to surgery. The radicular lower limb pain is generally more intensely painful than axial low back pain. Gadolinium-enhanced MRI of the lumbar spine must demonstrate epidural fibrosis around the suspected nerve root without evidence of other pathology such as neuroforaminal stenosis or a recurrent disc protrusion. If the physical examination reveals a new myotomal strength deficit or reflex change correlating with the distribution of radicular pain and MRI findings, a fluoroscopically guided therapeutic selective nerve root block is recommended to treat the involved nerve root. In the absence of these physical examination findings, a positive electrodiagnostic evaluation identifying new acute changes consistent with the involved nerve root level will diagnose the radiculopathy. A therapeutic selective nerve root block is then offered to treat the radiculopathy. An EMG is considered positive when the involved nerve root level has abnormal spontaneous activity at rest in the form of positive sharp waves and fibrillation potentials in the associated paraspinal musculature and in at least two muscles from the same myotomal, but different peripheral nerve innervation with neuropathic recruitment abnormalities.79 Although a positive EMG provides the diagnosis of radiculopathy, a negative EMG does not rule out nerve injury. It is not uncommon for patients with radicular pain to have normal electrodiagnostic findings or instances where only chronic changes are identified.80 If the electrodiagnostic study and physical examination are both negative in the setting of an abnormal imaging study with radicular complaints, a fluoroscopically guided diagnostic selective nerve root block is required.80–82 The diagnostic selective nerve root block is performed only with a small aliquot (1 cc or less) of local anesthetic to directly anesthetize only the suspected nerve root. Care must be taken to ensure that contrast only outlines the nerve root without epidural spread. Otherwise nearby structures in the epidural space will be inadvertently anesthetized, thus comprising the selective nature of this block and removing its diagnostic reliability. If there is at least an 80% or greater reduction of the postblock visual analog scale (VAS) when compared to the pre-block VAS several minutes post-injection, the diagnostic selective nerve root block is positive.81,83,84 This confirms that the radicular lower limb pain is emanating from the suspected nerve root, and a fluoroscopically guided therapeutic steroid selective nerve root block is then offered. The high sensitivity, ranging 99–100%,85,86 and high specificity, ranging 87–100%,85–90 of diagnostic selective nerve root blocks have been well documented by several studies. If the patient fails to improve with a fluoroscopically guided therapeutic steroid SNRB and seeks further treatment for persistent radicular lower limb pain due to epidural fibrosis, percutaneous epidural adhesiolysis under fluoroscopy is recommended by some. A dorsal column stimulator trial is reserved as the last resort if the patient is refractory to the aforementioned treatments.
SURGERY Most authors do not recommend reoperation when fibrosis is suspected to be the only cause of FBSS because the probability of longterm success after reoperation is low.1–7,43–48,91,92 Surgical outcomes have been reported to be between 10% and 30%.6,48 In a prospective case series, Jonssson and Stromqvist47 demonstrated that 62% of patients with FBSS secondary to neural fibrosis after discectomy undergoing reoperation were unchanged or worse. Neurolysis for epidural fibrosis not only yields dismal results and more expansive fibro-
1144
sis, but it also increases the risk of nerve root injury.45,48,93 The overall failure rate for neurolysis has been reported to be 62–83%.91,92,94–96 Outcomes are poor for eliminating scar tissue and significantly reducing pain from adhesive arachnoiditis, and may exacerbate symptoms by further damaging the neural elements.97,98 Exploratory surgery is not indicated in the absence of progressive neurologic deficit nor in patients whose pain can be controlled with nonsurgical treatment. Patients with high-grade arachnoiditis and those with preoperative dysesthesias have a worse prognosis for surgical success.99–102 In recent years, much attention has been focused on various biologic, pharmacologic, and synthetic materials to inhibit neural scarring and its intraoperative applications. Several materials have been used intraoperatively to inhibit scar; however, research related to their efficacy has been via animal models, and clinical results are not convincing. The ideal agent for scar inhibition remains to be identified. Fat free grafts have had the longest history of use and are generally accepted as a way to avoid possible postsurgical fibrosis. Again, its usefulness in epidural and perineural fibroses inhibition is uncertain. Fat graft is readily available with no additional cost, and it can become vascularized, nourishing the dura. The possible disadvantages of using this graft include seroma formation, indentations, and the fact that it is a space-occupying mass that may cause neural compression. The size of the graft is also important. A large graft may possibly result in neural compression, whereas if too thin it may be ineffective as the fat graft shrinks in size over time.103,104 Migration of the graft is also a concern and a few cases of cauda equina syndrome believed to result from migration have been reported.105,106 Generally speaking, surgeons prefer fat grafts, as they are easily available without additional costs and do protect the dura without excessive formation of fibrous tissue. Alternatives to fat grafts include a number of materials. Gelfoam is widely used as a hemostatic agent, but has also been shown to prevent scar adhesion when used in the epidural space after a laminectomy.107 Another gelatin-derived product is ADCONL. It was FDA approved in 1998 for inhibition of postsurgical fibrosis. Several cases of dural tears after use of ADCON-L in posterior lumbar surgeries were reported which has limited the widespread use of this material.108 There are several scar-inhibiting agents that are currently being evaluated in clinical trials.
PREVENTION Outcomes of nonoperative and surgical treatments for neural scarring are poor. Since there is no effective or curative treatment for neural scarring, preventative measures are critical. For example, more recent water-based contrast agents have replaced the oil-based agents for diagnostic imaging studies. In addition, preservative-free local anesthetic solutions are now readily available and are the standard of care when injecting local anesthetic agents into the epidural space. Similarly, with more widespread utilization of pharmacologic agents intrathecally and within the epidural space, minimizing the quantity and duration of these agents in contact with the thecal sac or epidural space and their respective contents is important to reduce the potential risk of neural scarring. From a surgical perspective, meticulous surgical technique can limit the extent of neural scarring by minimizing bleeding, infection, and dural and intrathecal insults.
SUMMARY The pathophysiology of radicular pain caused by epidural or intraneural fibrosis may be the result of inflammation, vascular compromise, mechanical compression, or tension of the spinal nerve roots. An accurate diagnosis of symptomatic neural scarring can be determined with a diagnostic algorithmic pathway incorporating a detailed
Section 5: Biomechanical Disorders of the Lumbar Spine
history, physical examination, electrodiagnostic testing, and fluoroscopically guided diagnostic selective nerve root blocks. Injection of glucocorticoids and local anesthetic agents has been proposed since these agents can indirectly stabilize neural membranes, reduce the local cellular immune response, inhibit inflammatory cytokines, decrease intraneural edema, and increase intraradicular blood flow. Nonsurgical and surgical outcomes for symptomatic neural scarring are poor. Treatment necessitates a multidisciplinary approach that also involves the patient’s social support network.
References 1. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, et al. Causes of failure of surgery on the lumbar spine. Clin Orthopaed Rel Res 1981; (157):191–199. 2. Ebeling U, Kalbarcyk H, Reulen HJ, Microsurgical reoperation following lumbar disc surgery. Timing, surgical findings, and outcome in 92 patients. J Neurosurg 1989; 70(3):397–404.
25. Bobcheko WP, Hirsch C. Autoimmune response to nucleus pulposus in the rabbit. JBJS 1965; 47B:574. 26. Gertzbein SD, et al. Autoimmunity in degenerative disc disease of the lumbar spine. 1975; 6(1):67–73. 27. Saal JS, et al. High levels of inflammatory phospholipase A2 activity in lumbar disc herniations. Spine 1990; 15:674–678. 28. Franson RC, Saal JS, Saal JA. Human disc phospholipase A2 is inflammatory. Spine 1992; 17(6 Suppl):S129–S132. 29. Byrod G, Rydevik B, Johansson BR, et al. Transport of epidurally applied horseradish peroxidase to the endoneurial space of dorsal root ganglia: a light and electron microscopic study. J Periph Nerv Sys 2000; 5(4):218–226. 30. Saal JS. The role of inflammation in lumbar pain. Spine. 1995; 20(16): 1821–1827. 31. Chen C, Cavanaugh JM, et al. Effects of phospholipase A2 on lumbar nerve root structure and function. Spine 1997; 22:1057–1064. 32. Muramoto T, Atsuta Y, et al. The action of prostaglandin E2 and triamcinolone acetonide on the firing activity of lumbar nerve roots. Int Orthop 1997; 21:172–175.
3. Slipman CW, Shin CH, Patel RK, et al. Etiologies of failed back surgery syndrome. Pain Med 2002; 3(3):200–214.
33. Ozaktay AC, Kallakuri S, et al. Phospholipase A2 sensitivity of the dorsal root and dorsal root ganglion. Spine 1998; 23:1297–1306.
4. Long DM. Failed back surgery syndrome. Neurosurg Clin N Am 1991; 2(4): 899–919.
34. Ross JS, Blaser S, et al. Gd-DTPA ehancement of posterior epidural scar: an exprimental model. AJNR 1989; 10:1083–1088.
5. Simmons ED. North American Spine Society annual abstracts, 1998.
35. Holt S, Yates PO. Cervical spondylosis and nerve root lesions. Incidence at routine necropsy. J Bone Joint Surg 1966; 48(3):407–423.
6. North RB, Campbell JN, James CS, et al. Failed back surgery syndrome: 5-year follow-up in 102 patients undergoing repeated operation. Neurosurgery 1991; 28(5):685–690. 7. Ross JS, Robertson JT, Frederickson RC, et al. Association between peridural scar and recurrent radicular pain after lumbar discectomy: magnetic resonance evaluation. ADCON-L European Study Group. Neurosurgery 1996; 38(4):855–861. 8. Annertz M, Jonsson B, Stromquist B, et al. No relationship between epidural fibrosis and sciatica in the lumbar postdiscectomy syndrome. A study with contrast-enhanced magnetic resonance imaging in symptomatic and asymptomatic patients. Spine 1995; (20)4:449–453. 9. McCarron R, et al. The inflammatory effect of nucleus pulposus: a possible element in the pathogenesis of low back pain. Spine 1987; 12:760–764. 10. Racz GB, Holubec JT. Lysis of adhesions in the epidural space. In: Racz GB, ed. Techniques of neurolysis. Boston: Kluwer Academic; 1989:57–72. 11. Prawl RP. Arachnoiditis and epidural fibrosis: the relationship to chronic pain. Curr Rev Pain 1998; 2:93–99.
36. Lindhal O, Rexed B. Histological changes in spinal nerve roots of operated cases of sciatica. Acta Orthop Scand 1951; 20:215–225. 37. Jayson MI. The role of vascular damage and fibrosis in the pathogenesis of nerve root damage. Clin Orthopaed Rel Res 1992; 279:40–48. 38. Jayson MI, Keegan A, Million R, et al. A fibrinolytic defect in chronic back pain syndromes. Lancet 1984; 2(8413):1186–1187. 39. Delamarter RB, Ross JS, Masaryk TJ, et al. Diagnosis of lumbar arachnoiditis by magnetic resonance imaging. Spine 1990; 15:304–310. 40. Ross JS, Masaryk TJ, Modic MT, et al. Lumbar spine: postoperative assessment with surface-coil MR imaging. Radiology 1987; 164:851–860. 41. Ross JS, Masaryk TJ, Modic MT, et al. MR imaging of lumbar arachnoiditis. Am J Roentgenol 1987; 149:1025–1032. 42. Hueftle MG, Modic MT, Ross JS, et al. Lumbar spine: postoperative MR imaging with gadolinium-DPTA. Radiology 1988; 167:817–824.
12. Barsa JE, Charlton JE. Diagnosis of epidural scarring and its possible contribution to chronic low back pain syndrome. Pain 1984; S4:376.
43. Fritsch EW, Heisel J, Rupp S. The failed back surgery syndrome: reasons, intraoperative findings, and long-term results: a report of 182 operative treatments. Spine 1996; 21(5):626–633.
13. Cook SD, Prewett AB, Dalton JE, et al. Reduction in perineural scar formation after laminectomy with polyactive membrane sheets. Spine 1994; 19:1815–1825.
44. Nykvist F, Hurme M, et al. Severe sciatica: A 13-year follow-up of 342 patients. Eur Spine J. 1995; 4:335–338.
14. Sunderland S. Meningeal–neural relations in the intervertebral foramen. J Neurosurg 1974; 40:756–763.
45. Finnegan WJ, Delin JM, et al. Results of surgical intervention in the symptomatic multiply-operated back patient, J Bone Joint Surg [Am] 1979; 61A:1077.
15. Hoyland JA, Freemont AJ, Jayson MI. Intervertebral foramen venous obstruction. A cause of periradicular fibrosis? Spine 1989; 14(6):558–568.
46. Law JD, Lehman RAW, et al. Reoperation after lumbar intervertebral disc surgery, J Neurosurg 1978; 48:259.
16. Spencer DL, Irwin GS, et al. Anatomy and significance of fixation of the lumbosacral nerve roots in sciatica. Spine 1983; 8:672–679.
47. Jonsson B, Stromqvist B. Repeat decompression of lumbar nerve roots. A prospective two-year evaluation. J Bone Joint Surg 1993; 75B(6):894–897.
17. Goddard, Reid JD. Movement induced by straight leg raising in the lumbosacral roots, nerves, and plexus, and in the intrapelvic section of the sciatic nerve. J Neurol Neurosurg Psychiatry 1965; 28:12–18.
48. Waddell G, Kummel EG, Lotto WN, et al. Failed lumbar disc surgery and repeat surgery following industrial injury. J Bone Joint Surg [Am] 1969; 61:201–207.
18. Parke WW, Watanabe R. The intrinsic vasculature of the lumbosacral spinal nerve roots. Spine 1985; 10:508–515. 19. Olmarker K, et al. Edema formation in spinal nerve roots induced by experimental study of the pig cauda equina. Spine 1989; 14:579–561 20. Horsley V, Sugar O, John Marshall. Nerve stretching, and the nervi nervorum. Surg Neurol. 1990; 34(3):184–187. 21. Cornefjord M, Sato K, Olmarker K, et al. A model for chronic nerve root compression studies. Presentation of a porcine model for controlled, slow-onset compression with analyses of anatomic aspects, compression onset rate, and morphologic and neurophysiologic effects. Spine 1997; 22(9):946–957. 22. Garfin SR, Rydevik B, et al. Spinal nerve root compression. Spine 1995; 20: 1810–1820. 23. Ebeling U, Reichenberg W, Reulen HJ. Results of microsurgical lumbar discectomy. Review on 485 patients. Acta Neurochir (Wien) 1986; 81(1–2):45–52. 24. Marshall LL. The lumbar disc. Med J Australia 1975; 2(1):10–12.
49. Wynn Parry CB, Girgis F. The assessment and management of the failed back, Part II. Int Disabil Stud 1988; 10(1):25–28. 50. Braverman DL, Slipman CW, Lenrow DA. Using gabapentin to treat failed back surgery syndrome caused by epidural fibrosis: A report of 2 cases. Arch Phys Med Rehabil 2001; 82(5):691–693. 51. Devulder J. Transforaminal nerve root sleeve injection with corticosteroids, hyaluronidase, and local anesthetic in the failed back surgery syndrome. J Spinal Disord 1998; 11(2):151–154. 52. Devulder J, Deene P, De Laat M, et al. Nerve root sleeve injections in patients with failed back surgery syndrome: a comparison of three solutions. Clin J Pain 1999; 15(2):132–135. 53. Slipman CW, Chow DW, et al. Outcomes of therapeutic selective nerve root block for painful symptoms of epidural and/or intraneural fibrosis following discectomy for a herniated disc: a preliminary report. (Submitted for publication.) 54. Kraemer J, Ludwig J, Bickert U, et al. Lumbar epidural perineural injection: a new technique. Eur Spine J 1997; 6:357–361.
1145
Part 3: Specific Disorders 55. Yabuki S, Kikuchi S. Nerve root infiltration and sympathetic block. An experimental study of intraradicular blood flow. Spine 1995; 20(8):901–906.
and lumbosacral radiculopathies: update in diagnosis and management. PM&R Clin N Am; 2002.
56. Cullen BF, Haschke RH. Local anesthetic inhibition of phagocytosis and metabolism of human leukocytes. Anesthesiology 1974; 40:142–146.
83. Anderberg L, Annertz M, Brandt L, et al. Selective diagnostic cervical nerve root block – correlation with clinical symptoms and MRI pathology. Acta Neurochir (Wien) 2004; 146(6):559–565.
57. Hoidal JR, White JG, Repine JE. Influence of cationic local anesthetics on the metabolism and ultrastructure of human alveolar macrophages. J Lab Clin Med 1979; 93:857. 58. Goldstein IM, Lind S, et al. Influence of local anesthetics upon human polymorphonuclear leukocyte function in vitro. J Exp Med 1977; 146:483–494. 59. Takahashi H, et al. Inflammatory cytokines in the herniated disc of lumbar spine. Spine 1996; 21:218–224. 60. Doita M, et al. Immunohistologic study of the ruptured intervertebral disc of the lumbar Spine 1996; 21:235–241. 61. Manchikanti L, Pakanati R, Bakhit CE, et al. Role of adhesiolysis and hypertonic saline neurolysis in management of low back pain. Evaluation of modification of Racz protocol. Pain Digest 1999; 9:91–96. 62. Manchikanti L, Pampati V, Fellows B, et al. Role of one day epidural adhesiolysis in management of chronic low back pain: a randomized clinical trial. Pain Phys 2001; 4(2):153–166. 63. Manchikanti L, Pampati V, Bakhit CE, et al. Non-endoscopic endoscopic adhesiolysis in post lumbar laminectomy syndrome. A one-year outcome study and cost effective analysis. Pain Phys 1999; 2:52–58. 64. Racz GB, Heavner JE, Raj PP. Percutaneous epidural neuroplasty. Prospective oneyear follow up. Pain Digest 1999; 9:97–102. 65. Heavner JE, Racz GB, Raj P. Percutaneous epidural neuroplasty. Prospective evaluation of 0.9% NaCl versus 10% NaCl with or without hyaluronidase. Reg Anesth Pain Med 1999; 24:202–207. 66. Arthur J, Racz G, Heinrich R, et al. Epidural space. Identification of filling defects and lysis of adhesions in the treatment of chronic painful conditions. In: Abstracts, 7th World Congress on Pain. Paris, IASP Publications, 1993:557. 67. Racz GB, Sabaonghy M, Gintautas J, et al. Intractable pain therapy using a new epidural catheter. JAMA 1982; 248:579–581.
85. Haueisen DC, Smith BS, Myers SR, et al. The diagnostic accuracy of spinal nerve injection studies. Clin Orthopaed Rel Res 1983; 198:179–183. 86. Van Akkerveeken PF. The diagnostic value of nerve root sheath infiltration. Acta Ortho Scand 1993; 64:61–63. 87. Dooley JF, McBroom RJ, Taguchi T, et al. Nerve root infiltration in the diagnosis of radicular pain. Spine 1994; 19:1125–1131. 88. Krempen JF, Smith BS. Nerve root injection: a method for evaluating the etiology of sciatica. J Bone Joint Surg [Am] 1974; 56A:1435–1444. 89. Schutz H, Lougheed WM, Wortzman G, et al. Intervertebral nerve-root in the investigation of chronic lumbar disc disease. Canadian J Surg 1973; 16:217–221. 90. Stanley D, McLaren MI, Euinton HA, et al. A prospective study of nerve root infiltration in the diagnosis of sciatica: A comparison with radiculography, computed tomography, and operative findings. Spine 1990; 6:540–543. 91. Ozgen S, Naderi S, Ozek MM, et al. Findings and outcome of revision lumbar disc surgery. J Spinal Disord 1999; 12(4):287–292. 92. Benoist M, Ficat C, Baraf P, et al. Postoperative lumbar epiduro-arachnoiditis. Diagnostic and therapeutic aspects. Spine 1980; 5(5):432–436. 93. Johnston J, Matheny J. Microscopic lysis of lumbar adhesive arachnoiditis. Spine 1978; 3:36–39. 94. Thomalske G, Galow W, Ploke G. Critical comments on a comparison of two series of lumbar disc surgery. Adv Neurosurg 1977; 4:22–27. 95. Johnston J, Matheny J. Microscopic lysis of lumbar adhesive arachnoiditis. Spine 1978; 3:36–39.
68. Racz GB, Heavner JE, Raj PP. Epidural neuroplasty. Semin Anesthesia 1997; 302–312.
96. Grane P. The post-operative lumbar spine. A radiological investigation of the lumbar spine after discectomy using MR imaging and CT. Acta Radiol Suppl 1998; 414:1–23.
69. Aldrete JA, Zapata JC, Ghaly R. Arachnoiditis following epidural adhesiolysis with hypertonic saline report of two cases. Pain Digest 1996; 6:368–370.
97. Quiles M, Machisello PJ, Tsairis P. Lumbar adhesive arachnoiditis: Etiologic and pathologic aspects. Spine 1978; 3:45–50.
70. Kim RC, Porter RW, Choi BH, et al. Myelopathy after intrathecal administration of hypertonic saline. Neurosurgery 1988; 22:942–922.
98. Coventry MB, Stauffer RN. The multiply operated back. In: American Academy of Orthopaedic Surgeons: Symposium on the Spine. St. Louis: CV Mosby; 1999: 132–142.
71. Lucas JS, Ducker TB, Perot PL. Adverse reactions to intrathecal saline injections for control of pain. J Neurosurg 197; 42:557–561.
99. Dolan RA. Spinal adhesive arachnoiditis. Surg Neurol 1993; 39:479–484.
72. Kushner FH, Olson JC. Retinal hemorrhage as a consequence of epidural steroid injection. Arch Ophthalmol 1995; 113:309–313.
100. Johnston J, Matheny J. Microscopic lysis of lumbar adhesive arachnoiditis. Spine 1978; 3:36–39.
73. Ling C, Atkinson PL, Munton CG. Bilateral retinal hemorrhages following epidural injection. Br J Ophthalmol 1993; 77:316–317.
101. Roca J, Moreta D, Ubierna MT, et al. The results of surgical treatment of lumbar arachnoiditis. Int Orthop 1993; 17:77–81.
74. Purdy EP, Ajimal GS. Vision loss after lumbar epidural steroid injection. Anesth Analg 1998; 86:119–122.
102. Wilkinson HA, Schuman N. Results of surgical lysis of lumbar adhesive arachnoiditis. Neurosurgery 1979; 4:401–409.
75. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to spread of anesthetic solution in epidural space. Anesth Analg 1967; 46:440–446.
103. Kanamori M, Kawaguchi Y, Ohmori K, et al. The fate of autogenous free-fat grafts after posterior lumbar surgery: part 1. A postoperative serial magnetic resonance imaging study. Spine 2001; 26(20):2258–2263.
76. Morris DA, Henkind P. Relationship of intracranial, optic-nerve sheath, and retinal hemorrhage. Am J Ophthalmol 1967; 64:853–859. 77. Manchikanti L, Bakhit CE. Removal of torn Racz catheter from lumbar epidural space. Reg Anesth 1997; 22:579–581. 78. York M, Paice JA. Treatment of low back pain with intraspinal opioids delivered via implanted pumps. Orthop Nurs 1998; 17(3):61–69. 79. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1997:231. 80. Slipman CW, Chow DW, Whyte WS, et al. An evidenced-based algorithmic approach to cervical spinal disorders. Crit Rev Phys Rehab Med 2001; 13(4): 283–299. 81. Huston CW, Slipman CW. Diagnostic selective nerve root blocks: indications and usefulness. Phys Med Rehabil Clin N Am 2002; 13(3):545–565. 82. Slipman CW, Chow DW. Therapeutic spinal corticosteroid injections for the management of radiculopathies (chapter 12). In: Dillingham TR, ed. Cervical, thoracic,
1146
84. Slipman CW, Plastaras CT, Palmitier RS, et al. Symptom provocation of fluoroscopically guided cervical nerve root stimulation: Are dynatomal maps identical to dermatomal maps? Spine 1998; 23(20):2235–2242.
104. Kanamori M, Kawaguchi Y, Ohmori K, et al. The fate of autogenous free-fat grafts after posterior lumbar surgery: part 2. Magnetic resonance imaging and histologic studies in repeated surgery cases. Spine 2001; 26(20):2264–2270. 105. Mayer PJ, Jacobsen FS. Cauda equina syndrome after surgical treatment of lumbar spinal stenosis with application of free autogenous fat graft. J Bone Joint Surg [Am] 1989; 71A:1090–1093. 106. Prusik VR, Lint DS, Bruder WJ. Cauda equina syndrome as a complication of free epidural fat-grafting. J Bone Joint Surg [Am] 1998; 70A:1256. 107. LaRocca H, Macnab I. The laminectomy membrane: studies in its evolution, characteristics, and prophylaxis in dogs. J Bone Joint Surg [Br] 1974; 56B: 545–550. 108. Le AX, Rogers DE, Dawson EG, et al. Unrecognized durotomy after lumbar discectomy: a report of four cases associated with the use of ADCON-L. Spine 2001; 26(1):115–117.
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar
CHAPTER
105
Postoperative Pseudomeningocele, Hematoma, and Seroma Kenny S. David, Raj D. Rao and Jeffrey S. Fischgrund
PSEUDOMENINGOCELE A pseudomeningocele is an extradural collection of cerebrospinal fluid (CSF) that has extravasated through a dural or arachnoid tear.1–3 Other terms used to describe this condition are ‘meningeal pseudocysts’ and ‘meningeal spurius’.4 Pseudomeningocele was first reported in the literature in 1946 following laminectomy for removal of a neoplasm.5
Epidemiology Among patients undergoing primary decompressive lumbar spine surgery, incidental durotomy occurs at an incidence of 9–12%, making it the most frequently reported complication of lumbar spine surgery.6,7 After cauda equina syndrome, dural tears are the most frequent underlying diagnosis in malpractice litigation involving lumbar spine surgery.8 Pseudomeningoceles are a rare consequence of dural injury. In a review of 1700 laminectomies, Swanson and Fincher reported pseudomeningocele formation in four patients.9 In a group of 400 postlaminectomy patients with persistent back pain and/or radicular symptoms, Teplick et al. found pseudomeningoceles in 8 patients (2%).3 Factors that predispose to a dural tear in surgery are prior surgery or irradiation, congenital spinal malformations, unrecognized dural adhesions, dural calcification contiguous with overlying lamina, and the absence of epidural fat.8,10,11 Severe spinal stenosis and large herniated discs make root dissection and dural retraction more difficult and can predispose to dural tears. Dural injuries and pseudomeningoceles are understandably more frequent with posterior than anterior approaches.
Pathogenesis Pseudomeningoceles generally develop following an intraoperative rent in the dura and arachnoid, but can occur following dural needle puncture procedures, especially after multiple punctures.9 The cerebrospinal fluid leaks dorsal to the lamina, into a space artificially created by dissection of the paravertebral musculature. The fluid cavity is lined by flattened connective tissue cells resting on loose, areolar connective tissue.2,4 An encysted pseudomeningocele refers to a CSF-filled herniation of an arachnoid lined cyst through a small rent in the dura. The narrow opening in the dura acts like a one-way valve leading to an increase in size of the CSF collection and formation of a pseudomembrane.2 The size of the dural defect, pressure of the inflowing CSF, and the resistance of the surrounding soft tissues all influence the size of a pseudomeningocele. Postoperative weakness of paraspinal muscles may be a reason contributing to expansion of the pseudomeningocele.12 Spinal fluid pressure keeps the dural defect open and prevents
healing. Herniation of nerve filaments into the original dural defect may be another factor responsible for keeping the dural opening patent (Fig. 105.1).4 Puncture of the dura can result in escape of large volumes of CSF, leading to intracranial hypotension and a demonstrable reduction in CSF volume. The adult subarachnoid pressure of 15 cmH2O can be reduced to 4 cmH2O or less. The rate of loss of CSF through a dural perforation following puncture with a 25-gauge or larger needle is generally greater than the rate of CSF production.13
Clinical features Cerebrospinal fluid leaks after needle procedures in the lumbar spine classically present with headache. There is evidence that CSF leaks may be inevitable following needle puncture of the thecal sac,14 and it is unclear why only some of these patients are symptomatic. The size of the dural leak has no direct relationship with the occurrence of headache.14 The actual mechanism of headache is also unclear. Some authors suggest that the lowering of CSF pressure following a leak causes traction on the intracranial structures in the upright position. These structures are pain sensitive, leading to the characteristic
Dura mater Arachnoid mater
Posterior longitudinal ligament
Entrapped nerve root Pseudomeningocele
Fig. 105.1 Meningeal layers involved in the formation of a pseudomeningocele, with schematic representation of nerve root entrapment at the site of the dural defect. 1147
Part 3: Specific Disorders
headache.13 Others authors report that the drop in intracranial pressure causes a compensatory intracranial venodilation, which causes the headache. The headache is generally localized to the frontal and occipital regions, with occasional radiation to the neck and shoulders. Other symptoms may include nausea, vomiting, tinnitus, and vertigo. While pseudomeningoceles may be asymptomatic, many present with local swelling, symptoms of CSF leak, or nerve root impingement. Local swelling15 may occasionally be the only suggestion of a pseudomeningocele.12 The swelling may vary in size, depending on whether the patient is standing or recumbent. There is no apparent correlation between the size of the pseudomeningocele, the size of the defect in the dura, and the degree of symptoms.4,16 Postural headache frequently occurs in patients with pseudomeningocele. Miller and Elder4 reported one patient whose postural headache could be increased by manual pressure directly over a large fluctuant meningocele. Back pain, with or without radicular leg symptoms, is commonly associated with pseudomeningocele. In a review of 10 patients with postoperative pseudomeningocele, Miller and Elder found that back pain was a common feature in all patients, with nine having radicular pain radiating into the lower limbs.4 Manual pressure over the paraspinal musculature on the side of the cyst may exacerbate the back pain.16 Coexisting worker’s compensation issues can lead to doubts being expressed as to the authenticity of such complaints in the postoperative patient.16 Radicular findings in patients with pseudomeningocele result from herniation and kinking of the nerve roots in the dural defect,17 adhesion of the nerve roots to the edges of the sac,18 or direct pressure of the pseudomeningocele on an adjacent nerve root. Eismont et al.19 reported a case of persistent postoperative radicular pain along with focal deficits following lumbar disc excision. Myelography revealed a pseudomeningocele involving the left fourth and fifth lumbar nerve roots. Intraoperatively, it was found that the L4 root had buttonholed through the site of the dural tear, while the pseudomeningocele was found to be compressing the L5 root. Ossification of a pseudomeningocele can rarely cause neural compression.20 In many patients an obvious site of nerve root entrapment is not identifiable.4 Asymptomatic meningoceles can become symptomatic after a precipitating event leading to nerve entrapment.21 Radicular pain in a previously asymptomatic patient can be precipitated by maneuvers that increase intracranial and intraspinal pressure, such as coughing, sneezing, or jugular compression.16 Unusual presentations associated with pseudomeningoceles include bone erosion of the posterior vertebral elements22 and chronic meningitis.23
A
1148
B
Investigations Myelography shows a characteristic pattern of dye extruding through the stalk of the pseudomeningocele, and a fluid level may be visible when the opening in the dura is large. Percutaneous injection of contrast material directly into the cyst cavity has been carried out when a palpable or visible mass is present at a surgical site.16 CT-myelography can effectively demonstrate the neck and outline of the pseudomeningocele although nerve root entrapment is not well visualized.18 MRI scans are very sensitive for CSF collections and pseudomeningoceles (Fig. 105.2). Some authors recommend a routine postoperative MRI scan following any repair of a durotomy, even in the absence of symptoms of a pseudomeningocele, in order to ensure that no further leakage is present.24 Digital subtraction myelography may occasionally reveal a pseudomeningocele when plain myelography, CT scan, and MRI show a fluid collection posterior to the dural sac, but no obvious connection between the two.25 In radionuclide cisternography, radionuclide contrast material is injected into the subarachnoid space followed by MRI evaluation. Areas filled with CSF show up as high-signal regions.26
Management of dural tear and pseudomeningocele In an attempt to reduce the incidence of postdural puncture CSF leak, numerous modifications have been made to spinal needles. Newer needle designs with narrow cutting tips and atraumatic bevels have resulted in a lower incidence of postspinal headache, neural irritation,13,27 and CSF leak.28 Spontaneous recovery from postdural puncture headache (PDPH) occurs in over 85% of patients within 6 weeks. Many forms of conservative management have been suggested and practiced, mostly without any scientific evidence to support their efficacy. Bed rest has been historically recommended, but does not lower the incidence of PDPH although it may delay its onset and decrease its intensity.29 Some authors suggest that bed rest may prevent further complications from traction and rupture of meningeal veins caused by intracranial hypotension.30 For severe and persistent headaches epidural blood patch (EBP) injections have been successfully used. Autologous blood is injected into the epidural space, where it forms a clot and seals the dural hole. Although over 90% of PDPH respond initially to EBP injections, a sustained and durable response has been identified in only 61–75%.31 Intraoperative durotomy is managed by primary dural repair, with a watertight suture of the dural defect. The key to prevention of
Fig. 105.2 (A) Parasagittal T2-weighted MRI of postoperative lumbar pseudomeningocele. (B) Axial T2-weighted MRI of the same patient, showing the pseudomeningocele communicating with the thecal sac.
Section 5: Biomechanical Disorders of the Lumbar Spine
postoperative pseudomeningocele is a meticulous primary repair of dural tears detected intraoperatively. Fine suture material such as 5-0 or 6-0 monofilament, braided or coated synthetic is suitable, although leakage of CSF can occur through the needle holes in the dura. A continuous running suture is quickest to perform, but may result in unraveling of the entire suture line if the tension is not perfect or the suture breaks. The use of magnification and coaxial illumination is essential for adequate repair. Local application of fibrin glue greatly reinforces a repair site.26,32 When a CSF leak is noticed postoperatively, surgical treatment is generally recommended for the immediate and definitive management of the lesion.19 Some authors recommend nonoperative management in a patient with a well-healed incision presenting with a soft subcutaneous bulge and no postural headache.33 Waisman and Schweppe treated seven patients by reinforcing the skin suture line, bed rest in the Trendelenburg position, and repeated puncture and drainage of the subcutaneous CSF collection. The CSF leakage stopped immediately after the incision was resutured, the subcutaneous fluctuation disappeared in 10–28 days, and an 8-year follow-up (clinical and ultrasound examination) revealed no pseudocyst formation.34 Eismont et al. reported one case where resuturing the skin stopped the CSF leakage through the incision. A symptomatic pseudomeningocele subsequently developed, and the authors recommends surgical repair of the dura for all dural leaks noted postoperatively.19 Closed subarachnoid drainage is frequently used in the management of CSF leaks33,35 and occasionally for established pseudomeningocele.36 The catheter is positioned in the subarachnoid space using fluoroscopic technique. Epidural catheter placement may be used for drainage of a pseudomeningocele.33 The proximal end of the catheter is connected to a sterile drainage system. The basis of this external CSF drainage is that a reduction of CSF pressure and preferential escape of the CSF through the catheter for 4–5 days generally allows the dural fistula to heal itself. Lumbar peritoneal shunting may play a role in the management of refractory CSF leaks.33,37 The dural opening is surgically repaired when feasible. A catheter is then introduced into the subarachnoid space, and a second catheter left in the meningocele cavity; both catheters are subcutaneously tunneled into the peritoneal cavity, where they are positioned under the diaphragm using laparoscopic assistance. The advantages of this technique including immediate mobilization of the patient, avoidance of complications of external drains and repeated aspirations, and a high success rate. The procedure is not in widespread use due to technically simpler and less invasive options being available. Occasionally, dural tears are lateral or ventral in position and not amenable to direct repair techniques. Thinned out or scarred dura adjacent to segments of thickened extradural scar tissue in the multiply operated back does not readily lend itself to direct repair. Some dural openings are irreparable after intradural procedures when the dura is abnormal or has to be partially resected. In such situations suturing fat, muscle graft, or autologous fascia lata graft over the repaired dural tear may reinforce the dural repair. Graft substitutes including cadaveric dura, silicone-coated Dacron, and bovine pericardium have been used, but are associated with the possibility of disease transmission and immunogenic tissue reaction. In previously irradiated tissue a vascularized myocutaneous flap can be rotated from an uninvolved area to the poorly vascularized defect and sutured to well-vascularized surrounding tissue. Newer techniques such as laser tissue welding are being investigated. Preliminary results show that primary repair combined with laser welding produces a higher leak pressure and tensile tissue strength than either technique used alone, with no evidence of underlying thermal tissue injury.38
Patients with established pseudomeningoceles who are not significantly disabled by their symptoms may be treated with observation alone. Follow-up MRI scans occasionally show complete resolution of small pseudomeningoceles.2 Sustained local pressure has been found to help control some symptoms of pseudomeningoceles. Leis et al.15 reported this form of treatment in a patient who was advised surgery but declined. The patient used a wide belt worn tightly around the waist and a folded towel under the belt so that it applied direct pressure over the swelling. This relieved the postural headache symptoms immediately. Repeat MRI scans done 8 weeks and 6 months after surgery showed progressive decrease in the size of the pseudomeningocele, till there was only a tiny focus of fluid left. The authors suggest a trial of focal compression for symptomatic relief of postural headache from pseudomeningocele. If symptomatic improvement is obtained, a more prolonged trial of mechanical compression may promote dural closure.15 Symptomatic pseudomeningoceles generally require surgical intervention.2,21 The operative procedure usually involves opening of the pseudomeningocele, followed by identification and closure of the dural defect with flaps from the cyst wall or a free graft. Augmentation of the repair with fibrin glue, muscle, fat, and fascial grafts is frequently necessary. Resection of overlying lamina is generally necessary for adequate visualization of the dural defect, and spinal fusion is indicated when excessive bone resection renders the spine unstable.4 Miller and Elder4 reported on the surgical treatment of 10 symptomatic pseudomeningoceles. The authors reported good results in seven patients, satisfactory results in two, and a poor result in one patient. Apart from surgical repair, the only other surgical option for pseudomeningocele is CSF diversion, a technique that is not always successful, especially when spinal fusion implants prevent the normal reapproximation of paraspinal tissues around the collection. In addition, a ball-valve mechanism at the dural fistula site may prevent complete drainage of CSF from the pseudomeningocele. The cavity could persist and reaccumulate CSF after the drain is removed.39 Complications of untreated pseudomeningocele include recurrence of radicular symptoms, the possibility of infection with resultant meningitis,23 ossification of the cyst wall producing canal stenosis and claudication,40 and rarely erosion of the bony vertebral elements from an expansile cyst.22
SPINAL HEMATOMA Introduction The term ‘hematoma’ when used in postoperative spine patients generally refers to a subcutaneous or subfascial incisional hematoma, and must be distinguished from a true spinal hematoma. The frequency of incisional hematomas depends on many factors, including the type and extent of surgery. An incidence of 0.08% (8.7 in 10 000) incisional hematomas was reported among 28 395 patients undergoing lumbar laminectomy,41 whereas rates of up to 12% have been reported following scoliosis surgery.42 True spinal hematomas occur most frequently in the epidural space (Table 105.1). The overall incidence of symptomatic spinal hematomas is very low, with a recent meta-analysis finding only 613 symptomatic patients over the past 170 years.43 Lawton et al.44 reported a 0.1% incidence (12 in 10 500) over a 14-year period comprising 10 500 spine surgery cases at one institution. Smaller asymptomatic hematomas occur more frequently than recognized in postoperative patients. When postoperative MRI is obtained, the reported incidence is 100%, even with procedures such as microdiscectomies.45 1149
Part 3: Specific Disorders
Table 105.1: Distribution of spinal hematomas according to anatomic localization43 Location
Number (n = 604)
%
Epidural
461
76.3
Subarachnoid
96
15.9
Subdural
25
4.1
Intramedullary
5
0.8
Combinations
17
2.8
The incidence of spinal hematoma following epidural/subarachnoid injection procedures is low. In a meta-analysis of 613 patients with spinal hematoma formation, Kreppel et al. reported that 10.3% (63 in 613) of these incidents occurred following lumbar puncture or spinal anesthesia.43 In a literature review of epidural hematomas after needle procedures, Adler et al. reported that 12 of 15 reported cases either had an abnormal bleeding profile or were on anticoagulant therapy.46 A review of subdural hematomas after lumbar injections showed similar results, with 17 of 19 reported patients receiving some form of anticoagulant therapy.46
Etiology In an extensive search of the literature on spinal hematomas, Kreppel et al. found a total 613 case studies reported over the last 170 years. Most cases had a multifactorial etiology, and no etiologic factor could be pinpointed in 29.7% of patients. Idiopathic spinal hematomas represented the most common category among all different age groups analyzed.43 Spontaneous epidural bleeds can arise following fibrinolytic therapy for coronary heart disease.47 Spinal hematomas also spontaneously develop from the lumbar facet joint48 and ligamentum flavum.49 The mechanism in these cases is presumed to be minor injury in the setting of degenerative changes. Arteriovenous malformations are another reported cause of spontaneous hematomas.50 Groen and Ponssen51 reported a spontaneous spinal epidural hematoma following rupture of the internal vertebral venous plexus. Spontaneous hematomas have also been reported in patients with liver disease and autoimmune conditions.52 Spinal hematomas occur rarely following spinal fractures, but are more prevalent with fractures in patients with ankylosing spondylitis.53 Spinal manipulation therapy is known to produce hematomas with resultant neurological deficits.54 Spinal injection procedures such as lumbar punctures, epidural and subdural anesthetic blocks, and therapeutic nerve root injections can lead to spinal hematoma formation. The hematomas are commonly epidural although there are a few reports of subdural hematomas. The common underlying factors in these reports are the coexistence of coagulation disorders, multiple punctures performed during the procedure, the insertion of a catheter, removal of a catheter, prior surgery, fibrosis, undetected spina bifida, and tethered cord syndrome. Preexisting coagulopathy may increase the likelihood of hematoma formation following spinal injection procedures, and the likelihood of back pain and neurologic deficit is also higher in these patients. Spinal hematoma is a recognized cause of postoperative worsening of neurological status in the first 24–48 hours following surgery. Kou et al.52 reviewed factors that predisposed to epidural hematoma formation in 12 patients who underwent lumbar laminectomy over a 10-year period. Multilevel procedures (p=0.037) and a preoperative coagulopathy (p=0.001) were significant risk factors. Age, body mass
1150
index, durotomy, and the use of postoperative drains were not statistically significant risk factors. In multilevel laminectomies, the increased exposure needed may increase the risk for bleeding from the paravertebral muscles. The larger exposures of the epidural space also increase the risk of insidious bleeding from the prominent internal vertebral venous plexus.52 The lordotic posture of the spine postoperatively may have a role in accentuating the pressure effects of a spinal hematoma. Ko and Kakiuchi55 reported on a patient who developed paraparesis 3 hours following decompressive surgery for lumbar spinal stenosis. Flexion of the spine was noticed to relieve the patient’s symptoms. The patient was positioned with the lumbar spine in sustained lumbar flexion and the deficits resolved within 5 days. Subdural spinal hematomas occur less frequently than epidural hematomas, and again are more likely with preexisting coagulopathy or following injection procedures. Accidental subdural spinal injection can occur in patients with postsurgical fibrosis causing obliteration of the epidural space, and mimics the radiographic appearance of epidural hematoma. Spinal subdural hematomas can also track down from a cranial subdural hematoma. The presence of blood within the dura may produce a fibroproliferative reaction of the leptomeninges, resulting in arachnoidal fibrosis and poorer prognosis.
Clinical features The presentation of spinal hematomas varies depending on the precipitating event, size of hematoma, canal dimensions, and location of the hematoma within the spinal column. Small hematomas are generally not evident clinically, and may be a universal phenomenon in the immediate postoperative period. Montaldi et al.56 found computed tomographic changes within the spinal canal suggestive of postoperative spinal hematoma or scar tissue in 84% of asymptomatic patients 1 week after lumbar discectomy. Kotilainen found MRI changes representing hematoma in 100% of asymptomatic patients following lumbar microdiscectomy on the first postoperative day.45 Neurologic deficits from larger spinal hematomas are infrequent. Patients with incomplete deficits fare better than those with complete paraplegia, and the location of the hematoma has a bearing on the clinical presentation as well as outcome. Spinal epidural hematomas at the lumbar cauda equina level usually fare better than hematomas at the spinal cord level. Spontaneous remission has been observed in hematomas at the cauda equina level with minor neurologic deficits.57 Spontaneous resolution has also been reported in two cases where the presentation was rapidly progressive over minutes.58 The symptoms resolved while investigations were being carried out over the next few hours. The authors suggested that while urgent decompression remains the treatment of choice in a symptomatic spinal epidural hematoma, conservative management may be indicated where there are definite signs of neurological improvement in the initial few hours. In patients who develop spontaneous spinal epidural hematomas without preceding trauma, an acute onset of local pain may be followed by radicular paresthesias. Within hours, signs of spinal cord compression can appear, presenting as progressive paraplegia and loss of sensory function. In 61 patients who developed spinal epidural hematomas after epidural puncture for anesthesia, and had been on anticoagulants, Vandermeulen et al. noted muscle weakness was the first sign in 28 of 61 patients, back pain in 23, and sensory deficit in 9.59 Paraplegia was recorded to occur within 14.5±3.7 hours after ending of the anesthetic. The most successful recovery following surgical decompression occurred in patients in whom surgical intervention was performed in less than 8 hours. In another review of five patients with spinal hematomas the authors found that four of five patients complained of acute back pain with paresthesias in both legs,
Section 5: Biomechanical Disorders of the Lumbar Spine
followed by rapidly progressive paraplegia.50 The fifth patient had an incomplete cauda equina syndrome. Slowly accumulating hematomas may result in delayed presentation up to a week following surgery. Long tract symptoms and findings may be seen if the hematoma impinges on the cervical spinal cord, following spinal manipulation or cervical epidural steroid injections. Although the clinical presentation of spinal epidural hematomas is relatively characteristic, other diagnoses need to be considered (Table 105.2)
Investigations Magnetic resonance imaging scanning is the diagnostic method of choice for evaluation of spinal hematomas (Fig. 105.3). MRI scans allow rapid evaluation of large sections of the spinal column and provide accurate information about the size and longitudinal extent of the lesion. Epidural hematomas have an isointense signal on T1weighted images. On T2-weighted images, acute hematomas show low-intensity signal in the periphery with a central high-intensity signal region. Beginning 4–14 days after the hematoma, the signal intensity increases from the periphery to the center due to the presence of methemoglobin derived from erythrocytes. Subdural hematomas can mimic epidural hematomas on MRI, but generally show high-intensity signals on both T1- and T2-weighted images. Preservation of the posterior epidural fat and visualization of the dural outline on axial images provide further clues to the subdural location of the hematoma. Intraspinal compressive lesions such as tumors or abscesses may be differentiated from subdural hematomas by virtue of a rim or uniform enhancement on MRI, whereas subdural hematomas rarely enhance. Some authors describe a 3-pointed star or ‘inverted Mercedes star’ appearance in lumbar subdural hematomas.60 CT scanning, myelography, and ultrasound have all been used to detect spinal hematomas, but do not have the sensitivity or specificity of MRI scanning.
Management An awareness of predisposing factors may substantially lower the incidence of spinal hematoma formation. For patients on anticoagulant therapy and undergoing spinal/epidural anesthetic procedures, the following guidelines may help reduce the occurrence of spinal hematoma:61 (1) atraumatic puncture, (2) a time interval of at least 60 minutes between spinal anesthesia and heparinization (based on the half-life period of heparin), and (3) close monitoring of coagulation parameters. Since the removal of epidural catheters is associated with a high incidence of bleeding complications, Sage62 recommended against the removal of spinal/epidural catheters in the first 2 hours following heparin administration, as many patients develop temporary blood concentration of heparin at this time. Following spine sur-
Table 105.2: Differential diagnosis of spinal epidural haematomas Intradural haemorrhage Spondylosis/disc herniation Infections Inflammatory pathologies Spinal cord infarction Spinal arterio-venous malformation Epidural varices
Fig. 105.3 Axial T2-weighted MRI of 83-year-old male with a thoracic epidural hematoma causing significant anteroposterior flattening of the spinal cord.
gery, most authors recommend at least 12 hours before restarting anticoagulant therapy.63 Although the use of postoperative suction drains following spine surgery is widespread, there is surprisingly limited evidence supporting this practice. In a recent Cochrane review of 21 studies in orthopedic literature on this subject, the authors found no difference in the rate of hematoma formation or other wound complications whether drains were used or not.64 Similar results were noted in a randomized trial on the efficacy of postoperative lumbar drainage on 200 patients after single-level nonfusion lumbar surgery. Patients were randomized into two groups of either receiving postoperative drains for 48 hours, or having no drain inserted. The authors found that no patient in either group developed a significant hematoma/ seroma requiring surgical drainage.65 The management of established spinal hematomas ranges from simple observation to emergency decompression surgery. The decision to treat a hematoma nonoperatively depends on the patient’s presenting symptoms, duration of symptoms, and evidence of clinical recovery in the early hours following onset of neurological deficit. In patients with no neurological deficits, nonoperative measures are reasonable. Even severe deficits have been treated with watchful expectancy and intravenous steroids when there are definite signs of neurologic improvement in the early hours following the onset of symptoms. The more spacious dimensions of the lumbar spinal canal, and the absence of spinal cord in this region lead to less damaging effects of a hematoma in the lumbar region. Younger patients with lumbar spine hematomas showing early evidence of neurological recovery can be considered for close observation. Most spinal hematomas presenting with acute neurological deficits are treated by emergency surgical decompression. The need for decompression of extrinsic cord compression has been demonstrated in experimental as well as clinical studies. Using an animal model, Delamarter et al.66 studied the effects of duration of spinal cord compression. Persistent pressure on the cord for 6 hours led to progressive necrosis within the cord, and neurologic recovery did not occur in this group following decompression. In a clinical review of 55 patients who developed spinal hematomas after spinal or epidural anesthesia and who were treated with emergency decompressive laminectomies, Vandermeulen et al found ‘good’ or ‘partial’ neurological recovery in 77% (10/13) of patients operated within 8 hours, 37.5% (3/8) of those treated within 8–24 hours, and only 17% (2/12) of those decompressed after 24 hours.59 Exceptions to the rule of urgent decompres-
1151
Part 3: Specific Disorders
sion may be made when: (1) a patient presents 48–72 hours after onset of neurologic involvement, and (2) significant recovery is noted in the initial few hours after onset of the deficit. Operative decompression should be carried out along the entire length of a hematoma to ensure adequate evacuation and maximize chances of neurologic recovery. In some cases of extensive spinal hematoma, a limited decompression may obtain similar results without the morbidity of an extensive decompression. Osmani et al. reported limited decompression for a patient who had a hematoma extending from T4 to L5. The authors performed laminectomies from T11 to L5, and then used an arterial embolectomy balloon catheter to extract the more proximally located epidural blood clots. The patient reportedly recovered ‘significant motor power’ at 2 months.67 Another option that may play a role in the future in extensive spinal hematomas is the use of thrombolytic agents locally. Thrombolysis and evacuation of hematoma is achieved by intermittent irrigation of the subdural space with recombinant tissue plasminogen activator (rt-PA), followed by saline lavage.68
SEROMA Introduction The incidence of seromas occurring after lumbar spine procedures varies from 2% to 16%, with higher rates after surgery in the elderly population.69,70 Seromas develop after various posterior spinal procedures, including scoliosis/deformity correction surgery, posterior lumbar interbody fusion, instrumented lumbar fusion procedures, and after paraspinal procedures for the treatment of CSF fistulas. Seroma also occur after implantation of spinal cord stimulators and pain pumps.
Clinical presentation In most cases, seroma formation presents with persistent clear drainage from the surgical suture line noticed in the immediate postoperative period that persists or increases in volume with time. In some cases the drainage appears from a small breakdown in an otherwise healed incision, 3–6 weeks following surgery. Complete wound dehiscence is a potential complication. Rarely, postoperative seromas can cause neural compression with recurrence or worsening of neurological deficits.
Management Attention to surgical technique with prevention of dead spaces during closure is of primary importance in the prevention of seromas. Particular attention needs to be paid to closure of the subcutaneous layer. Interrupted sutures are preferred to a running closure, to avoid the entire closure coming apart if integrity is lost at one site. The skin should not be unnecessarily undermined during the approach, in order to avoid a potential seroma cavity. A postoperative suction drain does not appear to affect the incidence of postoperative seromas.65 Wearing an abdominal binder may help prevent seroma formation after implantation of spinal cord stimulators or pain pumps.71 The diagnosis is self-evident in most cases. MRI signal characteristics of postoperative seromas include relatively well-defined lesions of low or intermediate signal intensity relative to adjacent muscle on T1-weighted images and very high signal intensity on T2-weighted images. Seromas are frequently successfully managed by one or two percutaneous needle aspirations. Sterile technique needs to be used, and the risk of bacterial contamination of the surgical incision makes this option unattractive. Gram-staining of the aspirate is recommended to rule out the possibility of infection, and antibiotic therapy insti1152
tuted if infection is detected. In situations where an infected seroma develops in the subcutaneous pocket housing a pain pump/spinal cord stimulator, antibiotic irrigation of the cavity is advised.71 Open debridement and implant removal need to be considered in all cases with recognized infection.
References 1. Barron JT. Radiologic case study. Lumbar pseudomeningocele. Orthopedics 1990; 13:603, 608–609. 2. Kumar AJ, Nambiar CS, Kanse P. Spontaneous resolution of lumbar pseudomeningocoele. Spinal Cord 2003; 41 470–472. 3. Teplick JG, Peyster RG, Teplick SK, et al. CT identification of postlaminectomy pseudomeningocele. Am J Roentgenol 1983; 140:1203–1206. 4. Miller PR, Elder FW Jr. Meningeal pseudocysts (meningocele spurius) following laminectomy. Report of ten cases. J Bone Joint Surg [Am] 1968; 50A:268–276. 5. Hyndman OR, Gerber WF. Spinal extradural cysts, congenital and acquired. Report of cases. J Neurosurg 1946; 3:474–486. 6. Benz RJ, Ibrahim ZG, Afshar P, et al. Predicting complications in elderly patients undergoing lumbar decompression. Clin Orthop Relat Res 2001; 384:116–121. 7. Silvers HR, Lewis PJ, Asch HL. Decompressive lumbar laminectomy for spinal stenosis. J Neurosurg 1993; 78:695–701. 8. Goodkin R, Laska LL. Unintended ‘incidental’ durotomy during surgery of the lumbar spine: medicolegal implications [comment]. Surg Neurol 1995; 43:4–12; discussion 12–14. 9. Swanson HS, Fincher EF. Extradural arachnoid cysts of traumatic origin. J Neurosurg 1947; 4:530–538. 10. Cammisa FP Jr, Girardi FP, Sangani PK, et al. Incidental durotomy in spine surgery. Spine 2000; 25:2663–2667. 11. Wiesel SW. The multiply operated lumbar spine. Instr Course Lect 1985; 34: 68–77. 12. Rinaldi I, Peach WF. Postoperative lumbar pseudomeningocoele. Report of 2 cases. J Neurosurg 1969; 30:504–506. 13. Turnbull DK, Shepherd DB. Post-dural puncture headache: pathogenesis, prevention and treatment. Br J Anaesth 2003; 91:718–729. 14. Iqbal J, Davis LE, Orrison WW Jr. An MRI study of lumbar puncture headaches. Headache 1995; 35:420–422. 15. Leis AA, Leis JM, Leis JR. Pseudomeningoceles: a role for mechanical compression in the treatment of dural tears. Neurology 2001; 56:1116–1117. 16. Rinaldi I, Hodges TO. Iatrogenic lumbar meningocoele: report of three cases. J Neurol Neurosurg Psychiatry 1970; 33:484–492. 17. O’Connor D, Maskery N, Griffiths WE. Pseudomeningocele nerve root entrapment after lumbar discectomy. Spine 1998; 23:1501–1502. 18. Hadani M, Findler G, Knoler N, et al. Entrapped lumbar nerve root in pseudomeningocele after laminectomy: report of three cases. Neurosurgery 1986; 19: 405–407. 19. Eismont FJ, Wiesel SW, Rothman RH. Treatment of dural tears associated with spinal surgery. J Bone Joint Surg [Am] 1981; 63A:1132–1136. 20. Ishaque MA, Crockard HA, Stevens JM. Ossified pseudomeningocoele following laminectomy: case reports and review of the literature. Eur Spine J 1997; 6: 430–432. 21. Nash L Jr, Kaufman B, Frankel VH. Postsurgical meningeal pseudocysts of the lumbar spine. Clin Orthop 1971; 75:167–178. 22. Lau KK, Stebnyckyj M, McKenzie A. Post-laminectomy pseudomeningocele: an unusual cause of bone erosion. Australas Radiol 1992; 36:262–264. 23. Koo J, Adamson R, Wagner FC Jr, et al. A new cause of chronic meningitis: infected lumbar pseudomeningocele. Am J Med 1989; 86:103–104. 24. Jamjoom AB, Tan JB. Subarachnoid haemorrhage related to a lumbosacral fusion: a case report. J Neurol Neurosurg Psychiatry 1990; 53:174–175. 25. Phillips CD, Kaptain GJ, Razack N. Depiction of a postoperative pseudomeningocele with digital subtraction myelography. Am J Neuroradiol 2002; 23:337–338. 26. Bosacco SJ, Gardner MJ, Guille JT. Evaluation and treatment of dural tears in lumbar spine surgery: a review. Clin Orthop Relat Res 2001; 389:238–247. 27. Sharma SK, Gambling DR, Joshi GP, et al. Comparison of 26-gauge Atraucan and 25-gauge Whitacre needles: insertion characteristics and complications. Can J Anaesth 1995; 42:706–710.
Section 5: Biomechanical Disorders of the Lumbar Spine 28. Cruickshank RH, Hopkinson JM. Fluid flow through dural puncture sites. An in vitro comparison of needle point types. Anaesthesia 1989; 44:415–418.
51. Groen RJ, Ponssen H. The spontaneous spinal epidural hematoma. A study of the etiology. J Neurolog Sci 1990; 98:121–138.
29. Chordas C. Post-dural puncture headache and other complications after lumbar puncture. J Pediatr Oncol Nurs 2001; 18:244–259.
52. Kou J, Fischgrund J, Biddinger A, et al. Risk factors for spinal epidural hematoma after spinal surgery. Spine 2002; 27:1670–1673.
30. Spencer HC. Postdural puncture headache: what matters in technique. Reg Anesth Pain Med 1998; 23:374–379; discussion 384–387.
53. Taggard DA, Traynelis VC. Management of cervical spinal fractures in ankylosing spondylitis with posterior fixation. Spine 2000; 25:2035–2039.
31. Duffy PJ, Crosby ET. The epidural blood patch. Resolving the controversies. Can J Anaesth 1999; 46:878–886.
54. Tseng SH, Chen Y, Lin SM, et al. Cervical epidural hematoma after spinal manipulation therapy: case report. J Trauma 2002; 52:585–586.
32. Shaffrey CI, Spotnitz WD, Shaffrey ME, et al. Neurosurgical applications of fibrin glue: augmentation of dural closure in 134 patients. Neurosurgery 1990; 26: 207–210.
55. Ko Y, Kakiuchi M. Extended posture of lumbar spine precipitating cauda equina compression arising from a postoperative epidural clot. J Orthop Sci 2001; 6: 88–91.
33. Freidberg SR. Surgical management of cerebrospinal fluid leakage after spinal surgery. In: Schmidek HH, Sweet WH, eds. Operative neurosurgical techniques – indications, techniques and results. Philadelphia: WB Saunders; 1995:2049–2054.
56. Montaldi S, Fankhauser H, Schnyder P, et al. Computed tomography of the postoperative intervertebral disc and lumbar spinal canal: investigation of twenty-five patients after successful operation for lumbar disc herniation. Neurosurgery 1988; 22:1014–1022.
34. Waisman M, Schweppe Y. Postoperative cerebrospinal fluid leakage after lumbar spine operations. Conservative treatment. Spine 1991; 16:52–53. 35. Kitchel SH, Eismont FJ, Green BA. Closed subarachnoid drainage for management of cerebrospinal fluid leakage after an operation on the spine. J Bone Joint Surg [Am] 1989; 71A:984–987. 36. Stambough JL, Templin CR, Collins J. Subarachnoid drainage of an established or chronic pseudomeningocele. J Spinal Disord 2000; 13:39–41. 37. Deen HG, Pettit PD, Sevin BU, et al. Lumbar peritoneal shunting with video-laparoscopic assistance: a useful technique for the management of refractory postoperative lumbar CSF leaks. Surg Neurol 2003; 59:473–477; discussion 477–478.
57. Egido Herrero JA, Saldana C, Jimenez A, et al. Spontaneous cervical epidural hematoma with Brown-Sequard syndrome and spontaneous resolution. Case report. J Neurosurg Sci 1992; 36:117–119. 58. Hentschel SJ, Woolfenden AR, Fairholm DJ. Resolution of spontaneous spinal epidural hematoma without surgery: report of two cases. Spine 2001; 26: E525–E537. 59. Vandermeulen EP, Van Aken H, Vermylen J. Anticoagulants and spinal-epidural anesthesia [comment]. Anesthes Analges 1994; 79:1165–1177.
38. Foyt D, Johnson JP, Kirsch AJ, et al. Dural closure with laser tissue welding. Otolaryngol Head Neck Surg 1996; 115:513–518.
60. Johnson PJ, Hahn F, McConnell J, et al. The importance of MRI findings for the diagnosis of nontraumatic lumbar subacute subdural haematomas. Acta Neurochir (Wien) 1991; 113:186–188.
39. McCormack BM, Taylor SL, Heath S, et al. Pseudomeningocele/CSF fistula in a patient with lumbar spinal implants treated with epidural blood patch and a brief course of closed subarachnoid drainage. A case report. Spine 1996; 21:2273–2276.
61. Vandermeulen EP, Vermylen G, Van Aken H. Epidural and spinal anaesthesia in patients receiving anticoagulant therapy. Baillieres Clin Anaesthesiol 1993; 7: 663–689.
40. Shimazaki K, Nishida H, Harada Y, et al. Late recurrence of spinal stenosis and claudication after laminectomy due to an ossified extradural pseudocyst. Spine 1991; 16:221–224.
62. Sage DJ. Epidurals, spinals and bleeding disorders in pregnancy: a review. Anaesth Intensive Care 1990; 18:319–326.
41. Ramirez LF, Thisted R. Complications and demographic characteristics of patients undergoing lumbar discectomy in community hospitals. Neurosurgery 1989; 25:226–230; discussion 230–231.
63. Uribe J, Moza K, Jimenez O, et al. Delayed postoperative spinal epidural hematomas. Spine J 2003; 3:125–129. 64. Parker MJ, Roberts C. Closed suction surgical wound drainage after orthopaedic surgery. Cochrane Database Syst Rev 2001; CD001825.
42. Cummine JL, Lonstein JE, Moe JH, et al. Reconstructive surgery in the adult for failed scoliosis fusion. J Bone Joint Surg [Am] 1979; 61A:1151–1161.
65. Payne DH, Fischgrund JS, Herkowitz HN, et al. Efficacy of closed wound suction drainage after single-level lumbar laminectomy. J Spinal Disord 1996; 9:401–403.
43. Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev 2003; 26:1–49.
66. Delamarter RB, Sherman J, Carr JB. Pathophysiology of spinal cord injury. Recovery after immediate and delayed decompression. J Bone Joint Surg [Am] 1995; 77A:1042–1049.
44. Lawton MT, Porter RW, Heiserman JE, et al. Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome [comment]. J Neurosurg 1995; 83:1–7. 45. Kotilainen E. Microinvasive lumbar disc surgery. A study on patients treated with microdiscectomy or percutaneous nucleotomy for disc herniation. Ann Chir Gynaecol Suppl 1994; 209:1–50. 46. Adler MD, Comi AE, Walker AR. Acute hemorrhagic complication of diagnostic lumbar puncture. Pediatr Emerg Care 2001; 17:184–188.
67. Osmani O, Afeiche N, Lakkis S. Paraplegia after epidural anesthesia in a patient with peripheral vascular disease: case report and review of the literature with a description of an original technique for hematoma evacuation. J Spinal Disord 2000; 13:85–87. 68. Little CP, Patel N, Nagaria J, et al. Use of topically applied rt-PA in the evacuation of extensive acute spinal subdural haematoma. Eur Spine J 2003; 12:12.
47. Harik SI, Raichle ME, Reis DJ. Spontaneously remitting spinal epidural hematoma in a patient on anticoagulants. N Engl J Med 1971; 284:1355–1357.
69. Greenfield RT 3rd, Capen DA, Thomas JC Jr, et al. Pedicle screw fixation for arthrodesis of the lumbosacral spine in the elderly. An outcome study. Spine 1998; 23:1470–5.
48. Nishida K, Iguchi T, Kurihara A, et al. Symptomatic hematoma of lumbar facet joint: joint apoplexy of the spine? Spine 2003; 28:E206–E208.
70. Rhee JM, Bridwell KH, Lenke LG, et al. Staged posterior surgery for severe adult spinal deformity. Spine 2003; 28:2116–2121.
49. Hirakawa K, Hanakita J, Suwa H, et al. A post-traumatic ligamentum flavum progressive hematoma: a case report. Spine 2000; 25:1182–1184.
71. Prager JP. Neuraxial medication delivery: the development and maturity of a concept for treating chronic pain of spinal origin. Spine 2002; 27:2593–2605; discussion 2606.
50. Alexiadou-Rudolf C, Ernestus RI, Nanassis K, et al. Acute nontraumatic spinal epidural hematomas. An important differential diagnosis in spinal emergencies [comment]. Spine 1998; 23:1810–1813.
1153
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar
CHAPTER
Epidural Adhesiolysis
106
Miles Day, Rinoo Shah, James Heavner and Gabor Racz
INTRODUCTION Chances are each of us will experience low back pain at some point in our lives. The usual course is rapid improvement, but 5–10% of patients develop persistent symptoms.1 In 1997, the total impact of low back pain on industry in the United States was estimated at US$171 billion.2 The medical treatment of low back pain in 1990 amounted to US$13 billion.3 Treatment varies from conservative therapy with medication and physical therapy to minimally and highly invasive pain management interventions. Surgery is sometimes required in those patients who have progressive neurological deficits or those who have failed other therapies. Surgery is successful in the majority of patients, but an unlucky few continue to have pain and neurological symptoms. A quandary arises as to whether a repeat surgery should be attempted or an alternative intervention should be sought. This is the exact quandary that the epidural adhesiolysis procedure was designed to address. It was developed to break down scar formation, deliver site-specific corticosteroids and local anesthetic drugs directly to the target, and reduce edema with hypertonic saline. Epidural adhesiolysis has afforded patients reduction in pain and neurological symptoms without the expense and sometimes long recovery period associated with repeat surgery, and often prevents the need for surgical intervention.
PATHOPHYSIOLOGY OF EPIDURAL FIBROSIS (SCAR TISSUE) AS A CAUSE OF LOW BACK PAIN WITH RADICULOPATHY The etiology of low back pain with radiculopathy is not well understood. Kuslich and colleagues addressed this issue when they performed 193 lumbar spine operations on patients given local anesthesia. Their study revealed that sciatica could only be produced by stimulation of a swollen, stretched, restricted (i.e. scarred) or compressed nerve root.4 Back pain could be produced by stimulation of several lumbar tissues, but the most common tissue of origin was the outer layer of the anulus fibrosus and posterior longitudinal ligament. Stimulation for pain generation of the facet joint capsule rarely generated low back pain, and facet synovium and cartilage surfaces of the facet or muscles were never tender.5 The contribution of fibrosis (scar tissue) to the etiology of low back pain has been debated.6–8 There are many possible etiologies of epidural fibrosis, including surgical trauma, an annular tear, infection, hematoma, or intrathecal contrast material.9 These etiologies are well documented in the literature. LaRocca and Macnab10 demonstrated the invasion of fibrous connective tissue into postoperative hematoma as a cause of epidural fibrosis, while Cooper and colleagues11 reported periradicular fibrosis and vascular abnormalities occurring with herniated intervertebral discs. McCarron et al.12 investigated
the irritative effect of nucleus pulposus upon the dural sac, adjacent nerve roots, and nerve root sleeves independent of the influence of direct compression upon these structures. Evidence of an inflammatory reaction was identified by gross inspection and microscopic analysis of spinal cord sections after homogenized autogenous nucleus pulposus was injected into the lumbar epidural space of four dogs. In the control group consisting of four dogs injected with normal saline, the spinal cord sections were grossly normal. Parke and Watanabe showed significant evidence of adhesions in cadavers with lumbar disc herniation.13 It is widely accepted that postoperative scar renders the nerve susceptible to injury via compressive phenomena.8 It is natural for connective tissue or any kind of tissue to form fibrous layers (scar tissue) as a part of the process that transpires after disruption of the intact milieu.14 Scar tissue is generally found in three components of the epidural space. Dorsal epidural scar tissue is formed by resorption of surgical hematoma and may be involved in pain generation.15 In the ventral epidural space, dense scar tissue is formed by ventral defects in the disc, which may persist despite surgical treatment and continue to produce low back pain/radiculopathy past the surgical healing phase.16 The lateral epidural space includes epiradicular structures outside the root canals, known as the lateral recess or ‘sleeves’ containing the exiting nerve root and dorsal root ganglia, which are susceptible to lateral disc defects, facet overgrowth, and neuroforaminal stenosis.17 Although scar tissue itself is not tender, an entrapped nerve root is. Kuslich et al.4 surmised that the presence of scar tissue compounded pain associated with the nerve root by fixing it in one position and thus increasing the susceptibility of the nerve root to tension or compression. They also concluded that no other tissues in the spine are capable of producing leg pain. In a study of the relationship between peridural scar evaluated by magnetic resonance imaging (MRI) and radicular pain after lumbar discectomy, Ross et al. demonstrated that subjects with extensive peridural scarring were 3.2 times more likely to experience recurrent radicular pain.18
RADIOLOGIC DIAGNOSIS OF EPIDURAL FIBROSIS Magnetic resonance imaging and computed tomography (CT) scanning are diagnostic tools with 50% and 70% sensitivity and specificity, respectively.14 CT-myelography may also be helpful. None of these imaging techniques can identify epidural fibrosis with 100% reliability. In contrast, epidurography is a technique used with considerable success and it is believed that epidural fibrosis is best diagnosed by performing an epidurogram.19–22 It can detect filling defects in good correlation with a patient’s symptoms in a real-time manner.22 A combination of more than one of these techniques will undoubtedly increase the ability to identify epidural fibrosis. 1155
Part 3: Specific Disorders
INDICATIONS FOR EPIDURAL ADHESIOLYSIS Although originally designed to treat radiculopathy secondary to epidural fibrosis following surgery, the use of epidural adhesiolysis has been expanded to treat a multitude of pain etiologies. These include:23 1. Postlaminectomy syndrome of the neck and back after surgery; 2. Disc disruption; 3. Metastatic carcinoma of the spine leading to compression fractures; 4. Multilevel degenerative arthritis; 5. Facet pain; 6. Spinal stenosis; and 7. Pain unresponsive to spinal cord stimulation and spinal opioids. Contraindications to epidural adhesiolysis include the following absolute contraindications: 1. 2. 3. 4. 5.
Sepsis; Chronic infection; Coagulopathy; Local infection at the site of the procedure; and Patient refusal.
A relative contraindication is the presence of arachnoiditis. With arachnoiditis, the tissue planes may be adhered to one another, increasing the chance of loculation of contrast or medication. It may also increase the chance of spread of the medications to the subdural or subarachnoid space, which can increase the chance of complications. Practitioners with limited experience with epidural adhesiolysis should consider referring these patients to someone with more experience.
Patient preparation Once epidural adhesiolysis has been deemed an appropriate treatment modality, the risks and benefits of the procedure should be discussed with the patient and an informed consent signed. The benefits are pain relief, improved physical function, and possible reversal of neurological symptoms. Risks include bruising, bleeding, infection, reaction to medications used (hyaluronidase, local anesthetic, corticosteroids, hypertonic saline), damage to nerves or blood vessels, no or little pain relief, bowel/bladder incontinence, worsening of pain, and paralysis. Patients with a history of urinary incontinence should have an evaluation by an urologist prior to the procedure to document the preexisting urodynamic etiology and pathology.
Anticoagulant medication Medications that prolong bleeding parameters should be withheld prior to performing epidural adhesiolysis. The length of time varies depending on the medication taken. A consultation with the patient’s primary physician should be obtained prior to stopping any of these medications. Nonsteroidal antiinflammatory drugs (NSAIDs) and aspirin should be withheld 4 days and 7–10 days prior to the procedure, respectively. Although there is much debate regarding these medications and neuraxial procedures, the authors tend to be on the conservative side. Clopidogrel (Plavix®) should be stopped 7 days prior to the adhesiolysis while ticlopidine (Ticlid®) is held 10–14 days prior.24 The warfarin (Coumadin®) withholding period is patient variable, but 5 days is usually adequate.24 Subcutaneous heparin administration should be stopped at a minimum of 12 hours prior to the procedure, while low molecular weight heparin requires a minimum of 24 hours.24 Over-the-counter medications that prolong bleeding parameters should also be withheld. These include vitamin E, gingko 1156
biloba, garlic, ginseng, and St. John’s Wort. In addition, a prothrombin time, a partial thromboplastin time, and a platelet function assay or a bleeding time is obtained to check for coagulation abnormalities. Any elevated value warrants further investigation and postponement of the procedure until those studies are complete.
Preoperative laboratory Prior to the procedure a complete blood count and a clean-catch urinalysis is obtained to check for any undiagnosed infection. An elevated white count and/or a positive urinalysis should prompt the physician to postpone the case and refer the patient to his/her primary care physician for further work-up and treatment. Adequate coagulation status can be confirmed by the prothrombin time, partial thromboplastin time, and a platelet function assay or bleeding time. The tests should be performed as close to the day of the procedure as possible. Tests performed only a few days after discontinuation of the anticoagulant medication may come back elevated, since not enough time has elapsed to allow the anticoagulant effects of the medication to resolve. The benefits of the procedure must be weighed against the potential sequelae of stopping the anticoagulant medication, and this should be discussed thoroughly with the patient.
TECHNIQUE This procedure can be performed in the cervical, thoracic, lumbar, and caudal regions of the spine. The caudal and transforaminal placement of catheters will be described in detail while highlights and slight changes in protocol will be provided for cervical and thoracic catheters. The authors’ policy is to perform this procedure under strict sterile conditions in the operating room. Prophylactic antibiotics with broad neuraxial coverage are given preprocedure. Patients will receive either ceftriaxone 1 g intravenously, or levaquin 500 mg orally in those allergic to penicillin. The same dose is also given on day 2. An anesthesiologist or nurse anesthetist provides monitored anesthesia care.
Caudal approach The patient is placed in the prone position with a pillow placed under the abdomen to correct the lumbar lordosis and a pillow under the ankles for patient comfort. The patient is asked to put his/her toes together and heels apart. This relaxes the gluteal muscles and facilitates identification of the sacral hiatus. After sterile preparation and draping, the sacral hiatus is identified via palpation or fluoroscopic guidance. A skin weal is raised with local anesthetic 1 inch lateral and 2 inches caudal to the sacral hiatus on the side opposite from the documented radiculopathy. The skin is nicked with an 18gauge cutting needle, and a 15- or 16-gauge RX Coude™ (Epimed International®) epidural needle is inserted through the nick at a 45° angle and guided fluoroscopically or by palpation towards the sacral hiatus. Once through the hiatus, the needle’s angle is dropped to approximately 30° and the needle is advanced. The advantages of the RX Coude™ over other needles are the angled tip, which enables easier direction of the catheter, and a less sharp tip. The back edge of the distal opening of the needle is designed to be a noncutting surface that allows manipulation of the catheter in and out of the needle. A Tuohy™ needle should never be used for this procedure as the back edge of the distal opening is a cutting surface and can easily shear a catheter. A properly placed needle will be inside the caudal canal below the level of the S3 foramen on anteroposterior (AP) and lateral fluoroscopic images. A needle placed above the level of the S3 foramen could potentially puncture a low-lying dura. The needle tip should cross the midline of the sacrum towards the side of the radiculopathy.
Section 5: Biomechanical Disorders of the Lumbar Spine
An epidurogram is performed using 10 mL of a non-ionic, watersoluble contrast agent. Confirm a negative aspiration for blood or cerebrospinal fluid (CSF) prior to any injection of contrast or medication. Omnipaque® and Isovue® are the agents most frequently used and are suitable for myelography.25,26 Do not use ionic, non-watersoluble contrast agents such as Hypaque® or Renagraffin® or ionic, water-soluble agents such as Conray®.27,28 These agents are not indicated for myelography. Accidental subarachnoid injections can lead to serious untoward events such as seizure and possible death. Slowly inject the contrast agent and observe for filling defects. A normal epidurogram will have a Christmas-tree pattern with the central channel being the trunk and the outline of the nerve roots making up the branches. An abnormal epidurogram will have areas where the contrast does not fill. These are the areas of presumed scarring and typically correspond to the patient’s back and radicular complaints. If vascular uptake is observed, the needle needs to be redirected. After turning the distal opening of the needle ventrolaterally, insert a TunL Kath™ or TunL-XL™ (stiffer) catheter (Epimed International®) with a bend on the distal tip through the needle. The bend should be 2.5 cm from the tip of the catheter and at a 30° angle. The bend will enable the catheter to be steered to the target level. Under continuous AP fluoroscopic guidance, advance the tip of the catheter towards the ventrolateral epidural space of the desired level. The catheter can be steered by gently twisting the catheter in a clockwise or counterclockwise direction. Avoid ‘propellering’ the tip, i.e. twisting the tip in circles, as this makes it more difficult to direct the catheter. Do not advance the catheter up the middle of the sacrum as this makes guiding the catheter to the ventrolateral epidural space more difficult. Ideal location of the tip of the catheter in the AP projection is in the foramen just below the midportion of the pedicle shadow (Fig. 106.1A). Check a lateral projection to confirm that the catheter tip is in the ventral epidural space (Fig. 106.1B). Under real-time fluoroscopy, inject 2–3 mL of additional contrast through the catheter in an attempt to outline the ‘scarred in’ nerve root. If vascular uptake is noted, reposition the catheter and reinject contrast. Preferably one should not have vascular run-off, but infre-
A
quently secondary to venous congestion an epidural pattern is seen with a small amount of vascular spread. This is acceptable as long as the vascular uptake is venous in nature and not arterial. Extra caution should be taken when injecting the local anesthetic to prevent local anesthetic toxicity. Any arterial spread of contrast always warrants repositioning of the catheter. The authors have never observed intraarterial catheter placement in 25 years of placing soft, spring-tipped catheters. Inject 1500 units of hyaluronidase dissolved in 10 mL of preservative-free normal saline (PFNS). This may cause some discomfort, so a slow injection is favorable. Observe for ‘opening up,’ i.e. visualization, of the ‘scarred in’ nerve root. A 3 mL test dose of a 10 mL local anesthetic/steroid (LA/S) solution is then given. Our institution uses 4 mg of dexamethasone mixed with 9 mL of 0.2% ropivacaine. Ropivacaine is used instead of bupivacaine for two reasons: the former produces a preferential sensory block, and is less cardiotoxic than racemic bupivacaine. Doses for other corticosteroids commonly used are 40–80 mg methylprednisolone (Depo-Medrol™), 25–50 mg triamcinolone diacetate (Aristocort™), 40–80 mg triamcinolone acetonide (Kenalog™), and 6–12 mg betamethasone (Celestone Soluspan™). If after 5 minutes there is no evidence of intrathecal or intravascular injection of medication, inject the remaining 7 mL of the LA/S solution. Remove the needle under continuous fluoroscopic guidance to ensure the catheter remains at the target level. Secure the catheter to the skin using nonabsorbable suture and coat the skin puncture site with antimicrobial ointment. Apply a sterile dressing and attach a 20 micron filter to the end of the catheter. Affix the exposed portion of the catheter to the patient with tape and transport the patient to the recovery area. A 20 minute period should elapse between the last injection of the LA/S solution and the start of the hypertonic (10%) saline infusion. This is necessary to ensure that a subdural injection of the local anesthetic/steroid solution has not occurred. A subdural block can mimic a subarachnoid block but takes longer to establish. If the patient develops a subarachnoid or subdural block at any point during the procedure, the catheter should be removed and the remainder of
B
Fig. 106.1 (A) Catheter tip at the left L4–5 foramen. (B) Catheter in the ventral epidural space at L5–S1. 1157
Part 3: Specific Disorders
the adhesiolysis canceled. The patient needs to be observed to document the resolution of the motor and sensory block and to document the absence of bladder/bowel dysfunction. Ten milliliters of hypertonic saline is then infused through the catheter over 30 minutes. If the patient complains of discomfort, the infusion is stopped and an additional 2–3 mL of 0.2% ropivacaine is injected and the infusion is restarted. Alternatively, 50–100 mg of fentanyl can be injected epidurally in lieu of the local anesthetic. After completion of the hypertonic saline infusion, the catheter is slowly flushed with 2 mL of preservative-free normal saline and the catheter is capped. Our policy is to admit the patient for a 23-hour observation status and do a second and third hypertonic saline infusion the following day. On postcatheter insertion day 2, the catheter is twice injected (separated by 4 hours) with 10 mL of 0.2% ropivacaine without steroid and infused with 10 mL hypertonic saline (10%) using the same technique and precautions as the day 1 infusion. At the end of the third infusion the catheter is removed and a sterile dressing applied. The patient is discharged home with 5 days of oral cefalexin at 500 mg twice a day or oral levaquin at 500 mg once a day in penicillin allergic patients. Clinic follow-up is in 30 days.
Transforaminal catheters Patients with an additional level of radiculopathy or those where the target level cannot be reached by the caudal approach may require placement of a second catheter. The second catheter is placed into the ventral epidural space via a transforaminal approach. After the target level is identified with an AP fluoroscopic image, the superior endplate of the vertebra that comprises the caudal portion of the foramina is ‘squared,’ i.e. the anterior and posterior shadows of the vertebral endplate are superimposed. The angle is typically 15–20° in a caudocephalad direction. The fluoroscope is then obliqued approximately 15° to the side of the radiculopathy and adjusted until the spinous process is rotated to the opposite side. This fluoroscope positioning allows the best visualization of
A
the superior articular process (SAP) that forms the inferoposterior portion of the targeted foramen. The image of the SAP should be superimposed upon the shadow of the disc space on the oblique view. The tip of the SAP is the target for needle placement. Raise a skin wheal slightly lateral to the shadow of the tip of the SAP. Pierce the skin with an 18-gauge needle and then insert a 16-gauge RX Coude™ needle and advance using gun-barrel technique towards the tip of the SAP. Continue to advance the needle medially towards the SAP until the tip contacts bone. Rotate the tip of the needle 180° laterally and advance about 5 mm. As the needle is advanced slowly, a clear ‘pop’ is felt as the needle penetrates the intertransverse ligament. Rotate the needle back medially 180°. Obtain a lateral fluoroscopic image. The tip of the needle should be just past the SAP in the posterior foramen. In the AP plane the tip of the needle should be just medial of the lateral border of the pedicle shadow. Under continuous AP fluoroscopy, insert the catheter slowly into the foramen and advance until the tip is past the medial border of the pedicle shadow (Fig. 106.2A). Confirm the catheter is in the anterior epidural space with a lateral image (Fig. 106.2B). Anatomically, the catheter is in the foramen above or below the exiting nerve root. If the catheter cannot be advanced, it usually means the needle is either too posterior or too lateral to the foramen. It can also indicate the foramen is too stenotic to allow passage of the catheter. The needle can be advanced a few millimeters anteriorly in relation to the foramen, and that will also move it slightly more medially into the foramen. If the catheter still will not pass, the initial insertion of the needle will need to be more lateral. Therefore, the fluoroscope angle will be about 20° instead of 15°. The curve of the needle usually facilitates easy catheter placement. Inject 1–2 mL of contrast to confirm epidural spread. When a caudal and a transforaminal catheter are placed, the 1500 units of hyaluronidase are divided evenly between the two catheters (5 mL of the hyaluronidase/saline solution into each). The LA/S solution is also divided evenly, but a volume of 15 mL (1 mL steroid and 14 mL
B
Fig. 106.2 (A) Transforaminal catheter at L1–2. The tip of the catheter is midline at the shadow of the spinous process. (B) Catheter in the ventral epidural space at L1–2. 1158
Section 5: Biomechanical Disorders of the Lumbar Spine
0.2% ropivacaine) is used instead of 10 mL. Remove the needle under fluoroscopic guidance to make sure the catheter does not move from the original position in the epidural space. Secure and cover the catheter as described above. The hypertonic saline solution is infused at a volume of 7.5 mL per catheter over 30 minutes. It behooves the practitioner to check the position of the transforaminal catheter under fluoroscopy prior to performing the second and third infusions. The catheter may advance across the epidural space into the contralateral foramen or paraspinous muscles or more commonly back out of the epidural space into the ipsilateral paraspinous muscles. This results in deposition of the medication in the paravertebral tissue rather than in the epidural space. As with the caudal approach, remove the transforaminal catheter after the third infusion.
Cervical lysis of adhesions The success of the caudal approach for lysis of adhesions led to the application of the same technique to the cervical epidural space. The indications and preprocedure work-up are the same as those for the caudal lysis technique, but there are a few differences in technique and volumes of medication used. The epidural space should be entered via the upper thoracic interspaces using a paramedian approach on the contralateral side. The most common levels are T1–2 and T2–3. Entry at these levels allows for a sufficient length of the catheter to remain in the epidural space after the target level has been reached. If the target is the lower cervical nerve roots, a more caudal interspace should be selected. We place the patient in the left lateral decubitus position, but use a prone approach in larger patients. A technique referred to as the ‘3-D technique’ is utilized to facilitate entry into the epidural space. The ‘3-D’ stands for Direction, Depth, and Direction. Using an AP fluoroscopic image, the initial Direction of the 15- or 16-gauge RX-Coude™ is determined. Using a modified paramedian approach with the skin entry one and a half levels below the target interlaminar space, advance and direct the needle toward the midpoint of the chosen interlaminar space with the opening of the needle pointing medially. Once the needle engages the deeper tissue planes (usually at 2–3 cm), check the Depth of the needle with a lateral image. Advance the needle towards the epidural space and check repeat images to confirm the Depth. The posterior border of the dorsal epidural space can be visualized by identifying the junction of the base of the spinous process of the vertebral body with its lamina. This junction creates a distinct radiopaque ‘straight line.’ The epidural space is just anterior to this ‘straight line.’ Once the needle is close to the epidural space, get an AP fluoroscopic image to recheck the Direction of the needle. If the tip of the needle has crossed the midline as defined by the spinous processes of the vertebral bodies, pull the needle back and redirect. The ‘3-D’ process can be repeated as many times as is necessary to get the needle into the perfect position. Using loss of resistance technique, advance the needle into the epidural space with the tip of the RX-Coude™ pointed caudally. Once the tip is in the epidural space, rotate the tip cephalad and inject 1–2 mL of contrast to confirm entry. Inject an additional 4 mL to complete the epidurogram. As with the caudal epidurogram, look for filling defects. It is extremely important to visualize spread of the contrast in the cephalad and caudal directions. Loculation of contrast in a small area must be avoided as this can significantly increase the pressure in the epidural space and can compromise the already tenuous arterial blood supply to the spinal cord. Place a bend on the catheter as previously described for the caudal approach and insert it through the needle. The opening of the needle should be directed towards the target side. Slowly advance the catheter to the lateral gutter and direct it cephalad. Redirect the catheter as needed and once
the target level has been reached, turn the tip of the catheter towards the foramen. Inject 0.5–1 mL of contrast to visualize the target nerve root. Make sure there is run-off of contrast out of the foramen (Fig. 106.3). Slowly instill 1500 units of hyaluronidase (Wydase™) dissolved in 5 mL of preservative-free normal saline (PFNS) (6 mL total). Follow this with 1–2 mL of additional contrast and observe for ‘opening-up’ of the ‘scarred-in’ nerve root. Give a 2 mL test dose of a 6 mL solution of LA/S. Our combination is 5 mL of 0.2% ropivacaine and 4 mg dexamethasone. If after 5 minutes there is no evidence of intrathecal or intravascular spread, inject the remaining 4 mL. Remove the needle, and secure and dress the catheter as previously described. Once 20 minutes have passed since the last dose of the LA/S solution and if there is no evidence of a subarachnoid or subdural block, start an infusion of 5 mL of hypertonic saline over 30 minutes. At the end of the infusion, flush the catheter with 1–2 mL of PFNS and cap the catheter. The second and third infusions are performed on the next day with 6 mL of 0.2% ropivacaine without steroid and 5 mL of hypertonic saline using the same technique and precautions described for the first infusion. The catheter is removed and prophylactic antibiotics are prescribed. Clinic follow-up is 30 days.
Thoracic lysis of adhesions The technique for entry into the thoracic epidural space for adhesiolysis is identical to that for the cervical region. Always remember the 3-D technique. Make sure to get a true lateral when checking the depth of the needle. This can be obtained by superimposing the rib shadows upon one another. The target is still the ventrolateral epidural space with the tip of the catheter in the foramen of the desired level. The major difference for thoracic lysis compared to the caudal and cervical techniques is the volumes of the various injectates. Volumes of 8 mL are used for the contrast, hyaluronidase, LA/S, and hypertonic saline.
Fig. 106.3 Cervical catheter and epidurogram. Note run-off of the contrast medium caudally and also out of the foramen. 1159
Part 3: Specific Disorders
Epidural mapping In patients with multilevel radiculopathy and complex pain, it can be difficult to determine from where the majority of the pain is emanating. We have been using a technique, which we have termed ‘mapping,’ to locate the most painful nerve root with stimulation and then carry out the adhesiolysis at that level. There are several references in the literature regarding the use of stimulation to confirm epidural placement of a catheter and for nerve root localization.29 The TunL Kath™ and the TunL-XL™ catheter can be used as stimulating catheters to identify the nerve root(s). After entering the epidural space, advance the catheter into the ventrolateral epidural space past the suspected target level. Make sure the tip of the catheter is pointing laterally towards the foramina, just below the pedicle. Pull the catheter stylet back approximately 1 cm. Using alligator clips, attach the cathode to the stylet and ground the anode on an EKG pad or a 22-gauge needle inserted into the skin. Apply electrical stimulation with a Medtronic® trail stimulating box with a rate of 50 pulses per second, a pulse width of 450 milliseconds, and an internal amplitude of 3 volts, dialing up the amplitude until a paresthesia is perceived. Inquire of the patient as to whether or not the paresthesia is felt in the area of the patient’s greatest pain. This process is repeated at each successive level until the most painful nerve root is identified. Once identified, the adhesiolysis is carried out at that level.
COMPLICATIONS As with any invasive procedure, complications are possible. These include: bleeding, infection, headache, damage to nerves or blood vessels, catheter shearing, bowel/bladder dysfunction, sexual dysfunction, paralysis, spinal cord compression from loculation of the injected fluids or hematoma, subdural or subarachnoid injection of local anesthetic or hypertonic saline, and reactions to the medications used. We also include on the permit that the patient may experience an increase in pain or no pain relief at all.
OUTCOMES Racz and Holubec first reported on epidural adhesiolysis in 1989.30 There were slight variations in the protocol compared to today’s protocol, namely the dose of local anesthetic and the fact that hyaluronidase was not used. Catheter placement was lesion-specific, i.e. the tip of the catheter was placed in the foramen corresponding to the vertebral level and side of the suspected adhesions. This retrospective analysis conducted 6–12 months postprocedure reported initial pain relief in 72.2% of patients (n=72) at time of discharge. Relief was sustained in 37.5% and 30.5% of patients at 1 and 3 months, respectively. Fortythree percent decreased their frequency and dosage of medication use and 16.7% discontinued their medications altogether. In total, 30.6% of patients returned to work or returned to daily functions. At a presentation at the 7th World Congress on pain, Arthur and colleagues reported on epidural adhesiolysis in 100 patients of whom 50 received hyaluronidase as part of the procedure.31 In the hyaluronidase group, 81.6% of the participants had initial pain relief, with 12.3% having persistent relief; 68% of the no hyaluronidase group had relief of pain, with 14% having persistent relief. In 1994, Stolker et al. added hyaluronidase to the procedure, but omitted the hypertonic saline. In a study of 28 patients, they reported greater than 50% pain reduction in 64% of patients at one year.32 They stressed the importance of patient selection and felt that the effectiveness of adhesiolysis was based on the effect of the hyaluronidase on the adhesions and the action of the local anesthetic and steroids on the sinuvertebral nerve. 1160
Devulder and colleagues published a study of 34 patients with failed back surgery syndrome in whom epidural fibrosis was suspected or proved with MRI.33 An epidural catheter was inserted via the sacral hiatus to a distance of 10 cm into the caudal canal. Injections of contrast dye, local anesthetic, corticosteroid, and hypertonic saline (10%) were carried out daily for 3 days. No hyaluronidase was used. Filling defects were noted in 30 of 34 patients, but significant pain relief was only noted in seven patients at 1 month, two patients at 3 months, and none at 12 months. They concluded that epidurography may confirm epidural filling defects for contrast dye in patients with filling defects, but a better contrast dye spread, assuming scar lysis, does not guarantee sustained pain relief. This study was criticized for lack of lesion-specific catheter placement resulting in non-specific drug delivery.34 Heavner and colleagues performed a prospective randomized trial of lesion-specific epidural adhesiolysis on 59 patients with chronic intractable low back pain.35 The patients were assigned to one of four epidural adhesiolysis treatment groups: (1) hypertonic (10%) saline plus hyaluronidase, (2) hypertonic saline, (3) isotonic (0.9%) saline, or (4) isotonic saline plus hyaluronidase. All treatment groups received corticosteroid and local anesthetic. Overall across all four treatment groups, 83% of patients had significant pain relief at 1 month compared to 49% at 3 months, 43% at 6 months, and 49% at 12 months. Manchikanti et al. performed a retrospective, randomized evaluation of a modified Racz adhesiolysis protocol in 232 patients with low back pain.36 The study involved lesion-specific catheter placement, but the usual 3-day procedure was reduced to a 2-day (group I) and 1-day (group II) procedure. Group I had 103 patients and group II had 129 patients. Other changes included changing the local anesthetic from bupivacaine to lidocaine, substituting methylprednisolone acetate or betamethasone acetate and phosphate for triamcinolone diacetate, and reduction of the volume of injectate. Of the patients in groups I and II, 62% and 58% had >50% pain relief at 1 month, respectively, with these percentages decreasing to 22% and 11% at 3 months, 8% and 7% at 6 months, and 2% and 3% at 1 year. Of significant interest is that the percentage of patients receiving >50% pain relief after four procedures increased to 79% and 90% at 1 month, 50% and 36% at 3 months, 29% and 19% at 6 months, and 7% and 8% at 1 year for groups I and II, respectively. Short-term relief of pain was demonstrated, but long-term relief was not. In a randomized, prospective study, Manchikanti and colleagues evaluated a 1-day epidural adhesiolysis procedure against a control group of patients who received conservative therapy.37 Results showed that cumulative relief, defined as relief greater than 50% with one to three injections, in the treatment group was 97% at 3 months, 93% at 6 months, and 47% at 1 year. The study also showed that overall health status improved significantly in the adhesiolysis group. Recently, Manchikanti et al. published their results of a randomized, double-blind, controlled study on the effectiveness of 1-day lumbar adhesiolysis and hypertonic saline neurolysis in treatment of chronic low back pain.38 Seventy-five patients whose pain was unresponsive to conservative modalities were randomized into one of three treatment groups. Group I (control group) underwent catheterization without adhesiolysis, followed by injection of local anesthetic, normal saline, and steroid. Group II consisted of catheterization and adhesiolysis, followed by injection of local anesthetic, normal saline, and steroid. Group III consisted of adhesiolysis, followed by injection of local anesthetic, hypertonic saline, and steroid. Patients were allowed to have additional injections based on the response, either after unblinding or without unblinding after 3 months. Patients without unblinding were offered either the assigned treatment or another treatment based on their response. If the patients in group I or II received
Section 5: Biomechanical Disorders of the Lumbar Spine
adhesiolysis and injection of hypertonic saline, they were considered withdrawn, and no subsequent data were collected. Outcomes were assessed at 3, 6, and 12 months using visual analog scale pain scores, Oswestry Disability Index, opioid intake, range of motion measurement, and P-3®. Significant pain relief was defined as average relief of 50% or greater. Seventy-two percent of patients in group III, 60% of patients in group II, and 0% in group I showed significant pain relief at 12 months. The average number of treatments for 1 year were 2.76 in group II and 2.16 in group III. Duration of significant relief with the first procedure was 2.8 ± 1.49 months and 3.8±3.37 months in groups II and III, respectively. Significant pain relief (=50%) was also associated with improvement in Oswestry Disability Index, range of motion, and psychological status.
EPIDURAL ENDOSCOPIC ADHESIOLYSIS Spinal endoscopy dates back to 1931 when Burman published the first experience with what was to become known as myeloscopy.39 Several more studies were published over the ensuing decades, and a historical review of said studies can be found in an article by Saberski and Brull.40 In 1991, Heavner and colleagues reported endoscopic evaluation of the epidural and subarachnoid spaces in rabbits, dogs, and human cadavers with aid of a flexible endoscope.41 Numerous articles followed over the next decade describing various aspects of spinal endoscopy, including clinical basis, protocol, safety, and costeffectiveness.42–45 Epidural endoscopic adhesiolysis is a minimally invasive technique for adhesiolysis and accurate placement of injectate intended for delivery in the epidural space.45–47 It is based on the premise that the epidural space can be accessed safely by using flexible fiberoptic catheters entering via the sacral hiatus.45 It facilitates three-dimensional visualization of the contents of the epidural space and provides the physician with the ability to steer the catheter toward structures of interest. This procedure allows examination of specific nerve root pathology and treatment by injection of medication onto the nerve root, along with the ability to expand the epidural space with normal saline. Indications and patient preoperative preparation are identical to those for epidural adhesiolysis. The epidural placement of an endoscope is most frequently performed via the sacral hiatus. This is based on anatomy, equipment, and experience.47 A midline entry of the epidural needle through the sacral hiatus is used instead of the usual paramedian approach. An epidurogram with water-soluble, non-ionic contrast is performed to visually assess the nerve roots. Insertion of the endoscope through the sacral hiatus will vary slightly depending on the type of endoscope used, but the Seldinger technique is the method of insertion used most frequently. Once inside the caudal epidural space, the endoscope is advanced using direct video and fluoroscopic guidance. There is a definite learning curve with epidural endoscopy and the operating physician should proceed with caution. In conjunction with gentle irrigation using normal saline, the myeloscope and catheter are manipulated and rotated in many directions to identify structures, namely nerve roots, at various levels. An endoscope with a working channel can facilitate placement of the epidural catheter. After the target level is reached, the epidural catheter is placed through the working channel and once it exits the distal end the endoscope is removed, leaving the catheter at the targeted nerve root (Fig. 106.4). Adhesiolysis is accomplished by the distention of the epidural space with the saline irrigation and by mechanical means using the endoscope and hyaluronidase. The LA/S and hypertonic saline protocol as previously described is then carried out.
Fig. 106.4 Endoscopic epidural adhesiolysis. Note the catheter exiting the working channel of the endoscope.
There is a paucity of literature with regards to epidural adhesiolysis with myeloscopy. Richardson et al. published a prospective case series in 34 patients with severe chronic low back pain.48 All had epidural scar tissue with 14 patients having dense adhesions. Followup over a 12-month period showed statistically significant reductions in pain score and disability. In two separate retrospective studies, Manchikanti and colleagues evaluated the effectiveness of endoscopic adhesiolysis in 85 patients with chronic low back pain with or without history of laminectomy and 60 patients with postlumbar laminectomy syndrome.45,49 In the first study, all 85 patients received significant pain relief (≥50%) in the first month, but this decreased to 77%, 52%, and 21% at 3, 6, and 12 months, respectively. All of the patients in the second study had significant analgesia in the first month which dwindled to 80%, 52%, and 22% at the 3-, 6-, and 12-month follow-up visits, respectively. As with adhesiolysis without endoscopy, short-term relief was afforded.
PHYSICAL THERAPY We routinely have our adhesiolysis patients engage in neural flossing exercises once the procedure is completed. These exercises involve performing repetitive, slow, rhythmic nonpainful distal initiation of dural movements (Fig. 106.5).50 The goal is to restore the normal movement of the involved nerve root in the foramen and to prevent adhesions from reforming. The patient is encouraged to do one set of ten repetitions of each of the three exercises twice a day. The patient is taught these exercises by a physical therapist prior to discharge from our facility.
CONCLUSION Epidural adhesiolysis has evolved over the years as an important treatment option for patients with intractable cervical, thoracic, and low back and leg pain. Studies show that patients are able to enjoy significant pain relief and restoration of function over several months. Manchikanti’s studies show that the amount and duration of relief can be achieved by repeat procedures. Endoscopy offers direct visualization of the affected nerve roots in addition to mechanical adhesiolysis, and may become more mainstream as the technique is 1161
Part 3: Specific Disorders
A
C
B
refined. More prospective, randomized, controlled studies need to be performed to further solidify epidural adhesiolysis’s position in the treatment algorithm of patients with intractable pain refractory to previous treatments.
References 1. Lawrence R, Helmick C, Arnett F, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 1998; 41(5):778–799. 2. Straus B. Chronic pain of spinal origin: the costs of intervention. Spine 2002; 27(22):2614–2619. 3. National Center for Health Statistics. National Hospital Discharge Survey. Report No. PB92-500818. Washington DC: US Department of Health and Human Services, Centers for Disease Control; 1990. 4. Kuslich S, Ulstrom C, Michael C. The tissue origin of low back pain and sciatica. Orthop Clin North Am 1991; 22:181–187. 5. Racz G, Noe C, Heavner J. Selective spinal injections for lower back pain. Curr Rev Pain 1999; 3:333–341. 6. Anderson S. A rationale for the treatment algorithm of failed back surgery syndrome. Curr Rev Pain 2000; 4:396–406. 7. Pawl R. Arachnoiditis and epidural fibrosis: the relationship to chronic pain. Curr Rev Pain 1998; 2:93–99. 8. Cervellini P, Curri D, et al. Computed tomography of epidural fibrosis after discectomy. A comparison between symptomatic and asymptomatic patients. Neurosurgery 1988; 6:710–713. 9. Manchikanti L, Staats P, Singh V. Evidence-based practice guidelines for interventional techniques in the management of chronic spinal pain. Pain Phys 2003; 6:3–81.
1162
Fig. 106.5 (A–C) Postepidural adhesiolysis exercises to prevent rescarring.
12. McCarron R, Wimpee M, Hudkins P, et al. The inflammatory effects of nucleus pulposus: a possible element in the pathogenesis of low back pain. Spine 1987; 12:760–764. 13. Parke W, Watanabe R. Adhesions of the ventral lumbar dura. An adjunct source of discogenic pain? Spine 1990; 15:300–303. 14. Viesca C, Racz G, Day M. Special techniques in pain management: lysis of adhesions. Anesthesiol Clin N Am 2003; 21:745–766. 15. Songer M, Ghosh L, Spencer D. Effects of sodium hyaluronate on peridural fibrosis after lumbar laminectomy and discectomy. Spine 1990; 15:550–554. 16. Key J, Ford L. Experimental intervertebral disc lesions. J Bone Joint Surg [Am] 1948; 30:621–630. 17. Olmarker K, Rydevik B. Pathophysiology of sciatica. Orthop Clin N Am 1991; 22:223–233. 18. Ross J, Robertson J, Frederickson R, et al. Association between peridural scar and recurrent radicular pain after lumbar discectomy: magnetic resonance evaluation. Neurosurgery 1996; 38:855–863. 19. Hatten H Jr. Lumbar epidurography with metrizamide. Radiology 1980; 137: 129–136. 20. Stewart H, Quinnell R, Dann N. Epidurography in the management of sciatica. Br J Rheumatol 1987; 26(6):424–429. 21. Devulder J, Bogaert L, Castille F, et al. Relevance of epidurography and epidural adhesiolysis in chronic failed back surgery patients. Clin J Pain 1995; 11:147–150. 22. Manchikanti L, Bakhit C, Pampati V. Role of epidurography in caudal neuroplasty. Pain Digest 1998; 8:277–281. 23. Day M, Racz G. Technique of caudal neuroplasty. Pain Digest 1999; 9(4):255–257. 24. Horlocker T, Wedel D, et al. Regional anesthesia in the anticoagulated patient: defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg Anesth Pain Med 2003; 28:172–197.
10. LaRocca H, Macnab I. The laminectomy membrane: studies in its evolution, characteristics, effects and prophylaxis in dogs. J Bone Joint Surgery 1974; 5613:545–550.
25. Omnipaque product insert. Princeton, NJ, Nycomed, Inc.
11. Cooper R, Freemont A, et al. Herniated intervertebral disc-associated periradicular fibrosis and vascular abnormalities occur without inflammatory cell infiltration. Spine 1995; 20:591–598.
27. Hypaque product insert. Princeton, NJ, Amersham Health, Inc.
26. Isovue product insert. Princeton, NJ, Bracco Diagnostics, Inc. 28. Conray product insert. Phillipsburg, NJ, Mallinckrodt, Inc.
Section 5: Biomechanical Disorders of the Lumbar Spine 29. Larkin T, Carragee E, Cohen S. A novel technique for delivery of epidural steroids and diagnosing the level of nerve root pathology. J Spinal Disord Tech 2003; 16(2):186–192. 30. Racz G, Holubec J. Lysis of adhesions in the epidural space. In: Raj P, ed. Techniques of neurolysis. Boston: Kluwer Academic; 1989:57–72. 31. Arthur J, Racz G, et al. Epidural space: identification of filling defects and lysis of adhesions in the treatment of chronic painful conditions. Abstracts of the 7th World Congress on Pain. Paris: IASP Publications; 1993.
39. Burman M. Myeloscopy or the direct visualization of the spinal canal and its contents. J Bone Joint Surg 1931; 13:695–696. 40. Saberski L, Brull S. Spinal and epidural endoscopy: a historical review. Yale J Biol Med 1995; 68:7–15. 41. Heavner J, Cholkhavatia S, Kizelshteyn G. Percutaneous evaluation of the epidural and subarachnoid space with the flexible endoscope. Reg Anesth 1991; 151:85. 42. Saberski L, Kitahata L. Direct visualization of the lumbosacral epidural space through the sacral hiatus. Anesth Analg 1995; 80:839–840.
32. Stolker R, Vervest A, Gerbrand J. The management of chronic spinal pain by blockades: a review. Pain 1994; 58:1–19.
43. Saberski L, Kitahata L. Review of the clinical basis and protocol for epidural endoscopy. Connecticut Med 1996; 60:70–73.
33. Devulder J, Bogaert L, Castille F, et al. Relevance of epidurography and epidural adhesiolysis in chronic failed back surgery patients. Clin J Pain 1995;1 1:147–150.
44. Saberski L. A retrospective analysis of spinal canal endoscopy and laminectomy outcomes data. Pain Phys 2000; 3:193–196.
34. Racz G, Heavner J. In response to article by Drs. Devulder et al. Clin J Pain 1995; 11:151–154.
45. Manchikanti L, Pakanati R, Pampati V, et al. The value and safety of epidural endoscopic adhesiolysis. Am J Anesthesiol 2000; 27:275–279.
35. Heavner J, Racz G, Raj P. Percutaneous epidural neuroplasty: prospective evaluation of 0.9% saline versus 10% saline with or without hyaluronidase. Reg Anesth Pain Med 1999; 24:202–207.
46. Addison R. Spinal endoscopy. Cur Rev Pain 1999; 3:116–120.
36. Manchikanti L, Pakanati R, Bakhit C, et al. Role of adhesiolysis and hypertonic saline neurolysis in management of low back pain: evaluation of modification of the Racz protocol. Pain Digest 1999; 9:91–96.
47. Manchikanti L, Singh V. Epidural lysis of adhesions and myeloscopy. Curr Pain Headache Reports 2002; 6:427–435. 48. Richardson J, McGurgan P, Cheema S, et al. Spinal endoscopy in chronic low back pain with radiculopathy. A prospective case series. Anaesthesia 2001; 56:454–460.
37. Manchikanti L, Pampati V, Fellow B, et al. Role of one day epidural adhesiolysis in management of chronic low back pain: a randomized clinical trial. Pain Phys 2001; 4:153–166.
49. Manchikanti L, Vidyasagar P, Bakhit C, et al. Non-endoscopic and endoscopic adhesiolysis in post lumbar laminectomy syndrome: a one-year outcome study and cost effectiveness analysis. Pain Phys 1999; 2:52–58.
38. Manchikanti L, Rivera J, Pampati V, et al. One day lumbar adhesiolysis and hypertonic saline neurolysis in treatment of chronic low back pain: a randomized, doubleblind trial. Pain Phys 2004; 7:177–186.
50. Sizer P, Phelps V, Dedrick G, et al. Differential diagnosis and management of spinal nerve-root related pain. Pain Practice 2002; 2:98–121.
1163
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar
CHAPTER
107
Spinal Cord Stimulation in Chronic Pain Robert E. Windsor, Markus Niederwanger and Steven Lobel
INTRODUCTION Since the first published paper on spinal cord stimulation (SCS) by Shealy in 1967 there have been a total of over 2000 articles, presentations, symposia, and abstracts on the topic of neuroaugmentation.88,92 The long-term results of SCS published in the 1970s were disappointing yet promising.28,30,32,93 Most of the studies published in the 1970s and early 1980s demonstrated success rates of approximately 40%.12 As with many new devices, problems included poorly designed hardware and software, inadequate patient selection criteria, and suboptimal surgical technique. Early on, the hardware typically consisted of a single or dual electrode system that was implanted epidurally. They provided a small electrical field and thus were unable to consistently stimulate the spinal cord. In addition, these systems were implanted via laminectomy or laminotomy with the patient under general anesthesia, thus eliminating the possibility of surgeon–patient interaction. The electrodes were commonly implanted in the high thoracic or lower cervical region for lumbar pain syndromes and patients were not consistently screened for psychological dysfunction, drug habituation, secondary gain issues, pain topography, and quality of pain. All of these factors have considerable impact on the overall efficacy of SCS. Significant advances in SCS have been made in recent years. The hardware is more durable and the electrode size and interelectrode distance have been improved. Improved software allows for more complex programming and multiple, simultaneously operating programs which generally allows for improved coverage and pain relief of difficult pain patterns. The devices may be implanted percutaneously under fluoroscopic guidance, which allows operator–patient interaction and may lead to more accurate positioning of SCS leads. Paddlestyle leads implanted via laminectomy may have certain advantages relating to energy consumption and long-term maintenance of back pain. Three decades of experience have provided improved patient selection criteria. The net result is an improved capacity to control chronic pain.12 This chapter will discuss the clinical indications, outcomes, complications, and other methods of implantation which may positively impact future outcomes and areas of study.
PAIN ANATOMY AND PHYSIOLOGY Pain is an uncomfortable sensation associated with an emotional response.35,106 The International Association for the Study of Pain (IASP) defined pain as ‘an unpleasant sensory and emotional experience associated with actual and potential tissue damage, or described in terms of such damage.’35 It may originate from stimulation of chemical, mechanical, or thermal receptors found in free nerve endings within injured tissue. This is known as afferent pain, and can occur in ligamentous or muscular injuries of the spine.11,47,54,90 Pain can also occur from direct injury to the peripheral nerve, which
results in burning or shooting pain in the distribution of the affected nerve. This is called peripheral deafferentation (neuropathic) pain and is demonstrated in conditions such as complex regional pain syndrome, peripheral neuropathy, or radiculopathy.30,64,65 Central deafferent pain appears after injury to certain structures within the central nervous system, such as the thalamus, that are responsible for the transmission of pain. Peripheral pain signals are transmitted by either thinly myelinated A-delta or unmyelinated C fibers. The A-delta fibers convey discrete, sharp, fast pain at approximately 15 m/sec, whereas the C fibers transmit vague, chronic, burning, slow pain at less than 1 m/sec.25,108 Pain fibers typically enter the spinal cord through the dorsal root and then ascend or descend two to six segments within the dorsolateral fasciculus (Lissauer’s tract)25,108 The A-delta fibers synapse with the dorsal gray horn neurons located in laminae 1, 2, 5, and 10, whereas the C fibers synapse with dorsal gray horn neurons located in laminae 1, 2, and 5. The majority of fibers then cross to the opposite ventrolateral portion of the spinal cord before ascending in the spinothalamic, spinoreticulothalamic, and spinomesencephalic tracts. The lateral spinothalamic fibers terminate in the thalamic ventralis posterolaterales and posteromedialis nuclei, from which fibers are projected into other areas of the thalamus and to the somatic sensory cortex. The medial spinothalamic, spinoreticulothalamic, and spinomesencephalic tracts end in the reticular activating system within the medulla, pons, midbrain, periaqueductal gray, hypothalamus, and thalamic medial and intralaminar nuclei (Fig. 107.1). The thalamus plays the primary role for conscious pain perception, and the cortex is involved in interpreting pain quality and locality. The A-delta fibers convey a distinctive, sharp pain, and C fibers conduct a characteristic diffuse, burning, or aching pain. This is likely a reflection of the A-delta fibers terminating at the cortical level versus C fibers, which end diffusely in the brain stem and diencephalon. In 1965, Melzack and Wall published their ‘gate control’ theory in which they hypothesized that a ‘gate’ system existed for pain modulation located in the dorsal gray horn within the substantia gelatinosa (laminae 2 and 3).60 They proposed that excess tactile signals traveling along the large myelinated A-delta fibers closed the gate, which then inhibited the propagation of pain impulses along the unmyelinated C fibers (Fig. 107.2). Although the pain pathway is still not completely understood, researchers have uncovered important parts of the neuronal system. This includes descending inhibitory influences from the brain, which have been shown to suppress transmission of pain.10,80,86 There is also evidence of an endogenous system of opioids that modulate sensory input.41,89,95 Today, there is a better awareness that the pain experience is not just physiologic but is also influenced by culture, religion, and psychological makeup.29,37,61,62 In order to provide appropriate 1165
Part 3: Specific Disorders VPM
LFS
VPL
MIT
H
Medial lemniscus Spinal nucleus of V
Periaqueductal gray Spinal nucleus of V
Mesencephalon
Reticular formation
Neotrigeminothalamic tract
Paleogeminothalamic tract
V
V IX
VII
Medulla X
IX X
Spinoreticular tract Dorsal column
Multisynaptic afferent systems
Spinomesencephalic tract Paleospinothalamic tract
Neospinothalamic tract
Spinocervical tract
A
B
Fig. 107.1 Neuroanatomic pathway for nociceptive pain transmission. (A) Lateral tracts and (B) medial tracts. In: Bonica JJ, ed. The Management of Pain. 2nd edn. Philadelphia: Lea & Febiger; 1990:89.
treatment, all of these factors must be taken into consideration when evaluating patients.
Central control
MECHANISM OF ACTION Gate control L
+ +
Input
T
SG –
S
– Action system
– +
Fig. 107.2 Melzack and Wall gate control theory of pain: large-diameter fibers (L), small-diameter fibers (S), substantia gelatinosa (SG), first central transmission cells (T). excitation (+), inhibition (–). From Melzack R, Wall PD. Pain mechanisms: A new theory. Science 1965; 150(699):971–979.
1166
Although the exact mechanism for pain control from SCS is not entirely understood, it is believed to result from direct or facilitated inhibition of pain transmission.28,30,32,40,60,92 There exist five mechanistic theories for SCS which should be noted: (1) gate control theory – segmental, antidromic activation of A-beta efferents; (2) SCS blocks transmission in the spinothalamic tract; (3) SCS produces supraspinal pain inhibition; (4) SCS produces activation of central inhibitory mechanisms influencing sympathetic efferent neurons; and (5) SCS activates putative neurotransmitters or neuromodulators.40 The gate control theory motivated Shealy et al. in 1967 to apply SCS as a means to antidromically activate the tactile A-beta fibers through dorsal column stimulation.92 Shealy et al. reasoned that sustained stimulation of the dorsal columns would keep the gate closed and provide continuous pain relief. While the theoretical model put forth by Melzack and Wall has been shown not to be
Section 5: Biomechanical Disorders of the Lumbar Spine
precisely accurate, pain gating or pain control has been shown to exist.28,30,32,60 Others believe that pain relief from SCS results from direct inhibition of pain pathways in the spinothalamic tracts and not secondary to selective large fiber stimulation.21 This theory has been supported by Hoppenstein, who showed that the posterolateral stimulation of the spinal cord provided effective contralateral pain relief with substantially less current than posterior stimulation.34 Some investigators speculate that the changes in blood flow and skin temperature from spinal cord stimulation may affect nociception at the peripheral level.11,17,27,54,55 This postulate is further supported in part by data from Marchand et al. who investigated the effects of SCS on chronic pain using noxious thermal stimuli.22,31,36,58,70,87 Since it was discovered that SCS causes vasodilation in animal studies, clinicians have used this modality for the treatment of chronic pain due to peripheral vascular disease and this is one of the leading indications for SCS in Europe today.31,36,40,87,100 The precise methods of action of pain modulation by SCS are still being elucidated. A better understanding of the pain system may lead to continued improvement in SCS hardware and software, implantation techniques, and even improved clinical outcomes.
SPINAL CORD STIMULATION LEADS Only three companies manufacture SCS systems in the United States: Medtronic, Inc. (Minneapolis, MN), Advanced Neuromodulation Systems (Dallas, TX), and Advanced Bionics (Sylmar, CA). Advanced Neuromodulation Systems (ANS) produces several leads for percutaneous placement with four or eight electrodes (Fig. 107.3A). The four-electrode lead has four 3 mm electrodes separated by an interelectrode distance of either 4 mm or 6 mm and spans a distance of either 24 mm or 30 mm. The eight-electrode lead has eight 3 mm electrodes with an interelectrode distance of 4 mm. The notion of spanning a larger distance is to help thwart the effects of possible migratory pain patterns which is thought to be a quality of complex regional pain syndrome type 1 or to provide programming redundancy in case of lead migration. The four-electrode lead spans
A
one average thoracic vertebral body while the eight-electrode lead spans two average vertebral bodies or three average cervical vertebral bodies. ANS also produces several different paddle electrodes for surgical implantation via laminotomy or laminectomy. They have a four-electrode Lamitrode Four, an eight-electrode Lamitrode 44 which has four electrodes side by side, and eight-electrode Lamitrode 8, and a 16-electrode Lamitrode 88 with eight electrodes side by side. ANS recently released curved contour laminotomy leads in dual quad, and dual Octrode configurations. The new curved contour laminotomy leads conform more accurately to the shape of the epidual space in the dorsal spinal canal and potentially provide more consistent service than previous laminotomy leads (Fig. 107.3B). Medtronic also manufactures leads designed for percutaneous or laminotomy implantation. The percutaneously implanted leads have either four or eight electrodes. They have a tough, polyurethane outer covering and a helicoil substrate making the leads very resilient with columnar strength and flexibility. There are three different four-electrode leads and one eight-electrode lead. They each have variable electrode lengths and interelectrode distances. The Pisces Quad Plus has four 6 mm electrodes with an interelectrode distance of 12 mm; the Pisces Quad lead has four 3 mm electrodes with an interelectrode distance of 6 mm; the Pisces Quad Compact lead has four 3 mm electrodes with an interelectrode distance of 4 mm; and the Octad has eight 3 mm electrodes with an interelectrode distance of 6 mm. In addition to these lead configurations, Medtronic has the capability to individually produce a wide variety of four- or eight-electrode leads to accommodate an individual physician’s specifications or to treat complex or difficult pain patterns. In general, the smaller the interelectrode distance, the less risk for rootlet stimulation. Medtronic also produces five electrodes for implantation via laminotomy: the Symmix, the dual-paddle Symmix, the Resume TL, the Resume, and the Specify. The Symmix, Resume TL, and the Resume leads have four electrodes each, the Specify has eight, and the dualpaddle Symmix has two paddles with two electrodes each. The Symmix has four electrodes arranged in a diamond pattern and the
B
Fig. 107.3 (A) Advanced Neuromodulation Systems percutaneous implantable lead types. This picture demonstrates an eight-electrode Octrode lead and two four-electrode leads. The electrodes on all leads are 3 mm long. The eight-electrode and one of the four-electrode leads have an interelectrode distance of 4 mm. The other four-electrode lead has an interelectrode distance of 6 mm. (B) Advanced Neuromodulation Systems laminectomy implantable lead types. This picture demonstrates four paddle-style leads implanted via laminectomy. There are two wide leads and two narrow leads. One of the narrow leads has eight electrodes and the other one has sixteen electrodes. There are two wide leads; one has eight electrodes and the other one has sixteen electrodes. 1167
Part 3: Specific Disorders
the IPG powered system is limited in that at this time it can only power a maximum of eight electrodes at a limited frequency and will require surgical replacement at some point in time. The RF receiver systems have the advantage of being externally powered, thus obviating the requirement for surgical replacement. The ANS receiver also has the capacity to run at a frequency of up to 1500 Hz, thus potentially allowing for a local anesthetic effect on the stimulated nerves.2,50 Both the ANS IPG and receiver have the capacity for complex programming and running several different programs simultaneously, which may have benefits when dealing with complex pain patterns, and has yet to be evaluated in a controlled study (Fig. 107.4).
Specify has a total of eight electrodes with four electrodes arranged side by side. Both of these electrode arrangements facilitate bilateral extremity stimulation. The dual-paddle Symmix has two separate paddles designed to allow implantation over two contact sites on the spinal cord to cover a more complex pain pattern. The Resume lead is the most commonly implanted paddle electrode. Both Medtronics and ANS have internally implanted batteries with pulse generators (internal pulse generator or IPG) and an externally powered radiofrequency (RF) controlled implanted receiver. Both IPG powered systems have the advantage of having the device completely internalized, which makes the system more flexible in that the patient can swim with it on if desired. However,
+
–
R
L
– +
A
–
+
R
L
+ B 1168
–
Fig. 107.4 (A) Advanced Neuromodulation Systems dual lead bipole. This picture demonstrates the electrical field experienced by the posterior spinal cord with a single active electrode on each percutaneously placed Octrode. Note that the bulk of the electrical field is biased to the left side, the cathode. (B) Advanced Neuromodulation Systems dual lead bipole. This picture demonstrates the electrical field experienced by the posterior spinal cord with a single active electrode on each percutaneously placed Octrode. Note that the bulk of the electrical field is biased to the right side, the side of the cathode.
Section 5: Biomechanical Disorders of the Lumbar Spine
+ – +
+
–
+
C
+
–
R
L
– + + D
Fig. 107.4—Cont’d (C) Advanced Neuromodulation Systems single lead guarded array. This picture demonstrates the electrical field experienced by the posterior spinal cord with a single-lead guarded array. This is a cathode with an anode on either side of it. Note that the bulk of the electrical field is biased in the center adjacent to the cathode. (D) Advanced Neuromodulation Systems transverse guarded array. This picture demonstrates the electrical field experienced by the posterior spinal cord with a transverse guarded array. This is a cathode on one lead with two anodes on the other lead. Note that the bulk of the electrical field is biased to the side of the cathode.
1169
Part 3: Specific Disorders
PATIENT SELECTION CRITERIA – INDICATIONS Proper patient selection is essential to the long-term success of a SCS system. Improper selection criteria were one of the main reasons for suboptimal results reported in the 1970s. During the 1970s and early 1980s, most studies evaluating the long-term efficacy of dorsal column stimulation quoted success rates of approximately 40%. Technical advances leading to improved hardware coupled with improved patient selection, have improved the rate of long-term efficacy to approximately 70%.12,92,93 An SCS system should be considered for patients who have failed all reasonable medical rehabilitation and inteventional spine techniques.12 An ideal patient should be motivated, compliant, and free of drug dependence.56 Psychological screening is recommended but not mandatory to exclude conditions that predispose to failure of the procedure. It is extremely important that the patient and the physician have a discussion regarding probable outcome prior to implantation and that the patient has realistic expectations. If a patient has unrealistic expectations of the intervention, the treating physician should not consider that patient for implantation. Diagnoses that are typical indications for this procedure in the United States include chronic radiculopathy, FBSS, neuropathic pain, and complex regional pain syndrome.8,16,25,43,59 In Europe, SCS is also used for peripheral vascular disease and angina that are not amenable to medical therapy with reportedly excellent results.6,31,36,87,97,100 Other indications for SCS include transformed migraines, perineal pain, and interstitial cystitis.4,83 When considering pain topography, extremity pain responds better than axial pain, and the more distal the extremity pain the greater the clinical response.73,103 Middle and upper lumbar pain as well as thoracic, cervical, and chest wall pain are difficult to adequately control and maintain long term. Pain, due to severe nerve damage superimposed upon cutaneous numbness (i.e. anesthesia dolorosa) is also difficult to treat with SCS. Central pain syndromes do not respond to SCS and are best treated by other modalities. The use of 3–7 day outpatient trials with an SCS system has proved helpful in determining which patients will respond well enough to warrant a permanent implantation.18,19,73,103 Absolute criteria that must be present for a patient to have a positive trial include tolerance of paresthesia, greater than 50% pain relief, and overall patient satisfaction. Relative requirements for a positive trial include improved functional level and reduced usage of pain medication. Long-term goals include reduced use of the medical system.
CLINICAL OUTCOMES Original long-term results of pain control from spinal cord stimulation in the late 1960s and 1970s were disappointing.28,30,32,93,96 This led to widespread disenchantment with SCS. Poor patient selection, inadequate equipment, and failure to perform implantations with the patient awake accounted for the disappointing results. The advent of new technology, careful patient selection, trial implantation, percutaneous placement or strict attention to positioning a paddle electrode in the same place as a percutaneously placed lead during a trial, and active physician–patient interaction during the procedure have all contributed to the success of spinal cord stimulation over the past 15 years. In 1998, Kumar et al. published a case series of 235 patients who had undergone an SCS implantation.44 The follow-up ranged from 6 months to 15 years after implantation with a mean of 5.6 years. One hundred and eighty-nine patients (80%) experienced satisfactory initial pain relief during a trial period of SCS and underwent 1170
a permanent SCS implant. The study population included 150 men and 85 women with a mean age of 51.4 years. Indications for SCS included FBSS (114 patients), peripheral vascular disease (39 patients), peripheral neuropathy (30 patients), MS (13 patients), RSD (13 patients) and other chronic pain etiology (26 patients). One hundred and eleven patients (59%) received satisfactory pain relief and 47 were gainfully employed (as compared with only 22 prior to implantation). Improvements in daily living as well as a decrease in analgesic usage were reported in successful outcomes. The shorter the duration of time to implantation after FBSS, the greater the rate of success. In the group with FBSS there were 101 successful stimulation trials and 13 unsuccessful stimulation trials. In this group, fiftytwo patients received long-term pain relief while 49 patients who underwent permanent implantation were classified as failure. Out of the 235 patients who underwent permanent implantation, 189 had a successful trial SCS and 111 (58.7%) were successful long term. In 2000, Villavicencio et al. published a retrospective nonrandomized case series comparing the long-term effectiveness of SCS using laminectomy-style electrodes versus percutaneously implanted electrodes.105 The etiology of pain was FBSS (n=24), CRPS (n=7), neuropathic pain (n=4) and other (n=6). Mean follow-up after implantation of SCS was 8.6 months for the laminectomy-type electrode and 10.3 months for the percutaneously placed electrodes. Twenty-seven of 41 patients (66%) participating in the trial SCS implantation went on to receive a permanent SCS implantation. The laminectomy-style electrodes were placed under general anesthesia, while the percutaneous ones were placed under local anesthesia. Outcome was measured per VAS scale via phone interview. Visual analogue scale scores decreased by an average of 4.6 points after laminectomy-style electrode stimulation and by 3.1 after percutaneously implanted electrode stimulation. Electrodes placed through laminectomy provided significantly greater long-term pain relief than percutaneously placed ones (p=0.02). Overall, 89% of patients had greater than 50% pain relief. Five of 12 patients in the laminectomy group and seven of 15 patients in the percutaneous group underwent revision due to loss of pain relief. All 3 patients under the age of 65 in the laminectomy group were able to go back to work. Of the four patients working in the percutaneous group, two were able to go back to work, one retired, and one remained disabled due to pain. In 2001, Leveque at al. published the results of a retrospective study involving 30 patients with FBSS who underwent permanent SCS.53 Each patient had had multiple spinal surgeries and was deemed to no longer be a candidate for traditional spine surgery. Each patient had back and leg pain and all patients underwent a screening trial of SCS prior to permanent implantation. Sixteen patients had greater than 50% pain relief during the trial SCS and underwent permanent implantation. Of the 16 patients who underwent permanent implantation, 9 were implanted with percutaneously implanted catheter-style leads and the remaining 7 patients underwent permanent implantation with a paddle-style lead via a laminectomy. Mean follow-up was 34 months with a range of 6–66 months. At last follow-up, 12 of the 16 patients continued to have at least 50% pain relief. All 6 patients who underwent implantation via laminectomy continued to have greater than 50% pain relief with or without narcotics while only 6 out of the 9 percutaneously implanted patients had greater than 50% pain relief with or without narcotics. The authors concluded that SCS is an effective means of treating intractable back pain in the FBSS population. They also suggested that paddle-style SCS leads placed via laminectomy may be superior for long-term efficacy to catheter-style leads placed percutaneously. In 2001, Ohnmeiss and Rashbaum published a retrospective study which evaluated patient satisfaction of SCS for predominant axial low back pain.79 The literature prior to this study does not support
Section 5: Biomechanical Disorders of the Lumbar Spine
the use of SCS for chronic spinal pain that is primarily limited to the low back. The patient sample included 41 patients who underwent SCS for axial low back pain of an average duration of 83 months. Inclusion criteria included failure of aggressive nonoperative care and patients were not considered surgical candidates. Thirty-eight out of forty-one patients had FBSS with back pain greater than leg pain. In all 41 patients, a SCS trial was performed for an average of 5.9 days. Five patients did not receive significant benefit from SCS trial and were not implanted. The remaining 36 patients were implanted with a Medtronics Mattrix system. Of the 36 patients, 4 later had the system removed due to lack of efficacy. The study included a mean follow-up of 10.5 months. Seventy percent of patients implanted reported being satisfied, 78.8% of patients would recommend SCS to others, and 75.8% would have the implantation again. Sixty percent of patients reported improvement, 33% of patients reported no change in their pain. And 6.1% of patients reported being worse off after the implant than before. The authors comment that much of the literature pertains to older devices no longer in use. They report a nonstatistically significant trend towards lower patient satisfaction with greater chronicity of symptoms pre-implantation. An interesting finding revealed in the questionnaire was that some patients dissatisfied with the results were still recommending the procedure to somebody else and would have the procedure done again. This may be due to overly inflated expectations of pain relief after SCS implantation. In 2001, Barolat et al. published a retrospective review of 44 patients who had undergone SCS implantation with a paddle-style electrode and a radiofrequency receiver via a laminectomy for the treatment of intractable low back pain.9 Only patients in whom further lumbar surgery was not indicated or those in whom medical conditions contraindicated surgery underwent implantation. All patients had leg pain in addition to their back pain. The study was a multicenter, prospective study with follow-up at 6, 12, and 24 months. Follow-up data were available in 41 patients. At 6 months, 91.6% of the patients reported fair to excellent pain relief in the lower extremities and 82.7% pain relief in the back. At 12 months, 88.2% of the patients reported fair to excellent pain relief in the lower extremities and 68.8% pain relief in the back. Significant improvement in function and quality of life was reported at both 6 and 12 months using the Oswestry and SIP, respectively. The majority of the patients report that the procedure was worthwhile and no patients considered the procedure not to be worthwhile. The authors concluded the SCS was beneficial in the treatment of intractable low back pain. The authors further opined that paddle-style electrodes may have an advantage over percutaneous catheter-style electrodes due to patient-reported broader coverage of stimulation and lower energy consumption. In 2001, Dario et al. published a five year retrospective analysis (1992–1997) of 49 patients treated for FBSS at the authors’ center.23 Twenty-one patients had predominantly leg pain, 22 had leg pain only, and six had back pain only. Outcome measures include change in VAS, Oswestry Scale, and Pain Disability Index as measured at entry and every three months for a period of 24–84 months with a mean duration of 42 months. The medical therapy was structured and all patients received the same protocol. After 6 months of medical therapy without significant benefit, patients underwent implantation of a Medtronic Itrel 2 or 3 SCS systems. Twenty-two patients had percutaneous leads implanted and 2 patients had laminectomy paddle-type leads implanted. The following measures were evaluated for SCS implanted patients: efficacy of therapy for leg and back pain, return to work status if previously employed, ADL activity if retired, and the concomitant use of medications and dosages after
implant. The results revealed medical therapy improved both back and leg pain with mean VAS decreasing from 76 to 25. Oswestry scale results dropped from 23 to 6, and PDI scores went from 42 to 4. Of the 22 patients who underwent SCS implant, the VAS results were broken down into leg pain only and back pain only. In the leg pain only group, VAS went from 85 to 22, whereas in the back pain only group the VAS went from 45 to 40. The overall SCS groups mean PDI went from 51 to 7 and the Oswestry scoring went from 12 to 9. The authors concluded that neurostimulation only partially resolved the need for chronic medical therapy. In 2002, North and Wetzel selected 26 patients with FBSS to undergo trial SCS.76 Selection criteria included FBSS with leg pain greater than back pain and one or more of the following: recent abnormal diagnostic imaging results, neurological deficit consistent with the patient’s complaints and history, and/or a well-documented history of surgery for appropriate indications. All patients underwent a percutaneous trial with a four-electrode SCS lead. Of the 26 patients trialed, 24 were chosen to undergo a permanent implantation at the same spinal level as the trial lead was placed. Twelve patients were implanted with a percutaneous four-electrode lead similar to the one temporarily implanted for the trial stimulation and the other twelve patients were implanted with an insulated four-electrode lead via laminectomy. The study demonstrated that the laminectomy-placed leads outperformed percutaneously placed leads with better patientreported pain coverage and lower amplitude requirements which should, according to calculations, yield a doubling of battery life. In 2002, Kumar et al. evaluated the overall cost-effectiveness of SCS therapy versus conventional pain therapy for a consecutive series of 104 patients with FBSS.45 Sixty patients with FBSS were treated with SCS versus 44 patients with conventional pain therapies (CPT). Outcome measures utilized included the Oswestry disability questionnaire at enrollment, yearly, and at 5-year follow-up. Cost of treatment was determined based on year 2000 Canadian dollars and expenditures were regulated by the Canadian Healthcare System. Treatment costs included primary care physician and specialist evaluations, imaging studies, surgery and devices for the interventional arm of the study and medication, physiotherapy, chiropractic, massage, and acupuncture for the control arm. The cumulative totals for the SCS arm were $29 123/patient compared to the control arm figure of $38 029/patient. The cost savings of SCS over the CPT group were realized at an average of 2.5 years due to the high initial cost of surgery and the device. After 2.5 years the savings of SCS versus CPT were realized through reduced drug use, reduced use of physical therapy services, and reduced use of the healthcare system in general. It is possible that in the US healthcare system the cost savings would be even greater. A prior study by Bell et al. puts the breakpoint at 2 years based on projected dollar values.13 In 2004, Turner et al. published a systematic review of the literature including the MEDLINE, EMBASE, Scientific Citation Index, Cochrane Controlled Trials Register, and Current Contents bibliographic databases back to their starting dates for articles published on the effectiveness of spinal cord stimulation (SCS) in treating failed back surgery syndrome (FBSS) and complex regional pain syndrome (CRPS) up to May 16, 2003.104 Seven of 583 articles met the inclusion criteria for review of SCS effectiveness (two CRPS, three FBSS, two mixed diagnoses) and 15 others met the criteria for the review of SCS complications. The average number of previous spine surgeries (in the three studies that reported it) ranged from 2 to 3.3. Mean follow-up time was 33.6 months (range 6–60 months) and an average of 72% (range 58–96%) of patients received the permanent implantation after trial implantation. The studies included different SCS implantation methods (percutaneous trial followed by percutaneous implantation, percutaneous trial followed 1171
Part 3: Specific Disorders
by implantation by laminectomy, and direct implantation by laminectomy without trial). Both FBSS studies (Dario23 and Ohnmeiss and Rashbaum79) that reported leg and back pain separately found greater improvement in the leg pain than the back pain with SCS. Due to the study design of the seven publications, no conclusions could be drawn regarding effectiveness of SCS in returning patients to work. There was a suggestion that pain relief after SCS implantation decreases over time; however, no prospective study with a control group was available. Among 40 FBSS patients in an Ohnmeiss et al. study done in 1996, benefit from SCS decreased from 83% after 12 month to 70% after 24 months.78 One large prospective multicenter study published in 1996 by Burchiel et al. with 182 FBSS patients who received a permanent SCS was excluded due to the fact that only 70 completed the follow-up.19 In this study, a one-year follow-up, showed statistically significant pain decrease and improvement in quality of life measures, but not in medication use or work status. However, due to the large number of patients lost in the follow-up, it is unclear if the patients at follow-up were representative of the original sample. Also, in 2004, Mailis-Gagnon et al. performed a systematic review of the medical literature from 1980 to September 2003 regarding the efficacy of SCS in relieving certain types of chronic pain, its complications, and its adverse effects.57 Studies that were only descriptive or observational were excluded. Primary outcome measure was pain relief. Secondary outcomes were indirect statements about pain relief, e.g. well-being, happiness, functional status, etc. A total of 1629 titles and abstracts were screened, 18 papers were retrieved, 16 of those were excluded, and two were included: one by Kemler et al.38 and one by North et al.74 Both studies were randomized, controlled trials but the Kemler et al. study was a truly prospective study while the North et al. study used a cross-over design. The Kemler et al. study evaluated CRPS type I and had 12-month follow-up while the North et al. study evaluated FBSS and had a 6-month cross-over between SCS and operation. Kemler et al. concluded that SCS is more effective and less expensive than standard treatments protocols for chronic CRPS and North et al. concluded that SCS should be considered prior to operation of the spine on a repeat disc herniation at a previously operated segment. The conclusion of Mailis-Gagnon et al. was that there is limited evidence in favor of SCS for FBSS and CRPS type I. Further, they felt that more trials were needed to confirm whether SCS is an effective treatment for certain types of chronic pain. The most common SCS application in North America today is in the treatment of chronic low back and lower extremity pain due to chronic radiculopathy despite surgery.19,46,78,91,95,103 The largest SCS study incorporates 320 consecutive patients who underwent either temporary or permanent implants at the Johns Hopkins Hospital between 1971 and 1990.40 This series included follow-up on 205 patients, the majority of whom had the diagnosis of failed back surgery syndrome. Permanent SCS implants were placed in 171 of these patients. At follow-up (mean interval 7.1±4.5 yrs), 52% of patients had at least 50% continued pain relief, and 58% had a reduction or elimination of analgesic intake. About 54% of patients younger than 65 were working at the time of follow-up; 41% had been working preoperatively. The percentage of patients having long-term pain relief is similar in the majority of large published SCS series of implants for FBSS. The success rate in most of these studies, which is generally reported as 50% or more pain relief, is approximately 50–60%.9,20,23,43,52,53,68,79,81,85 Some studies report success rates as high as 88% and others as low as 37%.39,94 Although these latter studies differ in implantation technique and screening protocols, the success rate for pain reduction generally remains the same. 1172
More recently published reviews have specifically looked at the efficacy of SCS in FBSS for pain control, reduction in narcotic consumption, function, and work status.24,50 69,70,84,105 According to these studies, long-term pain reduction (at least 2 years after implantation) can be expected to range 50–70% in approximately 60% of SCS patients. In 50–90% of individuals, there will be an elimination or reduction in the use of opioids. The return to full employment rate after SCS reported by two studies is 25–59%, which is significant when comparing it to the usual return to work rate in this population of 1–5%.50,70 Reasons for the disparity between pain reduction and return-to-work rates appear to reflect the high percentage of unskilled laborers among this population, the prolonged periods of disability and the attendant socio-behavioral changes tend to take place in chronic pain patients. Despite this disparity, there is a general increase in function and activities of daily living.
COMPLICATIONS There are rarely any serious complications from of SCS implantation.7 In one study, one nonfatal pulmonary embolism and one case of paraplegia lasting 3 months occurred.49 The latter resulted during the laminectomy placement of a paddle-style lead. Other rarely reported complications include sphincter disturbance and gait abnormality.82 Most complications from SCS devices include reduced or altered paresthesia, lead migration, lead fracture, pain at the pocket site or connection site, infection, nerve injury, and epidural hematoma.6,7,25,26,42,66,70,96,99,109 In a comprehensive summary of different publications, lead migration or displacement varied from 3.7% to 69% although most studies reported migration between 16% and 25%.7 Rates of lead fractures were reported in various series from less than 1% to more than 20% and superficial infections occurred in 2–12% of cases. Serious surgical infections were rare as were clinically apparent epidural hematomas. Cerebrospinal fluid leakage was found in one series in 2% of patients. In a more recent study, Kumar et al. published a case series of 235 patients who had undergone a SCS implantation.45 Complications included hardware malfunction (n=8), electrode displacement (n=65, of which 35 were repositioned and 30 were replaced), infection (4% of implanted devices; n=11 of which 8 required removal), CSF leak (n=2, resolved spontaneously), 1 SQ hematoma at the site of the pulse generator, 3 electrical leaks, and 8 electrode fractures. Development of tolerance was thought to be responsible for most of the 79 long-term failures. In 2000, Heideche et al. published a retrospective review of 42 patients with FBSS who had undergone a permanent SCS implantation for the purposes of identifying the types and frequency of hardware failures.33 The patients were followed for 6–74 months. Thirty-five patients had undergone implantation with a single quadripolar SCS lead percutaneously placed and attached to a Medtronic X-trel receiver; three patients were implanted with dual leads attached to a Mattrix receiver; and the other four patients were implanted with a Medtronics Resume lead via laminectomy. In this study, lead breakage or insulation disruption (n=8) was the most frequently encountered hardware failure with receiver leakage being second most common (n=4). In 2004, Turner et al. performed a systematic review of the literature involving SCS and found 583 articles.104 After screening for pertinent articles, they reviewed 21 studies. An average of 34% (range 0–81%) of patients had one or more complications after the implantation of the permanent SCS during the study follow-up period. Complications included superficial infection (mean 4.5%, range 0–12%), deep infection (one case), pain in the region of the stimulator components (mean 5.8%, range 0–40%), and equipment
Section 5: Biomechanical Disorders of the Lumbar Spine
failure (mean 10.2%, range 0–40%). The median rate for equipment failure of 6.5% may be more accurate, since one study in 2002 by Alo et al. had higher than usual equipment failure rates, which may have skewed the rate upwards.5 Other complications include a need for stimulator revision, mostly due to dislodged or displaced electrodes and a need for stimulator removal.5,104
THE FUTURE Authors of several of the current outcome studies have pointed out that older outcome studies bear little relevance to today’s outcomes due to improved patient selection, improved technology, and improved understanding of implantation techniques. In addition, recently published outcome studies have focused on the antegrade placement of percutaneous or paddle leads in the lower thoracic spine for the treatment of chronic back and leg pain. Other methods of lead placement exist that have anecdotally proven effective in the treatment of back and leg pain but that have not yet been subjected to controlled trials. The retrograde placement of percutaneously placed leads has proven effective in the treatment of low back and leg pain (Fig. 107.5).2 This technique typically involves the cephalocaudal advancement of a lead into the lower lumbar or sacral spine via an epidural needle placed at the L2–3 or L3–4 level. Using this technique, the lead may be placed over one or two adjacent nerve roots or actually fed into a particular foramen. This technique allows for a very stable, focused paresthesia along one or a few nerve roots at very low amplitudes. When the lead is entered into a foramen it tends to be very stable and allows for very little positional or activity-related change in paresthesia. Thus, if a patient has a poor result from a SCS trial with a traditionally placed SCS lead, then the placement of a SCS lead via a retrograde approach may be indicated. In selected cases, it is the authors’ experience that by applying this method in lieu of or in addition to a traditionally placed lead, clinical outcomes will improve. Peripheral nerve stimulation (PNS) is a technique that is considered to be very similar to SCS except that the neural elements being stimulated lie outside of the spinal column. This method has
A
Fig. 107.5 Retrograde placement of spinal cord stimulator leads. This picture of a radiograph demonstrates two quadripolar leads percutaneously placed in a cephalocaudal direction. Note that the distal ends of both leads are entering the ipsilateral L2–3 foramen bilaterally. This array succeeded in managing this patient’s low back and bilateral lower extremity pain when two quadripolar leads placed in an antegrade manner failed despite adequate coverage of the patient’s pain pattern with paresthesia.
been successfully applied in the treatment of refractory transformed migraines.5 It has also been successfully applied in an anecdotal manner by the authors and others for the treatment of focal, intense low back pain. This technique involves the placement of an epidural needle immediately beneath the skin peripheral to the center of a focal region of pain (Fig. 107.6A). The needle is then directed into the long axis of the pain so that the distal 5 cm of the needle crosses through the middle of the most intense pain. An eight-channel SCS lead is then advanced into the needle and the needle is removed. The
B
Fig. 107.6 (A) Peripheral nerve stimulation. This picture demonstrates an epidural needle being placed beneath the skin peripheral to a focal region of pain in a patient with a failed back surgery syndrome in preparation for a trial peripheral nerve stimulator. (B) Peripheral nerve stimulation. This picture demonstrates an epidural needle in the L1–2 epidural space with a SCS lead appropriately placed. There is also an epidural needle placed subcutaneously traversing the long axis of a focused region of pain.
(Continued) 1173
Part 3: Specific Disorders
C
D
Fig. 107.6—Cont’d (C) Peripheral nerve stimulation. This picture of a radiograph demonstrates two eight-electrode leads placed subcutaneously along the long axis of a patient’s central low back pain. (D) Peripheral nerve stimulation. This picture of a radiograph demonstrates a hybrid system in which an eight-electrode lead is in the epidural in traditional position and another eight-electrode lead is placed subcutaneously along the long axis of a focused region of pain.
lead is then trialed for efficacy in a manner similar to an SCS trial. This method of PNS provides a very dense, focused paresthesia and is often successful at relieving intense low back pain when SCS alone fails. As a result, when a patient with an intense, focused region of low back pain has a poor result from a trial SCS, a PNS trial should be considered in lieu of or in addition to a traditional SCS trial (Fig. 107.6B–D). The authors have had several anecdotal cases in which a combination of PNS and SCS has succeeded in patients who have had a poor result from the antegrade placement of a percutaneously placed lead despite coverage of the patient’s pain pattern with paresthesia. Studies focused on the combination of PNS and SCS in selected cases may improve long-term success rates.
CONCLUSION Spinal cord stimulation has been demonstrated to be effective at managing pain in selected patients and selected conditions. Hardware, software, and implant technology have improved outcomes and consistency over time. Paddle-style leads implanted via laminectomy may have slight advantage over percutaneously implanted leads when managing back pain over time; however, there does not appear to be a difference in efficacy when managing hip or lower extremity pain. To date, studies have evaluated only leads placed in an antegrade manner either via a laminectomy or percutaneous technique. The efficacy of retrograde lead placement and peripheral nerve stimulation have not been evaluated either alone or in combination with each other or with antegrade lead placement. Finally, the efficacy of complex programming has not been evaluated and may improve consistency and efficacy over time.
References 1. Abram SE. Pain pathways and mechanisms. Sem Anesth 1985; 4:267–274. 2. Alo K, Yland M, Radko R, et al. Lumbar and sacral nerve root stimulation (NRS) in the treatment of chronic pain: A novel anatomical approach and neurostimulation technique. Neuromodulation 1999; 2(1):23–31. 3. Alo K, Ziddan A. Selective nerve root stimulation in the treatment of end-stage, diabetic, peripheral neuropathy: A case report. Neuromodulation 2000; 3(4): 201–208.
1174
4. Alo K, McKay E. Selective nerve root stimulation (SNRS) for the treatment of intractable pelvic pain and motor dysfunction: a case report. Neuromodulation 2001; 4(1):19–24. 5. Alo K, Redko V, Charnov J. Four year follow up of dual electrode spinal cord stimulation for chronic pain. Neuromodulation 2002; 5(2):79–88. 6. Augustinsson LE, Carlsson CA, Holm J, et al. Epidural electrical stimulation in severe limb ischemia. Pain relief, increased blood flow, and a possible limb-saving effect. Ann Surg 1985; 202(1):104–110. 7. Augustinsson LE. Avoiding difficulties in spinal cord stimulation. In: Waldman SD, Winnie AP, eds. Interventional pain management. 1st edn. Philadelphia: WB Saunders; 1996:427–430. 8. Barolat G, Schwartzman R, Woo R. Epidural spinal cord stimulation in the management of reflex sympathetic dystrophy. Stereot Funct Neurosurg 1989; 53(1): 29–39. 9. Barolat G, Oakley J, Law J, et al. Epidural spinal cord stimulation with a multiple electrode paddle lead is effective in treating intractable back pain. Neuromodulation 2001; 4(2):59–66. 10. Basbaum AI, Fields HL. Endogenous pain control systems: Brainstem spinal pathways and endorphin circuitry. Ann Rev Neurosci 1984; 7:309–338. 11. Bayliss WM. On the origin from the spinal cord of the vasodilator fibres of the hind-limb, and on the nature of these fibres. J Physiol 1901; 26(3):173–209. 12. Bedder MD. Spinal cord stimulation and intractable pain: patient selection. In: Waldman SD, Winnie AP, eds. Interventional pain management. 1st edn. Philadelphia: WB Saunders; 1996:412–418. 13. Bell GK, Kidd D, North RB. Cost-effectiveness analysis of spinal cord stimulation in treatment of failed back surgery syndrome. J Pain Symptom Manag 1997; 13(5):286–295. 14. Bonica JJ. Anatomic and physiologic basis of nociception and pain. In: Bonica J, ed. The management of pain. Vol 1, 2nd edn. Philadelphia: Lea & Febiger; 1990: 28–94. 15. Bowsher D. Pain mechanisms in man. Res Staff Phys 1983; 29:26–34. 16. Broseta J, Roldan P, Gonzalez-Darder J, et al. Chronic epidural dorsal column stimulation in the treatment of causalgia pain. Appl Neurophysiol 1982; 45 (1–2):190–194. 17. Broseta J, et al. Spinal cord stimulation in peripheral arterial disease. J Neurosurg 1986; 64:71–80. 18. Burchiel KJ, Anderson VC, Wilson BJ, et al. Prognostic factors of spinal cord stimulation for chronic back and leg pain. Neurosurgery 1995; 36(6):1101–1110. 19. Burchiel KJ, Anderson VC, Brown FD, et al. Prospective, multicenter study of spinal cord stimulation for relief of chronic back and extremity pain. Spine 1996; 21(23):2786–2794.
Section 5: Biomechanical Disorders of the Lumbar Spine 20. Burton CV. Session on spinal cord stimulation: Safety and clinical efficacy. Symposium on the safety and clinical efficacy of implanted neuroaugmentative devices. Neurosurgery 1977; 1:214–215. 21. Campbell JN. Examination of possible mechanisms by which stimulation of the spinal cord in man relieves pain. Appl Neurophysiol 1981; 44(4):181–186.
49. Law JD. Percutaneous spinal cord stimulation for the ‘failed back surgery syndrome.’ Pain Manage Update 1990; l(l):12. 50. Law JD, Kirkpatrick AF. Update: Spinal cord stimulation. Am J Pain Manage 1992; 2(l):34–42. 51. LeDoux MS, Langford KH. Spinal cord stimulation for the failed back syndrome. Spine 1993; 18(2):191–194.
22. Crue BL. The neurophysiology and taxonomy of pain. In: Brena SF, Chapman SL, eds. Management of patients with chronic pain. Jamaica, NY: Spectrum; 1983: 21–31.
52. LeRoy PL. Stimulation of the spinal neuraxis by biocompatible electrical current in the human. Appl Neurophysiol 1981; 44(4):187–193.
23. Dario A, Fortini G, Bertollo D, et al. Treatment of failed back surgery syndrome. Neuromodulation 2001; 4(3):105–110.
53. Leveque J, Villavicencio A, Bulsara K, et al. Spinal cord stimulation for failed back surgery syndrome. Neuromodulation 2001; 4(1):1–9.
24. De La Porte C, Van de Kelft E. Spinal cord stimulation in failed back surgery syndrome. Pain 1993; 52(1):55–61.
54. Linderoth B, Fedorcsak I, Meyerson BA. Is vasodilatation following dorsal column stimulation mediated by antidromic activation of small diameter afferents? Acta Neurochirurg Supple 1989;46:99–101.
25. Devulder J, De Colvenaer L, Rolly G, et al. Spinal cord stimulation in chronic pain therapy. Clin J Pain 1990; 6(1):51–56. 26. Erickson DL, Long DM. Ten-year follow-up of dorsal column stimulation. Advin Pain Res Ther 1983; 6:583–589.
55. Linderoth B. Dorsal column stimulation and pain: Experimental studies of putative neurochemical and neurophysiological mechanisms (thesis). Stockholm: Karolinska Institute; 1992.
27. Fedorcsak I, et al. Peripheral vasodilation due to sympathetic inhibition induced by spinal cord stimulation. In: Proceedings of the IBRO World Congress of Neurosciences, Paris, France, 1991:126.
56. Loeser JD, Parker G. Assessment and investigation of the patient with chronic pain at the University of Washington Multidisciplinary Pain Center. In: Loeser JD, Egan KJ, eds. Pain management. New York: Raven Press; 1989:21–34.
28. Feldman RA. Patterned response of lamina V cells: Cutaneous and dorsal funicular stimulation. Physiol Behav 1975; 15(1):79–84.
57. Mailis-Gagnon A, Furlan AD, Sandoval JA, et al. Spinal cord stimulation for chronic pain (Cochrane Review). In: The Cochrane Library, Issue 3, 2004. Chichester, UK: John Wiley; 2004.
29. Fields H. Depression and pain: A neurobiological model. Neuropsychiatry, Neuropsychol Behav Neurol 1991; 4:83–92. 30. Foreman RD, Beall JE, Coulter JD, et al. Effects of dorsal column stimulation on primate spinothalamic tract neurons. J Neurophysiol 1976; 39(3):534–546.
58. Marchand S, Bushnell MC, Molina-Negro P, et al. The effects of dorsal column stimulation on measures of clinical and experimental pain in man. Pain 1991; 45(3):249–257.
31. Groth DE. Spinal cord stimulation for the treatment of peripheral vascular disease. Adv Pain Res Ther 1985; 9:861–870.
59. Meglio M, Cioni B, Rossi GF. Spinal cord stimulation in management of chronic pain: A 9-year experience. J Neurosurg 1989; 70(4):519–524.
32. Handwerker HO, Iggo A, Zimmerman M. Segmental and supraspinal actions on dorsal horn neurons responding to noxious and non-noxious skin stimuli. Pain 1975; 1(2):147–165.
60. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965; 150(699): 971–979.
33. Heideche V, Rainov N, Burket W. Hardware failures in spinal cord stimulation for failed back surgery syndrome. Neuromodulation 2000; 3(1):27–30. 34. Hoppenstein R. Percutaneous implantation of chronic spinal cord electrodes for control of intractable pain. Preliminary report. Surg Neurol 1975; 4(1):195–198. 35. International Association for the Study of Pain. Classification of chronic pain: Descriptions of chronic pain syndromes and definitions of pain terms. Pain Suppl 1986; 3:S1–S225. 36. Jacobs MJ, Jorning PJ, Joshi SR, et al. Epidural spinal cord electrical stimulation improves microvascular blood flow in severe limb ischemia. Ann Surg 1988; 207(2):179–183. 37. Jensen MP, Turner JA, Romano JM, et al. Coping with chronic pain: A critical review of the literature. Pain 1991; 47(3):249–283. 38. Kemler M, Barendse G, van Kleef M, et al. Spinal cord stimulation in patients with chronic reflex sympathetic dystrophy. N Engl J Med 2000; 343(9):618–624. 39. Kolin MT, Winkelmuller W. Chronic pain after multiple lumbar discectomies – significance of intermittent spinal cord stimulation. Pain 1990; 40(5):S241. 40. Krames ES. Mechanisms of action of spinal cord stimulation. In: Waldman SD, Winnie A, eds. Interventional pain management. 1st edn. Philadelphia: WB Saunders; 1996:407–411. 41. Krieger DT, Martin JB. Brain peptides. N Eng J Med 1981; 304(15):876–885.
61. Melzack R, Casey KL. Sensory, motivational, and central control determinates of pain. In: Kenshalo DR, ed. The skin senses. Springfield: Charles C Thomas; 1968:423–443. 62. Melzack R. Psychological aspects of pain: implications for neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd ed. Philadelphia: JB Lippincott; 1989:845–860. 63. Melzack R. Anatomy and physiology of pain: clinical correlates. In: Waldman SD Winnie AP, eds. Interventional pain management. 1st edn. Philadelphia: WB Saunders; 1996:1–9 64. Meyerson BA. Electric stimulation of the spinal cord and brain. In: Bonica JJ, ed. The management of pain. 2nd edn. Philadelphia: Lea & Febiger; 1990: 1862–1877. 65. Meyerson BA, Linderoth B, Lind G. Spinal cord stimulation in chronic neuropathic pain. Lakartidningen 1991; 88(9):727–732. 66. Mullet KR. Design and function of spinal cord stimulators – theoretical and developmental considerations. Pain Digest 1992; 1:281–287. 67. Nagase Y, Moritani M, Nakagawa S. Serotonergic axonal contacts on identified cat trigeminal motor neurons and their correlation with medullary raphe nucleus stimulation. J Compar Neurol 1997; 384(3):443–455. 68. Nielson KD, Adams JE, Hosobuchi Y. Experience with dorsal column stimulation for relief of chronic intractable pain. Surgi Neurol 1975; 4(1):148–152.
42. Kumar K, Wyant G, Ekong C, et al. Epidural spinal cord stimulation for relief of chronic pain. Pain Clin 1986; 1(2):91–99.
69. North RB, Ewend MG, Lawton MT, et al. Failed back surgery syndrome: 5-year follow-up after spinal cord stimulator implantation. Neurosurgery 1991; 28(5): 692–699.
43. Kumar K, Nath RK, Wyant GM. Treatment of chronic pain by epidural spinal cord stimulation: 10-year experience. J Neurosurg 1991; 75(3):402–407.
70. North RB, Ewend MG, Lawton MT, et al. Spinal cord stimulation for chronic, intractable pain: superiority of ‘multi-channel’ devices. Pain 1991; 44(2):119–130.
44. Kumar K, Toth C, Nath RK, et al. Epidural spinal cord stimulation for treatment of chronic pain – some predictors of success: a 15-year experience. Surg Neurol 1998; 50(2):110–121.
71. North RB, Fowler K, Nigrin D, et al. Patient-interactive, computer-controlled neurological stimulation system: Clinical efficacy in spinal cord stimulator adjustment. J Neurosurg 1992; 76(6):967–972.
45. Kumar K, Malik S, Demeria D. Treatment of chronic pain with spinal cord stimulation versus alternative therapies: cost-effectiveness analysis. Neurosurg 2002; 51(1):106–116.
72. North RB, Kidd D, Zahurak M. Spinal cord stimulation for chronic intractable pain: Experience over two decades. Neurosurgery 1993; 32(3):384–394.
46. Kupers RC, Van den Dever R, Van Houdenhove B, et al. Spinal cord stimulation in Belgium: a nation-wide survey on the incidence, indications and therapeutic efficacy by the health insurer. Pain 1994; 56(2):211–216.
73. North RB, Kidd D, Lee MS, et al. A prospective, randomized study of spinal cord stimulation vs. reoperation for failed back surgery syndrome: initial results. Stereot Funct Neurosurg 1994; 62(1–4):267–272.
47. Larson SJ, Sances A, Riegel DH, et al. Neurophysiological effects of dorsal column stimulation in man and monkey. J Neurosurg 1974; 41(2):217–223.
74. North RB, Kidd D, Piantadosi S. Spinal cord stimulation versus reoperation for failed back surgery syndrome: a prospective, randomized study design. Acta Neurochirurg Suppl 1995; 62(1–4):273–278.
48. Law JD. Spinal stimulation: Statistical superiority of monophasic stimulation of narrowly separated, longitudinal bipoles having rostral cathodes. Appl Neurophysiol 1983; 46(1–4):129–137.
75. North B, Kidd D, Wimberly RL, et al. Prognostic value of psychological testing in patients undergoing spinal cord stimulation: A prospective study. Neurosurgery 1996; 39(2):301–311.
1175
Part 3: Specific Disorders 76. North RB, Wetzel FT. Spinal cord stimulation for chronic pain of spinal origin. Spine 2002; 27(22):2584–2591. 77. North RB, Kidd DH, Olin JC, et al. Spinal cord stimulation electrode design: prospective randomized, controlled trial comparing percutaneous and laminectomy electrodes. Part I: technical outcomes. Neurosurgery 2002; 51(2):381–390. 78. Ohnmeiss D, Rashbaum R, Bogdanffy GM. Prospective outcome evaluation of spinal cord stimulation in patients with intractable leg pain. Spine 1996; 21(11): 1344–1350. 79. Ohnmeiss D, Rashbaum R. Patient satisfaction with spinal cord stimulation for predominant complaints of chronic, intractable low back pain. Spine J 2001; 1(5):358–363. 80. Oliveras JL, Redjemi G, Guilbaud G, et al. Analgesia induced by electrical stimulation of the inferior centralis of the raphe in the cat. Pain 1975; 1(2):139–145.
95. Snyder SH. Opiate receptors in the brain. N Engl J Med 1977; 296(5):266–271. 96. Spiegelmann R, Friedman WA. Spinal cord stimulation: a contemporary series. Neurosurgery 1991; 28(1):65–71. 97. Steude U, Abendroth D, Sunder-Plassamann L. Epidural spinal electrical stimulation in the treatment of severe arterial occlusive disease. Acta Neurochirurg Suppl 1991; 52:118–120. 98. Stinson L, Roderer G, Cross N, et al. Peripheral subcutaneous electrostimulation for control of intractable post-operative inguinal pain: a case series. Neuromodulation 2001; 4(3):99–104.
81. Pineda A. Dorsal column stimulation and its prospects. Surg Neurol 1975; 4(1):157–163.
99. Sweet WH, Wepsic JG. Stimulation of the posterior column of the spinal cord for pain control: indications, technique and results. Clin Neurosurg 1974; 21: 278–310.
82. Pineda A. Complications of dorsal column stimulation. J Neurosurg 1978; 48(1):64–68.
100. Tallis RC, Illis LS, Sedgwick EM, et al. Spinal cord stimulation in peripheral vascular disease. J Neurol Neurosurg Psychiatry 1983; 46(6):478–484.
83. Popeney CA, Alo KM. Peripheral neurostimulation for the treatment of chronic, disabling transformed migraine. Headache 2003; 43(4):369–375.
101. Tasker RR. Deafferentation in central pain. In: Wall PD, Melzack R, eds. Textbook of pain. 2nd edn. Edinburgh: Churchill-Livingstone; 1989:154–180.
84. Racz GB, McCarron R, Talboys P. Percutaneous dorsal column stimulator for chronic pain control. Spine 1989; 14(1):1–4.
102. Thienhaus O, Cole BE. The classification of pain. In: Weiner RS, ed. Pain Management: a practical guide for clinicians. 5th edn. Boca Raton: St. Lucie Press; 1998:19–26.
85. Ray CD, Burton C, Lifson A. Neurostimulation as used in a large clinical practice. Appl Neurophysiol 1982; 45(1–2):160–166. 86. Reynolds DV. Surgery in the rat during electrical analgesia induced by focal brain stimulation. Science 1969; 164(878):444–445. 87. Robaina FJ, Dominguez M, Diaz M, et al. Spinal cord stimulation for relief of chronic pain in vasospastic disorders of the upper limbs. Neurosurgery 1989; 24(1):63–67. 88. Robb LG, Spector G, Robb MP. Spinal cord stimulation: neuroaugmentation of the dorsal columns for pain relief. In: Weiner RS, ed. Pain management: a practical guide for clinicians. 5th edn. Boca Raton: St. Lucie Press; 1998:271–293. 89. Ruda MA. Opiates and pain pathways: Demonstration of enkephalin synapses on dorsal horn projection neurons. Science 1982; 215(4539):1523–1525. 90. Saade NE, Tabet MS, Soueidan SA, et al. Supraspinal modulation of nocioception in awake rats by stimulation of the dorsal column nuclei. Brain Res 1986; 369(1–2):307–310.
103. Turner JA, Loeser JD, Bell KG. Spinal cord stimulation for chronic low back pain: a systematic literature synthesis. Neurosurgery 1995; 37(6):1088–1096. 104. Turner JA, Loeser JD, Deyo RA, et al. Spinal cord stimulation for patients with failed back surgery syndrome or complex regional pain syndrome: a systematic review of effectiveness and complications. Pain 2004; 108:137–147. 105. Villavicencio AT, Leveque JC, Rubin L, et al. Laminectomy versus percutaneous electrode placement for spinal cord stimulation. Neurosurgery 2000; 46(2): 399–405. 106. Wall PD, Melzack R. Introduction. In: Wall PD, Melzack R, eds. Textbook of Pain. 2nd edn. Edinburgh: Churchill-Livingstone; 1989:1–18. 107. Yaksh TL. Neurological mechanisms of pain. In: Cousins MJ, Bridenbaugh PO, eds. Neural blockade in clinical anesthesia and management of pain. 2nd edn. Philadelphia: JB Lippincott; 1988:791–844.
91. Segal R, Stacey BR, Rudy TE, et al. Spinal cord stimulation revisited. Neurolog Res 1998; 20(5):391–396.
108. Yaksh TL. Anatomy of the pain processing system. In: Waldman SD, Winnie AP, eds. Interventional pain management. 1st edn. Philadelphia: WB Saunders; 1996:10–18.
92. Shealy CN, Mortimer JT, Reswick JB. Electrical inhibition of pain by dorsal column stimulation. Anesth Analg 1967; 46(4):489–491.
109. Young RF. Evaluation of dorsal column stimulation in the treatment of chronic pain. Neurosurgery 1978; 3(3):373–379.
93. Shealy CN, Mortimer JT, Hagfors NR. Dorsal column electroanalgesia. J Neurosurg 1970; 32(5): 560–564.
1176
94. Siegfried J, Lazorthes Y. Long-term follow-up of dorsal column stimulation for chronic pain syndrome after multiple lumbar operations. Appl Neurophysiol 1982; 45(1–2):201–204.
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar
CHAPTER
Neuraxial Drug Administration to Treat Pain of Spinal Origin
108
Joshua P. Prager
INTRODUCTION Advances in neurobiology serve as the basis for current and evolving implantable pain modalities, consisting of neurostimulation and neuraxial drug administration systems. Both neurostimulation and intrathecal drug administration systems are reversible and nondestructive neuromodulatory techniques that can reduce pain of spinal origin. Neurostimulation is preferred over neuraxial drug delivery when the patient’s problem is amenable to both techniques because drug delivery systems require regular medication refills. Neuraxial medication delivery is indicated when side effects of systemic analgesics limit the ability to deliver effective doses of medications. Prager and Jacobs provide a comprehensive review of patient selection for these neuromodulatory techniques.1
RATIONALE The discovery of opioid receptors2,3 provided a rational basis for the delivery of opioid drugs intraspinally. By 1979, reports of epidural4 and intrathecal5 opioid delivery in humans had entered the peerreviewed literature. Intraspinal infusions delivered drugs directly to opioid receptors, limited systemic exposure, and by decreasing the opioid dosage required for pain relief, generally reduced side effects, which facilitated the provision of greater analgesia. The benefits of short-term spinal analgesia, primarily for patients with intractable cancer pain, led to investigation of longer-term continuous subarachnoid opioid infusions for the management of both cancer pain6–17 and noncancer pain, such as that produced by failed back surgery syndrome.18–30 Pain specialists currently are successfully using opioids to treat patients with chronic noncancer pain, noting that such patients can benefit from sustained analgesia and better function without becoming addicted.31 The key to appropriate treatment of pain is proper diagnosis. Pain can be characterized as nociceptive (e.g., somatic pain), neuropathic (pain from nerve injury), or idiopathic. Pure nociceptive pain usually responds well to systemic opioids. Neuropathic pain responds to opioids at higher doses and often is responsive to a large number of antineuropathic medications (Table 108.1). Failed back surgery syndrome (FBSS) pain usually is a mixed type of pain that is both nociceptive and neuropathic. Nociceptive pain arises from disc or bone injury, reaction to hardware or graft harvesting, or reactive spasm. Neuropathic FBSS pain can arise from nerve injury before surgery, chronic compression, chemical irritation, nerve injury during surgery, scar tissue formation, or arachnoiditis. The challenge in treating FBSS pain is that of treating this mixed etiology of pain. Pain from spinal cord injury may be predominantly neuropathic in nature, whereas mechanical pain such as that in the patient with severe osteoporosis is more nociceptive.
In appropriately selected patients, intraspinal therapy has been refined through accumulated experience from treating tens of thousands of cases (more than 25 000 with implantable pumps32), improved drug delivery systems, and new pharmacologic approaches, making it an effective technique for the control of intractable pain.
INTRASPINAL DRUG DELIVERY SYSTEMS Intraspinal drug delivery can be accomplished by a variety of means including percutaneous catheter, percutaneous catheter with subcutaneous tunneling, implanted catheter with subcutaneous injection site, totally implanted catheter with implanted reservoir and manual pump, and totally implanted catheter with implanted infusion pump.33 The choice of the system depends on the indication for intraspinal therapy, the need for bolus versus continuous infusion, the patient’s general medical condition, available support services, ambulatory status, life expectancy, and cost. In general, percutaneous tunneled catheters, external pumps, and implanted passive reservoirs can be more cost-effective when life expectancy is a matter of weeks to months. A fully implanted pump becomes economical if life expectancy is longer than 3 months.34 The first ‘permanent’ catheter for intraspinal drug delivery was developed by DuPen et al.35 in the 1980s. They adapted Broviac catheter technology to create an exteriorized, permanent, three-piece, silicone epidural catheter. The catheter was implanted in 55 cancer patients who had metastatic disease and intractable pain. After 3891 days of catheter use, there were no catheter infections and 18 minor side effects. The rate of hospitalization for pain control was decreased by 90% in these patients. In one series of 350 reported implantations of the DuPen catheter, there were 30 superficial catheter infections, 8 deep catheter infections, and 15 epidural or intrathecal catheter infections, representing a 15.1% infection rate. The DuPen catheter continues to be marketed for use with an external pump. It may represent a cost-effective alternative for patients with a short life expectancy, such as patients with severe metastatic disease to the spine. However, the DuPen catheter and similar external systems have limited applicability in treating noncancer pain of spinal origin. Two types of implantable drug delivery systems are marketed currently in the United States.34,36 The first commercially available implantable pump delivered medication at a fixed rate and consisted of two chambers separated by a flexible bellows in addition to a side port for bolus injections.3 Outflow was regulated by compressed Freon gas, so changes in altitude and temperature affected drug flow. Because the pump ran at a fixed rate, changes in the rate of medication delivery could be accomplished only by emptying the pump and refilling it with a different concentration of medication. This pump was approved by the Food and Drug Administration (FDA) for epidural administration of preservative-free morphine. The original pump has been superseded by a new model,2 which has a single 1177
Part 3: Specific Disorders
Table 108.1: Updated pain treatment interventions and medications32,36 Exercise Meditation, relaxation, yoga, traditional biofeedback and neurobiofeedback Over-the-counter medications (aspirin, traditional nonsteroidal antiinflammatory drugs) and cyclooxygenase inhibitors Antineuropathic adjunctive medications (tricyclic antidepressants, selective serotonin reuptake inhibitors, GABAergic drugs, other antispasmodics, anticonvulsants, local anesthetics, calcium-channel blockers, substance P-depleting amines, α2 agonists, NMDA receptor antagonists, tramadol) and other adjunctive medications: corticosteroids Physical rehabilitation: physical therapy, work hardening, occupational therapy, Pilates Somatic and sympathetic nerve blocks Cognitive and behavioral therapies Opioid medications combined with adjuvants Pure high-potency, time-released opioid medications with breakthrough short-acting opioid medications Spinal cord stimulation if pain is segmental Intraspinal infusion analgesia Neurodestructive procedures
raised septum and no side port. Although essentially the same, the new pump was modified by removing the side port to minimize the potential for overdose. A special needle with a needle shaft aperture and a closed needle tip is used to deliver fluid directly into the catheter rather than the drug reservoir.33 A second and third fixed-rate pump are now available. The third type of implantable delivery system is a programmable electronic pump powered by batteries, which last up to 7 years depending on flow rate.4 Two pumps are FDA approved and contain either 10 or 18 mL collapsible reservoirs, a volume activated valve and a pump or 20 or 40 mL reservoirs, a pressure activated valve and a pump, both of which push medication through a bacteriostatic filter and catheter. Comparison of these pumps is found in Table 108.2. The newer pump, the SynchroMed II has the advantage of having a smaller size with a slightly larger reservoir volume or a vastly greater effective reservoir volume at approximately the same size as its predecessor, the SynchroMed EL. At the time of this writing, both pumps are available for implantation. The SynchroMed II allows for more sophisticated programming, stores more important information, and has a slightly longer battery life expectancy. The newer pump costs approximately 10% more. These pumps are FDA approved for epidural or intrathecal infusion of preservative-free morphine sulfate for chronic, intractable pain, and baclofen for chronic spasticity. Ziconotide was FDA approved for intrathecal use for pain in these pumps in 2004. Both pumps are programmed, using noninvasive telemetry to control medication concentration, volume, and dosage. The programmable feature allows flexible dosing options over time and permits precise dose titration. Both pump types require refilling under sterile conditions at least every several months, depending on flow rate.37 In deciding whether to implant a programmable pump or a fixedrate pump, several factors should be considered, including their specific attributes. Table 108.3 compares the attributes of the two pump types. The programmable pumps provide greater flexibility of medication delivery and are more adjustable. However, a programmable pump is more expensive and needs to be replaced when the battery fails. Hardware is but one component of the entire implantation cost, and when all costs are aggregated, the percentage difference in cost
1178
diminishes. As a rule of thumb, programmable pumps are implanted when dosage titration and regulation is anticipated, and fixed-rate pumps may provide a cost-effective choice when dosage is expected to be stable. In practical terms for the patient with chronic pain of spinal origin, dosage regulation should be anticipated. Thus, a programmable pump serves the patient better initially. If the patient stabilizes on a regimen, a fixed-rate pump may be considered for replacement to minimize expense. However, the current and future flexibility of programmable pumps make them a superior choice for most important factors, excluding expense.
PATIENT SELECTION AND SCREENING TRIALS The literature is virtually unanimous in emphasizing the importance of appropriate patient selection if intraspinal pain therapy is to be successful.1 Patients with chronic pain are subject to neurophysiologic, emotional, and behavioral influences, which govern their perception of pain and of pain relief. Therefore, treatment of chronic noncancer pain is multidisciplinary, drawing on cognitive and behavioral psychological therapies, functional rehabilitation, orthopedic and neurologic surgery, medications, nerve blockade, neuroaugmentive and sometimes neurodestructive procedures. The pain treatment continuum in Table 108.1 lists these interventions and the antineuropathic medications currently used to treat intractable pain.32 Indications and contraindications for intraspinal opioid therapy appear in Table 108.4.34 Intraspinal drug delivery has been used primarily for patients with nociceptive pain, which has proved to be opioid responsive. Experience in intraspinal treatment of neuropathic pain is more limited, although several studies indicate that neuropathic pain may respond to intraspinal delivery of escalating doses of opioids, or to nonopioid medications.34,38 Finally, a screening trial allows both physician and patient to assess intraspinal drug delivery before committing to pump implantation. Numerous screening protocols exist. Trials can incorporate epidural or intrathecal administration, bolus injection, a series of injections, or continuous infusion, and they can be conducted on an inpatient or outpatient basis. Pure opioid or a mixture containing opioid can be administered. The duration of the trials varies from 24 hours to longer
Section 5: Biomechanical Disorders of the Lumbar Spine
Table 108.2: Comparison of SynchroMed EL with SynchroMed II implantable pumps PUMP COMPARISON SynchroMed EL
SynchroMed II
Reservoir volume
10 mL pumps residual volume 1.2 mL 18 mL pumps residual volume 2.4 mL
20 mL pumps residual volume 1.4 mL 40 mL pump residual volume 1.4 mL
Pump displacement volume
10 mL pumps 107 mL 18 mL pumps 125 mL
20 mL pump 91 mL 40 mL pump 121 mL
Drug stability
Morphine: Lioresal* intrachecal (baclofen injection): FUDRs: Methotrexane:
90 days 90 days 56 days 56 days
Morphine: Lioresal* intrathecal (baclofen Injection): FUDRs: Methotrexane:
180 days 180 days 56 days 56 days
Reservoir fill port
4.75 mm diameter
6.8 mm diameter
Flow rate accuracy
Flow rate accurate until pump reservoir reaches 2 mL
Flow rate accurate until pump reservoir reaches 1 mL
Catheter access port (CAP)
CAP not included on all models. Mesh screen over port allows 25-gauge or smaller needle.
CAP included on all models. Single-hole, funnel design allows 24-gauge or smaller needle.
Pump rollers
Two rollers.
Three rollers. One roller arm has a
Pump tubing volume
Pumps with CAP 0.26 mL to 0.36 mL Pumps without CAP 0.23 mL to 0.32 mL
0.199 mL to 0.289 mL
• Volume-activated valve. • Expanding drug reservoir bellows pulls valve seem onto a metal seat, forming a seal • Upon activation, requires continuous aspiration and time as release.
• Pressure–activated valve. • As pressure diaphragm flatters, a spring pushes valve seem onto a metal seat, forming a seal • Release immediately upon aspiration.
One tone that sounds approximately every 15 seconds when activated.
Critical alarm – louder two-some alarm that indicates:
Alarm indicates:
• Empty reservoir • End of service (EOS) • Motor stall • Stopped pump duration exceeds 48 hours • Critical pump memory error
radiopaque marker.
Reservoir valve
Alarms
• Low reservoir volume reached • Low battery • Pump memory error Can disable (silence) or postpone some alarms.
Non-critical – louder single-tone alarm that indicates: • Low resroir volume reached • Elective replacement indicator (ERI) • Non-critical pump memory error Interval between sounds is adjustable. Some alarms can be silenced once they have sounded. Continued 1179
Part 3: Specific Disorders
Table 108.2: cont’d Comparison of SynchroMed EL with SynchroMed II implantable pumps Warming
Warming to body temperature required before implantation.
No warming required before implantation.
Pump Purge
Pump purge required to confirm pump operation before implantation.
No pump purge before implantation and purge infusion mode not available.
Suture Loops/Mesh Pouch
Suture loops not included on all models.
Suture loops included on all models. Mesh pouch not provided in pump package. May be ordered separately as an accessory (8590–1 Mesh Pouch Accessory).
Mesh pouch provided in pump package for pumps without suture loops. Information Management
The pump stores:
The pump stores:
• Pump model • Patient ID (3 characters) • 1 Drug (5 characters) • Drug concentration • Infusion prescription • Calibration constant
• Patient demographics • Pump information • Catheter information • Drug name (up to 5 drugs, 25 characters each) • Drug concentration (for each drug entered) • Physician notes • Time-stamped event log • Infusion prescription • Calbration constant Notes: Telemetry takes longer because there is more data to transmit between the pump and programmer. A typical session takes 30 seconds for pump interrogation and 30–90 seconds for pump update.
Longevity
Approximately 6.5 years at 0.5 mL per day – determined by battery depletion.
7 years at 0.5 mL per day - determined by a combination of battery depletion, motor revolutions and time.
Radiopaque Identifier
None.
Identifies pump model under fluoroscopy or X-ray.
Battery Composition
Lithium thionyl chloride.
Lithium-hybrid cathode.
Internal Bacterial-retentive Filter
0.22 μm.
0.22 μm.
SynchroMed EL
SynchroMed II
Programmer
Programmer models 8840, 8821, 8820 and 8810 can be used. Magnet accessory required on releme try head of the 8840 N’Vision Programmer.
Only the 8840 N’Vision Programmer can be used. Do not use the magnet accesory on the telemetry head. It will present relemetry with a SynchroMed II pump.
Infusion prescription
Complex continuous infusion mode available.
Flex infusion mode available – has a repeating cycle of 24 hours. Allows 2 different drug delivery pattern over a 7-day week. Can program a bolus to run between flex or simple continuous infusion modes. Bridge bolus can be programmed to-and-from any infusion mode. Minimum rare infusion mode available (non-therapeutic rate of approximately 6 microliters/day).
PROGRAMMING COMPARISON
Periodic bolus infusion mode available. Can program a bridge bolus only with simple continuous infusion mode. Limited bridge bolus duration.
Programmer therapy stop key
1180
Does not obtain pump status before stopping the pump. Programs pump to stopped pump (0 microliters/day)
Obtains pump status before stopping the pump. Programs pump to minimum rate (6 microliters/day)
Section 5: Biomechanical Disorders of the Lumbar Spine
Table 108.3: Comparison of implanted pump characteristics39 Consideration
Programmable pump
Fixed-rate pump
Cost
More expensive hardware* Needs to be replaced† Can change rate without changing medication Requires programmer
Less expensive hardware Can be permanent Rate change requires removal of medications to be replaced with different concentration Larger reservoir can reduce number of refills
Environment factors
Will not run when cold‡
Rate affected by pressure and temperature changes
Flexibility
Can run at multiple rates or deliver periodic boluses Can change rate without changing concentration for short term or long term Can be turned off temporarily
Fixed-rate (some have a fixed rate selectable at time of implantation)
MRI compatibility
Compatible§
Compatible
Reservoir volume
18 mL and 10 mL reservoirs or 20 and 40 mL reservoirs
Can have much larger reservoirs Can be smaller
Other features
Programmer displays pump information (rate, medication, concentration last fill, refill date, etc.) Potential for some patient control for incident pain Potential to collect longitudinal information with programming
* Hardware cost is one component of overall implantation costs. Other costs include operating suite, recovery room, radiology facility and professional fees, anesthesiology professional fees, surgical professional fees, and medications. When considering total cost, hardware cost represents only a small amount. † Battery lifespan is estimated to be up to 7 years. Surgical costs are incurred for replacement. ‡ Only a factor in pump preparation, not at physiological temperatures. § Please see recently distributed guidelines.
Table 108.4: Updated indications and contraindications for intraspinal drug delivery34,36,39 INDICATIONS Chronic pain with known pathophysiology Sensitivity of pain to medication being used Failure of more conservative therapy Favorable psychosocial evaluation Favorable response to screening trial CONTRAINDICATIONS Systemic infection Coagulopathy Allergy to medication being used Inappropriate drug habituation (untreated) Failure to obtain pain relief in a screening trial Unusual observed behavior during screening trial Poor personal hygiene Poor patient compliance
than 1 week. No protocol can be considered superior or definitive on the basis of current research. However, approximating the conditions of long-term therapy during the trial would seem to offer the best chance for assessing efficacy and tolerance. Table 108.5 compares the advantages of each trial technique.39 The choice of protocol is influenced by the patient’s overall condition, the physician’s preference and experience, the available facilities and resources, the practice environment, and the payer coverage. Medicare reimbursement, for example, requires ‘a preliminary trial of intraspinal opioid drug administration … with a temporary intrathecal/epidural catheter.’40 The question of epidural versus intrathecal administration continues to be debated, although no study has directly compared the two routes of administration. Although the epidural route is more convenient, an epidural dose must be roughly 10 times an intrathecal dose to provide equivalent analgesia. Proponents of intrathecal administration argue that the larger epidural dose may induce more severe side effects, deterring some patients from agreeing to intrathecal therapy that might be both beneficial and tolerable. For patients with chronic pain of spinal origin, an intrathecal trial optimizes the chance for uniform drug delivery and simulates actual effect more accurately. Two questions are fundamental. Is the patient’s pain responsive to opioid therapy? Can the patient tolerate the planned drug and dosage?36 The physician and patient should agree in advance on the goals of the trial and on the measures to be used for assessment of the outcome. For example, if returning to work is a goal of long-term intraspinal drug therapy, the patient should be evaluated by a rehabilitation specialist during the screening trial. In general, candidates should not proceed to implantation unless their pain can be reduced by at least 50%.9,41 Behavioral observation during the trial adds to the
1181
Part 3: Specific Disorders
Table 108.5: Comparison of neuraxial trial techniques 39 Epidural Trial Decreased risk of intrathecal infection Lower incidence of post-dural puncture headache (PDPH) No risk of CSF drainage through catheter from disconnect More common for outpatient administration
Intrathecal Trial Most accurately simulates permanent catheter Lower dosage required Smaller needle produces less severe PDPH Even distribution of medication in FBSS
Bolus Trial Ease of administration Does not require pump for trial Decreased trial expense if additional bolus is not necessary
Continuous Infusion Trial Most accurately simulates permanent implant Can be titrated Required by some carriers Does not produce peaks and troughs of medications Facilitates longer trial Fewer side effects by avoiding peaks Can incorporate placebo without need for second procedure Opioid with Adjuvant Medication Trial May more realistically predict long-term administration
Pure Opioid Trial Predicts the effect of pure opioid No need to discern which medication had salutary or untoward effects Inpatient Trial Better monitoring may enhance safety Easier to observe patient Sterile technique more likely
Outpatient Trial More accurately simulates normal activities Facilitates longer trial More opportunity for titration Less expensive per day
Pure Percutaneous Catheter Trail Less procedure-related pain during the trial Simpler to perform Less invasive Twenty-four Hour Trial Less expensive
Tunneled Catheter Trial Decreases chance of CNS infection Facilitates longer trial Decreases chance of catheter dislodgement
Longer Trial Can more accurately simulate normal activities More accurately predicts long-term result Decreases placebo response Withdraw Systemic Medications during Trial Use of Current Systemic Medications during Trial Eliminates possible systemic abstinence syndrome (abstinence symptoms can confound results)
information used for making decisions regarding permanent implantation.42 A psychological interview is valuable during or after the trial to discuss if and how the trial met expectations.
SURGICAL IMPLANTATION Device manufacturers provide recommended surgical procedures, which can be adapted to surgeon and institutional preference. The surgical procedure has two steps: placement of the catheter and implantation of the reservoir or pump. Implantation technique varies widely, even for a single type of pump, as Krames and Chapple43 reported in their review of 202 patients in 22 centers. Most of the catheters were inserted between L2 and L4 (87.2%), introduced through the midline (65.1%), or positioned with their tips at T10 to T12 (64.1%). Also, 95% of the catheters were anchored, 43.8% with a right-angled anchor and 44.8% with a butterfly anchor. Catheter position was confirmed in 94.8% of the cases. Follett et al. analyzed catheter-related complications and determined that paramedian insertion, appropriate anchoring, and placement with redundant loops reduced the chance of complications.44 1182
Can observe the effect and side effects of neuraxial medication without additive effect of systemic medications
DRUG SELECTION Intraspinal drugs must be preservative free. Alcohol, phenol, formaldehyde, and sodium metabisulfite, common drug preservatives, are all toxic to the central nervous system. Any drug packaged in a multidose vial probably contains preservatives and should not be used for intraspinal administration.45 Preservative-free morphine sulfate is the only drug approved by the FDA for intraspinal delivery for pain relief. Its long history of clinical use, long duration of action (12–24 hours), and relative ease of use explain why it remains the gold standard for intraspinal therapy. If morphine is poorly tolerated, other opioids (hydromorphone, meperidine, methadone, fentanyl, and sufentanil) also can be used intraspinally. Care must be taken to ensure that the medication preparation is compatible with the pump tubing, and that the medication is pure and preservative free. Some meperidine preparations have rendered the SynchroMed pump (Medtronic, Minneapolis, MN) inoperable by damaging internal tubing (personal communication with Medtronic personnel). The pharmacokinetic properties of various drugs (their lipid solubility, pH, pKa, molecular weight, and opioid receptor affinity) determine time to onset of
Section 5: Biomechanical Disorders of the Lumbar Spine
action, duration of action, uptake and distribution, and side effects. Lipophilic medications such as sufentanil do not spread more than several neurotomes beyond the delivery site at the catheter tip, whereas hydrophilic medications such as morphine circulate throughout the cerebrospinal fluid (CSF). Furthermore, the site of drug delivery (epidural versus intrathecal) affects distribution. Drugs delivered epidurally must first cross the dura and arachnoid membranes before diffusing to their site of action, whereas drugs delivered intrathecally diffuse passively to the spinal cord. Morphine, which has low lipid solubility and high receptor affinity, diffuses slowly and remains bound for prolonged periods. Unfortunately, the risk of central nervous system side effects (sedation, nausea and vomiting, and respiratory depression) is greater with hydrophilic drugs, such as morphine, than with lipophilic drugs, such as fentanyl or sufentanil. These lipophilic drugs have a rapid onset and prolonged duration of action.32,36,37 Dosing of intraspinal drugs is highly individual and depends on the patient’s pain type, age, previous need for analgesia, and previous use of opioid medication. Usually, patients with neuropathic pain require higher doses of opioids than patients with nociceptive pain if an opioid is the only medication administered. One advantage with the use of continuous infusion or increasing-dose bolus injections during the screening trial is that dosage can be more precisely titrated. Drug admixtures can help patients who experience side effects associated with the increasing doses required to provide analgesia or outright tolerance to opioids. Combining drugs with different mechanisms of action can produce synergy, as in the case of morphine combined with bupivacaine. In theory, synergy reduces morphineassociated side effects by decreasing the opioid dose required for analgesia. One caveat applies: although use of admixtures is increasingly popular and often produces increased analgesia, safety data on many of the combinations are scarce. In fact, there is a paucity of literature even demonstrating the stability of various admixtures in the pump at body temperature up to 3 months. Satisfactory results with a morphine–bupivacaine combination have been reported in several studies of cancer and noncancer pain, although high concentrations of epidural morphine were required and side effects included transient paresthesias, motor blockade, and gait disruption.34 The study of van Dongen et al.46 followed a group of cancer patients treated with intrathecal morphine and bupivacaine through a tunneled percutaneous catheter. Of 17 patients treated with this admixture because morphine alone was insufficient to relieve pain, 10 improved significantly and four moderately. The three patients who experienced no improvement also had clinical signs of severe depression. No serious complications were reported. A more recent study by a similar group found that intrathecal morphine and bupivacaine slowed the progression of morphine dose, as compared with morphine given alone. These authors attributed the diminished morphine dosage to the synergistic analgesic effect of bupivacaine.47 Although bupivacaine is a commonly used adjuvant medication, care should be taken to avoid concentrations greater than 0.75% in noncancer patients because neurotoxicity has been demonstrated at higher concentrations in rats receiving long-term infusions. Lidocaine (a local anesthetic) and clonidine (an alpha-adrenergic agonist) also have been given with morphine. The morphine–clonidine combination seems to be particularly effective for patients with neuropathic or mixed nociceptive–neuropathic pain.32,36 In the mid-1990s, the Epidural Clonidine Study Group evaluated 85 patients with severe cancer pain who were taking large doses of opioids without significant pain relief or suffering from severe side effects. They were randomly assigned to receive 30 μg/ hour of epidural clonidine or placebo for 14 days and had access to rescue epidural morphine. Pain was documented by visual analog score, McGill Pain Questionnaire, and daily epidural morphine use. Successful analgesia was reported by 45% of patients receiving
clonidine, and by 21% receiving placebo. Among the patients with neuropathic pain, 56% receiving clonidine reported successful analgesia, as compared with only 5% receiving placebo. Pain scores were lower at the end of the study for the patients with neuropathic pain who received clonidine rather than placebo, and morphine use was unaffected. Serious hypotension occurred in two patients receiving clonidine and one receiving placebo.48 Clonidine has not yet been approved for intrathecal infusion in the United States, but in European and Australian studies, intraspinal infusion was well tolerated for 6–12 months.49,50 Dexmedetomidine, a highly selective new α2 adrenergic agonist, is known to produce sedation and analgesia in humans.51 Given intrathecally to rats, it is a very potent antinociceptor.52 Alpha-2 agonists also seem to potentiate the analgesic effects of opioids. One study in rats evaluated the interactions between systemically (subcutaneous, intravenous, and intraperitoneal) and spinally (epidural and intrathecal) administered α2 agonists (medetomidine, dexmedetomidine, xylazine, clonidine, and detomidine) and opioids (fentanyl or sufentanil).53 All of the tested α2 agonists potentiated the effects of opioids by reducing the amount of opioid needed to reach specified levels of analgesia and prolonging the duration of analgesia with a fixed dose of opioid. The potentiation appeared to be independent of the route of administration. Dexmedetomidine was second only to medetomidine in its ability to produce deep surgical analgesia when combined with fentanyl. Recent research that elucidates the neurobiology of pain suggests other methods of pain control. Nerve and tissue damage leads to changes in both the peripheral and central nervous system. Drugs specifically targeted at steps in the neuropathologic cascade are being investigated for properties of reducing both pain perception and side effects. One such drug is ziconotide, a highly selective, potent, and reversible blocker of neuronal N-type voltage-sensitive calcium channels that produces antinociception in animals. Ziconotide is the third medication to receive FDA approval for continuous intrathecal administration via a SynchroMed pump. In one study, ziconotide exhibited substantial neuroprotective activity in a model of traumatic diffuse brain injury in rats.54 The effect of intrathecally administered ziconotide and morphine on nociception also has been studied in rats.55 After a 7-day intrathecal infusion, ziconotide enhanced morphine analgesia, but had no effect on ziconotide antinociception. Whereas chronic intrathecal morphine infusion led to rapid tolerance, ziconotide had no loss of analgesic potency during the infusion period. Ziconotide administered with morphine produced a synergistic analgesic effect, but did not prevent morphine tolerance.55 In humans, ziconotide has been administered intrathecally to control acute postoperative pain.56 Mean daily morphine dosage (administered by patient-controlled analgesia) was significantly less in patients receiving ziconotide than in those receiving placebo 24–48 hours after surgery (p>0.040). Patient pain perception (measured by visual analog scale) also was markedly lower in patients treated with ziconotide than in patients treated with placebo. Four of six patients receiving the high dose of ziconotide (7 μg/hour) experienced adverse events including dizziness, blurred vision, nystagmus, and sedation, all of which resolved after drug discontinuation. Ziconotide has also been used to treat cancer and AIDS patients experiencing pain not responsive to opioids.57 Intrathecal ziconotide has demonstrated analgesic efficacy, and the initial reports indicated that adverse events could be controlled with symptomatic treatment. An expert panel convened in July 2000 released clinical guidelines for intraspinal drug selection, dosage, and administration.58 The panel found wide variation in practice patterns on the basis of an Internet survey of physicians using implantable pumps. The guidelines reflect the best available evidence, as judged by experienced clinicians. 1183
Part 3: Specific Disorders
In 2003, a similar meeting was convened and data from the intervening period were reviewed.59 The treatment recommendations are summarized in Figure 108.1. In 2007, a third panel met to review data from the intravening four years.59a The highlights of the new consensus statement include a change in the first line of therapy to include morphine, hydromorphone and ziconotide. The second line of therapy recommendations will also include ziconotide as an adjuvant option along with clonidine and bupivacaine. The panel also ranked other drugs in order of scientific support and clinical utility. A new important component was also developed for the 2007 version of the consensus panel which includes special recommendations for end of life care.59a The panel noted that the extensive preclinical and clinical data obtained as part of a formal drug development program exceeds the data available for other drugs used for intrathecal infusion and will probably lead to placement of ziconotide on an upper line of the algorithm, unless accumulating experience suggests a narrow therapeutic index in practice. Although the FDA approved ziconotide as an intrathecal monotherapy with a starting dose of 2.4 μg/d, a different, but overlapping consensus of experts expect that this medication will be used in conjunction with other intrathecal medications at a significantly lower staring dosage.60
Efficacy Studies on the efficacy of intraspinal morphine report widely ranging success rates for pain relief (Table 108.6).3,4–6,7,9,11–15,18,24,26,30, 31,38,42,57,61–69 In general, pain relief for cancer patients occurred
Morphine
Line 1
a
more frequently (in approximately 80% of cases) and consistently than for noncancer patients. Some studies also included other measures of efficacy, such as improvement in activities of daily living, employment status, and quality of life. In a cancer study, Smith et al. recently compared neuraxial delivery of morphine to maximum analgesic medical therapy in cancer patients and found that in addition to receiving better analgesia, the patients who received intrathecal morphine had greater longevity.69 Several key studies have examined the efficacy and reliability of intraspinal drug delivery. Winkelmüller and Winkelmüller68 investigated the long-term effects of continuous intrathecal infusion for chronic noncancer pain. They followed 120 patients for 6months to 5.7 years, 73 of whom were FBSS patients with mixed nociceptive–neuropathic pain from multiple lumbosacral operations, including spondylolysis. The best long-term results occurred in the management of deafferentation pain and neuropathic pain with pain reduction (measured by a visual analog scale) of 68% and 62%, respectively. The mean morphine dosage was 2.7 mg/d initially, which rose to 4.7 mg/d after an average of 3.4 years. Among 28 patients treated more than 4 years, 18 (64.3%) were maintained on constant doses, and 10 (35.7%) required increases to more than 6 mg/d 1 year after therapy began. Tolerance developed in seven patients, three of whom had the pump removed. During the follow-up period, 74.2% of the patients benefited from intrathecal opioid delivery. The average pain reduction was 67.4% after 6 months and 58.1% at last follow-up examination. Most patients (92%) were satisfied with therapy, and 81% Neuropathic pain
Hydromorphone b
Morphine (or Hydromorphone) + Bupivacaine d
Line 2
c
Morphine (or Hydromorphone) + Clonidine
Line 3
Line 4
* Z i c o n o t i d e
Morphine (or Hydromorphone) + Bupivacaine + Clonidine
e
Fentanyl, Sufentanil, Midazolam, Baclofen f For selected patients only
Line 5
Neostigmine, Adenosine, Ketorolac g
Line 6
Ropivacaine, Meperidine, Gabapentin, Buprenorphine, Octreotide, other**
* The specific line to be determined after FDA review ** Potential spinal analgesics: Methadone, Oxymorphone, NMDA antagonists a. If side effects occur, switch to other opioid. b. If maximum dosage is reached without adequate analgesia, add adjuvant medication (Line 2). c. If patient has neuropathic pain, consider starting with opioid monotherapy (morphine or hydromorphone) or, in selected patients with pure or predominant neuropathic pain, consider opoid plus adjuvant medication (bupivacaine or clonidine) (Line 2). d. Some of the panel advocated the use of bupivacaine first because of concern about clonidine-induced hypotension. e. If side effects or lack of analgesia on second first-line opioid, may switch to fentanyl (Line 4). f. There are limited preclinical data and limited clinical experience; therefore, caution in the use of these agents should be considered. g. There are insufficient preclinical data and limited clinical experience; therefore, extreme caution in the use of these agents should be considered. Fig. 108. 1 Clinical guidelines for intraspinal infusion, 2003.59 (The reader is referred to an updated recommended algorithm for intrathecal polyanalgesic therapies in a forthcoming publication, 2007.59a) 1184
Section 5: Biomechanical Disorders of the Lumbar Spine
Table 108.6: Studies of intraspinal morphine for intractable pain 39 Studies (listed in order of publication)*
Patient population (nonmalignant/ malignant pain)
Route of administration
Efficacy
Side effects
Behar et al.
6
Epidural
3 complete relief 3 >50% reduction in pain
Wang et al.
8
Intrathecal
2 complete relief from separate saline and morphine injections 6 complete relief from morphine alone
Coombs et al.
10 (5/5)
Intrathecal
5 cancer patients: significantly reduced pain 5 noncancer patients: poor pain reduction
Krames et al.
17(1/16)
Intrathecal/epidural
1 noncancer patient: poor pain relief 16 cancer patients: 50–70% reduction in pain
Auld et al.
32
Epidural
66% good 3% side effects
Auld et al.
20 (15 patients with nonmalignant pain)
Epidural
Of 15 patients, 2 had excellent relief, 6 good relief, 1 fair relief, 2 poor relief, 4 no relief
Brazenor
26
Intrathecal
20 had excellent relief, 3 good relief, 1 poor, 1 none, 1 comatose
Penn and Paice
43 (8/35)
Intrathecal
8 noncancer patients: all good or excellent pain relief 35 cancer patients: 80% good or excellent pain relief
Onofrio and Yaksh
53 (0/53)
Intrathecal
67% good or excellent; 19 of 33 improved ambulation Average parenteral opiate doses fell significantly
Hassenbusch et al.
69
Intrathecal
41 patients reduced mean pain scores from 8.6 to 3.4
Follett et al.
37 (2/35)
Intrathecal
35 cancer patients: good pain relief 2 noncancer patients: most good pain relief
Spinal headache (31%), nausea (26%, not necessarily attributable to pump implantation), and lethargy (15%) most common
Kanoff
15
73% good to excellent 40% of patients returned to work
20% catheter-related
Hassenbusch et al.
18
Intrathecal
61% fair to good
33%
Winkelmüller and Winkelmüller
120
Intrathecal
74% 67% had pain reduction at 6 months 58% at last follow-up 92% of patients satisfied with treatment 81% of patients reported improved quality of life
17%
6% complications, mostly catheter-related
Early pump failure problems in 6 units were corrected by device modification
*See original article 39 for references to the studies. Continued 1185
Part 3: Specific Disorders
Table 108.6: cont’d Studies of intraspinal morphine for intractable pain 39 Studies (listed in order of publication)*
Patient population (nonmalignant/ malignant pain)
Route of administration
Efficacy
Side effects
Paice et al.
429 (289/140)
Intrathecal
95% good to excellent 28 patients returned to work
22%
Tutak and Doleys
26
Intrathecal
77% good to excellent
35% catheter-related
Doleys et al.
36
Intrathecal
60.8% subjective improvement 76.7% decreased oral medications 47.8% improved function 83% of patients rated outcome as good or excellent
Nausea was the most frequent side effect (27.8%) 33% catheter problems requiring surgery Three pumps removed, none for mechanical failure
Anderson and Burchiel
30
Intrathecal
50% had at least 25% pain reduction after 24 months Activities of daily living improved for at least 12–18 months
20% device-related
Smith et al.
0/71 compared
Intrathecal
58% achieved 20% pain and toxicity reduction, overall 52% pain reduction. Improved survival compared to conventional medical therapy (54% vs. 37%)
22% device pump to medical Rx
*See original article 39 for references to the studies.
reported improvement in quality of life. Angel et al.70 studied 11 patients (9 with FBSS) referred to a neurosurgery clinic and treated with intrathecal morphine. The patients were observed for up to 3 years. Overall, a good to excellent analgesic response was seen in 73% (8/11) of the patients. Unfortunately, the three patients judged to have poor results all had FBSS. The effective response among all the FBSS patients was 67% (6/9). Bladder dysfunction requiring pump removal occurred in two patients. The authors concluded that intrathecal morphine delivery was a viable alternative in the management of FBSS despite its limitations. They cautioned that it should be a last-choice option. In the most recent study in FBSS patients, The National Outcomes Registry for Low Back Pain collected prospective data on 136 patients with chronic low back pain treated using intraspinal infusion via implanted devices, 81% of whom received morphine. Oswestry Low Back Pain Disability Scale ratings after 12 months improved by 47% in patients with back pain and by 31% in patients with leg pain.71 The largest study, a retrospective, multicenter study, surveyed physicians in the United States regarding intrathecal morphine delivered by the SynchroMed pump.64 In this study, 35 physicians provided 429 case reports detailing screening methods, outcomes, dosing, and adverse effects. Each of the physicians contacted had implanted at least five pumps. Among these patients, 33% were being treated for cancer pain and 67% for noncancer pain. The average length of treatment was 14.6±0.57 months. The patients with somatic pain had the degree of pain relief. After initial dose titration, intrathecal morphine doses increased only twofold, from 5.84±0.65 mg/d to 13.19±1.76 mg/d. The patients being treated for cancer pain had a higher initial dose, which escalated quickly and then reached a plateau. Patients with noncancer pain had a gradual, linear increase in dosage. Adverse
1186
drug effects were not frequent, but catheter or system malfunction occurred in 21.6% of the cases. Although most implantable drug delivery systems are used to treat nociceptive pain, in the Hassenbusch et al. study38 of intraspinal drug therapy for patients with severe neuropathic pain, 11 of 18 patients (61%) had good or fair pain relief after more than 2 years. Average numerical pain scores declined by 39±4.3%, although long-term pain relief eventually fai™led for 7 of 18 patients (39%). The authors concluded that long-term intrathecal opioid infusions could be effective for treating neuropathic pain, but at higher doses than used for treating nociceptive pain. A recent prospective study examined the long-term safety and efficacy of intrathecal morphine for patients with severe noncancer pain.61 Of 40 patients, 30 experienced pain relief during a screening trial and had an intraspinal delivery system implanted. Patients had mixed neuropathic–nociceptive pain (50%), peripheral neuropathic pain (33%), deafferentation pain (13%), or nociceptive pain (3%). Half of the patients (11/22) reported at least a 25% reduction on the visual analog scale after 24 months of treatment. The results of the McGill Pain Questionnaire and Chronic Illness Problem Inventory showed improvement in sleep, social activities, inactivity levels, and medication use throughout the follow-up period. Device-related problems requiring additional surgery were experienced by 20% of the patients.
COMPLICATIONS The complications of intraspinal therapy fall into several categories: procedure-related complications, drug-related side effects, and equipment-related problems. Immediate drug-related side effects include nausea and vomiting, urinary retention (more common in men with benign prostatic hypertrophy), pruritus, and respiratory
Section 5: Biomechanical Disorders of the Lumbar Spine
depression. Each of these conditions can be managed medically with antiemetics, intermittent catheterization, antihistamines, or naloxone, respectively. Respiratory depression, the most serious of these side effects, is relatively rare in patients already exposed to opioids. Delayed side effects include constipation, myoclonus, edema, arthralgias, facial flushing, and diaphoresis. Clinicians increasingly recognize suppression of the hypothalamic–pituitary axis producing endocrine changes. Examples include decreased testosterone production resulting in decreased libido and suppression of thyroid function resulting in hypothyroidism. For this reason, serum lipids, androgens or estrogens, 24-hour urinary cortisol, and serum IGF-1 levels should be monitored during intrathecal therapy.72 Intraspinal therapy requires conscientious follow-up evaluation, with doses adjusted to balance pain relief against side effects. Many side effects respond to symptomatic treatment.37 Unintentional overdosing can be disastrous. Symptoms of massive morphine overdose include muscle rigidity, severe myoclonus, seizure activity, hypertension, cardiovascular collapse, and severe respiratory depression. Should an overdose occur, the patient should be hospitalized immediately. Replacing some CSF with saline and administering naloxone if signs of respiratory depression occur may help.36 Catheter-related problems are common, occurring in 10–40% of cases. Any abrupt change in pain can signal a catheter problem.34,37 Troubleshooting for equipment problems demands all of a physician’s diagnostic and management skills. A radiograph of the pump and catheter will disclose many catheter problems, but not whether the tip is obstructed or a CSF leak has occurred. Often, surgical inspection and correction are required.36 Meticulous surgical technique can help to prevent some catheter problems. Catheter position can be checked fluoroscopically, CSF flow confirmed at each step during implantation, and the catheter secured with a purse-string suture at the interspinous ligament, and again with a plastic fixation device.34 A recent prospective study of 202 patients in 22 centers in the United States and Europe examined results from the use of a catheter5 modified to overcome some drawbacks of earlier designs.42 The patients in this study were being treated for noncancer pain (60.4%), spinal spasticity (21.8%), cancer pain (12.4%), or other conditions. The catheter implantation technique varied widely with regard to catheter entry site and tip position, spinal introducer position, and catheter anchoring. Based on 3112.8 months of patient use, the overall catheter-caused complication rate was 0.3% per patient per
month. More than 89% of the physicians rated the new catheter as superior to previously available catheters. Table 108.7 lists the nonmedication-related complications associated with this new catheter. Cerebrospinal fluid leaks are inevitable during intrathecal catheter placement, leading to postspinal headache in up to 20% of patients. Persistent CSF leaks should be treated with autologous epidural blood patching. Cerebrospinal fluid hygromas usually resolve spontaneously, but surgical intervention may be necessary if fluid persistently leaks through the suture line after more conservative measures have failed.36 Catheter-tip granulomas, often associated with neurologic sequelae, may develop after intraspinal catheter placement.72 Granulomas are relatively rare. In a survey of 519 US physicians who implanted drug delivery systems, 31 reported a total of 19 cases, 6 of which had not been previously reported in the literature.65 Two reported cases involved patients with FBSS.73,74 Patients with a granulomatous mass may present with new pain, numbness, weakness, or changes in bowel and bladder habits. A recent study analyzed reports of catheter-tip inflammatory masses (granulomas) in 39 patients who received intrathecal morphine or hydromorphone, either alone or mixed with other drugs.75 The authors noted that patients whose mass was diagnosed during the administration of drugs other than intrathecal morphine had probably been exposed to morphine earlier in their clinical course. Subsequently, based on this and preclinical studies, Hassenbusch led a consensus conference that recommended positioning of the catheter tip in the lumbar thecal sac, minimizing opioid dosage and concentration to the extent possible, and providing attentive follow-up of patients to encourage early diagnosis and to reduce the risk of neurological injury.76 This must be weighed against the potential efficacy and reduction of side effects produced by strategic placement of the catheter tip near the level where pain signal enter the cord. If placement of the tip is considered outside the lumbar area, consistent follow-up is essential and unusual neurological symptoms warrant a thorough, immediate evaluation. The diagnosis of granuloma is confirmed by a neurologic examination and MRI. Treatment consists of surgical decompression and removal of the mass and spinal catheter.72 Prevention trumps treatment in the management of surgical infections. Prophylactic cephalosporin or vancomycin administration is recommended, along with strict sterile technique. A wound should never be closed in the presence of uncontrolled bleeding because hematomas are
Table 108.7: Summary of complications related to a new intrathecal catheter72 Complication
Procedure-related
Patient-related
Mechanical
Total
Dislodged
4
5
1
10
Cut during placement
2
0
0
2
CSF leak/hygroma
2
1
0
3
Pain during insertion
1
0
0
1
Occlusion
0
5
0
5
Disconnection
1
1
0
2
Break
1
2
0
3
Kink
0
1
0
1
Pump pocket/site
3
0
0
3
Total
14
15
1
30
Rate per patient month of follow-up
0.45%
0.48%
0.03%
1.0%
1187
Part 3: Specific Disorders
active breeding grounds for infections. Epidural hematoma, diagnosed by MRI or computed tomography (CT), should be treated as an emergency if it impairs neurologic function. Superficial wound infections can be treated with appropriate antibiotics. The implant must be removed if infection invades the catheter or implant pocket. After exploration, the wound should be packed and left open to heal. Intrathecal infections are rare, although many patients spike a fever within the first 3 days after implantation. The most recent information regarding intrathecal granuloma is summarized in the paper from the Polyanalgesic Consensus Conference 200772a. Of note is the fact that the lowest incidence of granuloma is reported with intrathecal fentanyl and baclofen (possibly concentration related). If the complete blood count is normal, the CSF shows only leukocytosis, and the fever falls within 48–72 hours, meningitis probably is not a concern. Untreated epidural infections can abscess and compress the thecal sac, potentially leading to paralysis. Diagnosis relies on clinical signs and symptoms, confirmed by MRI or CT studies. Epidural abscess is treated by removing the pump and catheter and administering antibiotics. Consultation with an infectious disease specialist can be helpful in the selection of antibiotics.36 Many patients notice pump pocket seroma for several months after implantation. The use of postoperative abdominal binders may decrease the incidence and severity of this problem. When seroma persists, fluid can be aspirated for Gram staining if infection is suspected. Intravenous antibiotics and antibiotic irrigation of the pocket can be performed for proven bacterial infection. Patients should be monitored carefully for the spread of infection during treatment, and the device must be removed if the infection does not respond to treatment.36
TROUBLESHOOTING FOR LACK OF EFFICACY When a patient presents with lack of efficacy from a neuraxial drug delivery system, an algorithm for troubleshooting must be used. The clinician must consider possible tolerance to medication or a change in the patient’s back problem as the possible etiology. When these are ruled out, troubleshooting of the system should be initiated. The system can fail to deliver adequate medication when the reservoir volume drops below a critical level, improper programming has occurred, the catheter kinks or obstructs, the catheter becomes dislodged or migrates, the pump malfunctions, or the pump actually stalls. If the clinician approaches troubleshooting in a systematic
A
fashion, the task becomes relatively simple. The first step involves ensuring that the pump has an adequate amount of medication in its reservoir. If the pump is programmable, a scan of the pump should show whether the pump is programmed properly. Once these basics have been covered, the catheter is evaluated. If the pump has a side port, this can be aspirated to determine whether fluid can be obtained from the catheter. Radiography, particularly fluoroscopic radiography, is a valuable tool for evaluating catheter position. If there is any question regarding catheter function after these preliminary steps, a contrast study can be performed by injecting contrast through the side port of pumps so equipped.
Caveat 1 When performing a contrast study through the side port of the pump, the clinician should be careful not to administer a bolus to the patient while medication is contained in the catheter. If it is not possible to aspirate fluid back before injecting, it may not be advisable to inject contrast medium through the catheter.
Caveat 2 When injecting contrast solution into the intrathecal space, the clinician should use contrast medium indicated only for intrathecal administration. Failure to use an appropriate contrast medium can result in adverse events such as seizures and death. Less-severe complications include extreme pain and cramps. Distribution of the contrast solution can demonstrate proper flow within the CSF, verifying catheter function. Pump function (proper pump roller rotation) can be observed under fluoroscopic guidance. Figure 108.2A demonstrates the original position of the pump rotor prior to rotor rotation. Figure 108.2B demonstrates rotation of the rotor. For cases in which conventional contrast radiography leads to a confusing picture, radiolabeled indium can be injected, with the result that serial scans over the ensuing 12–24 hours will show diffusion through the CSF if the catheter is positioned intrathecally.
IMPLANTED PUMPS AND RADIOLOGIC PROCEDURES Patients with FBSS may require diagnostic procedures such as CT or MRI scans. Questions frequently arise regarding the advisability of performing scans for patients with implanted devices. There are no
B
Fig. 108.2 Radiograph of implanted pain pump. (A) Labeled rotor before rotation. (B) Rotor after rotation. Notice the change in the movement of the rotor indication that the pump is turning.39 1188
Section 5: Biomechanical Disorders of the Lumbar Spine
special implications for plain radiographs or CT scans. With modern fixed-rate pumps, exposure of pumps to MRI fields of 1.51 Tesla has demonstrated no impact on pump performance and a limited effect on the quality of the diagnostic information. For patients with implanted programmable pumps, the manufacturer recently released a document stating that the magnetic field of the MRI scanner will temporarily stop the rotor of the pump motor and suspend drug infusion for the duration of MRI exposure. The pump should resume normal operation on termination of MRI exposure. Before MRI, the physician should determine if the patient could safely be deprived of drug delivery. If the patient cannot be safely deprived of drug delivery, alternative delivery methods for the drug can be used during the time required for the MRI scan. If there is concern that suspension of drug delivery during the MRI procedure may be unsafe for the patient, medical supervision should be provided while the MRI is conducted. Before scheduling an MRI scan and on completion of the MRI scan, or shortly thereafter, the pump status should be confirmed using the SynchroMed programmer. In the unlikely event that any change to the pump status has occurred, a Pump Memory Error message will be displayed and the pump will sound a Pump Memory Error Alarm (double tone). The pump should then be reprogrammed and Technical Services notified.66 High doses of radiation can damage a pump’s circuitry. Care should be taken to exclude the pump from the radiation field during radiation therapy.
CONCLUSION Neuraxial medication delivery is now a proven and sophisticated method for managing complex intractable pain, such as that experienced by patients with FBSS. This treatment should be considered when other methods short of neurodestructive procedures have failed. With proper patient selection and medication trial, neuraxial medication delivery is a reversible, nondestructive technique that can benefit patients with FBSS by providing improved pain relief while reducing systemic side effects. Intrathecal medication administration not only can reduce pain while reducing side effects but can play a significant role in functional rehabilitation for the patient with pain of spinal origin. Intraspinal medication delivery has become an effective technique for control of intractable pain in appropriately selected patients seen by spine surgeons.
References 1. Prager J, Jacobs M. Evaluation of patients for implantable pain modalities: medical and behavioral assessment. Clin J Pain 2001; 17:206–214. 2. Hughes J, Smith TW, Kosterlitz HW, et al. Isolation of two related pentapeptides from brain with potent opiate activity. Nature 1975; 258:577–580. 3. Pert CB, Snyder S. Opiate receptors demonstration in nervous tissue. Science 1973; 179:1011–1014. 4. Behar M, Olshwant D, Magor F, et al. Epidural morphine in treatment of pain. Lancet 1979; 1:527–529.
FUTURE CHALLENGES
5. Wang JF, Nauss LA, Thomas JE. Pain relief by intrathecally applied morphine in man. Anesthesiology 1979; 50:149–151.
During the past decade, intraspinal therapy for intractable pain has evolved into a useful clinical treatment. Nevertheless, many challenges remain. Large-scale, well-controlled studies could answer some perplexing questions regarding efficacy in patients with noncancer or neuropathic pain. Patient selection criteria undoubtedly will be refined and validated as more patients are treated. In addition, further investigation of specifically targeted agents or drug combinations for intraspinal use could reduce side effects and expand indications. Basic science is elucidating pain mechanisms, providing a basis for the development of new medications and a rationale for new off-label uses of existing medications. With this in mind, clinicians planning new intrathecal catheter placement should consider a location close to the site where pain information enters the spinal cord so that lipophilic medications can achieve optimal effect. Vigilance must be exercised to observe long- and short-term side effects of medications introduced into the spinal fluid. New combinations of medications provide a huge potential for increased efficacy through additive effects and synergy, but the stability of these admixtures and their neurologic impact must be studied. Microprocessors and miniaturization have enhanced pump development. Programmable pumps are now limited by battery life constraints and size. Improvements in power sources will expand the lifespan of programmable pumps and decrease their size, allowing for larger reservoir volume. At this writing, only one implantable intrathecal system provides an element of patient control and it is not FDA approved for use in the United States. The current pumps are effective in treating baseline pain, but a system that allows patient control for breakthrough pain is essential. Finally, given the contrast in the pharmacokinetics and pharmacodynamics of the various medications that will be used simultaneously in pumps in the future, a system that can deliver different medications at different rates would be desirable. A review of experimental drugs undergoing study can be found in the Intradisciplinary Polyanalgesic Consensus Conference 2007.77
6. Brazenor GA. Long-term intrathecal administration of morphine: A comparison of bolus injection via reservoir with continuous infusion by implanted pump. Neurosurgery 1987; 21:484–491. 7. Coombs DW, Saunders RL, Gaylor MS, et al. Relief of continuous chronic pain by intraspinal narcotics infusion via an implanted reservoir. JAMA 1983; 250:2336–2339. 8. Dennis GC, DeWitty RL. Management of intractable pain in cancer patients by implantable morphine infusion systems. J Natl Med Assoc 1987; 79:939–944. 9. Follett KA, Hitchon PW, Piper J. Response of intractable pain to continuous intrathecal morphine: A retrospective study. Pain 1992; 49:21–25. 10. Harbaugh RE, Coombs DW, Saunders RL, et al. Implanted continuous epidural morphine infusion system. J Neurosurg 1982; 56:803–806. 11. Krames ES, Gershow J, Glassberg A, et al. Continuous infusion of spinally administered narcotics for the relief of pain due to malignant disorders. Cancer 1985; 56:696–702. 12. Onofrio BM, Yaksh TL. Long-term pain relief produced by intrathecal infusion in 53 patients. J Neurosurg 1990; 72:200–209. 13. Penn RD, Paice JA. Chronic intrathecal morphine for intractable pain. J Neurosurg 1987; 67:182–186. 14. Shetter AG, Hadley MN, Wilkinson E. Administration of intraspinal morphine sulfate for the treatment of cancer pain. Neurosurgery 1986; 18:740–747. 15. Spaziante R, Cappabiance P, Ferone A. Treatment of chronic cancer pain by means of continuous intrathecal low-dose morphine administration with a totally implantable subcutaneous pump. J Neurosurg Sci 1985; 29:143–151. 16. Varga CA. Chronic administration of intraspinal local anesthetics in the treatment of malignant pain. Proc Am Pain Soc 1989; 71. 17. Zimmerman CG, Burchiel KM. The use of intrathecal opiates for malignant and nonmalignant pain: Management of thirty-nine patients. Proc Am Pain Soc 1991; 97. 18. Auld AW, Maki-Jokela A, Murdoch DM. Intraspinal narcotic analgesia in the treatment of chronic pain. Spine 1984; 10:777–781. 19. Barolat G, Schwartzman RJ, Aries I. Chronic intrathecal morphine infusion for intractable pain in reflex sympathetic dystrophy. Proc Am Pain Soc 1988; 17. 20. Bedder MD, Olson KA, Flemming BM, et al. Diagnostic indicators for implantable infusion pumps in nonmalignant pain. Proc Am Pain Soc 1992; 111. 21. Burchiel KJ, Johans TJ. Management of postherpetic neuralgia with chronic intrathecal morphine. Proc Am Pain Soc 1992; 136. 22. Goodman RR. Treatment of lower extremity reflex sympathetic dystrophy with continuous intrathecal morphine infusion. Appl Neurophysiol 1987; 50:425–426. 23. Hadley MN, Shetter AG. Intrathecal opiate administration for analgesia. Contemp Neurosurg 1986; 8:1–6.
1189
Part 3: Specific Disorders 24. Hassenbusch SJ, Stanton-Hicks MD, Soukup J, et al. Sufentanil citrate and morphine/bupivacaine as alternative agents in chronic epidural infusions for intractable noncancer pain. Neurosurgery 1991; 29:76–82. 25. Jacobson L. Clinical note: Relief of persistent postamputation stump and phantom limb pain with intrathecal fentanyl. Pain 1989; 37:317–322.
54. Berman RF, Verweu BH, Muizelaar JP. Neurobehavioral protection by the neuronal calcium channel blocker ziconotide in a model of traumatic diffuse brain injury in rats. J Neurosurg 2000; 93:821–828.
26. Kanoff RBL. Intraspinal delivery of opiates by an implantable, programmable pump in patients with chronic, intractable pain of nonmalignant origin. J Am Osteopath Assoc 1994; 94:487–493.
55. Wang YX, Gao D, Pettus M, et al. Interactions of intrathecally administered ziconotide, a selective blocker of neuronal N-type voltage-sensitive calcium channels, with morphine on nociception in rats. Pain 2000; 84:271–281.
27. Krames ES, Lanning RM. Intrathecal infusion analgesia for nonmalignant pain. Proc Am Pain Soc 1991; 98.
56. Atanassoff PG, Hartmannsgruber MW, Thrasher J, et al. Ziconotide, a new N-type calcium channel blocker, administered intrathecally for acute postoperative pain. Reg Anesth Pain Med 2000; 25:274–278.
28. Krames ES, Lanning RM. Intrathecal infusional analgesia for nonmalignant pain: Analgesic efficacy of intrathecal opioid with or without bupivacaine. J Pain Symptom Manage 1993; 8:539–548.
57. Penn RD, Paice JA. Adverse effects associated with the intrathecal administration of ziconotide. Pain 2000; 85:291–296.
29. Lamb SA, Hosobuchi Y. Intrathecal morphine sulfate for chronic benign pain, delivered by implanted pump delivery systems. Proc Intl Assoc Study Pain 1990; S120.
58. Bennett G, Burchiel K, Buchser E, et al. Clinical guidelines for intraspinal infusion: Report of an expert panel. J Pain Symptom Manage 2000; 20:S37–S43.
30. Prager JP, DeSalles A, Wilkinson A, et al. Loin pain hematuria syndrome: Pain relief with intrathecal morphine. Am J Kidney Dis 1995;25:629–31.
59. Hassenbusch S, et al. Polyanalgesic Consensus Conference 2003: An update on the management of pain by intraspinal drug delivery- report of an expert panel. J Pain Symptom Manage 2004; 27(6):540–563.
31. Portenoy RK. Current pharmacotherapy of chronic pain. J Pain Symptom Manage 2000; 19(1 Suppl):S16–S20. 32. Krames ES, Olson K. Clinical realities and economic considerations: Patient selection in intrathecal therapy. J Pain Symptom Manage 1997; 14:S3–S13.
59a. Deer T, Krames ES, Hassenbusch S, et al. Polyanalgesic Consensus Conference 2007: Recommendations for the Management of Pain by Intrathecal (Intraspinal) Drug Delivery. Report of an Intradisciplinary Expert Panel. In Press 2007.
33. Ferrante FM. Neuraxial infusion in the management of cancer pain. Oncology 1999; 13(5 Suppl 2):30–36.
60. Willis D, et al. Expert Consensus of dosing and use of Ziconotide [Editorial in press]. Neuromodulation June 2005.
34. Levy RM, Salzman D. Implanted drug delivery systems for control of chronic pain. In: North RB, Levy RM, eds. Neurosurgical management of pain. New York: Springer-Verlag: 1997:302–324.
61. Anderson VC, Burchiel KJ. A prospective study of long-term intrathecal morphine in the management of chronic nonmalignant pain. Neurosurgery 1999; 44:289–301.
35. DuPen SL, Peterson DG, Bogosian AC, et al. A new permanent exteriorized epidural catheter for narcotic self-administration to control cancer pain. Cancer 1987; 59:986–993. 36. Krames E. Intraspinal opioid therapy for chronic nonmalignant pain: Current practice and clinical guidelines. J Pain Symptom Manage 1996; 11:333–352. 37. Gianino JM, York MM, Paice JA. Intrathecal drug therapy for spasticity and pain. New York: Springer-Verlag; 1996. 38. Hassenbusch SJ, Stanton-Hicks M, Covington EC, et al. Long-term intraspinal infusions of opioids in the treatment of neuropathic pain. J Pain Symptom Manage 1995; 10:527–543. 39. Prager JP. Neuraxial medication delivery. the development and maturity of a concept for treating pain of spinal origin. Spine 2002; 27:2593–2605. 40. Medicare Conditions for Coverage, Medicare Coverage Issues Manual, February. Transmittal No. 67, Section 40-14, 1994. 41. Caudill MA, Holman GH, Turk D. Effective ways to manage chronic pain. Patient Care 1996; 31:154–166. 42. Prager J, et al. Behavioral evaluation of patients for significant pain interventions. Presented at the American Pain Society Professional Development Course, October, 2000. 43. Krames ES, Chapple I, the 8703 W Catheter Study Group. Reliability and clinical utility of an implanted intraspinal catheter used in the treatment of spasticity and pain. Neuromodulation 2000; 3:7–14. 44. Follett KA, Burchiel K, Deer T, et al. Prevention of intrathecal drug delivery catheterrelated complications. Neuromodulation 2003; 6(1):32–41. 45. York M, Paice JA. Treatment of low back pain with intraspinal opioids delivered via implanted pumps. Orthop Nurs 1998; 17:61–69. 46. van Dongen RT, Crul BJ, DeBock M. Long-term intrathecal infusion of morphine and morphine/bupivacaine mixtures in the treatment of cancer pain: A retrospective analysis of 51 cases. Pain 1993; 55:119–123. 47. van Dongen RT, Crul BJ, van Egmond J. Intrathecal coadministration of bupivacaine diminishes morphine dose progression during long-term intrathecal infusion in cancer patients. Clin J Pain 1999; 15:166–172. 48. Eisenach JC, DuPen S, Dubois M, et al. Epidural clonidine analgesia for intractable cancer pain. Pain 1995; 61:391–399. 49. Hassenbusch SJ. Epidural and subarachnoid administration of opioids for nonmalignant pain: Technical issues, current approaches, and novel treatments. J Pain Symptom Manage 1996; 11:357–362. 50. Krames ES. Intrathecal infusion therapies for intractable pain: Patient management guidelines. J Pain Symptom Manage 1993; 8:36–46. 51. Guo TZ, Jiang JY, Buttermann AE, et al. Dexmedetomidine injection into the locus ceruleus produces antinociception. Anesthesiology 1996; 84:873–881. 52. Kalso EA, Poyhia R, Rosenberg PM. Spinal antinociception by dexmedetomidine, a highly selective alpha 2-adrenergic agonist. Pharmacol Toxicol 1991; 68:140–143.
1190
53. Meert TF, De Kock M. Potentiation of the analgesic properties of fentanyllike opioids with alpha 2-adrenoceptor agonists in rats. Anesthesiology 1994; 81:677–688.
62. Auld AW, Maki-Jokela A, Murdoch DM. Intraspinal narcotic analgesia: Pain management in the failed laminectomy syndrome. Spine 1987; 12:953–954. 63. Doleys DM, Coleton, Tutak U. Use of intraspinal infusion therapy with non-cancer pain patients: Follow-up and comparison of worker’s compensation vs. nonworker’s compensation patients. Neuromodulation 1998; 1:149–159. 64. Paice JA, Penn RD, Shott S. Intraspinal morphine for chronic pain: A retrospective, multicenter study. J Pain Symptom Manage 1996; 11:71–80. 65. Schuchard M, Lanning R, North R, et al. Neurologic sequelae of intraspinal drug delivery systems: Results of a survey of American implanters of implantable drug delivery systems. Neuromodulation 1998; 1:137–148. 66. Schueler BA, Parrish TB, Lin J-C, et al. MRI compatibility with and visibility assessment of implantable medical devices. J Magn Reson Imaging 1999; 9:596–603. 67. Tutak U, Doleys DM. Intrathecal infusion systems for treatment of chronic low back and leg pain of noncancer origin. South Med J 1996; 89:295–300. 68. Winkelmüller M, Winkelmüller W. Long-term effects of continuous intrathecal opioid treatment in chronic pain of nonmalignant etiology. J Neurosurg 1996; 85:458–467. 69. Smith TJ, Staats PS, Deer T, et al. Randomized clinical trial of an implantable drug delivery system compared with comprehensive medical management for refractory cancer pain: Impact on pain, drug-related toxicity, and survival. J Clin Oncol 2002; 20:4040–4049. 70. Angel IF, Gould HF, Carey ME. Intrathecal morphine pump as a treatment option in chronic pain of nonmalignant origin. Surg Neurol 1998; 49:92–98. 71. Deer T, Chapple I, Classen A, et al. Intrathecal drug delivery for treatment of chronic low back pain: Report from the National Outcomes Registry for Low Back Pain. Pain Med 2004; 5:6–13. 72. Naumann C, Erdine S, Koulousakis A, et al. Drug adverse events and system complications of intrathecal opioid delivery for pain: Origins, detection, manifestations, and management. Neuromodulation 1999; 2:92–107. 72a. Deer T, Krames ES, Hassenbusch S, et al. Management of intrathecal catheter-tip inflammatory masses: an updated 2007 Consensus Statement from an Expert Panel. In Press, 2007. 73. Koulousakis A, Imdahl M, Weber M. Continuous intrathecal application of morphine in cancer pain. Proceedings of the 8th World Congress, 1998. 74. North RB, Cutchis PN, Epstein JA, et al. Spinal cord compression complicating subarachnoid infusion of morphine: Case report and laboratory experience. Neurosurgery 1991; 29:778–784. 75. Coffey RJ, Burchiel K. Inflammatory mass lesions associated with intrathecal drug infusion catheters: Report and observations on 41 patients. Neurosurgery 2002; 50:78–87. 76. Hassenbusch S, Burchiel K, Coffey R, et al. Management of intrathecal catheter-tip inflammatory masses: A consensus statement. Pain Med 2002; 3:313–323. 77 Deer T, Krames ES, Hassenbusch S, et al. Experimental drugs for intrathecal pain management: a review and update from the Interdisciplinary Polyanalgesic Consensus Conference 2007. In press, 2007.
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic and Lumbar
CHAPTER
Spinal Ablative Techniques for the Treatment of Chronic Pain Conditions
109
Julius Fernandez and Claudio A. Feler
INTRODUCTION
The diagnosis of pain
The interruption of pathways of the nervous system concerned with pain is a classical approach to the relief of intractable pain disorders, which stems from neurosurgeons having been trained with a primary understanding of anatomy and, to a lesser extent, an appreciation of neurophysiology. While successful when implemented in the correct clinical setting, there have also been significant complications with these procedures, including return of pain and sometimes worsening of pain, and/or the evolution of neuropathic pain syndromes in many patients treated with these procedures. The use of ablative techniques has long been a viable treatment option in many patients; however, today there is reluctance in implementing these procedures in favor of neuromodulation. The latter methods of pain management offer the benefits of reversibility and increased safety. Though many of the alternative ablative techniques have become infrequently used, they can continue to play a role in chronic pain management. The purpose of this chapter is to provide to the reader an overview of chronic pain as well as to revisit neurosurgical ablative techniques in the spinal axis that may be of utility when attempting to manage patients. Procedures to be revisited are: spinal rhizotomies and ganglionectomies; dorsal root entry zone lesioning (DREZ); open and pecutaneous anterolateral cordotomy; midline/ commissural myelotomy; cordectomy; sympathectomy; and facet rhizotomy.
The primary phase in evaluating a patient experiencing pain begins with a targeted history and physical examination. This will lead to a better understanding of the abnormal physiologic and anatomic structures as a first step to appreciating and treating the pathologic state in the patient. The use of vague terms such as ‘failed back surgery syndrome’ or ‘cancer pain’ is of limited use. A full appreciation of taxonomy and classification of painful conditions is required in order to define specific therapy in any given patient. Patients may present to a pain management physician for reasons other than somatic pain. The physician will need to navigate through both psychologic and physical issues that a pain patient may have. The duration of pain is an extremely important issue as this may point to a chronic versus acute condition. Following the chronicity of pain, the location must be noted to help guide the specific intervention as well as occasional subtle elements of those interventions. Treatments aimed at and useful for appendicular pain may not be as useful for midline pain as, for example, unilateral cordotomy. The use of pain descriptors during the targeted history, such as sharp, electriclike, numb, dull, aching, and burning are crucial in focusing on the pain physiology and generators in the patient. Long before the different mechanisms of chronic pain were defined, neurosurgeons distinguished between chronic pain due to cancer and chronic pain of ‘benign’ origin. Currently, a more helpful way to differentiate chronic pain is through physiology: namely, nociceptive and neuropathic pain syndromes. The difference between these two categories is the absence of a continuous nociceptive input through pain receptors in neuropathic pain syndromes. It is key to recognize that a given patient may have features of more than one pain physiology. Weir Mitchell first described and named causalgia as a regional pain disorder associated with both motor and sensory disturbance.9 Since then, many and often confusing terms have been used to describe chronic neuropathic pain syndromes. In 1994, the International Association for the Study of Pain (IASP) adopted the term complex regional pain syndrome (CRPS) to replace the terms reflex sympathetic dystrophy (RSD) and causalgia.10 Complex regional pain syndrome is further divided into type 1 and type 2, representing RSD and causaglia, respectively. CRPS may exist in a state of flux and, regardless of whether the patient suffers from CRPS 1 or 2, there may be sympathetically maintained and independent features involved. While many theories exist, the definitive pathophysiology and etiology of CPRS remains unclear. A correct physiologic diagnosis can only be obtained through detailed history and physical examination. It may be necessary to obtain diagnostic studies such as computed tomography (CT) scan, margnetic resonance imaging (MRI), and electromyogram/nerve conduction velocity (EMG/NCV). Diagnostic spinal procedures such as
Historical aspects of pain management The origin of the word ‘pain’ is the Latin word poena, meaning punishment. The early concept of pain as a form of punishment for sinful activities is as old as humankind.1 Early healers used a wide range of modalities to attempt the control of pain, including herbal medicines and the application of electric fish.2 Decartes’ description of pain conduction from peripheral damage through nerves to the brain led to the first scientific understanding of pain.3 The first plausible surgical management of pain was on an anatomic basis where nerves were cut in attempts to denervate the painful areas of the body. These methods were a direct byproduct of the understanding of pain transmission during the scientific revolution. It was not until the Wall and Melzack Gate Control Theory that a sound scientific basis for pain mechanism was formulated.4 Shortly thereafter, initial efforts were made to modulate pain at peripheral nerve, spinal cord,5,6 and other targets such as brain stem7 and, more recently, the cerebral cortex.8 Despite their long history, destructive pain techniques may continue to fall into disuse as further understanding of the pain system and its physiology becomes more sophisticated.
1191
Part 3: Specific Disorders
selective root blocks, sympathetic blocks, and discography will often further aid the clinician. There is no confirmatory test or procedure for CRPS 1, and this diagnosis can only be attained through a clinical examination. An early and specific refinement of the pain diagnosis is necessary and valuable, as it directs care of the patient.
cated for treating extremity pain in a functional limb, as complete or near-complete functional paralysis will occur because of absence of sensory input. Extensive sectioning of sacral posterior root also needs to be performed with selectivity as interference with sphincter and sexual function can occur.
Preablative therapy evaluation
Pertinent anatomy
Prior to performing an ablative technique on any patient, one should perform a thorough history and physical examination and a review of the available studies before a presumptive clinical diagnosis can be made. A series of diagnostic blocks can then be utilized to further develop a line of reasoning supportive of an ablative technique. It is imperative to distinguish patients experiencing nociceptive pain and those who present with neuropathic pain syndromes. The successful treatment of chronic pain should follow a logical algorithm, beginning with the correct diagnosis. Failure to select the appropriate treatment for a patient will lead to inadequate pain relief and unsatisfactory patient care. Simulation of the ablation can be accomplished through pharmacology and should always precede destructive and irreversible procedures. To best serve a patient, these authors believe that the diagnostic blocks necessary should be performed by the physician who will ultimately perform the definitive ablation so that correct patient selection and therapy can be rendered.
The spinal root anatomy begins with the formation of the anterior roots, which are formed by three to five rootlets emerging from the anterolateral sulcus; the posterior roots are formed by three to ten rootlets which penetrate into the dorsolateral sulcus (Fig. 109.1). The dorsal and ventral roots are separated by the dentate ligaments, though they are grouped together prior to leaving the thecal sac. Microscopic anastomotic branches exist that pass from one rootlet to another. As the roots approach the intervertebral foramen, both the ventral and dorsal roots are situated in a common dural sleeve. In the intervertebral foramen the dorsal ganglion can be identified. At this point the subarachnoid space is sealed by the arachnoid trabeculae and no cerebrospinal fluid (CSF) is contained.19 Distal to the dorsal ganglion and lateral to the foramen, the spinal nerve is formed which will then bifurcate into ventral and dorsal branches.
SPINAL RHIZOTOMIES AND GANGLIONECTOMIES Historical background Dorsal root rhizotomy was first attempted for the relief of intractable pain by Abbe in 1889.11 The operation was based on the concept that afferent signals are conveyed via the dorsal roots while efferent signals are conveyed via the ventral roots.12,13 There now exists a large body of evidence supporting the existence of as much as 30% afferent axons passing through the ventral roots.14–16 Dorsal rhizotomies or ganglionectomies are primarily indicated for treatment of pain syndromes involving the neck, trunk, abdomen, and perineal region. Persistent post-thoracotomy or postlaparotomy pain is a frequent indication for these procedures, as well as treating malignant pain syndromes from pleural based or apical lung lesions. Several variations of spinal root surgery have been developed over the century, though the methods have experienced a long decline due to the disappointing outcomes of most series.17,18 The procedure is contraindi-
Procedure Prior to the procedure, a selective nerve root block may aid in determining if rhizotomy or ganglionectomy may provide any benefit. The operation is performed under general anesthesia with the patient in the prone position and may be performed via an intradural (dorsal rhizotomy) or extradural (ganglionectomy) approach. The desired spinal segments are exposed. In the case of dorsal rhizotomies, laminectomies are performed and a midline dural opening is made. The dorsal rootlets of the desired segments are then sectioned sharply. A technique described by Sindou in 1972 aimed to interrupt selectively small-diameter nociceptive fibers at their radicular entrance into the spinal cord.20 This technique of selective dorsal root rhizotomy allows for preservation of lemniscal fibers that may avoid secondary appearance of pain and leave intact substrates that can be utilized for neuromodulatory procedures.21 For ganglionectomies, foraminotomies are performed to expose the desired dorsal root ganglia. The ganglia are then carefully dissected free from the surrounding tissue and the dorsal root is divided proximal to the ganglion. Following this, the ganglion is gently elevated and the distal connection to the root is sectioned. In most cases, the ventral root can be spared. Important aspects from a purely technical point of view include verification of the level of lamienctomy, root identification by anatomical, radiographic,
Fig. 109.1 Pertinent anatomy. 1192
Section 5: Biomechanical Disorders of the Lumbar Spine
and physiological means, selection of roots by stimulation, recognition of anastomoses between roots, and sparing of radicular arteries. Other technical variants exist such as extradural spinal root ganglion resection as described by Scoville in 1966, which avoid the opening of the dura. An alternative to the open surgical technique’s proximal radiofrequency thermocoagulation of primary spinal trunk and ganglion has been described; Uematse et al. proposed a percutaneous technique for lesioning the dorsal root ganglion and rootlets.22
Outcomes The variability of clinical results of posterior rhizotomy and ganglionectomy warrants the cautious use of these denervation interventions and should only be used after nondestructive techniques have been exhausted. For lumbar radiculopathies, there is about a 30% success rate at 1 year.23 The results for postherpetic neuralgia are no better, with success rates at less than 30%.24 And the results for non-specific relief of chronic pain are extremely poor in the long term.25 A review of the literature reveals that results are generally less than 50% for good pain reduction with limited long-term follow-up. Unfortunately, these procedures produce a complete denervation of one or more spinal segments, thus precluding the patient from potential future neuromodulation. Because of this, and the general availability of long-acting opiate analgesics, these procedures are not generally recommended.
DORSAL ROOT ENTRY ZONE LESIONS (DREZOTOMY)
Dorsal root rhizotomy Dorsal root ganglion Spinal nerve
Ganglionectomy
Gray rami communicantes White rami communicantes Thoracic paravertebral sympathectomy Sympathetic trunk Dorsal ramus Thoracic sympathetic ganglion Greater splanchnic nerve Facet denervation
Historical background During the early 1960s, research into pain focused attention on the dorsal root entry zone (DREZ) as the first level of modulation for the cessation of pain.26 What is known of these pathological mechanisms is that the cells in the dorsal root ganglion become hyperactive and send nociceptive impulses via the spinothalamic pathways. Based on this understanding, Sindou performed the first DREZ operation in 1972 for pain caused by Pancoast-Tobias syndrome.27 Others such as Nashold and Ostdahl placed thermal lesions into the substantia gelatinosa of the spinal cord for the treatment of nonmalignant pain.28 In view of the complex anatomy and lack of histological confirmation, the target was referred to as the DREZ. This region in the spinal cord is currently recognized as a sophisticated structure for the modulation of pain and continues to be utilized for ablative techniques, either open or percutaneous.
Pertinent anatomy Using cytoarchitectural criteria, in 1952 Rexed divided the gray matter of the spinal cord of the cat into ten separate cell layers. Similar laminar patterns were confirmed by Schoenen.29 The uppermost lamina (I–V) are pertinent to the DREZ procedure. The major nociceptive input is distributed to layers I, II, and V (layers I and II representing the substantia gelatinosa), with their second-order neurons giving rise to the spinothalamic tract. Neurons in layers III and IV receive non-noxious inputs from the periphery and project to the dorsal column nuclei. Situated dorsolateral to the dorsal horn is the tract of Lissauer, an intersegmental longitudinal spinal tract with multiple collaterals to Rexed layers I and II. This tract plays an important role in the intersegmental modulation of the nociceptive afferents. Its medial part transmits the excitatory effects of each dorsal root to the adjacent segments and its lateral part conveys inhibitory influences to the substantia gelatinosa.30 The DREZ procedure is directed
Lesion locations = Fig 109.2 Thoracic spine anatomy.
at destroying the Rexed layers I, II, and V and the medial portion of the tract of Lissauer which coordinates sensory information.
Procedure The surgical technique of thermal coagulation for DREZ lesions has been described in detail by Nashold and collaborators and extensively published.31 With the patient placed under general anesthesia and in the prone position, laminectomies or hemilaminectomies are performed over the involved regions of the spinal cord. In the cervical region, the localization of the appropriate level is one level rostal to the dermatomal localization, and in the thoracic region two to three veterbral segments rostal to the affected dermatomes (Fig. 109.2). Lumbar and sacral segments are localized through laminectomies at T10 through L1 for exposure of the conus medullaris. The operating microscope is utilized throughout the procedure following the dural opening. Each dorsal root is composed of several small rootlets which enter the cord at the postointermediolateral sulcus at the margin of the dorsal columns. Identification of the root and corresponding cord level can be confirmed with electrophysiologic monitoring. Following the identification of the rootlets of each root, though this may be difficult at the level of the conus, the lesions are made in the dorsal root entry zone. The lesions are created over an additional one to two segments above and below the affected roots to ensure adequate coverage of the painful segments. Bilateral lesioning should be avoided in patients with 1193
Part 3: Specific Disorders
good neurologic function below the lesion, as deterioration in proprioception, motor, or bladder and bowel function can occur. Methods for lesioning include: argon and CO2 laser; radiofrequency; bipolar coagulation; and ultrasound. The authors’ preferred method is radiofrequency (RF) ablation, as it allows for uniform size and depth of lesioning. The electrode used is 2 mm in length and 0.25 mm in diameter. It is typically inserted at a 25° angle; however, the point of exit of each dorsal root and its angulation from the spinal cord is the best guide for introduction of the RF electrode. Lesions are made at 75°C for 15 seconds and are made at 1 mm intervals along the length of the spinal cord and segments. Rapid tissue heating, thermal vaporization of the spinal parenchyma, and tissue scaring at the electrode should be avoided. Care must also be taken not to injure any vasculature of the spinal cord in order to avoid ischemic changes or new neurological deficits that may include weakness.
Outcomes The DREZ procedure has been implemented for a large series of deafferentation pain syndromes. Results from several series report a 54–79% success rate for the procedure.32–34 Probably the single best indication for the DREZ lesioning is pain following brachial plexus avulsion. Long-term pain relief for this procedure for brachial plexus avulsion pain reaches 70%.35 The major complication with thoracic spinal DREZ operation is weakness in the ipsilateral leg due to injury of the corticospinal tract; this is seen in 5–10% of patients,36–38 though this may occur with other sites of DREZotomy. While the DREZ operation has been used in an attempt to treat a multitude of pain conditions, its current indications are very specific. It is best used to treat deafferentation pain (as seen with brachial plexus avulsion), limited cancer pain (as seen with a Pancoast tumor), segmental pain after spinal cord injury, peripheral nerve pain (seen with nerve injuries and phantom limb or stump pain), and postherpetic pain.39 These authors do not utilize this procedure, however, for other than segmental pain following spinal cord injury because neuromodulation is commonly usable in most of the other painful phenomenon listed and neuromodulation has a superior safety profile.
OPEN ANTEROLATERAL CORDOTOMY Historical background In 1889, Edinger40 first described the anatomy of the spinothalamic tracts, though functional correlation was not discovered until Spiller reported his findings in 1905.41 The first anterolateral tractotomy was performed by Martin at the suggestion of Spiller in 1911 for management of pain in man.42 Eventually, both in Europe and America, the surgical cordotomy became a standard neurosurgical procedure for the treatment of pain. Mullan43 developed the technique for percutaneous cordotomy using a radioactive strontium needle in 1963 where the lesion can be made without the necessity of general anesthesia. Rosomoff44 further refined the technique using a radiofrequency needle electrode system. Additional refinements to the procedure have included myelography45 to outline landmarks, CT guidance,46 and electrical impedance monitoring.47 While the operation has remained in essence the same as that introduced by Spiller and Martin, much effort over the decades has continued to be devoted to lesioning the anterolateral quadrant of the spinal cord. Both open and percutaneous techniques will be discussed.
Pertinent anatomy Neuroanatomical and physiological aspects of nociceptive pathways have been extensively studied in animals and humans. Within close proximity to the spinothalamic tract lie many other ascending and 1194
descending tracts, damage to which leads to many of the complications of cordotomy. The corticospinal tract is located posteriorly and injury to it results in ipsilateral weakness. Overlying the spinothalamic tract is the ventral spinocerebellar tract and injury of that pathway may produce an ipsilateral ataxia of the arm. Knowledge of the location of descending respiratory pathways is not just theoretical, as one of the most feared complications of a high bilateral cordotomy is respiratory dysfunction. Typically, the patient is capable of voluntary but not involuntary respiration, and consequently dies during sleep because of destruction of the system for automatic respiration (Ondine’s Curse).48
Surgical cordotomy procedure The basic open surgical cordotomy has not changed much since it was first described by Spiller and Martin in 1912.42 The technique is relatively simple; however, it is important to note that the vertebral and spinal cord segments do not correspond. Functional segments of the spinal cord tend to lie two to three levels lower than the vertebrae. The authors’ practice is to perform open cordotomy at the T1–2 or T2–3 segments. Following the laminectomy, the dura is opened in a semicircular manner paramedian to the midline. In order to facilitate rotation of the spinal cord, a dorsal root may be incised as the dentate ligaments above and below the segment are sectioned. The cut end of the dentate ligament is then grasped and the cord is rotated 45° to allow visualization of the anterolateral surface. The origin of the dentate ligament from the cord is a valid landmark for the dorsal extent of the crossed spinothalamic tract. If necessary, a dental mirror can be used to better identify the anterior spinal artery or the medial limits of the ventral rootlets. A cordotomy knife is then inserted at the origin of the ligament, and an incision is made to a point just medial to the emergence of the most medial fibers of the ventral rootlets. Poletti’s technique has increased safety, as he incises the tough pia with a knife and then completes a tractotomy with a ball hook.49 The incision should be deep enough into the cord to transect a pie-shaped segment of about 90°.
Percutaneous cervical cordotomy procedure Mullan et al., in 1963, introduced a procedure to percutaneously perform an anterolateral cordotomy.43 Since the first description, there are have been few technical advances such as CT guidance17 and impedence monitoring.18 The target in percutaneous cordotomy is the lateral spinothalamic tract, located in the anterolateral part of the spinal cord at the C1–2 level, since the interspace is large enough. The patient is placed in the supine position with the upper cervical spine being kept exactly horizontal. Image guidance may consist of either biplanar fluoroscopy or CT scanning. Following the injection of local anesthetic into the skin, the cordotomy needle is inserted inferior to the tip of the mastoid process in a vertical plane perpendicular to the axis of the spinal cord. The needle is then aimed at the location of the dentate ligament, usually the middle of the C1–2 space halfway between the anterior and posterior bony margins. The needle is then further advanced to perforate the ligamentum flavum and dura. Upon perforating the dura, a contrast medium is injected into the subarachnoid space to outline the anatomy of the cord and dentate ligaments. Originally, strontium radioactive source was used, later modified by Rosomoff50 to incorporate radiofrequency ablation. Many authors currently recommend impedance monitoring. An electrode can be inserted through the needle, and impedance measurements taken to confirm the location as the needle passes from CSF into the spinal cord. Electrical impedance measures about 400 ohms when the electrode is in CSF and rises to about 1000 ohms once the cord is
Section 5: Biomechanical Disorders of the Lumbar Spine
entered. Further physiologic localization can then be performed with stimulation. With appropriate localization, contralateral warm or cold sensory effects are induced at 100 Hz. Ideal placement is generally 1–3 mm anterior to the dentate ligament, with upper extremity fibers tending to be more anterior. A test lesion is then generally made with an electrode tip temperature of 50–60°C. Close monitoring of contralateral motor function must be performed. If no untoward side effects are noted, a permanent lesion is then made at 70–80°C for 60 seconds. It is highly recommended following high cervical cordotomy to monitor these patients’ respiratory status for approximately 5–7 days, as an unintended unilateral lesion may actually represent a bilateral lesion.
Lower cervical cordotomy procedure Lin et al. describe an anterior approach for percutaneous lower cervical cordotomy, thus attempting to avoid phrenic nerve fibers and the dreaded respiratory complications of high cervical cordotomies.51 It involves an anterior transdiscal approach to the lower anterolateral cervical cord, producing a lesion in the spinothalamic tract. This transdiscal technique can be difficult to achieve if the needle should be redirected in the event it does not hit the target. The patient is positioned supine with the neck slightly extended. The needle is then inserted under local anesthetic between the carotid sheath and tracheoesophageal complex. CT or biplanar fluoroscopy is used for guidance. The needle is usually directed towards the C5–6 disc space. Once the needle is passed through the disc space and dura, contrast can be injected into the subarachnoid space. For pain involving the lower extremity, the target is 8 mm lateral and 5 mm anterior to the posterior wall of the canal. For trunk pain, the lesion is 3 mm lateral and 8 mm anterior to the posterior wall. The trajectory is either calculated or determined graphically. As with the high cervical cordotomy, impedance monitoring and stimulation can be performed to confirm physiological localization. The RF lesion is then created as described above.
Outcomes These procedures are not commonly employed for benign chronic pain syndromes, as newer therapies that include long-acting opiates delivered through intraspinal or intraventricular routes or neuromodulation techniques have become first-line therapies. The results for the various cordotomy procedures are fairly similar; however, lower complication rates are seen with the percutaneous approach.52 For open surgical cordotomy, approximately 50% of patients with cancer pain have complete relief and an additional 25% will have significant reduction in pain.20 By 6 months, however, pain will return in half of the initially successfully treated patients.21 After high percutaneous cordotomy, 60–70% have complete relief and 80–90% have significant relief.53–55 As with surgical cordotomy, these results tend to drop at 1 year.28,56 The results for low anterior cordotomy are similar, with 75–80% of patients experiencing significant pain relief.57 Although cordotomy has initially been used to treat all types of pain, it is now reserved for pain of malignant origin. Studies show that 80% of patients undergoing cordotomy have significant relief of their pain, though at 1-year follow-up only 40% have any pain reduction.36,58 The highest level of analgesia that can be reliably and persistently obtained with high cervical cordotomy is the C5 dermatome and is generally not effective for pain due to head and neck cancers. Lesions above C5 may be treated with a mesencephalic tractotomy. Bilateral cordotomy is reserved primarily for midline abdominal and pelvic pain or bilateral lower extremity pain, though not recommend secondary to the risk of Ondine’s Curse.37,59
The complication rates of the various techniques differ, though with surgical cordotomy there is an 8% mortality rate27 and 13% incidence of lower extremity weakness.38 Complications for high cervical cordotomy include a 1–5% mortality rate,60 4–8% incidence of lower extremity paresis or ataxia,34 and a 5% incidence of bladder dysfunction.34 The complications for low cervical cordotomy are similar to the higher posterior approaches with except of the phrenic and respiratory tract injury.32
MIDLINE/COMMISSURAL MYELOTOMY Historical background Midline or commissural myelotomy is a procedure in which the decussating fibers of the spinothalamic tract are interrupted as they cross in the anterior white commissure of the spinal cord. The procedure was conceived as an alternative to bilateral anterolateral cordotomy in patients in whom a bilateral area on analgesia was sought. The procedure was first described by Hitchcock in 1970.61 During a planned percutaneous cervical cordotomy, the electrode was inadvertently inserted into the center of the spinal cord in the upper cervical region. The patient had immediate relief of pain, and the relief lasted when only a small lesion was made at the site. This target was adopted for central myelotomy, and other patients had similar successful relief of pain with this technique. The results tended to be best in those patients with midline or visceral pain. This led some to conclude that a previously undescribed pathway ascends at the center of the spinal cord and carries predominately visceral pain perception. The technique was later refined by Gildenberg and Hirshberg,62 who felt that there was no advantage to making a high cervical lesion for patients with pelvic or perineal pain. Interruption of the central cord at the lumbothoracic level provided similar results. Today, limited myelotomy is most commonly performed for pelvic pain related to rectal or uterine cancer.
Pertinent anatomy On the anterior surface of the spinal cord there can be identified a deep anterior median fissure which penetrates the spinal cord. On the posterior surface, a small posterior median sulcus is continuous with a glial partition. The spinothalamic fibers cross in the anterior white commissure in a decussion that involves several spinal segments and ascend contralaterally. The intent of the myelotomy is to interrupt the paleospinothalamic tract, producing analgesia with preserved ability to localize and discriminate between sharp and dull sensation.63
Procedure It is important to note that the vertebral and spinal cord segments do not correspond. Functional segments of the spinal cord tend to lie two to three levels lower than the vertebrae. With this in mind, the lamina overlying the spinal segments targeted for denervation are identified with the aid of fluoroscopy. Laminectomies are then performed and the dura is opened to expose the spinal cord. The midline can be identified by the vessels diving into the posterior median sulcus between the posterior columns. The pia is then opened sharply and the posterior median septum is identified. The septum is a single fibrous layer that lies between the posterior columns, and one can dissect along either side of it to the central canal area. Dissection continues until the anterior median septum is encountered. This represents the ventral extent of the myelotomy, as further dissection risks injury to the anterior spinal artery. Various other techniques have been reported, including radiofrequency and carbon dioxide laser techniques.64 1195
Part 3: Specific Disorders
Outcomes Midline myelotomy is most effective for pain in the lower portion of the body, especially midline visceral pain. The overall efficacy of midline myelotomy has been reported in the order of 70%.65–67 There are, however, several undesirable side effects of the procedure, such as hyperesthesia, diminished proprioception, parasthesias, and incoordination of gait.68 A reduction in side effects has been reported by performing a limited myelotomy versus the classic midline myelotomy technique. The difficulty with comparing reports stems from the controversy of the depth of cut. Neither the limited and classic myelotomy technique is performed with any frequency, limiting the role of these techniques for chronic pain management.
CORDECTOMY Historical background Armour, in 1916, performed the first cordectomy for pain in a posttraumatic paraplegic.69 Prior to this, cordectomy had been formed for other indications including intramedullary spinal cord tumors, severe spasticity, and post-traumatic syringomyelia.
Procedure The technique for cordectomy is rarely performed, as many of the indications for this procedure have found newer nondestructive therapies. Intrathecal baclofen pumps have rendered cordectomy obsolete for uncontrolled leg spasticity. Shunts have also supplanted the cordectomy for the therapy of syringomyelia. There are several techniques of cordectomy, though the majority of techniques have described multilevel segmental resection of spinal cord at the level of injury. Segments have been reported from 2.5 cm to 21 cm of spinal cord. In the literature there is no standard technique, as the number of cases performed is few.
Outcomes The clinical indications for cordectomy are varied, including posttraumatic syringomyelia, uncontrollable leg spasticity, and post-traumatic spontaneous neurogenic leg pain. The operation of selective spinal cordectomy is rarely performed. Jefferson, in 1983, reported his series of 19 cases of cordectomy with adequate pain relief in traumatic paraplegics.70 Clinical results in the patients with syringomyelia and uncontrollable leg spasticity have been excellent, though cordectomy did not provide permanent relief in the patients with neurogenic leg pain.71
SYMPATHECTOMY Background Surgery on the sympathetic nervous system dates to the late nineteenth century. The functional role of the autonomic nervous system was poorly understood, and early sympathectomies were performed for such varied disorders as epilepsy, vascular disease, and spasticity. By 1930, thoracic and lumbar sympathectomies were being performed for angina, hypertension, and pain.72 While many of these are no longer indications due to the advent of modern pharmaceuticals and surgical techniques, sympathetically maintained pain remains one of the few indications for a sympathectomy other than hyperhidrosis. Currently, sympathetic denervation for pain is carried out for three main sites of pain: the heart, the limbs, and the abdominal viscera. Sympathetically mediated pain includes a wide spectrum of disorders that share in common the factor that the pain can be relieved through sympathetic block or interruption.73 The most common indications for the procedure are reflex sympathetic dystrophy (RSD)/ Sudeck’s 1196
atrophy, causalgia, and ischemic pain states from occlusive vascular disorders. These conditions can be sympathetically mediated pain syndromes and generally respond to sympathetic blocks with local anesthetics. Sympathectomy should not be considered unless there is good relief with the diagnostic block. Often, lasting relief can be achieved with a series of blocks if they are performed early in the progression of the disease. Visceral pain secondary to unresectable cancers of the abdominal visera and painful relapsing chronic pancreatitis are some of the indication for sympathectomy.46,74 Pancreatic afferents travel bilaterally through the splanchnic chain and into the lower thoracic sympathetic ganglia. The biliary tract is supplied by the right splanchnic nerves and each kidney is supplied unilaterally by the nerves on that side. Attempts at chemical sympathectomy of the celiac plexus and splanchnic nerves during exploratory laparotomy, or percutaneously, have had good initial pain relief though poor localization, and the diffuse target make it difficult to assess the completeness of denervation.75
Pertinent anatomy The paravertebral sympathetic trunk extends from the coccyx to the base of the skull. The cervical sympathetic can be divided into three regions: superior, middle, and cervicothoracic (stellate) ganglia. The stellate ganglion is a fusion of the lower cervical and first thoracic ganglia located at the level of the sixth cervical vertebra. The sympathetic innervation to the upper extremity is from preganglionic fibers exiting the T2–10 roots and traveling through the sympathetic chain to the upper thoracic and cervical ganglia. The sympathetic innervation to the lower extremity arises in the lower thoracic cord and travels down the chain into five lumbar ganglia. The splanchnic nerves receive their sympathetic supply from the T4–12 segments, with the lesser splanchnic nerve being mostly from T10–12 and the greater from T4–9. Denervation of the pancreas can be accomplished by bilateral resection of the T9–12 ganglia along with the greater, lesser, and least splanchnic nerves.
Upper thoracic ganglionectomy procedure Sympathetic activity can be interrupted by lesioning the paravertebral sympathetic chain along its course. This can be achieved either by direct/endoscopic surgical resection or through chemical or radiofrequency ablation. Resection of the T2 and T3 ganglia should result in complete sympathetic denervation to the upper extremity.76,77 The most common surgical approach is through a midline incision with the patient in the prone position, which allows for bilateral exposure and lesioning. After a subperiosteal dissection of the muscles, the T3 lamina and rib are identified with the use of fluoroscopy. The transverse process and medial portion of the rib are then resected. The second and third sympathetic ganglia should be found in the paravertebral fat and sectioned at the ganglia; a Horner’s syndrome can generally be avoided. Alternative approaches include the anterior transthoracic, percutaneous radiofrequency, and transaxillary exposure.78 Here, a rib-spreading incision is made low in the axilla between the third and fourth ribs, and the lung must temporarily be collapsed. The thoracic chain can be identified beneath the pleura alongside the vertebrae. Lastly, the procedure can be performed through a supraclavicular approach.48 The lower cervical and upper thoracic sympathetic ganglia can be found in the fatty tissues deep and medial to the sublclavian artery.
Lumbar sympathectomy procedure The operation is performed through a retroperioneal approach through a flank incision.46,79 The external oblique, internal oblique, and transverse muscles are divided in the direction of their fibers in order
Section 5: Biomechanical Disorders of the Lumbar Spine
to reach the retroperitoneal space alongside the psoas muscle. The ureter is identified and carefully elevated from the vertebral column. The sympathetic chain should be encountered between the psoas and vertebral bodies. The ganglia and their rami communicantes can then be segmentally resected. Removal of the L2 and L3 sympathetic ganglion is usually adequate to remove sympathetic tone from the lower extremities. Male patients should be warned that sexual dysfunction may occur with bilateral lumbosacral sympathectomy.
Splanchnicectomy procedure The upper abdominal viscera sends numerous amounts of nociceptive afferents into the spinal cord via the greater and lesser splanchnic nerves. This allows for the effective treatment of pain by denervation of sympathetic tone to the viscera. The patient is positioned prone and an oblique incision is made over the eleventh rib approximately 5 cm from midline. Six centimeters of rib are then resected, starting just lateral to the transverse process. The pleura is carefully stripped away to visualize the lateral aspects of the vertebral bodies. The sympathetic ganglia are identified ventral to the intercostal nerves. The sympathetic chain and T9–12 ganglia, along with the three splanchnic nerves, are then resected. For pancreatic pain, the procedure must be done bilaterally.46,47,80 Further modifications have been reported with the use of endoscopic procedures performed by thoracic surgeons.
Outcomes The indications for open sympathectomy have decreased steadily over the past decades as pharmacological substances have supplanted these aggressive surgical techniques. The results of sympathectomy for pain disorders have yielded modest success. Most authors report sustained pain relief in less than two-thirds of patients at 2 years, and about one-third at 5 years.46,47,51,81,82 The adequate and limited long-term outcomes should give consideration to either repetitive blocks or other neuromodulatory methods that are nondestructive.
RADIOFREQUENCY FACET DENERVATION Historical background Shealy first described the application of radiofrequency to the facet joint for the treatment of spinal pain.83 Prior to Shealy, Goldthwait 84 and others85,86 initiated interest in the neuroanatomy of the facet joint and its origin of nociceptive lumbar pain. In 1971, Rees published a specific method of attempting facet denervation to modulate back pain.87 Others later suggested that the knife that had been used by Rees was, however, too short to have produced a lesion to the innervation of the facet, being long enough to only produce a myofasciotomy.88 In 1979 and 1980, Bogduk and Long went on to describe a more anatomically correct approach to facet denervation, and their approach is the one used today.89,90 The clinical aspects of facet pain are often non-specific, deep aching paravertebral low back pain referred to a nondermatomal distribution. Because of the non-specific symptoms and lack of confirmatory images or examinations, all patients should undergo a diagnostic block.
Pertinent anatomy The facet joint innervation arises from the posterior ramus of multiple nerve roots. The nerve which appears to be most closely associated with the joint is the medial branch of the dorsal primary ramus. The dorsal ramus branches off the segmental nerve immediately after
exiting the foramen. It then continues posteriorly by piercing the intertransverse ligament and subsequently divides into a medial and lateral branch. The medial branch runs caudally and dorsally, lying against the bone at the junction of the root of the transverse process and superior articular process.
Procedure The procedure is performed percutaneously and is usually preceded by temporary pharmacological blocks. The patient is positioned in the prone position with a pillow or foam wedge supporting the lower abdominal region. Fluoroscopy is utilized throughout for adequate anatomic localization of the target. Intravenous sedation is typically employed to remove any anxiety during the procedure. The transverse processes (or sacral ala in the case of L5–S1) of the levels to be denervated are identified. Local anesthetic is then infiltrated into the skin and the introducer cannula is inserted to the superior and medial border of the transverse processes (or into the groove between the ala of the sacrum and the superior articular process at the L5–S1 level). This is performed using anteroposterior fluoroscopy; however, it sometimes may be useful to obtain an oblique image (10–15°) to better visualize the medial border of the transverse process. A lateral fluoroscopic image is obtained to ensure that the cannula is not approaching the foraminal canals. Once the cannula is in correct position, electrical stimulation is performed at 50 Hz. Paresthesia to the back, paravertebral, or hip region should be noted when the medial branches at these levels are stimulated. Adequate stimulation should be noted at less than 1 volt at 50 Hz. Next, electrical stimulation is performed at 2 Hz and lower extremity motor fasiculations should be absent at 3 volts. At this point, 1 cc of local anesthetic is injected through each cannula in preparation for the lesion. Thermal lesions are then created at each level for a duration of 90 seconds at a temperature of 80°C.
Outcomes The only randomized, double-blind study on this topic was conducted by Wedley et al; it demonstrated that lumbar facet denervation is clearly superior to placebo.91 The results from radiofrequency facet denervation series vary greatly; however, most studies report success rates of 45–80%.92–95 The wide range of outcomes is likely due to many factors, including differing techniques and localization of target. Result from facet rhizotomies have a tendency to diminish over time96 and may be explained through the regeneration of the medial branch. This relapse of symptoms may be due to regeneration of the medial branch nerve of the posterior ramus. The most common complications are superficial infections and reactions to local anesthetic, though serious complications with root injury may occur with the malpositioning of electrodes.
CONCLUSIONS A systematic multidisciplinary approach is required to treat patients with chronic pain. While ablative spinal techniques offer pain relief in many patients, the use of these methods should be cautiously utilized. Once destructive therapies have been employed, neuromodulatory procedures may be rendered ineffective. With the sophistication of understanding pain physiology, many of these ablative techniques will likely become historical, although several of the aforementioned techniques can continue to play a role in current pain management. We hope that this chapter has presented a procedurally oriented overview of the spinal ablative techniques for the treatment of chronic painful conditions with a major emphasis on clinical decision-making, indications, and efficacy. 1197
Part 3: Specific Disorders
References 1. Procacci P, Maresca M. Evolution of the concept of pain. In: Sicuteri F, ed. Advances in pain research and therapy, vol 20. New York: Raven Press; 1984. 2. Sheon RP. Transcutaneous electrical nerve stimulation. From electric eels to electrodes. Postgrad Med 1984; 75(5):71–74. 3. Schiff M, Lehrbuch der physiologie, muskel, and nervenphysiologie. Schavenberg, Germany: Lahr, 1848. 4. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965; 150(3699):971– 979. 5. Sweet WH, Wepsic JG. Treatment of chronic pain by stimulation of fibers of primary afferent neuron. Trans Am Meurol Ass 1968; 93:103–105. 6. Shealy CN, Mortimer JT, Reswick JB. Electrical inhibition of pain by stimulation of the dorsal columns. Anesth Analg 1967; 46:489–491. 7. Adams JE, Hosobuchi Y. Stimulation of internal capsule for relief of chronic pain. J Neurosurg 1974; 41:740–747. 8. Nguen JP, Lefaucher JP, Le Guerinal C, et al. Motor cortex stimulation in the treatment of central and neuropathic pain. Arch Med Res 2000; 31:263–265. 9. Mitchell SW. Gunshot wounds and other injury of the nerves. Philadelphia: JB Lippincott: 1864. 10. Merskey H, Bogduk N. Classification of chronic pain, 2nd edn. Seattle: IASP Press; 1994. 11. Abbe R. A contribution to the surgery of the spine. Med Rec 1889; 35:149–152. 12. Bell C. Ideas of a new anatomy of the brain. London: Strahan & Preston; 1811. 13. Magendie, F. Experiences sur les functions de raciness des nerfs rachidiens. J Physiol [Paris] 1882; 2:246–279. 14. Light AR, Metz CB. The morphology of the spinal cord efferent and afferent neurons contributing to the ventral root of the cat. J Comp Neurol 1978; 179:501–516. 15. Coggeshall RE, Applebaum ML, Fazen M, et al. Unmyelinated axons in human ventral roots, a possible explanation for the failure of dorsal rhizotomy to relieve pain. Brain 1975; 98:157–166. 16. Frykholm R, Hyde J, et al. On pain sensations produced by the stimulation of ventral roots in man. Acta Physiol Scand 1953; 106:455–469. 17. Scoville WB. Extradural spinal sensory rhizotomy. J Neurosurg 1966; 24:94–95. 18. Smith FP. Trans-spinal ganglionectomy for the relief of intercostal pain, J Neurosurg 1970; 32:574–577. 19. McCabe JS, Low FN. The subarachnoid angle: an area of transition in peripheral nerves. Anat Rec 1969; 164:15–34. 20. Sindou M, Daher A. Spinal coablation procedures for pain. In: Dubner, Gebhart, Bond, eds. Pain research and clinical management, vol 3. 1988:447–495. 21. Sindou M, Kervel Y. Analgesie par la methode d’electrostimulation transcutaanee. Neurochirurgie 1980; 26:153–157. 22. Uematsu S. Percutaneous electrotherrmaocoagulation of spinal truck, ganglion and rootlets. In: Schmidek HH, Sweet WH, eds. Operative neurosurgical techniques; indications, methods and results, vol 2. New York: Grune and Stratton; 1982: 1177–1198. 23. Bernard TN, Broussard TS, et al. Extradural sensory rhizotomy in the management of chronic lumbar spondylosis with radiculopathy. Orthop Trans 1987; 11:23–27. 24. Onofrio B, Campa H. Evaluation of rhizotomy. J Neurosurg 1972; 36:751–755. 25. Loeser JD. Dorsal rhizotomy for the relief of chronic pain. J Neurosurg 1972; 36:745. 26. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965; 150:971–979. 27. Sindou M. Etude de la jonction radiculo-medullaire posterieure: la radicellotomie posterieure selective dans la chirurgie de la douleur. Lyon: These Med; 1972. 28. Nashold BS Jr, Urban B, Zorub DS. Phantom pain relief by focal destruction of the substantia gelatinosa of Rolando. Adv Pain Res Ther 1976; 1:959–963. 29. Schoenen J. Organisation neuronale de la moelle epiniere de l’homme; these, Liege. 1980. 30. Denny-Brown D, Kirk EJ, Yanagisawa N. The tract of Lissauer in relation to sensory transmission in the dorsal horn of spinal cord in the macaque monkey. J Comp Neurol 1973; 151:175–200.
1198
33. Thomas DGT, Kitchen ND. Long-term follow-up of dorsal root entry zone lesions in brachial plexus avulsion. J Neurol Neurosurg Psychiatry 1994; 57:737–738. 34. Rath SA, et al. Results of DREZ-coagulations for pain related to plexus lesions, spinal cord injuries, and post-herpetic neuralgia. Acta Neurochir 1996; 138:364–369. 35. Ostdahl R. DREZ surgery for brachial plexus avulsion pain. The American Association of Neurolgical Surgeons Publications Committee, 1996. 36. Cowie RA, Hitchcock ER. The late results of antero-lateral cordotomy for pain relief. Acta Neurochir 1982; 64:39–50. 37. Rosomoff HL, et al. Effects of percutaneous cervical cordotomy on pulmonary function. J Neurosurg 1969; 31:620–627. 38. White JC, Sweet WH: Pain and the neurosurgeon. A forty year experience. Springfield: Charles C Thomas; 1969. 39. Iskandar BJ, Nashold BS. Spinal and trigeminal DREZ lesion. In Gildenberg PL, Tasker RR, eds. Textbook of stereotactic and functional neurosurgery. New York: McGraw-Hill; 1998. 40. Edinger L. Vergleichend-entwicklingsgeschichtliche und anatomische Studien im Beriche des Central-nervensystems. II Uber die Forsetzung der hinten Ruckenmarkswurzlen zum Gehirn. Anat Anz 1889; 4:121–128. 41. Spiller WG. The location within the spinal cord of the fibers for temperature and pain sensations. J Nerv Ment Dis 1905; 32:318–320. 42. Spiller WG, Martin E. The treatment of persistent pain of organic origin in the lower part of the body by division of the anterolateral column of the spinal cord. JAMA 1912; 58:1489–1490. 43. Mullan S, et al. Percutaneous interruption of spinal-pain tracts by means of strontium-90 needle. J Neurosurg 1963; 20:931–939. 44. Rosomoff HL, et al. Percutaneous radiofrequency cervical cordotomy. J Neurosurg 1965; 23:639–644. 45. Onofrio BM. Cervical spinal cord and dentate delineation in percutaneous radiofrequency cordotomy at the level of the first to second cervical vertebrae. Surg Gynecol Obstet 1971; 133:30–34. 46. Kanpolat Y, et al. CT-guided extralemniscal myelotomy. Acta Neurochir 1988; 91:151–152. 47. Gildenberg PL, et al. Impedance monitoring device for detection of penetration of the spinal cord in anterior percutaneous cordotomy. J Neurosurg 1969; 30:87–92. 48. Hitchcock E, Leece B. Somatotopic representation of the respiratory pathways in the cervical cord in man. J Neurosurg 1967; 27:320–329. 49. Poletti, CE. Open cordotomy: new technique. In: Schmidek HH, Sweet WH, eds. Operative neurosurgical techniques: indication, methods and results, vol 2. 1982:1119–1136. 50. Rosomoff HL, Carroll F, Brown J. Percutaneous radiofrequency cervical cordotomy technique. J.Neurosurg 1965; 23:639–644. 51. Lin PM, et al. An anterior approach to percutaneous lower cervical cordotomy. J Neurosurg 1966; 25:553. 52. White JC, Sweet WH. Anterolateral cordotomy: Open versus closed comparison of end results. Adv Pain Res 1979; 3:911–919, 53. Lorenz R. Method of percutaneous spinothalamic tract section. In: Krayenbuhl H, Brihaye J, ed. Advances and technical standards in neurosurgery, vol 3. Vienna: Springer-Verlag; 1976:123–154. 54. Sindou M, et al. Ablative neurosurgical procedures for the treatment of chronic pain. Neurophysiol Clin 1990; 20:399–423. 55. Tasker RR. Outcomes of surgery for movement disorders and pain. In: Wilden JN, ed. Outcomes of neurological and neurosurgical disorders. Cambridge, MA: Cambridge University Press; 56. Rosomoff HL, Papo I, Loeser JD, et al. Neurosurgical operations on the spinal cord. In: Bonica JJ, ed. The management of pain, 2nd edn. Philadelphia: Lea and Febiger; 1990:2067–2081. 57. Lin PM. Percutaneous lower cervical cordotomy. In: Gildenberg PL, Tasker RR, eds. Textbook of stereotactic and functional neurosurgery. New York: McGraw-Hill; 1998:1403–1409. 58. Nathan PW. Results of antero-lateral cordotomy for pain in cancer. J Neurol Neurosurg Psychiatry 1963; 26:353–362.
31. Nashold BS, Pearlstein R, eds. The DREZ operation, The American Association of Neurological Surgeons Publications Committee, 1996.
59. Rosomoff HL. Bilateral percutaneous cervical radiofrequency cordotomy. J Neurosurg 1969; 31:41–46.
32. Friedman AH, Nashold BS, Bronec PR. Dorsal root entry zone lesions for the treatment of brachial plexus avulsion injuries: A follow-up study. J Neurosurg 1988; 22:369–373.
60. Tasker RR. Percutaneous cordotomy for persistent pain. In: Gildenberg PL, Tasker RR, eds. Textbook of stereotactic and functional neurosurgery. New York: McGrawHill; 1998:1491–1505.
Section 5: Biomechanical Disorders of the Lumbar Spine 61. Hitchcock ER. Stereotactic cervical myelotomy. J Neurol Neurosurg Psychiatry 1970; 33:224–230.
79. Gybels JM, Sweet WH; Sympathectomy for pain. In: Neurosurgical treatment of persistent pain. New York: Karger; 1984:257–282.
62. Gildenberg PL, Hirshberg RM. Limited myelotomy for the treatment of intractable cancer pain. J Neurol Neurosurg Psychiatry 1984; 47:94–96.
80. Hardy RW. Surgery of the sympathetic nervous system. In: Schmidek HH, Sweet WH, eds. Operative neurosurgical techniques: indications, methods and results, vol. 2. New York: Grune and Stratton; 1982:1045–1061.
63. Schvarcz JR. Stereotactic extralemniscal myelotomy. J Neurol Neurosurg Psychiatry 1976; 39:53.
81. Dawson DM, Katz M. Reflex sympathetic dystrophy. Neurol Chron 1993; 8:1–6.
64. Fink RA. Neurosurgical treatment of nonmalignant intractable rectal pain: microsugical commissural myelotomy with the carbon dioxide laser. Neurosurgery 1984; 14:64.
82. Schwartzman RJ, McLellan TL. Reflex sympathetic dystrophy: a review. Arch Neurol 1987; 44:555–561.
65. Adams JE, Lippert R, Hosobuchi Y. Commissural myelotomy. In: Schmidek HH, Sweet WH, eds. Operative neurosurgical techniques: indications, methods, and results, vol. 2, 2nd edn. Philadelphia: WB Saunders; 1988:1185–1189.
83. Shealy CN. Percutaneous radiofrequency denervation of spine facets, treatment of chronic back pain and sciatica. J Neursurg 1978; 43:448–451.
66. Broager B. Commissural myelotomy. Surg Neurol 1974; 2:71–74.
84. Goldthwait JE. The lumbo-sacral articulation: an explanation of many cases of ‘lumbago,’ ‘sciatica,’ and paraplegia. Boston Med Surg J 1911; 164:365–372.
67. Cook AW, Kawakami Y. Commissural myelotomy. J Neurosurg 1977; 47:1–6.
85. Putti V. New conceptions in the pathogenesis of sciatic pain. Lancet 1927; 2:53–60.
68. Gybels JM, Sweet WH. Neurosurgical treatment of persistent pain. pain and headache, vol 11. Basel: Karger; 1989.
86. Ghormley RK. Low back pain. J Am Med Assoc 1933; 101:1773–1777.
69. Armour D. Surgery of the spinal cord and its membranes. Lancet 1927; I:691–697. 70. Jefferson A. Cordectomy for intractable pain in paraplegia. In: Lipton, Miles, eds. Persistant pain: modern methods for treatment, vol. 4. 1983:115–132. 71. Durward QJ, Rice GP, et al. Selective spinal cordectomy: clinicopathogical correlation. J Neurosurg. 1982; 56(3):359–367. 72. Greenwood B. The origins of sympathectomy. Med Hist 1967; 11:166–169. 73. Sweet WH. Sympathectomy for pain. In: Youmans JR, ed. Neurological surgery, 3rd edn. Philadelphia: WB Saunders; 1990:4086–4107. 74. Sadar ES, Cooperman MA. Bilateral thoracic sympathectomy–splanchnicectomy in the treatment of intractable pain due to pancreatic carcinoma. Cleve Clin Q 1974; 41:185–188.
87. Rees WE. Multiple bilateral subcutaneous rhizolysis of segmental nerves in the treatment of the intervertebral disc syndrome. Ann Gen Pract 1971; 26:126–127. 88. King JS, Lagger R. Sciatica viewed as a referred pain syndrome. Surg Neurol 1976; 5:46–50. 89. Bogduk N, Long DM. The anatomy of the so-called ‘articular nerves’ and their relationship to facet denervation in the treatment of low back pain. J Neurosurg 1979; 51:172–177. 90. Bogduk N, Long DM. Percutaneous lumbar medial branch neurotomy: a modification of facet denervation. Spine 1980; 5:193–200. 91. Wedley JR, Gallagherr J, Hamann W, et al. An evaluation of facet joint denervation in the management of low back pain. Pain 1986; 24:67–73. 92. Shealy CN. Percutaneous radiofrequency denervation of spinal facets. J Neurosurg 1979; 43:448–451.
75. Flanigan DP, Kraft RO. Continuing experience with palliative chemical splanchnicectomy. Arch Surg 1978; 113:50–51.
93. Burton CV. Percutaneous radiofrequency facet denervation. Appl Neurophysiol 1976; 39:80–86.
76. Mattassi T, Miele F. Thoracic sympathectomy: Review of indications, results, and surgical techniques. J Cardiovasc Surg 22:336–339.
94. Lora J, Long D. So-called facet denervation in the management of intractable back pain. Spine 1976; 1:121–126.
77. Shih CJ, Wang YC. Thoracic sympathectomy for palmar hyperhydrosis: Report of 457 cases. Surg Neurol 1978; 10:291–296.
95. North RB, et al. Radiofrequency lumbar facet denervation: analysis of prognostic factors. Pain 1994; 57:77–83.
78. Berguer R, Smit R. Transaxillary sympathectomy (T2 to T4) for relief of vasospastic/sympathetic pain of upper extremities. Surgery 1981; 89:764–769.
96. Ignelzi RJ, Cummings TW. A statistical analysis of percutaneous radiofrequency lesions in the treatment of chronic low back pain and sciatica. Pain 1980; 8:181–187.
1199
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBBS-Cervical, Thoracis, and Lumbar ■ i: Functional Restoration
CHAPTER
110
History and Principles of Pain Rehabilitation Hubert L. Rosomoff, Renee Steele-Rosomoff and Elsayed Abdel-Moty
INTRODUCTION Pain rehabilitation is a specific form of rehabilitation medicine applied to the management of chronic pain. To qualify, it is important to distinguish between acute and chronic pain. Acute pain is a self-limiting form of noxious stimulation following tissue injury that persists during that period of time during which the body would be expected to repair itself and recover to its preexistent biological status. Chronic pain is a condition which lasts beyond the reparative phase. Secondary physical and behavioral effects develop that create disability and an inability to function. A variety of adverse events tend to be associated with the development of chronic pain including drug abuse, further decreased function, psychiatric abnormalities, multiple unsuccessful surgical interventions, social and economic isolation, and even suicide.1 Through the early 1970s, the primary medical discipline responsible for the treatment of intractable chronic pain fell mainly to neurosurgeons. Their singular focus entailed the performance of complex ablative surgical procedures to destroy neural pain transmission systems. Anesthesiologists complemented this treatment approach with an assortment of nerve blocks. Ultimately, this paradigm failed to produce successful long-term results. As well, the associated side effects and risks of the procedures were often too adverse to justify their routine use. These failures amplified the crux of the problem which was that no single discipline could manage the multifaceted nature of the problem. Recognition of these issues led to the development of an interdisciplinary approach in 1973–1974 by Bonica and associates at the University of Washington in Seattle, and a multidisciplinary approach by Rosomoff and colleagues in Florida at the University of Miami. Soon afterwards, pain societies were founded and pain medicine evolved, accompanied by the growing science of pain and its clinical applications. The road was difficult, because insurers and governmental agencies were reluctant to pay for treatment regimens or evolving techniques which were then too neophytic to have accumulated the data to support medical necessity. More than a decade passed until Medicare, in 1988, published its Appendix §35-21.1, Coverages Issues – Medical Procedures of Pain Rehabilitation, which set the first standard and, ultimately, criteria which other payors would use for reimbursement. Unfortunately, surgical disciplines confounded this approach by developing more complicated operative remedies for which success was claimed, but whose supportive data base was questionable. The burgeoning world of anesthesiologic interventional techniques also claimed success, again unsupported by scientifically reliable data. The rehabilitation model appears to have produced the most acceptable data and, at least, has equal or better outcome results without the risks attending all interventional applications.2
THE NEUROPHYSIOLOGICAL BASIS OF PAIN REHABILITATION In principle, pain is a signal received by the central nervous system from an anatomical, physiological, or pathological source producing a noxious impulse. Correction and restoration of function will result in diminution and cessation of pain perception. Pain rehabilitation enables patients with chronic pain to return to a productive lifestyle. Pain centers or clinics are facilities where patients are sent for the treatment of chronic pain, after conventional management has failed and no further directed disease-oriented care is deemed appropriate.3 Patients who are considered candidates for pain rehabilitation have chronic pain, illness, disability conviction, and are physically and functionally impaired. Pathological abnormalities must be distinguished from dysfunction. Activation must occur before pain is resolved.4,5 Functional restoration is a keystone to pain rehabilitation. It must be multidisciplinary as compared to single treatments or exercises. Stretching, strengthening, physical modalities, aerobic activities, resistive exercises, education, conditioning, mobilization, pacing, biofeedback, relaxation, and other components are included as treatment individually and in combination. Although a pain rehabilitation program is designed for individuals with measurable functional deficit, it may also be appropriate for either the physically active individual or for someone with severe disability where optimization of residual capacities is needed. Patients with chronic pain present a clinical challenge because of the vast time and the diagnostic and therapeutic resources they consume. The pain management approach must be capable of properly identifying patients’ problems whether sensory, perceptual, psychological, psychosocial, environmental, or biomechanical in nature. Treatment goals are to reduce chronicity, prevent re-injury or disability, and restore function, as well as to return the patient to a productive lifestyle.6 The original concept that nerve root compression from a herniated disc produces pain was challenged decades ago when Rosomoff7 presented a series of observations together with clinical and experimental evidence that supported the contention that alternative nonsurgical methods will provide successful treatment even for manifest disc herniations or lumbar stenosis. Physiologic studies demonstrated that, except for a transient painful impulse when the nerve is first impacted, sustained nerve root compression or ‘pinching’ does not produce pain.8 There could be numbness or loss of function, but this is not a painful event. From inspection of human anatomy, it is inescapably clear that all low back injuries must have associated soft tissue abnormalities. Even if the forces causing the injury reach sufficient magnitude to herniate
1201
Part 3: Specific Disorders
or rupture an intervertebral disc, the force must be transmitted first through the surrounding soft tissue that binds the spine together as a functional unit. These tissues, when injured, undergo a breakdown of the cell membranes to arachidonic acid, from which biosynthesis of prostaglandins and associated products ensues. One important issue in this process is the induction of a state of hyperalgesia, following which a pain signal will evolve when excessive mechanical stimulation occurs or when compounds of reaction to injury, such as histamine or bradykinin, are produced.9 The nerve itself does not originate the pain signal; nociceptors are stimulated to initiate the transmission of the signal. It is our thesis that the disordered musculoskeletal system is responsible for initiating these phenomena.3,7,10 These structures are in the surrounding paraspinal muscles, buttocks, hips, and legs. These peripheral sites are treatable by alternative medical approaches. Treatment will restore function and alleviate pain, often without the need for correcting intraspinal abnormalities that have traditionally been designated as the pain generator. Further, a study carried out in 45 000 patients with low back pain indicated that only 1 in 200 of patients may actually need surgical intervention;11 in our experience the number of patients is 1 in 500. Muscular and fascial abnormalities are called myofascial syndromes. They have been well described by Travell and Simons.12 Abnormal movements of the back, restricted ranges of motion in the hips or legs, or the presence of muscle tenderness and/or trigger points, are
seen with myofascial syndromes. These can perpetuate mechanical dysfunction, continued strain, muscle fatigue, and pain.
ALGORITHM FOR PAIN REHABILITATION Although it can be described in discrete phases, rehabilitation is a continuous process of evaluation, treatment, conditioning, and reevaluations. The intensity and duration of each process depends on a variety of parameters including patient’s response, rate of progress, the presence of comorbidities, and the number and type of objectives to be met. The algorithm is depicted in Figure 110.1 and the elements are described below.
Admission criteria To enter the system, the patient undergoes evaluation over a 3-day period. The rehabilitation team attempts to identify the medical, behavioral, vocational, financial, social, and other significant problems. The approach is comprehensive and holistic. Patient selection criteria are broad. The patient must have the ability to understand and carry out instructions, must be compliant and cooperative, and must not have aggressive or disruptive behavior that would disturb the milieu. Patients with schizophrenia, manic-depression, or other major psychiatric disorders are not precluded as long as they are receiving treatment which renders them stable. The patient, the family, and significant others,
START: EARLY REFERRAL TO A MULTIDISCIPLINARY PAIN CENTER WITH FUNCTIONAL RESTORATION COMPONENT
RESTORATION
Phase I
MEDICAL / PHYSICAL Evaluation by physician (request consults if needed)
FUNCTIONAL
Evaluation by physical & massage therapy, MDE
Evaluation by occupational therapy
BEHAVIORAL / EMOTIONAL
Evaluation by psychology
Evaluation by psychiatry
VOCATIONAL Vocational / ergonomic evaluation (if applicable)
2−3 days Contruct and formalize interdisciplinary plan of treatment. Develop key indicators for each area
Phase II 1−2 weeks
Monitor and supervise treatment plan, address comorbidities
Restore ROM, resolve trigger (TP) points & soft tissue management
Restore functional tolerances. Teach body mechanics, pacing, etc.
Council patient and family in pain impact. Teach relaxation
Taper off narcotic medications
Establish goals with patient & employer
Monitor progress and key idicators. Adjust plan of treatment if necessary
Phase III 1−2 weeks
Interventional procedures for unresolved TP
Strengh and endurance traininng
Implement functional circuits, ADL/ IADL training
Train in stress management. Guide through treatment
Monitor compliance with tapering
Finalize multidisciplinary discharge planning / return to work planning / maintenance program
FINISH: RETURN TO WORK OR PRIOR FUNCTION Fig. 110.1 Algorithm for pain rehabilitation.
1202
Job simulation, work conditioning, job site visit
Section 5: Biomechanical Disorders of the Lumbar Spine
such as the lawyer, the employer, and the insurer must be accepting of vthe program. Worker compensation, liability cases, multiple surgeries, long histories of invalidism, or drug abuse are not exclusionary conditions. Although integral, the financial, legal, and administrative aspects of patient admission are beyond the scope of this chapter. Upon entry, patients are oriented to the program and are made aware of rules, policies, and expectations. Evaluations and observations are made by the various disciplines in order to: 1. Decide if the patient meets the criteria for inclusion into the program; 2. Determine the appropriate diagnosis based on previous medical records and the additional medical, physical, and psychological assessments; 3. Establish a baseline of abilities, limitations, and goals; and 4. Medication intake, dependence, and use must be determined, particularly as it pertains to narcotics. The multidisciplinary team consists of physicians, psychologists, occupational and physical therapists, massage therapists, ergonomists, nurses, vocational counselors, and biofeedback therapists. Assessment of the injured individual by these disciplines considers not just the injury history but also the patient’s physical and behavioral status and vocational issues, if applicable. The outcome of the exhaustive assessment is a constructed, formalized care plan detailing problem areas, treatment strategies, and expected outcomes. Due to the large number of possible findings upon initial assessment, a set of ‘key indicators’ is used to monitor progress towards the final goals. Key indicators may include (1) pain level; (2) number of hours of sleep; (3) pain medications; (4) lifting, carrying, sitting, standing, walking tolerances; (5) ranges of motion of the neck and trunk; (6) straight leg raise; (7) composite hip range of motion; (8) posture; (9) strength; (10) gait; (11) and key behavioral and vocational problems. These indicators are updated on a weekly basis. Phase I may take 2–3 days for interviews and/or evaluations. A team meeting is then held, findings are discussed, and team recommendations are presented to the Medical Director. In a multidisciplinary conference, the Medical Director discusses the findings with the patient and significant other. Team recommendations, clarification of medical concerns, and diagnosis are addressed. Patient questions,
misconceptions, and expectations are also discussed. Admission to the program is contingent upon the patient’s full consent to participate in the process, including tapering from narcotics or other dependence-producing substances.
Activation and physical restoration During this phase, treatment is initiated. A variety of therapeutic approaches are used to restore ranges of motion, resolve trigger points, taper off narcotic medications, and begin the process of education and relearning. Stretching, physical agent modalities, body mechanics training, and behavioral interventions are used to guide the patients through what is probably the most difficult phase of the program. Patients must surmount hurdles of fear, anger, mistrust, and past misconceptions about diagnosis in order to proceed with confidence and acceptance. Education includes topics such as myofascial pain syndrome, relaxation, stress management, and healthy lifestyles. Simultaneously, the patient’s medication is reviewed and a rigorous management program is initiated and monitored, including tapering from narcotics or other dependence-producing drugs. The use of ice and other modalities to alleviate pain are introduced. A daily treatment schedule is designed to accommodate the various treatments and disciplines. A typical treatment schedule for one patient is shown in Table 110.1. The contents of each patient’s schedule vary on a daily basis depending on the stage (week) in treatment, level of activation, and progress. Treatment is provided on a daily basis including Saturdays. At nighttime, patients are assigned ‘homework’; i.e. evening self-paced exercises determined by the treating therapist and monitored by nursing staff. A very effective tool in this phase is the concept of daily goals, final goal setting, and self-monitoring. Computerized modeling is used to determine optimal pathways a patient should follow during rehabilitation. The model utilizes statistical projection methods, which take into consideration the patient’s initial performance level and the desired goals.13 This nonlinear model derives its coefficients from retrospective data collected from over 1000 patients with chronic pain who successfully completed the 4-week rehabilitation and functional restoration program, and who have returned to a productive lifestyle. Once initial levels of performance have been
Table 110.1: Typical daily treatment schedule Patient name
___________________________________
Time
Activity
8:00–8:30
Movement therapy, warm up, low-impact aerobics
8:30–10:00
Physical therapy, stretching, modalities, back exercises, functional electrical stimulation, active exercises, gait training, flare-up procedures
10:00–11:30
Occupational therapy, body mechanics training, biofeedback, functional circuits, pacing, walking, climbing, lifting, carrying, pushing/pulling, reaching, safety, joint protection, ADL training
11:30–12:00
Psychological counseling, family counseling, stress management, breathing exercises, hypnosis, vocational counseling, vocational preparation, case management
12:00–1:00
Lunch break
1:00–1:30
Strength and cardiovascular training
1:30–2:00
Neuromuscular massage therapy
2:00–3:00
Occupational therapy, upper extremity activities exercises, educational activities, work simulation
3:00–4:00
Group activity, educational sessions
4:00
Evening activities, recreational activities
1203
Part 3: Specific Disorders
measured and treatment goals have been determined, the daily goals are assigned to provide a personalized print-out of the expected ‘daily’ performance. The daily goals program provides daily increments for the patient’s therapeutic activities. The optimal progression printout from initial tolerances to final goals is used by the patient and the treating staff to determine effects needed to achieve the desired daily performance throughout treatment. On a weekly basis or sooner, if necessary, a team conference reviews the patient’s progress and level of participation; and the team determines if the program should be continued, modified, or terminated. Behavioral issues are addressed early. The patient must be in agreement with the treatment plan. The building blocks for the postdischarge maintenance program also start during this phase.
Rehabilitation for lifestyle and work restoration Job simulation is an important concept with respect to return to work. In conjunction with the vocational counselor, job tasks are reviewed with the patient to determine which must be simulated if there is to be a successful return to work. Conferences with the employer and job site visits may be necessary to form the plan. Once the simulation demands are determined, the patient is taught to perform tasks safely to restore confidence and prevent reinjury. This allows the treating physician to certify that the patient can safely handle the job. If a patient’s care plan does not include return to work, functional circuits and realistic lifestyle simulations are utilized to return the patient to those functional levels that will allow comfort and safety.
EVALUATION OF FUNCTIONAL DISABILITY Objective measurements are utilized to determine physical condition, functional abilities, behavioral health, vocational parameters, and other patient attributes relevant to the rehabilitation process. Methods of measuring functional capacity fall under three main categories: (1) patient’s self-report of functional levels, which provides information about the perception of how much the patient believes he can or cannot do; (2) medical examination to provide an estimate of medical impairment; and (3) assessment of abilities or limitations producing quantifiable measures reflecting the level of performance, in comparison with performance levels of healthy subjects (e.g. norms) or the match to job/task demands.
Physician evaluation The entry to evaluation and treatment is through the physician. The physician must obtain a detailed, accurate history. The mechanism of injury and the precise location of the pain at onset are critical. A neurologic examination evaluates reflexes, muscle strength, and sensory status to document the presence or absence of neurologic deficits.14 Although neurologic screening is essential, it is most often not significantly positive. In fact, only 1% of individuals have neurologic dysfunction which is reversible usually and, therefore, should not be considered as a pathological deficit. The soft tissue examination must be sophisticated and thorough.15 All musculoskeletal and myofascial abnormalities must be identified. This is particularly important, since myofascial syndromes may simulate neurological syndromes, particularly radiculopathies. The straight leg raising (SLR) test may produce leg pain considered to be indicative of irritated nerve roots, but this occurs even more regularly with myofascial syndromes. Contractures of the hip musculature, particularly the hip rotators, are common and disabling with standing or walking, so that restricted ranges of motion about the hips are not necessarily an indicator of articular disease. Palpable soft tissue tenderness by itself, again, is thought by some to be less specific or reliable, but, to reiterate, tender/trigger 1204
points and restricted ranges of motion are the hallmark of myofascial syndromes and must be sought so they can be identified and treated. They are, in fact, objective findings. Simple laboratory tests, including blood count and erythrocyte sedimentation rate, are sufficiently inexpensive and efficacious for use as initial tests when there is suspicion of back-related pathology, such as tumor or infection. Lastly, special tests such as radiographs, imaging techniques, electrodiagnostics, thermography, and discography should be reviewed or recommended, if deemed necessary, but should be interpreted with extreme caution.10
Motor dysfunction evaluation This is a method developed to identify and effectively treat ‘motor’ dysfunction in patients with chronic pain conditions.16 This innovative testing utilizes on-line computerized electromyographic (EMG) methods to study recruitment of muscles involved in a chain of motor activities.17 This method may detect functional muscular abnormalities that cannot be identified by clinical examination, even by experienced observers. The EMG signals of the various muscles are examined for baseline activity, symmetry, magnitude, frequency contents, synchrony, timing, and patterns. Patients’ behaviors are also observed. Motor dysfunction evaluation (MDE) findings are then compared to relevant clinical findings. Patient-specific, as well as condition-specific, multidisciplinary approaches are then generated to deal with the problems during daily treatment. The overall objective is to improve function and accelerate restoration. This is accomplished through using EMG and other electrically assisted methods to increase sensory perception of muscles and joints; increase neuromuscular recruitment; increase strength and endurance; and reestablish synchrony, symmetry, pattern, and synergy of muscle activity, thereby increasing functional capacities and reduction of pain.
Physical therapy evaluation This type of evaluation emphasizes the different aspects of the soft tissues and the musculoskeletal system such as muscle tone and strength, ranges of motion, gait, spasm, swelling, pain pattern, etc. Physical examination in this category evaluates muscle strength, which is reported on a scale from 0 (no strength) to 5 (normal strength). While yielding numerical data, these measurements are to some degree subjective. Recently, new technology has enabled the introduction of testing equipment such as electronic goniometers and muscle testing machines that permit quantitative measurement of human functions.
Occupational therapy evaluation Occupational therapy evaluation determines functional levels, such as sitting, standing and walking tolerances; posture, balance and coordination; risk of falling; stair climbing; carrying and lifting, pushing and pulling; self-care, especially activities of daily living, socialization, driving, and other vocational and leisure activities. Descriptive information about the degree of independence, physical tolerances, endurance, speed, and attitude of the patient are established. The assessment of proper body mechanics is key.
Behavioral therapy/psychological evaluation This examination reveals a great deal about the patient’s mental state, behaviors, coping styles, and the effects of pain or injury on personality. Behavioral analysis considers compliance, achievement level before injury, activity level after injury, functional capacities, anxiety, depression, personality disorders, marital status, role reversal, and family dysfunctional states. There are psychological tests designed to elicit
Section 5: Biomechanical Disorders of the Lumbar Spine
responses which can be translated into numerical values and compared with the performance of other persons, such as the Minnesota Multiphasic Personality Inventory and the Millon Behavioral Health Inventory Assessment. These instruments test psychogenic attitudes, such as chronic tension, recent stress, premorbid pessimism, future despair, social alienation, and somatic anxiety. They are not a predictor of outcome, nor should they be used for that purpose. We no longer use these instruments, but depend heavily on individual interview assessments.18 If utilized, it should be for the purpose of finding out how the treating staff can interact with the individual in an effective manner to allow the patient to accept the rehabilitation plan. The patient has to be a partner in the rehabilitative process; otherwise, the effort will fail. Psychological services offer biofeedback, relaxation training, coping skills training, assertiveness, stress management, and self-hypnosis. Group and family therapy deal with social interactions, return to environment, employment, and disability versus wellness with an emphasis on function, not pain. Psychological evaluations are tailored to document these issues. They work with the vocational counselors concerning return to work issues.
Vocational evaluation The objectives of vocational evaluations are: 1. Assessment of education level, training and work history, vocational abilities, transferable skills, job satisfaction, interests, goals, and interpersonal relations at work; 2. Identification of vocational goals and motivation to return to work, same job, modified job, different job and job seeking skills; and 3. Establishment of the role of the significant other, family, employer, attorney as it pertains to return to work issues.1,19
COMPONENTS OF PAIN REHABILITATION (INTERVENTIONS) Pain rehabilitation programs utilize a multimodal, cognitive–behavioral, goal-oriented aggressive physical approach within a supportive environment in which patients learn pain management techniques and work toward clear and achievable goals. Within such a complex paradigm, customization, individualization, communication, collaboration, planning, and flexibility become important characteristics. The program is carried out by experts in pain management and rehabilitation from different specialties. Pain physicians coordinate and oversee the program, including the prescription of medication. Physical medicine and rehabilitation directs the application of all physical medicine modalities and treatments. Nurses trained in rehabilitation and behavior monitor patient progress and education, and reinforce the teachings of all disciplines, provide direct nursing care and medication, manage tapering from narcotics, and serve as case managers. The behavioral division is headed by a psychiatrist; doctorate-level psychologists are assigned to each patient. They do individual and group counseling, administer biofeedback, behavioral modification, stress management, time management, coping methods, self-hypnosis, or other applicable techniques. The vocational rehabilitation division evaluates and directs job readiness, goal setting for job placement, and return to work. The ergonomic division simulates the job and adapts the patient and/or work site while computing daily achievement goals. Functional capacities are measured regularly. The average program will last 4 weeks on an inpatient or outpatient basis or a combination thereof. Inpatient status is preferred for the medically and behaviorally difficult, complicated case, but it is
not always possible, as the healthcare reimbursement system may dictate the circumstances of treatment. In a tertiary referral center, few ‘simple,’ early primary care-type patients are seen. Our program receives the most complex, ‘court of last resort,’ salvage cases.
Medication/narcotics Narcotics have been the first line of treatment for intractable pain since time immemorial. These agents are not particularly effective with chronic pain, even when pursued vigorously as has happened during the past decade. If this statement were not true, then why would patients come to our center, in pain, having been given escalating doses of analgesics, to the daily equivalent of 12 000 mg of morphine? This would seem almost unbelievable, if it were not for the fact this experience has been repeated at our center on numerous occasions. Drug therapy is the primary mode of management for both acute and chronic pain, and conventionally can be classified into three categories: (a) nonopioid analgesics, (b) opioid analgesics, and (c) coanalgesics. Nonopioid analgesics such as salicylates, acetaminophen, nonsteroidal antiinflammatory drugs (NSAIDs) are indicated for pain involving inflammation, although acetaminophen lacks clinically useful peripheral antiinflammatory activity. NSAIDs are both analgesic and antiinflammatory and, therefore, are useful also for the treatment of pain not involving inflammation. NSAIDs differ from morphinetype analgesics in that there is an analgesic dose ceiling above which adverse effects increase, but additional analgesia does not result; NSAIDs do not produce physical or psychological dependence; NSAIDs are antipyretic. The primary mechanism of NSAID action is inhibition of the enzyme cyclooxygenase, inhibiting the formation of prostaglandins which sensitize peripheral nerves and central sensory neurons to painful stimuli. These time-honored agents have been used extensively, but do require caution in that they may produce gastrointestinal side effects such as ulceration or bleeding. Drugs such as ibuprofen, naproxen, ketoprofen, indometacin, ketorolac and others in this group which have their advocates will actually serve good purpose but, in chronic pain, may not produce total relief. The more recent COX-2 group were thought to be more effective, but currently are under scrutiny and have even been banned because of complicating features such as cardiac disease in addition to adverse hematological effects, renal effects, and even occasional central nervous system dysfunction. The opioid analgesics have shown increased use throughout the later decades because of the continuing quest for pain relief in contradistinction to pain control. There have been, and continue to be, opposing views on how these drugs should be used. There are those who take the more standard approach of following the PDR recommendations. Others believe that pain is such an intolerable condition that whatever is required to produce control should be prescribed. Unfortunately, if one carries that thesis to conclusion, it will often turn out that the escalating high-level dose approach will also result in an inability to function because of sedation or other physical side effects and, therefore, prove useless, at least for the noncancer patient. It has always been the philosophy of our center that every effort should be made to taper and discontinue narcotic analgesics in favor of pain rehabilitation. So much of the disability is mechanical in origin as compared to chemical. In fact, throughout the years, there have been very few patients in whom successful tapering and cessation of narcotic use cannot be effected, to the betterment of their physical and psychological status. It would be rare for us to complete our rehabilitation program and prescribe ‘maintenance narcotic.’ This may represent a minority view, but it has been our experience, and it remains our philosophy, unchanged throughout three decades of pain management. 1205
Part 3: Specific Disorders
The coanalgesic group of drugs may be used to enhance the effect of opioids or NSAIDs, have independent analgesic activity in certain situations, or counteract the side effects of analgesics. Neuropathic pain represents 30–40% of this treatment group. This is pain which has a burning, prickling quality which has been called dysesthetic pain as compared to the sharp, toothache-like pain managed with standard analgesics. Included in this group would be the tricyclic antidepressants, the antiepileptic drugs, local anesthetics, glucocorticoids, skeletal muscle relaxants, antispasmodial agents, antihistamines, benzodiazepines, caffeine, phenothiazines, and topical agents.
Physical therapy restoration Physical medicine has the goal of restoring body function to normal or its closest equivalent. Because myofascial contracture is the common denominator in the low back disorders, the first phase of management is muscle stretching and restoration of full range of motion in the joints of the hips, back, and lower extremities. This therapy includes gait retraining because of acquired maladaptive patterns, postural adjustment, proper use of effective modalities, elimination of adaptive equipment when possible, and strength and endurance conditioning with instruction of flare-up management. Modalities, when evaluated as unimodal therapy, may not show clear-cut evidence of effectiveness. However, they appear to be useful in combination which, unfortunately, makes statistical evaluation more difficult. Nonetheless, scientific rationale exists for some. Ice application with lowering of temperature is known to decrease nerve conduction to the point of anesthesia, and the inflammatory reaction is contained with a reduction of chronic changes.20,21 To be effective, the body part must be packed in ice for periods in excess of 30 minutes. Trigger point desensitization is indicated. Liberal use of ice is the preferred method of treatment. Heat does seem to soften muscle preparatory to stretching. An adjunct vapocoolant helps to block the stretch reflex and makes lengthening easier. Mechanical traction is useful for certain specific indications. Conceptually, we apply traction to stretch muscle groups, not to distract the spine or to release nerve entrapment. We do not believe that distraction can be effected with the weights that are used, and the principle of entrapment is not tenable. Therefore, traditional pelvic or leg traction is not employed. Gravity traction is applied for iliopsoas contractures in the patient with a spinal flexion deformity and/or failure to extend the back. Autotraction is an important technique, which allows threedimensional placement of the spine by rotating, flexing, or extending the unit as the patient imposes his or her own body force by pushing and pulling. The self-applied force of autotraction will not exceed that which could be potentially injurious, but it will release tight paraspinal muscles. Autotraction does not decompress the nerve root, as was the concept of its originators.22,23 Most stretching is manual and labor intensive, since it is important that the therapist feels the tissue during treatment. Massage also is used as adjunct treatment to enhance muscle lengthening and supple movement. There are over 200 forms of massage and bodywork. Swedish, shiatsu, rolfing, cranio-sacral release, Alexander technique, sports massage, neuromuscular therapy, seated massage, and Thai massage are several examples. For the purpose of functional restoration and pain reduction, neuromuscular therapy uses advanced concepts in pressure therapy to break the stress–tension–pain cycle. It aims to relax muscle so that the body will return to normal neuromuscular integrity and balance. Neuromuscular massage is essential to resolve trigger points. But trigger point resolution by massage may not be sustained unless progress is made towards restoring normal ranges of motion, flexibility, and mobility. Transcutaneous electrical neural stimulation (TENS) is used infrequently and only with patients who are TENS responders and who
1206
can be assisted with a difficult drug taper for which TENS may give short-term relief as the drugs are withdrawn. TENS will not be given to the patient beyond this period of time; it has no role in long-term therapy. Conceptually, it is to be emphasized that we are aiming for resolution of the painful disorder by physical restitution, not by an attempt at distraction, masking the pain, or at coping by ‘learning to live with pain.’ Passive, then active ranging of motion is essential, especially about the hips and, in particular, the hip rotators. Hamstring lengthening is another mandate, because hamstring tightness will affect back movement. Full ranges of back motion are the ultimate goal, so flexion and extension exercises are instituted without prejudice for the proponents of either type. Both flexion and extension exercises are needed. A full compendium of exercises is employed, as described in any standard physical therapy textbook, to establish full ranges of motion throughout the lower body with supple muscles and fluid movement. As this is being achieved, muscle strengthening and endurance/cardiovascular conditioning are added to the regimen with monitoring of those patients who have associated medical problems. Movement (dance) therapy is an interesting adjunct, because patients with pain will often perform effortlessly to music when, seemingly, without music, pain will be a limiting factor. It helps to diminish the fear of moving/activation.
Functional electrical stimulation When a specific muscle group is weak, functional electrical neuromuscular stimulation and muscle reeducation are implemented.24,25 This technique can produce rapid and dramatic increases in muscle recruitment patterns and muscle strength; footdrop braces can be discarded. Functional electric stimulation (FES) is used when minimal muscle recruitment or reduced voluntary control are detected upon muscle testing. With FES, muscles can be strengthened ‘passively’ without placing excessive demands on the patient, especially in the presence of pain. FES is the process of applying an external electrical stimulus to a muscle or muscle groups in order to induce muscle contraction. We also use FES successfully to treat conversion-disorders-type paralysis, for electric testing of motor responses, and as a motor dysfunction treatment method. FES allows the induction of maximal muscular contraction without any voluntary effort on the part of the treated individual. This latter aspect is of value for patients with chronic pain whose pain is often aggravated through exercise or who are unable to initiate voluntary effort necessary for muscular conditioning due to disuse. Studies on FES indicate that this passive intervention strategy can be quite effective.25 It should be emphasized here that FES is not a substitute for regular exercise. FES is used to ‘jump start’ the neuromuscular system. Once the patient has gained sufficient power to initiate voluntary movement comfortably, the patient engages in active resistive exercises for strengthening and endurance training.
Motor dysfunction treatment Strategies for treating motor dysfunctions identified upon evaluation (see MDE above) are patient specific, as well as condition specific. The overall objective is to improve functional capabilities. Motor dysfunction treatment (MDT) is incorporated into regular patient treatment to address problems such as depressed muscle activity, increased muscle tension (hyperactivity), significant EMG asymmetry or asynchrony, and nondistinctive EMG activity patterns (work versus rest cycles). For example, in order to restore function to muscle with depressed EMG activity, the MDT protocol will consist of monitoring the target muscle while the patient performs selected therapeutic maneuvers designed to recruit that muscle compared to
Section 5: Biomechanical Disorders of the Lumbar Spine
its contralateral partner. If EMG recruitment is found to be minimal, functional electrical stimulation is used to increase strength and power of the affected muscle. As soon as the patient demonstrates ability to recruit the muscle(s) voluntarily, active EMG interventions using methods of muscle reeducation and biofeedback commence. Motor dysfunction treatment also involves educating the patient as to muscle compensation/isolation, and improving strength, endurance, and muscle tone through progressive resistive training and massage. It also involves increasing kinesthetic awareness in order to reestablish proper motor recruitment patterns. Establishment of proper recruitment patterns becomes essential in order for the patient to perform with proper body mechanics during functional activities and work simulations.
Occupational therapy restoration Occupational therapy concentrates on body mechanics, activities of work and daily living, and on functional circuits. Sitting, standing, walking, lifting, climbing, and reaching tolerances are established and brought to normal levels of function. Pacing of activity and energy-saving techniques are taught. Adaptive equipment is used infrequently and only on specific indication. Posture and gait are corrected, as most patients are found to have poor posture and maladaptive gaits. Proper motor vehicle entry, seating, transfers, and luggage management are taught. Recreational activities are reviewed and eye/hand/ leg coordination and tolerances are established. Vocational goals are set in conjunction with the vocational counselor and ergonomist for job simulation.
Postural correction Awkward postures cause fatigue, strain, and eventually pain; they need to be corrected. Poor postures will result in pain, loss of stability, and falls.26 Faulty posture and poor body alignment develop slowly and may not be apparent to the individual. Poor posture is found with obesity, leading to weakened muscles, emotional tension, and poor body attitudes in the workplace. The incidence of pain increases in predominantly sitting work activities, especially with the use of computers. Ideally, patients do best when they can alternate activities among walking, standing, and sitting.27 It is recognized that when the body is not in correct alignment, static loading on muscles and joints results in awkward positions that are not healthy.26 Prolonged forward bending of the head and trunk, stooped postures, forced postures, and postures causing constant deviation from neutral alignment are but a few examples of poor postures. Even sleeping postures must be assessed.28 Programs must address the factors contributing to poor postures from both the physical as well as the engineering perspective. On the physical level, deficiencies in human structural capabilities can be considered in the design and selection of products and tools. Patients are taught, through practice and the use of biofeedback, to choose proper equipment, to modify their working environment thus encouraging good postural habits, and to alternate activities to avoid postural fatigue.
Body mechanics interventions Proper body mechanics provides the basis for the safest way to perform daily tasks. Corrective training to alleviate and prevent mechanical stressors and improper habits for sitting, standing, walking, lifting,
carrying etc. is provided. Biofeedback may be a helpful adjunct. It is important that body mechanics techniques are taught with sufficient generalization to allow patients to accommodate specific body mechanics technique in the presence of conditions other than pain and as the task demands change. Modification of proper body mechanics must be taught if the task does not lend itself to ideal technique.
Job simulation and work readiness This is the ultimate goal of achievement for the working-aged group, but it does not exclude students or elderly persons, who also require instruction for their needs. The physician, the occupational and physical therapists team with vocational counselors and ergonomists to develop the treatment plan. It is essential that the patient advise the job simulation team of the job activities which provoke the pain. Physical and occupational treatments are highly structured, task-focused to the job requirements, goal oriented, individualized, and multidisciplinary in nature. Patients should not begin this phase of treatment until they possess the necessary tools, such as increased awareness of posture and body mechanics; increased flexibility and mobility; adequate strength and endurance; good stress management skills; good pain control and safety techniques; and positive attitude towards employment, and return to work.
Ergonomic restoration The thrust of the ergonomic approach to injury management and pain rehabilitation is ‘to design effective intervention strategies for the restoration of functional abilities, control of pain, and immediate return to work and productive lifestyle.’ Another objective is to avert further aggravation of an existing condition or injury. This philosophy was adopted by the University of Miami Comprehensive Pain and Rehabilitation Center as early as 1982 when ergonomics was first introduced into a multidisciplinary pain management team. This marked the beginning of a new era for ergonomics research and application in healthcare systems and pain treatment.
Workplace design This type of ergonomic intervention aims at assessing the relationship between human characteristics (e.g. posture, body mechanics) and musculoskeletal stresses with emphasis on work issues.29 The task of the ergonomist is to assist the patient or employer to design or modify the workstation to insure proper engineering design and good body mechanics when performing job tasks. The process of workplace design within a functional restoration program consists of the following components: 1. The patient’s job description, the employee’s job description, and a description of a ‘typical’ work day; 2. Evaluation of essential job tasks is to identify tasks that are potentially stressful/painful. Analysis of video graphic data is used to isolate the critical risk factors; and 3. Intervention phase. Interventions specific to reducing or resolving the risk factors are developed. Ergonomic analysis aims at adjusting, modifying, changing, and/or replacing current heights, layout, equipment, tools, and design characteristics. It is not always necessary to recommend new equipment or adaptive technologies (e.g. cushions, ergonomic chairs, etc.). In most cases, workplaces can be reasonably accommodated to meet ergonomic needs. The patient’s set-up may not be an ‘ideally correct’ setup. It is the responsibility of the ergonomist to teach patient methods of improving safety and comfort without need for expensive adjustments or equipment.
1207
Part 3: Specific Disorders
A tool which we have used in the process of analyzing and recommending workplace adjustments and modifications is Sitting Workplace Analysis and Design (SWAD).30 SWAD is a computer program resembling artificial intelligence. The inputs to the program are workplace user demographics, 16 anthropometric dimensions, workplace dimensions, work tools, and the priority and frequency of use of each work element. SWAD then combines this information with a ‘knowledge base’ of ergonomic principles and guidelines and a set of inference procedures. The output of SWAD is the recommended workplace dimensions, heights, reaches, footrest, chair parameters, VDT parameters, and optimal placement of all work tools. It enables customization of workstation adjustment without trial and error.
Electromyogram biofeedback A carefully processed EMG signal can be a useful tool in the quantitative measurement of muscular performance, for reeducation and in the evaluation of patient’s response to specific treatments.17 Biofeedback is the process of using specialized instruments to give people information about their biological systems (temperature, heart rate, muscle activity, etc.). It is a set of training techniques used to increase awareness and voluntary control of biological conditions and relate them to human physical and emotional well-being. Biofeedback (BF) is useful in the relief of stress, tension, headaches, muscular dysfunction, and for the reduction of muscle tension, which correlates well with a reduction in pain and improvement of muscle strength.31,32 Using EMG biofeedback, patients perform therapeutic maneuvers while affected muscles are monitored. The information is used to facilitate patient awareness of muscular performance. These methods can then be used to improve the patient’s ability to coordinate muscle activity, reestablish proper reciprocal inhibition, reestablish functional synergy including appropriate force couples and sequential contractions, decrease the need for inappropriate muscular or postural compensations, and achieve recruitment levels beyond baseline activity.
Vocational rehabilitation A vocational rehabilitation professional counsels the patient throughout the program to address all vocational issues. The vocational professional will work with the psychologist and ergonomist, and share essential information with the treating team. The vocational counselor is the liaison to outside parties such as case managers, insurers, and employers. The vocational professional addresses the traditional activities such as skills, obstacles to return to work, transferable skills, job readiness, and all skills needed to return to employment. The vocational goal is full functional activity and return to previous employment, when possible. Even the heaviest physical activity capacities have been achievable in most patients. If limitations are inevitable, the counselor works with the patient on possible transferable skills.
Behavioral modification Behavioral management is a key issue. Nearly 20% of Americans suffer one or more emotional disorders, so at the least patients with low back injury may have these disturbances as a preexistent condition. Patients with chronic pain perceive their pain as a disability limiting their functional status. The perception of pain as a disability is such a national problem that the Social Security Administration Commission on the Evaluation of Pain recommended the development of a listing ‘impairment due primarily to pain.’33 An abnormal psychological profile is inherited by the treatment team, insurer, and all others concerned. Our study of pain-population
1208
patients found 62.5% to have anxiety disorders and 56.2% to have current depression.34 These conditions were comingled with other less prevalent disorders. Only 5.3% of 283 patients were found to have no psychiatric diagnosis. Pure psychogenic pain is probably rare when presented as mental events giving rise to pain. However, all pain, as perceived by the patient, is real, regardless of cause. Most bodily pain is a combination of factors, e.g. physical stimuli and mental events. Abnormal mental and emotional states may arise from a background of past personal experiences with pain, or from personality characteristics. A history of physical abuse is not uncommon in patients with chronic pain. Individual counseling is given when needed, including sexual counseling. Every patient has an assigned doctoral-level psychologist, who monitors daily progress and reinforces the goal of physical restoration. Relaxation training includes coping approaches, muscle reeducation, meditation and distraction, guided imagery, autosuggestion, especially to be used with physical activity, and tape supplements, which enhance ‘live’ therapy. Stress management is incorporated into the behavioral sessions. Hypnotherapy is utilized on selected cases. Weekly family groups explore the goals of the patient with the spouse and/or other family members. How to respond to pain without fear is discussed as well as how to gain control over pain and their lives. Effective communication is an important subject. The roles of the various family members are defined, both as to distribution and as to responsibility. Experiences and frustrations are shared. These sessions facilitate the return to home, hopefully to an environment which will now foster wellness, not disability. The behavioral staff address the ‘fall out’ and behavioral responses to tapering from narcotics. Intense activation will produce endorphin release that helps ameliorate withdrawal.35 Most important of all, we do not teach people how to live or cope with their pain. Our goal is reduction or elimination of pain, and for the patient, to control any painful flare-ups. The pain is thereby no longer catastrophic; hence, it does not control the patient’s life.
Role of psychiatry Patients with chronic pain being treated at pain centers have been reported to suffer a wide range of psychiatric conditions. These include depression, anxiety, drug dependence/abuse, irritability and/ or anger, physical or sexual abuse, suicidal or homicidal ideation, and memory or concentration problems. These data are supported by epidemiological community studies, which indicate a strong relationship between chronic pain and depression.36–39 Depression is not only a potential target for treatment, but coping strategies may differ in depressed patients with chronic pain. Patients with chronic pain may over-rely on passive avoidance coping activities in response to life’s stresses, including pain; these coping activities may be a function of depressed mood.40 Severe depression is an indication for pain treatment facility referral. A facility with on-site psychiatric treatment should be chosen, since levels of anxiety, depression, etc. change rapidly during the treatment program. This necessitates an immediate response. Drug abuse, dependence, and addiction are reported in the range of 3.2–18.9%.41 These diagnoses are reported in a significant percentage of chronic pain patients, but evidence of addictive behaviors is not common. The dependence occurs as a result of the pain, not addiction. At issue is whether patients with physician-perceived drug problems are best treated at a pain treatment facility or at a substance abuse facility. Detoxification in pain treatment facilities where simultaneous pain treatment is available appears to be the
Section 5: Biomechanical Disorders of the Lumbar Spine
better route.37 Detoxification is not realistic unless pain alleviation occurs simultaneously. Management of pain medications and controlled substances should parallel physical and functional restoration.
Role of nursing Nurses are an integral part of the multidisciplinary team. Nurses are involved at every level as programs director, nurse manager, admissions liaison, admitting nurses and staff nurses who work in therapy areas with the patients and team throughout the treatment day. They support the physicians, do crisis management, medication management, monitor underlying medical problems, and provide 24-hour continuity of care when in the inpatient unit. They teach, counsel patients, families and case managers, and are involved with discharge planning. They supervise evening exercises assigned by the therapists.
HEADACHES AND PAIN REHABILITATION Headache is a frequent comorbid condition in patients with chronic pain. These headaches are mostly classified as migraines. However, a considerable number of patients with chronic pain present with injury-related headaches. In one study,42 10.5% of the chronic pain patients had headache interfering with function. Of these, 55.8% related their headaches to an injury and 83.7% had neck pain. Migraine headache was most common (90.3%) with cervicogenic being second (33.8%). Of the total, 44.2% had more than one headache diagnosis. The most frequent headache precipitants were mental stress, neck positions, and physical activity utilizing the neck muscles. Of the total group, 74.6% had a neck tender point. Discriminate analysis found the following symptoms as the most common predictors of headache: (1) onset of severe headache beginning at the neck tender point and numbness in arms and legs; (2) headache brought on by neck positions and arms overhead; and (3) cervical pain with a tender point in the neck. Taut muscle bands and cervical tender/trigger points perpetuate head and neck pain. Successful rehabilitation efforts must address both the headache component through effective medications and physical medicine management of the cervical abnormality.
GERIATRIC PAIN REHABILITATION While generally thought of as a worker compensation injury-related model, the concept of pain rehabilitation applies to patients of all age groups. As American workers age, the number of expected disabled workers is also expected to increase. Older workers and those who do become disabled can respond well to well-designed, customized programs tailored to their levels, goals, and expectations.43 Many studies have reported significant improvement in functional abilities of patients with pain irrespective of their age group.30,44,45 Even when the outcome of return to work in older patients was not achieved (e.g. Mayer and Gatchel4), the consensus is that older patients should not be denied access to pain rehabilitation after onset of injury.30
OUTCOME EVALUATION OF THE PAIN REHABILITATION MODEL Are multidisciplinary pain centers effective? The answer is ‘yes,’ by virtue of increase in functional activity, return to work, decreased use of the healthcare system, elimination of opioid medication, closure of disability claims, pain reduction, and proved cost-effectiveness.46
Evidence from well-designed outcome studies indicates that: (1) multidisciplinary pain facilities do return patients with chronic pain to work; (2) the increased rates of return to work are due to treatment; and (3) the benefits of treatment are not temporary.2,47–49 In one study, our center reported that 86% of all patients treated returned to full activity, with 70% fully employed and another 16% who were physically capable of full employment but could not return to work because jobs were not available.50 Among the 86% who were fully active, there was no clear-cut difference between compensation and noncompensation class cases.14 In a more recent study, the return rate to full function and work was again 86%, albeit the patients had some residual discomfort that eventually remitted or was controlled at a low level of intensity.2 The 14% who failed to return to full function were highly complex patients with major behavioral problems. Treatment at multidisciplinary pain clinics, based on a metaanalysis of 3080 patients, found savings in medical expenditures equal to US$9 548 000, savings in indemnity expenditures equal to US$175 225 000, with a total savings of US$184 772 050! Our data showed a 92% improvement in functional status, a 66% reduction in pain, and a 62% return to employment or a work-ready state. A 93% patient satisfaction rate with treatment is strong testimony to the effectiveness of multidisciplinary pain center treatment. Despite the perceived high cost, multidisciplinary pain rehabilitation programs are cost-effective by reducing long-term utilization of medical services and by returning patients early to employment or previous lifestyle.
SUMMARY AND CONCLUSIONS The problem of chronic pain is a powerful practical example of the complexity of an illness or injury when compounded by patient’s beliefs, cultural aspects, experience, the family, the workplace, the community, as well as the healthcare system. Seen from this perspective, it is predictable that these multifaceted problems are more amenable to a multidisciplinary treatment approach than to a series of single therapeutic interventions. These patients are too complex to be successfully treated by a single discipline. The treatment must be integrated and concurrent. Team communication is essential. The management of back injuries is far from simple, especially for those classified as having non-specific pain. An early referral to a competent pain center may prevent that simple sprain from becoming a catastrophe leading to total disability. The labeled ‘low back loser’ is a victim of the healthcare delivery system. Early multidisciplinary rehabilitation treatment is cost-effective. The healthcare system, therefore, must be capable of identifying the problems early and then dealing with them in a concise, comprehensive, goal-oriented way. We conclude that early referral can prevent the sensory, perceptual, behavioral, psychosocial, biomechanical consequences, and disability that are certain to develop if chronicity becomes established. Although this chapter concentrates on ‘spinal pain,’ pain rehabilitation does not limit its application to musculoskeletal disorders, spinal problems, or work injuries. If one accepts the hypothesis that chronic pain of any etiology produces a dysfunctional state, the mechanical issues of the myofascia loom large as a major contributing factor to the loss of function and its painful consequences. It then becomes clear that pain rehabilitation as described herein would be applicable to all conditions in which myofascial abnormality is found. The holistic, collaborative philosophy of optimizing the physical, functional, behavioral, cognitive, and occupational abilities makes pain rehabilitation the best choice for the patient from the humane, medical, and financial perspective.
1209
Part 3: Specific Disorders
References 1. Rosomoff RS. The pain patient. State of the Art Reviews. Spine 1990; 5(3): 417–428. 2. Cutler RB, Fishbain D, Rosomoff HL, et al. Does nonsurgical pain center treatment of chronic pain return patients to work? A review and meta-analysis of the literature. Spine 1994; 19:643–652. 3. Rosomoff HL, Rosomoff RS. A rehabilitation physical medicine perspective. In: Cohen MJM, Campbell JN, eds. Pain treatment centers at a crossroads: a practical and conceptual reappraisal, progress in pain research and management. Ch. 4, vol. 7. Seattle: IASP Press; 1996: 47–58.
26. Khalil TM, Abdel-Moty E, Rosomoff RS, et al. Ergonomics in back pain. A guide to prevention and rehabilitation. New York: Van Nostrand Reinhold; 1993:81–86. 27. Khalil TM, Abdel-Moty E, Steele-Rosomoff R et al. The role of ergonomics in the prevention and treatment of myofascial pain. In: Rachlin ES, ed. Diagnosis and comprehensive treatment of myofascial pain: handbook of trigger point management. New York: Mosby Year Book; 1993:487–523.
4. Mayer TG, Gatchel RJ. Effect of age on outcomes of tertiary rehabilitation for chronic disabling spinal disorders. Spine 2001; 26(12):1378–1384.
28. Khalil TM, Abdel-Moty E, Steele-Rosomoff R et al. The role of ergonomics in the prevention and treatment of myofascial pain. In: Rachlin ES, ed. Diagnosis and comprehensive treatment of myofascial pain: handbook of trigger point management. New York: Mosby Year Book; 1993:487–523.
5. Rosomoff HL, Fishbain D, Goldberg M, et al. Physical findings in patients with chronic intractable benign pain of the back and/or neck. Pain 1989; 37: 279–287.
29. Khalil TM, Abdel-Moty E, Steele-Rosomoff R, et al. Ergonomic programs in post injury management. In: Karawowski W, Marras WS, eds. The occupational ergonomics handbook. New York: CRC Press; 1999:1269–1289.
6. Rosomoff HL, Rosomoff RS. Comprehensive multidisciplinary pain center approach to the treatment of low back pain. Neurosurg Clin N Am 1991; 2(4):877–890.
30. Abdel-Moty E, Khalil TM, Rosomoff RS et al. Ergonomics considerations and interventions. In: Tollison CD, Satterthwaite JR, eds. Painful cervical trauma: diagnosis and rehabilitative treatment of neuromusculoskeletal injuries. Philadelphia: Williams & Wilkins; 1990:214–229.
7. Rosomoff HL. Do herniated disks produce pain? Clin J Pain 1985; 1:91–93. 8. Wall PD. Physiological mechanisms involved in the production and relief of pain. In: Bonica JJ, Procacci P, Pagni CA, eds. Recent advances on pain: pathophysiology and clinical aspects. Springfield, IL: Charles C. Thomas; 1974:36–63. 9. Vane JR. Pain of inflammation: an introduction. In: Bonica JJ, Lindblom U, Iggo A, eds. Advances in pain research and therapy, vol. 5. New York: Raven Press: 1983:597– 603. 10. Rosomoff HL, Rosomoff RS. Assessment and treatment of chronic low back pain: the multidisciplinary approach. In: Rucker KS, Cole AJ, Weinstein SM, eds. Low back pain: a symptom-based approach to diagnosis and treatment. Boston: Butterworth-Heinemann; 2000:343–362. 11. Spitzer WO, LeBlanc FE, Dupuis M, et al. Scientific approach to the assessment and management of activity-related spinal disorders: a monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spine 1987; 12:51–59.
31. Asfour SS, Khalil TM, Waly S, et al. Biofeedback in back muscle strengthening. Spine 1990; 15(6):510–513. 32. Khalil T, Asfour SS, Waly SM, et al. Isometric exercise and biofeedback in strength training. In: Asfour SS, ed. Trends in ergonomics/human factors, IV. New York: Elsevier Science; 1987:1095–1101. 33. Turk DC, Rudy TE, Stieg RL. The disability determination dilemma: towards a multi-axial solution. Pain 1988; 34:217–229. 34. Fishbain DA, Goldberg M, Meagher R, et al. Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain 1986; 26:181–197. 35. Carr DB, Bullen BA, Skrinar GS, et al. Physical conditioning facilitates the exerciseinduced secretion of beta-endorphin and beta-hypoprotein in women. N Engl J Med 1981; 305:560–563.
12. Travell JG, Simons DG. Myofascial pain and dysfunction: the trigger point manual. Baltimore: Williams and Wilkins; 1983.
36. Fishbain DA, Cutler R, Rosomoff HL, et al. Chronic pain-associated depression: antecedent or consequence of chronic pain? A review. Clin J Pain 1997; 13:(2) 116–137.
13. Abdel-Moty E, Khalil T, Steele-Rosomoff R et al. Maximizing progress during low back pain rehabilitation. In: V. Nielsen R, Jorgensen K, eds. Advances in industrial ergonomics and safety. London: Taylor & Francis; 1993:331–335.
37. Fishbain DA, Cutler RB, Rosomoff HL, et al. Pain facilities: a review of their effectiveness and referral selection criteria. Psychiatr Manage Pain 1997; 1:(2) 107–116.
14. Rosomoff HL, Green CJ, Silbret M, et al. Pain and low back rehabilitation program at the University of Miami School of Medicine. In: Ng LKY, ed. New approaches to treatment of chronic pain: a review of multidisciplinary pain clinics and pain centers. National Institute on Drug Abuse Research Monograph Series 36. Washington DC: US Government Printing Office; 1981:92–111.
38. Fishbain DA. Somatization, secondary gain, and chronic pain: Is there a relationship? Curr Rev Pain 1998; 6:101–108.
15. Rosomoff H.L, Rosomoff RS. Myofascial pain syndromes. In: Follett KA, ed. Neurosurgical pain management. Philadelphia: WB Saunders; 2004:57–72. 16. Headley B. Assessing muscle dysfunction from active trigger points. Adv Physical Therap 1997; 8:21–22. 17. Khalil TM, Abdel-Moty E, Diaz E, et al. Electromyographic symmetry pattern in patients with chronic low back pain and comparison to controls. In: Karwowski W, Yates JW, eds. Advances in industrial ergonomics & safety, III. London: Taylor and Francis; 1991:483–490. 18. Fishbain DA, Turner D, Rosomoff H, et al. Millon Behavioral Health Inventory scores of patients with chronic pain associated with myofascial pain syndrome. Pain Med 2001; 2:1328–1335. 19. Steele-Rosomoff R, Rosomoff HL, Abdel-Moty E. Vocational rehabilitation and ergonomics. In: Burchiel KJ, ed. Surgical management of pain. New York: Thieme; 2001:171–180. 20. Rosomoff HL. The effects of hypothermia on the physiology of the nervous system. Surgery 1956; 40:328–336. 21. Rosomoff HL, Clasen RA, Hartstock R, et al. Brain reaction to experimental injury after hypothermia. Arch Neurol 1965; 13:337–345. 22. Lind GAM. Auto-traction: treatment of low back pain and sciatica. Sweden: Sturetryckeriet; 1974. 23. Natchev E. A manual on autotraction treatment for low back pain. Folksam Scientific Council Publ, B 1984; 171. 24. Abdel-Moty E, Khalil TM, Rosomoff RS, et al. Computerized electromyography in quantifying the effectiveness of functional electrical neuromuscular stimulation. In: Asfour SS, ed. Ergonomics/human factors, IV. New York: Elsevier Science; 1987:1057–1065.
1210
25. Abdel-Moty E, Fishbain D, Goldberg M, et al. Functional electrical stimulation treatment of postradiculopathy associated muscle weakness. Arch Phys Med Rehabil 1994; 75:680–686.
39. Fishbain DA, Cutler BR, Rosomoff HL, et al. Comorbidity between psychiatric disorders and chronic pain. Psychiatr Manage Pain 1998; 2:(1)1–10. 40. Weickgerant AL, Slater MA, Patterson TL, et al. Coping activities in chronic low back pain: relationship with depression. Pain 1993; 53:95–103. 41. Fishbain DA, Steele-Rosomoff R, Rosomoff HL. Drug abuse, dependence, and addiction in chronic pain patients. Clin J Pain 1992; 8:77–85. 42. Fishbain DA, Cutler R, Cole B, et al. International Headache Society headache diagnostic patterns in pain facility patients. Clin J Pain 2001; 17:178–193. 43. Khalil TM, Abdel-Moty E, Zaki A M, et al. Reducing the potential for fall accidents among the elderly through physical restoration. In: Kumar S, ed. Advances in industrial ergonomics & safety, IV. London: Taylor & Francis; 1992:1127–1134. 44. Khalil TM, Abdel-Moty E, Diaz E, et al. Efficacy of physical restoration in the elderly. Experimental Aging Research 1994; 20(3):189–199. 45. Cutler RB, Fishbain DA, Lu Y, et al. Prediction of pain center treatment outcome for geriatric chronic pain patients. Clin J Pain 1994; 10:(1)10–17. 46. Turk DC. Efficacy of multidisciplinary pain centers in the treatment of chronic pain. In: Cohen MJM, Campbell JN, eds. Pain treatment centers at a crossroads: a practical and conceptual reappraisal. Progress in pain research and management, vol. 7. Seattle: IASP Press; 1996:257–273. 47. Fishbain DA, Cutler RB, Rosomoff HL, et al. Movement in work status after pain facility treatment. Spine 1996; 21:(2)2662–2669. 48. Fishbain DA, Cutler R, Rosomoff HL, et al. Impact of chronic pain patients’ job perception variables on actual return to work. Clin J Pain 1997; 13:197–206. 49. Fishbain DA, Cutler RB, Rosomoff HL, et al. Pain facility treatment outcome for failed back surgery syndrome. Curr Rev Pain 1999; 3:10–17. 50. Cassisi JE, Sypert GW, Salamon A, et al. Independent evaluation of a multidisciplinary rehabilitation program for chronic low back pain. Neurosurgery 1989; 25:877–883.
Section 5: Biomechanical Disorders of the Lumbar Spine
Further Reading Abdel-Moty E, Fishbain D, Khalil T, et al. Functional capacity and residual functional capacity and their utility in measuring work capacity. Clin J Pain 1993; 9:168–173.
Moty EA, Khalil T, Asfour S, et al. On the relationship between age and responsiveness to rehabilitation. In: Das B, ed. Proceedings of the Annual International Industrial Ergonomics and Safety Conference. Advances in Industrial Ergonomics and Safety 11. Philadelphia: Taylor & Francis; 1990: 49–56.
American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain 2003; 73.
Rosomoff HL, Fishbain DA, Goldberg M, et al. Are myofascial pain syndromes (MPS) physical findings associated with residual radiculopathy? Pain 1990; Suppl 5:S396.
Fishbain DA, Rosomoff HL, Cutler B, et al. Opiate detoxification protocols. A clinical manual. Ann Clin Psychiatry 1993; 5:(1)53–65.
Rosomoff RS, Rosomoff HL. Hospital-based inpatient treatment programs. In: Tollison CD, ed. Handbook of pain management, Ch. 51, 2nd edn. Baltimore: Williams & Wilkins; 1994:686–693.
Fishbain DA, Cutler RB, Rosomoff RS, et al. The problem-oriented psychiatric examination of the chronic pain patient and its application to the litigation consultation. Clin J Pain 1994; 10:28–51. Fishbain DA, Cutler RB, Rosomoff HL, et al. Validity in self-reported drug use in chronic pain patients. Clin J Pain 1999; 15:3184–3191. Fishbain DA, Cutler RB, Rosomoff HL, et al. Does the Conscious Exaggeration Scale detect deception within patients with chronic pain alleged to have secondary gain? Pain Med 2002; 3:139–146. Fishbain DA, Cutler RB, Rosomoff HL, et al. Are opioid-dependent/tolerant patients impaired in driving-related skills? A structured evidenced-based review. J Pain Symptom Manage 2003; 25(6):559–577. Fishbain DA, Cutler RB, Rosomoff HL, et al. Is pain fatiguing? A structured evidencebased review. Pain Med 2003; 4(1):51–62. Gunn CC. Treatment of chronic pain intramuscular stimulation for myofascial pain of radiculopathic origin, 2nd edn. New York: Churchill Livingstone; 1996:165. Khalil TM, Goldberg ML, Asfour SS, et al. Acceptable maximum effort (AME): a psychophysical measure of strength in back pain patients. Spine 1987; 12(4): 372–376. Khalil TM, Asfour SS, Martinez LM, et al. Stretching in the rehabilitation of low-back pain patients. Spine 1992; 17:(3)311–317.
Rosomoff HL, Rosomoff RS, Fishbain D. Chronic low back pain. J Back Musculoskel Rehab 1997; 9(3):201–208. Rosomoff HL, Rosomoff RS, Fishbain DA. Types of pain treatment facilities referral selection criteria: are they medically & cost effective? J Florida Med Assoc 1997; 84:(1)41–45. Rosomoff HL, Steele-Rosomoff R. Surgery for the herniated lumbar disk with nerve root entrapment; are alternative treatments to surgical intervention effective? Curr Rev Pain 1998; 2:121–129. Steele-Rosomoff R, Rosomoff HL. Hospital-based inpatient treatment programs. In: Tollison CD, Satterwaite JR, Tollison JW, eds. Practical pain management, Ch. 53. Philadelphia: Lippincott Williams & Wilkins; 2002:782–790. US Department of Labor, Employment and Training Administration. Selected characteristics of occupations defined in the DOT. Washington, DC: US Government Printing Office; 1981. US Department of Labor, Employment and Training Administration. Dictionary of occupational titles, 4th edn. Washington, DC: US Government Printing Office; 1986. Yeomans SG, Liebenson C. Applying outcomes management to clinical practice. JNMS 1997; 5(1):1–14.
1211
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBBS-Cervical, Thoracic, and Lumbar ■ i: Functional Restoration
CHAPTER
Deconditioning
111
Terry C. Sawchuk and Eric K. Mayer
INTRODUCTION Most patients with an episode of low back pain will improve significantly in a relatively short period of time, while others with seemingly minor injuries and often times minimal imaging abnormalities go on to develop chronic low back pain and significant disability. It is believed that there is a reduced level of physical activity associated with their pain leading to a decreased level of fitness or deconditioning. In recent years there has been great interest in why some develop chronic pain and subsequent disability and deconditioning. There is also great interest in what is occurring from a physical as well as a psychological perspective. Deconditioning, or its related terms detraining and disuse, is a multifactorial process that occurs in multiple body systems and is often secondary to an inciting event. Medline lists more than 2.6 million articles published since 1996 related to deconditioning of the heart, vessels, cardiovascular set-points, bone, cognition, affect, and muscles. The common factor for the pathologic change to these varied systems revolves around exercise or, more precisely, a lack of exercise exacerbating pathology. Though deconditioning is a common search term, it is not an entity defined in Steadman's Medical Dictionary. Moreover, existing literature has used the term in various related manners, depending upon whether the investigator is a physiologist, neurologist, physiatrist, or orthopedic surgeon. The favorite terms in the literature associated with deconditioning are: decreased exercise tolerance, decreased VO2 max, decreased ability of adaptation to functional demands, and general decreased performance in occupation and/or activities of daily living. With such an array of connotations and denotations, is it any wonder that the literature is conflicting at times? Since most of those who become disabled are of working age, the costs of their lost productivity and treatment is shouldered by all of society. It now appears evident that chronic low back pain (CLBP) is not merely a function of incomplete healing after an injury. While there certainly may be residual pain, most recover sufficiently to continue working and functioning in daily life. Understanding the reasons behind the development of chronic pain, deconditioning, and disability as well as the physical, psychosocial, and socioeconomic consequences holds significant promise for improved treatment, reduced pain, suffering and disability, and potentially enormous cost savings. A pure physical or anatomic model fails to adequately explain chronic pain and the associated disability and deconditioning. As a result, chronic pain is now conceptualized as a multifactorial phenomenon with biological, psychological, and socioeconomic variables interplaying. Our discussion here will include a review of deconditioning-related physiologic changes such as muscle atrophy, osteoporosis, and obesity as well as deconditioning-related functional changes such as a reduced cardiovascular capacity, a decrease in muscle strength and impaired coordination or motor control in
the presence of CLBP. Psychological variables such as fear-avoidance beliefs and depression and their relationship with CLBP and deconditioning are also reviewed. Chronic low back pain is one of the most costly as well as the one of the most common diseases affecting industrialized societies today. While the incidence of lower back injuries has not changed over time, disability rates have increased sharply over the past 20 years.1 It has been estimated that a percentage as small as 20% of low back pain patients account for 90% of the costs.2 The enormous costs for the treatment including lost productivity and worker replacement has been estimated as high as US$837 billion3,4 secondary to chronic spinal disorders. It has been proposed that with chronic pain there comes inactivity, disuse, and deconditioning. Kottke5 in 1966 stated, ‘The functional capacity of any organ is dependent within physiologic limits upon the intensity and frequency of its activity. Although rest may be protective for a damaged organ it results in progressive loss of functional capacity for normal organs.’ The decrease in function will be proportional to the duration, degree, and type of limitation of activity. Hasenbring et al.6 proposed physical disuse as a risk factor for chronicity in lumbar disc patients. Disuse or disuse syndrome and deconditioning are terms associated with this loss of functional capacity. The disuse syndrome was first described by Bortz in 1984.7 He pointed out how our society had become progressively more sedentary, adhering to an anthropologic law called the Principle of Least Effort. This, stated simply, says when an organism has a task to perform it will seek that method of performance that demands the least effort. Focusing on the long-term adverse consequences of inactivity, he described the identifying characteristics of the syndrome as cardiovascular vulnerability, obesity, musculoskeletal fragility, depression, and premature aging. He did not consider the reasons for inactivity but observed that disuse is physically, mentally, and spiritually debilitating. Mayer and Gatchel8 introduced the term ‘deconditioning syndrome’ in 1988. They felt deconditioning may be a response mediated physically by the injury as well as psychologically by a variety of secondary factors. Some of these include injury-imposed inactivity, neurologically mediated spinal reflexes, iatrogenic medication dependence, nutritional disturbance, and psychologically mediated responses to prior psychiatric distress, vocational adjustment problems, and/or limited social coping resources.9 As a result of inactivity, physical deconditioning represented by muscle inhibition/atrophy, decreased cardiovascular conditioning, decreased neuromuscular coordination, decreased ability to perform complicated repetitive tasks, and musculotendinous contractures ensues. They use the term ‘deconditioning syndrome’ to represent the cumulative disuse changes, physical and psychological, produced in the chronically disabled patient suffering from spinal and other chronic musculoskeletal disorders.
1213
Part 3: Specific Disorders
We will review the physical and psychological consequences of inactivity or disuse in patients with CLBP. Physical measurements have addressed muscle function or strength and endurance isometrically, isokinetically, and isotonically. Methods such as magnetic resonance imaging (MRI), computed tomography (CT) scanning, and electromyography have been utilized to measure changes in muscle composition and function. Cardiovascular capacity and motor control or coordination have also been measured in CLBP patients. Psychosocial issues or variables such as distress, depression, anxiety, and fear-avoidance beliefs and their relationship with CLBP will be reviewed.
DECONDITIONING: A HISTORICAL PERSPECTIVE Original interest in a deconditioning syndrome was prompted primarily by two things. First, as part of the practice of medicine at one time, bed rest was often a prescribed treatment. However, physicians began to realize a multitude of adverse consequences secondary to this imposed immobility. Second, as the space program evolved, astronauts spent longer periods of time in a weightless environment, stimulating further interest on the affects of immobilization. Sixty years ago Dietrick et al.10 studied the effects of immobilization by placing four normal men in plaster casts from the umbilicus to the toes for 6 weeks and then followed them through a 4–6 week recovery period. They and other investigators observed a multitude of physiologic and metabolic changes. While our patients with CLBP certainly have not been immobilized to such a degree, a short review of that literature is enlightening. During exercise, cardiac output, heart rate, and left ventricular function all increase. Even with moderate exercise cardiac output may triple, heart rate may double, and left ventricular effort may more than triple. Oxygen uptake with heavy exercise rises six times higher than that seen at rest. With inactivity, physical fitness decreases rapidly. Resting heart rate was reported to increase by 0.4 beats per minute during an immobilization period.11 Stroke volume decreased by as much as 30% during maximal exercise following a period of immobilization.11 The maximal oxygen uptake (VO2 max) is felt to be the most sensitive measure of physical fitness. A decrease in VO2 max of 21% after 30 days of bed rest was observed by Greenleaf.12 Pulmonary function as measured by total lung capacity, forced vital capacity, forced expiratory volume, alveolar–arterial oxygen tension difference, and membrane diffusing capacity remained unchanged or showed decreases only in proportion to decreases in cardiovascular output and maximal oxygen uptake.10,11 In these studies the immobilization was virtually absolute and cognitive, emotional, and social effects were observed as well as the physiologic and metabolic effects. With immobilization, skeletal muscle obviously undergoes atrophy as well as decreased strength, endurance, and coordination. Muller13 reported strength loss of approximately 3% per day for the first 7 days in the muscle of the upper extremity immobilized in a cast. Little further strength loss was observed with further immobilization. Bone marrow content is lost during immobilization, resulting in osteopenia or osteoporosis.14 This skeletal calcium loss is associated with increased urinary calcium excretion which begins to rise on the second or third day of immobilization.10,14 Decreased physical activity alone without actual confinement to bed may result in skeletal calcium loss.15 Gaber et al.16 have shown that patients with CLBP have an increased incidence of osteopenia and osteoporosis. Another metabolic consequence is a negative nitrogen balance with losses of 29–83 grams during 6–7 weeks of immobilization. This loss reflects the equivalent of 1.7 kilograms of muscle protoplasm.10
1214
Before beginning our discussion of a deconditioning syndrome as it relates specifically to patients with CLBP, there are several terms should be defined. Verbunt et al.17 defined ‘disuse’ as performing at a reduced level of physical activity in daily life. They described ‘physical deconditioning’ as a decreased level of physical fitness with an emphasis on the physical consequences of inactivity for the human body, whereas Mayer and Gatchel8 included the psychological effects secondary to inactivity or disuse along with the physical consequences as part of their definition of the deconditioning syndrome. Verbunt chose to include the term ‘disuse syndrome’ in their discussion as well. The ‘disuse syndrome’ is defined as a result of long-term disuse, which is characterized by both physical and psychosocial effects of inactivity. Our discussion here will include a review of the literature on disuse or what is actually known about the level of physical activity in daily life of patients with CLBP. We have chosen to utilize the term deconditioning syndrome as defined by Mayer and Gatchel to represent the cumulative changes secondary to disuse, both physiological and psychological, produced in the patient suffering from CLBP. Thus, we can see how disuse leads to the deconditioning syndrome. The assumption is that we can show a significantly reduced level of physical activity resulting in deconditioning in patients with CLBP.
DISUSE In 1946, Young18 described the effects of use and disuse on nerve and muscle. Introducing the term disuse into the medical literature, he described it as not using the musculoskeletal system during periods of immobility. Then Bortz in 1984 referred to the disuse syndrome and included many of the adverse consequences of inactivity in his definition beyond those affecting muscle and nerve. For purposes of this discussion we will define disuse as performing at a reduced level of physical activity.17 We are sure many of us hold the belief that our patients with CLBP are leading a very sedentary existence with an activity level significantly below that of the norm. But, in actuality, what is known about the activity level of these patients? In a group of patients with chronic pain (but not specifically low back pain) the Baecke Total Physical Activity Score was significantly higher in female than in male patients, a finding not observed in healthy controls.19 This study also revealed a statistically significant reduction in a physical work capacity index of 34% in males and only a 17% reduction in found in women, which hardly reached the significance level. The authors concluded that chronic pain may have a greater impact on activity level in male patients than in female patients, whereas Protas20 and Verbunt et al.21 found that physical activity in the daily life of patients with CLBP did not differ significantly from healthy age- and gendermatched controls. The physical activity in daily life expressed as whole-body acceleration measured with a triaxial accelerometer and as the ratio between average daily metabolic rate, measured by the doubly labeled water technique, and resting metabolic rate, measured by ventilated hood, was reported by Verbunt et al.21 Both techniques were used simultaneously for 14 days. They noted that the mean level of physical activity did not differ in CLBP patients when compared with healthy controls. Thus, they could not confirm the presence of disuse in this group of patients. Given that 77% of the patients in this study were employed despite their back problems, it is possible that the patients participating in this study were in relatively better physical condition than other patients with CLBP. Further measurements revealed no difference in percentage of body fat and body mass between patients and controls. They found it remarkable that although patients felt disabled because of
Section 5: Biomechanical Disorders of the Lumbar Spine
their back pain as shown in their Rowland Disability Questionnaire scores, their level of physical activity as actually measured was not decreased in comparison with controls. They also noted there was no correlation between pain intensity and physical activity levels. Several theories as to the reasons for the differing results with regards to the presence or absence of disuse have been offered. Work status may indeed have a significant impact on physical activity levels. On the one hand, in the study by Verbunt et al.21 77% of the CLBP subjects were working, whereas in Neilens and Plaghki's studies19,22,23 only 20–34% of subjects had a paying job. Different methods for assessment of the degree of inactivity have also been employed. While Verbunt utilized physiologic measurements, others used self-reporting to assess physical activity levels. A discrepancy in reported functioning by patients and actual functioning has been reported.24,25 Physical activity levels as reported by patients with CLBP and as reported by their physical therapists revealed that the patients significantly underestimated their level of activity.25 It also has been shown that patients with CLBP have greater difficulty actually estimating their level of exertion during a performance test.24 From these studies, it would appear that self-reporting of activity levels in patients with CLBP is unreliable. In summary, it is surprising that so few studies have been performed on the level of physical activities in daily life or disuse in patients with CLBP. The results have been equivocal and thus, despite what our beliefs may be about the activity level of these CLBP patients, the literature does not support the definitive presence of a reduced activity level. This lack of a decreased activity level particularly seems to be the case, at least in patients with CLBP, who continue to work. The study by Verbunt et al.21 is the most scientifically well designed of these and they were unable to confirm the presence of disuse in a group of CLBP patients. The work status and/or varying methods of reporting activity level may offer some explanation for the inconclusive results reported here.
DECONDITIONING IN CHRONIC LOW BACK PAIN The presence of disuse or a reduced level of physical activity in daily life has not been definitively supported by the literature. However, since deconditioning is felt to be a result of disuse, the presence of deconditioning in CLBP may be used as supportive evidence of a low level of activity. There may be both physiological as well as psychosocial changes associated with the deconditioning syndrome. Physical consequences of inactivity may include decreased cardiovascular endurance, decreased strength and muscular atrophy, impaired coordination, osteoporosis, metabolic changes and obesity. Psychosocial changes may include distress, depression, anxiety, or behaviors consistent with the fear-avoidance model.
Cardiovascular capacity Endurance or cardiovascular capacity in patients with CLBP has been measured utilizing various methods. The most widely accepted measure of cardiovascular fitness is maximal oxygen uptake (VO2 max). The various methods of measurement have included measurement of VO2 max as well as utilizing submaximal exercise testing. Interestingly, the results have not led to a definitive conclusion about the cardiovascular capacity of patients with CLBP. In measuring parameters such as predicted VO2 max utilizing a symptom-limited treadmill test or bicycle ergometer some studies have shown significantly lower levels of cardiovascular fitness in patients24,26–28 whereas Wittink et al.29 and several others have failed to
demonstrate a significantly reduced level of aerobic fitness in patients with CLBP.30–32 A lower cardiovascular capacity was shown for men compared with controls but not for women in some studies.19,22,23 Wittink et al.29 tested a sample of 50 patients with CLBP with a mean duration of symptoms of 40 months. Oxygen consumption (VO2) was measured during a symptom-limited modified treadmill test. Prediction equations were employed to estimate VO2 max. The mean observed VO2 max values for men and women with CLBP were consistent with those found in earlier studies that tested normal subjects. Given these results, they concluded that rather than being a group of significantly deconditioned subjects, at least from an aerobic standpoint, this group of patients with CLBP represented a sample of moderately fit individuals. Furthermore, their data suggest that aerobic fitness levels are independent of diagnosis, duration of pain, pain intensity, work status, or smoking. Previously, Wittink et al.33 had subjects with CLBP perform three symptom-limited maximal exercise tests: a treadmill, an upper extremity ergometer, and a bicycle ergometer test. The treadmill test was found to be by far the best test for measuring aerobic fitness in these patients. Wittink et al.34 went on to show that there is no significant relation between aerobic fitness and pain intensity in patients with CLBP and that a lack of cardiovascular fitness therefore does not contribute to pain intensity in patients with CLBP. In a follow-up sample, patients reported significantly less pain before and after treadmill testing at the end of a functional restoration program compared with their pain intensity with testing before the program. Since their predicted VO2 max had not changed, the authors noted that there had been a decreased pain intensity independent of aerobic fitness levels. Hurri et al.32 measured VO2 max in 245 subjects with CLBP, 81 who were treated as inpatients, 88 treated as outpatients, and 76 controls with a history of CLBP but who were still working. They performed bicycle ergometer tests four times over a 30-month period. The estimated VO2 max of their patients was not significantly different than reference values of healthy persons. Battie et al.30 noted that aerobic fitness did not affect the risk of back injury in a prospective study. He did observe that it might affect the response to the problem and subsequent recovery. Cady et al.,35 in his oft quoted study from 1979 on a group of firefighters, showed a graded and statistically significant protective effect for increasing levels of fitness and conditioning. A criticism of Cady's study was that fitness level included both cardiovascular or endurance parameters as well as strength measures, making it impossible to isolate the benefits of these individually. On the other hand, some investigators have shown what most of us would believe to be true, that indeed there is a significantly decreased level of cardiovascular fitness in CLBP patients. Brennan et al.26 used bicycle ergometry to determine a predicted VO2 max in 40 patients with herniated discs with an average duration of symptoms of 87 days. Comparing these results with those of a matched control group revealed a significantly reduced predicted VO2 max for the patients. Others,24,27 in addition to van der Velde and Meirau,28 have also shown diminished cardiovascular capacity in patients with CLBP. Their original experimental objective was to determine the effects of 6 weeks of exercise on aerobic capacity and on measures of pain and disability in patients with CLBP.28 Baseline measurements determined that the percentile rank of aerobic capacity for the patients with CLBP was statistically significantly lower than those measures for the controls. Patients who completed a 6-week program of aerobic, muscular endurance, and flexibility exercises showed a statistically significant improvement in the mean percentile rank for aerobic capacity. In addition, they showed significant decreases in pain and disability after completion of the exercise program.
1215
Part 3: Specific Disorders
We can see that despite what our preconceived ideas may be regarding a decreased aerobic capacity in patients with CLBP, the literature is inconclusive. Instead, it reveals that a decreased aerobic capacity may or may not actually be present in these individuals. Work status again has been offered as a possible reason why the results have varied so, the thought being that even in the presence of CLBP those individuals continuing to work are more likely to possess a fitness level equal to the norm. Unfortunately, information pertaining to work status is not available for all of the studies considered here. It is notable that in most studies where no difference in cardiovascular capacity was reported, most of the subjects being studied were still working. The cardiovascular capacity was better for CLBP patients who were working compared with those who were not in one study.36 In several studies19,22,23 male subjects had decreased cardiovascular capacity when compared with controls, whereas females did not. Speculation as to why this may be so centered on the idea that when men lose their job there is a greater degree of inactivity, whereas in the case of women they remain more active at home with tasks such as cooking, cleaning, and childcare. This keeps them at an activity level equivalent to that of healthy females.
Muscle changes: composition and performance Skeletal muscle has incredible plasticity associated with it. It can adapt to almost any array of functional demands we place upon it. The level by which muscle function declines with inactivity depends upon the level of training before inactivity began and the duration of inactivity. In discussing muscle, it is important to understand the function of muscle subtypes. Type II (predominantly subtypes a and b) fibers are generally ‘fast twitch.’ They can track fast and are maximally powered by glycolysis, and therefore fatigue quickly. They are usually recruited late when the body needs to exert ‘maximal effort.’ Type I fibers are generally ‘slow twitch.’ They contrast slowly and are metabolically inexpensive, utilizing aerobic metabolism. In the acute period (14–30 days), fiber type is preserved even with activity reduction greater than 75% given the absence of an associated neuromuscular injury (i.e. foot drop such as from an L4 nerve root impingement).37,38 In the subacute period (30–90 days), large progressive shifts of type IIa fibers to type IIb fibers (both fast twitch fibers) occur at a rate of 5–19%.39 This shift can precede fatty replacement of muscle (apoptosis) in animal models. There is also a 15% decrease in the number as well as the size of type I (efficient slow twitch muscle fibers).40 In chronic detraining (90 days to 9 months), power lifters showed oxidative muscle (type I) fibers increased by 1.4 times,41 while type II fibers (fast twitch) decreased by 60% in axial muscles.42,43 It has been noted that the very young (less than 20 years old) may exhibit a certain immunity to fiber-type change in the face of detraining.44,45 A changed fiber cross-sectional area (atrophy) also occurs with deconditioning and detraining. In athletes both type I and type II fibers decreased in size by 9–23% in as little as 6 weeks of detraining.46 In a chronic period (7 months) there can be as much as 37% atrophy across all muscle fiber types.41 Mayer et al.47 noted in CT that CLBP patients (in both operative and nonoperative segments) had significantly decreased muscle bulk with evidence of fatty replacement of muscle. The authors further correlated this observational qualitative finding of atrophy with a quantitative finding of greater than 50% mean reduction in strength testing for the atrophied spinal muscle group compared to age- and gender-matched controls. Several other studies have shown smaller cross-sectional areas of the paraspinal muscles by CT or MRI scanning in subjects with CLBP.48–50 It remains debatable, but some papers have shown that larger muscles (postural 1216
muscles of the back and lower extremities) become atrophic at a faster rate than extremity muscles. Few authors have actually correlated strength performance to atrophy, but generally strength is largely preserved during short periods of convalescence although eccentric strength decreases earlier than other aspects of neuromuscular performance (7–21 days). In the subacute period (4–12 weeks) there are declines in strength, measured by both force and power, of 7–15%.51,52 For chronic periods, decreases in power were 40–60% for trained muscles in the arms and legs, but less dramatic decreases of 15–37% were noted in the contralateral untrained arm.37,53 Muscle endurance times are also decreased with deconditioning. Decreased strength as well as decreased endurance for trunk/spinal musculature was seen in patients with chronic low back pain despite having similar physical activity levels as age- and gender-matched controls.49,54 Mayer et al.55 demonstrated significant strength deficits for both trunk flexors and extensors for a group of CLBP patients utilizing a Cybex prototype sagittal trunk strength tester. Using a dynamic isokinetic lifting device, Kishino et al.56 show significantly decreased isokinetic as well as isometric lifting capabilities for patients with CLBP. Houston et al.37 have noted a capillary density diminution in as few as 15 days after training cessation. However, other authors have noted that even after 90 days of detraining, capillarization remained largely unchanged with only minor decreases in VO2 max.57 Mujika and Padilla, who have analyzed much of the existing data, surmise that capillaries and muscles are preserved in trained athletes and may account for their greater speed to reach previous training levels than in sedentary individuals.58,59 Rapid and progressive reduction in mitochondrial oxidative enzymes creates a rapid decrease in the efficiency of muscle cells to manufacture APT.59 Further, ‘run-time exhaustion’ or subthreshold muscle failure is associated with decreased mitochondrial density and/or efficiency.60 Deconditioned, formerly trained individuals retain higher enzymatic and mitochondrial numbers than sedentary individuals and will reach peak performance levels faster when they resume activity.61 Motor control is also adversely affected in the presence of CLBP. Performing a standardized reach task, postural control in patients with CLBP was more affected in those with severe low back pain compared with moderate pain.62 Patients with CLBP showed a delayed-onset contraction of abdominal muscles during motion of the upper extremities.63,64 Patients with low back pain were shown to have decreased trunk motion patterns while performing a repetitive wheel rotation task.65 Haines66 showed immobility, as well as decreased coordination and balance. Several surface EMG studies have shown reduced recruitment patterns and lower maximum integrated electromyography in paraspinal muscles in CLBP patients.67,68 Moreover, studies of movement patterns have shown the delayed onset of contraction of the transversus abdominis indicating a deficit of motor control, hypothesized to result in inefficient muscular stabilization of the spine.69 Thus, it appears that in the presence of CLBP there is muscular atrophy with a subsequent decrease in strength and endurance. In addition, altered recruitment patterns may affect muscular stabilization of the spine.
Obesity Several studies have addressed the issue of obesity in the presence of chronic pain and deconditioning, some specifically in a population of patients with CLBP. In an experimental study where subjects (not necessarily patients with CLBP) were placed at bed rest, it was shown that lean body mass decreases during 30 days of bed rest whereas body weight did not change.12 This finding suggests that the percentage of body fat will increase as the percentage of muscle mass decreases. During a period of reconditioning, this inverse relationship
Section 5: Biomechanical Disorders of the Lumbar Spine
was confirmed.70 Furthermore, it has been shown that with increasing aerobic fitness there is a significant decrease in the percentage of body fat. Verbunt et al.21 showed that the percentage of body fat of CLBP patients did not differ from controls, which is in agreement with the findings of others.49 Toda et al.71 was able to show that in female patients with CLBP there was an increase in the percentage of body fat when compared to healthy age- and gender-matched controls but were unable to show this same difference in men. Given the study design, it is impossible to state that this information provides definitive scientific evidence that an increased body fat percentage is the result of deconditioning in CLBP. Obesity itself may actually contribute to the occurrence of back pain and was already present before back pain began.
Psychosocial changes Why some patients develop CLBP and significant disability has become an evermore perplexing question. This small percentage of patients with oftentimes seemingly minor injuries and imaging studies comparable to others who recover as expected with little or no disability end up consuming a great majority of the dollars spent on treatment. The fear-avoidance model as an explanation of how and why some individuals with musculoskeletal disorders develop a chronic pain syndrome was first proposed by Lethem et al.72 in 1983. They described how fear of pain and avoidance of it result in the perpetuation of pain behaviors and experiences, even in the absence of demonstrable organic pathology. Fear-avoidance refers to the avoidance of movements or activities based on the fear of increased pain or re-injury. Thus, it is thought to play a role in the development of the deconditioning syndrome. Avoidance is a type of learned behavior which postpones or averts the presentation of an adverse event. Vlaeyen et al.73–75 have proposed a fear-avoidance model with two opposing behavioral responses: confrontation and avoidance, and present possible pathways by which injured patients get caught in a downward spiral of increasing avoidance, disability, and pain. The model predicts several ways that pain-related fear can lead to disability: 1. Negative appraisals about pain and its consequences, such as catastrophic thinking, are considered a potential precursor of pain related fear. 2. Fear is characterized by escape and avoidance behaviors, such that daily activities are diminished, resulting in functional disability. 3. Because avoidance behaviors occur in anticipation of pain rather than as a response to pain, they may persist, resulting in decreasing opportunities to correct them. 4. Longstanding avoidance and physical inactivity have a detrimental impact on the musculoskeletal and cardiovascular systems, leading to disuse and deconditioning. Avoidance also means withdrawal from essential reinforcers, thus increasing mood disturbances such as depression. Depression and disuse have been shown to be associated with decreased pain tolerance.76,77 5. Pain-related fear interferes with cognitive functioning just as other forms of fear and anxiety do, making those affected less able to shift their attention away from pain-related information, at the expense of other important tasks including coping with problems of daily life. 6. Pain-related fear will be associated with increased psychophysiological reactivity when the individual is confronted with situations that are appraised as dangerous. It has been proposed that there is a subgroup of CLBP patients who have a tendency to cope with pain using endurance strategies as opposed to avoidance strategies.6 In this fear-avoidance model of
chronic pain, patients appear to ignore their pain and ‘stick it out’ despite the pain. This ‘stick it out/grit their teeth’ behavior also results in complaints of persistent pain. These individuals are likely to report a physical activity level that fluctuates greatly over time as a reaction to their pain. They will tend to persevere or push on until increasing pain prevents it. This period of increased activity is then followed by a period of rest or reduced activity followed again by resumption of increased activity. This has been referred to as ‘all or nothing’ behavior, representing the so-called ‘overactivity/underactivity’ cycle seen in many chronic pain patients.78,79 What do we know about the effect of pain-related fear on physical performance? A significant correlation was found between painrelated fear and range of motion measured with a flexometer.80 Using a simple task such as lifting a 5.5 kg weight in the dominant arm and holding it until pain or physical discomfort made it impossible to continue, Vlaeyen et al.73 found a significant correlation between lifting time and results from the Tampa Scale for Kinesiophobia (TSK). The TSK was developed as a measure of fear of movement/(re)injury.81 The term kinesiophobia refers to an excessive, irrational, and debilitating fear of physical movement and activity resulting from a feeling of vulnerability to painful injury or re-injury. Using the knee extension–flexion unit (KEF, Cybex 350 system) Crombez et al.82 found a significant association between performance level and pain-related fear, but no relationship between performance and pain intensity in a group of patients with CLBP. They had chosen the knee extension–flexion test specifically because patients believed it put minimal strain on their backs. In a follow-up study utilizing trunk extension–flexion and a weight lifting task, they showed that painrelated fear was the best predictor of behavioral performance.83 They felt the study also supported the idea that pain-related fear is more disabling than pain itself. These studies provide evidence that painrelated fear is associated with escape/avoidance of physical activities, resulting in poor behavioral performance. Somewhat surprising then are the results of Wittink et al.84 who performed a maximal symptom-limited modified treadmill test in patients with CLBP. The Short Form - 36 mental health (MH) scale results were correlated with results from treadmill testing. The results showed that the reason to stop testing and time walked on the treadmill were determined by pain intensity increase and not by low mental health. Although patients with low mental health were more likely than patients with high mental health to stop testing because of pain, the results did not reach statistical significance. How pain-related fear affects daily activities and the development of disability has been studied as well. Waddell et al.85 developed the Fear-Avoidance Beliefs Questionnaire (FABQ) in 1993. It was developed based on theories of fear and avoidance behavior and focused specifically on patients' beliefs about how physical activity and work affected their low back pain. The FABQ is a self-report questionnaire of 16 items where each is answered on a seven-point Likert scale from strongly disagree to strongly agree. Answer analysis indicated a two-factor structure. Factor 1 (FABQ1) concerns fear-avoidance beliefs about the relationship between low back pain and work while Factor 2 (FABQ2) concerns fear-avoidance beliefs about physical activity in general. The two main findings of this study were: first, there was little direct relationship between pain and disability; and the second main finding is the strength of the relationship between fear-avoidance beliefs about work and both work loss and disability in activities of daily living. Waddell et al. concluded that ‘fear of pain and what we do about it is more disabling than the pain itself.’ In a study comparing people matched for pain intensity and duration, fear-avoidance beliefs were found to be an important factor discriminating people with considerable 1217
Part 3: Specific Disorders
sick leave from those with no sick leave.86 Vlaeyen et al.74 have shown that fear of movement (re)injury is a better predictor of selfreported disability levels as measured with the Rowland Disability Questionnaire than either via medical findings or pain intensity levels. Disability was most strongly correlated with the more specific pain-related fear measures as compared to more general measures of anxiety.87 Verbunt et al.88 were able to show that a fear of injury correlated significantly with disability as measured with the Roland Disability Questionnaire. They found no statistically significant association between disability and aerobic fitness or fear of injury and aerobic fitness. Thus, while fear of injury correlated with disability, they were unable to demonstrate that fear of injury leads to physical deconditioning. Prospective studies have attempted to address whether fearavoidance beliefs are a precursor to chronic pain or a consequence of the pain. Work by Klenerman et al.89 supports the idea that pain-related fear is a precursor of disability. In a large prospective cohort study, Linton et al.90 observed that individuals who scored above the median score on a modified version of the FABQ had twice the risk of having an episode of pain during the following year. While not a prospective study, Fritz et al.91 showed that fearavoidance beliefs were present in some patients with acute low back pain of less than 3 weeks' duration. The presence of these beliefs did not explain a significant amount of the variability in the initialdisability levels; however, they were significant predictors of 4-week disability and work status. In a prospective study of 252 patients presenting with low back pain in an effort to isolate risk factors for the development of chronic pain the results did not support the fear-avoidance concept as such a risk factor.92 The information from these studies suggests that there is a subgroup of patients with fear-avoidance beliefs prior to an injury or who develops the beliefs shortly thereafter. Evidence presented in this section suggests that pain-related fear leads to poor physical performance and that these effects also extend to activities of daily life including those in the workplace. In addition, fear-avoidance beliefs may be an important predictor of who may go on to develop chronic low back pain or as a predictor of who is at risk for a pain episode. Fear of injury/re-injury has been shown to correlate significantly with disability. Other psychosocial variables such as distress, depression, and anxiety have been mentioned in the deconditioning syndrome and have been studied in the presence of CLBP. A systematic review of prospective cohort studies in low back pain to evaluate the evidence implicating psychological factors in the development of chronicity in low back pain was recently undertaken by Pincus et al.93 Only six studies met their acceptability criteria for methodology, psychological measurement, and statistical analysis. They concluded that it was not possible to differentiate between psychological distress, depressive symptoms, and depressive mood and therefore chose to use the term distress to represent a composite of these parameters. The most consistent finding was that distress is a significant predictor of unfavorable outcome, particularly in the primary care setting. They also concluded from their review that somatization as well as distress was confirmed as having a role in the progression to chronicity in low back pain. The supporting evidence was felt to be strong for the role of psychological distress/depression and moderate for the role of somatization. They felt the evidence for fear/anxiety is surprisingly scarce in that the single acceptable study that looked at fearavoidance found it had no significant predictive power when analyzed together with other parameters.92 For a group of patients specifically diagnosed with acute radicular pain and a disc prolapse or protrusion, Hasenbring et al.6 looked at various psychological predictors, somatic predictors, and social predictors. Results of multivariate or 1218
regression analysis indicated that depressive mood and specific paincoping strategies are high-risk factors for the development of persistent pain. Relevant coping strategies were extreme tendencies to cope with physical and mental efforts, avoiding behavior on the one hand, extreme tendency to stick it out or to bagatellize on the other, or the nature of communication of the pain experience to others. An example of a maladaptive coping strategy was the tendency toward nonverbal/motoric expressive behavior such as groaning, twisting their faces, or rubbing the painful areas during pain. The extent of disc displacement was the only significant predictor of persistent pain among somatic predictors. Sitting occupation and social status were shown to be high-risk factors of chronicity of pain among the social variables investigated. Polatin et al.94 evaluated 200 patients with CLBP using a structured clinical interview. They reported a 45% point prevalence and a 64% lifetime prevalence of a major depressive episode. They further found that 55% of those who had concurrent major depressive disorder developed it before the onset of the low back pain but 45% became depressed after the onset of their pain.94 In a meta-analysis of studies of chronic pain and depression, 21 of 23 articles related the severity of pain to the degree of depression.95 The authors also concluded that the duration of pain was related to the development of depression in three of three studies of patients with diverse kinds of pain symptoms. They found that depression following the onset of pain was supported in 15 of 15 studies attempting to address this issue but that it preceded the onset of pain in 3 of 13 studies reviewed. Depressed subjects were found to have a reduced work capacity in one study.70 On the other hand, aerobically fit people were found to have reduced psychosocial stress responses in a review of 34 studies on the relationship between physical fitness and stress response.96 Selfreported stress was decreased and scores for subjective health and well-being were improved in 100 healthy police officers following their participation in an aerobic training program which resulted in improved physical fitness.97 Higher levels of physical activity were associated with a better mood, whereas inactive but fit subjects reported a poorer mood than inactive and unfit individuals.98 The authors concluded that the positive relationship between physical activity and mental mood was less mediated by improved fitness and more by participation in the performance of physical activity as a social event. A meta-analysis of the available literature in 1991 concluded that aerobic but not anaerobic exercise was associated with lower levels of anxiety.99 In summary then, it appears that CLBP is associated with increased depression, that depression becomes more common after the onset of pain, and that in the presence of CLBP depression may precede or follow the onset of pain. In addition, it is suggested that an improved level of physical fitness is associated with better mood and less distress while inactivity is associated with increased distress. Depression has been associated with a reduced physical work capacity and a decreased pain tolerance. While treatment is beyond the scope of this chapter and will be covered elsewhere, a brief mention of treatment specifically related to fear-avoidance beliefs seems warranted here. These beliefs and fear of movement/(re-)injury in particular have been shown to be strong predictors of physical performance and pain disability. Given this association, research has begun to be carried out on the effects of treatment specifically aimed at fear-avoidance behaviors. In a small study of six patients Vlaeyen et al.100 showed that improvements in pain-related fear and pain catastrophizing occurred only during a period of exposure in vivo and not during graded activity. Decreases in pain-related fear also concurred with decreases in pain disability and pain vigilance, and an increase in physical activity levels. Further, all
Section 5: Biomechanical Disorders of the Lumbar Spine
improvements remained at 1-year follow-up. Woby et al.101 found that reductions in fear-avoidance beliefs about work and physical activity, as well as increased perceptions of control over pain, were uniquely related to reductions in disability even after controlling for reductions in pain intensity, age, and sex. However, changes in the cognitive factors were not significantly associated with changes in pain intensity in a group of patients with CLBP. In a recent investigation, patients were treated with operant behavioral treatment plus cognitive coping skills treatment or operant behavioral treatment plus group discussion.102 Patients improved with respect to level of depression, pain behavior, and activity tolerance post-treatment and at 12-month follow-up. Treatment also resulted in a short- and long-term decrease in catastrophizing and enhancement of internal pain control. Klaber et al.103 treated patients in an exercise program of eight 1-hour sessions held twice per week designed to encourage movement of the back and strengthen and stretch all the main muscle groups in the body but not focusing on the back. The treatment program also included cognitive–behavioral principles. They compared patients treated with this program versus those allocated to ‘normal general practitioner care.’ High fear-avoiders fared significantly better in the exercise program with behavioral–cognitive principles than in usual general practice care at 6 weeks and 1 year. Those who were distressed or depressed were significantly better off at 6 weeks, but benefits were not maintained at 1 year. In a randomized clinical trial of patients with low back pain of less than 8 weeks' duration, George et al.104 showed that patients who initially had elevated fear-avoidance beliefs appeared to have less disability following fear-avoidance-based physical therapy when compared to those receiving standard physical therapy. However, patients with lower fear-avoidance beliefs appeared to have more disability from fear-avoidance-based physical therapy when compared to those receiving standard physical therapy. The fear-avoidance treatment group also had a significant improvement in fear-avoidance beliefs. There are only a few investigations in this area and conclusions should be drawn cautiously. Given that, it appears as if there is a group of patients possessing fear-avoidance beliefs who may derive greater benefit from treatment programs which address these behaviors.
CONCLUSION It is interesting that when the information available regarding disuse and a deconditioning syndrome in the presence of CLBP is reviewed, a clearer picture does not emerge. Clearly, it has been shown that complete bed rest or immobilization has profound and deleterious affects both physical and psychosocial. Less clear is whether patients with CLBP develop such a condition. With an injury, temporary suppression or cessation of domestic or professional responsibilities may initially be essential to the process of healing. The longer the period of decreased activity or disuse the greater the opportunity to create physical capacity deficits leading to decreased human performance or a deconditioning syndrome. When attempting to objectively confirm the presence of disuse or a decreased level of physical activity, several of the studies reviewed showed no difference between patients with CLBP and matched controls. Methods of activity measurement and working status have been offered as possible explanations for this lack of a discrepancy. If a decreased cardiovascular capacity measured by VO2 max is perceived as the gold standard for deconditioning, the available literature fails to definitively demonstrate its presence in patients with CLBP. Again, work status is proposed as a possible explanation for why results have varied. Muscle atrophy, weakness, and impaired coordination have been demonstrated in the presence of CLBP. As might be expected, there appears to be a significant role for the
presence of psychosocial issues. Particularly interesting appears to be the role of fear-avoidance beliefs. Whether these beliefs precede or follow the onset of pain is unknown and both scenarios may exist. The presence of such behaviors has been demonstrated in the acute phase (0–4 weeks). Their presence acutely has been associated with increased absenteeism from work later. In addition, a high point prevalence and lifetime prevalence of depression has been reported. Clearly, further research regarding disuse and a deconditioning syndrome in the presence of CLBP is needed. Attempts to define and document their presence in patients with CLBP have lead to inconclusive results.
References 1. Cats-Baril W. The cost of low back pain. Travelers Insurance Low Back Symposium, St. Louis, 1996. 2. Cats-Baril W, Frymoyer J. Identifying patients at risk of becoming disabled because of back pain: the Vermont rehabilitation engineering center predictive model. Spine 1991; 16:605–607. 3. United States Bureau of Labor Statistics. Survey of occupational injuries and illnesses, 1996, Washington, DC: United States Government Printing Office; 1998:1–56. 4. United States Bureau of Labor Statistics. BLS Issues 1996 Lost-work-time injuries and illnesses survey. American College of Occupational and Environmental Medicine Report 1998; 98–5:6–7. 5. Kottke FJ. The effects of limitation of activity upon the human body. JAMA 1966; 196:117–122. 6. Hasenbring M, Marienfeld G, Kuhlendahl D, et al. Risk factors of chronicity in lumbar disc patients. A prospective investigation of biologic, psychological, and social predictors of therapy outcome. Spine 1994; 19(24):2759–2765. 7. Bortz WM. The disuse syndrome. West J Med 1984; 141:691–694. 8. Mayer TG, Gatchel RJ. In: Functional restoration for spinal disorders; the sports medicine approach. Philadelphia: Lea and Febiger; 1988:8–9. 9. Polatin P, Kinney R, Gatchel R, et al. Psychiatric illness and chronic low back pain: the mind and the spine – which goes first? Spine 1993; 18:66–71. 10. Dietrick JE, Whedon GD, Shor E. Effects of immobilization upon various metabolic and physiologic functions of normal men. Am J Med 1948; 4:3. 11. Saltin B, Blomgvist G, Mitchell JH, et al. Response to exercise after bed rest and after training. Circulation 1968; 38 (Suppl VII):1. 12. Greenleaf JE. Intensive exercise training during bed rest attenuates deconditioning. Med Sci Sports Exerc 1997; 29:207–215. 13. Muller, EA. Influence of training and of inactivity of muscle strength. Arch Phys Med Rehab 1970; 51:449. 14. Schneider VS, McDonald J. Skeletal calcium homeostasis and countermeasures to prevent disuse osteoporosis. Calcif Tissue Int 1984; 36:151. 15. Uhthoff HK, Jaworski ZFG. Bone loss in response to long-term immobilization. J Bone Joint Surg 1978; 60:420–429. 16. Gaber TA, McGlashan KA, Love S, et al. Bone density in chronic low back pain: a pilot study. Clin Rehabil 2002; 16(8):867–870. 17. Verbunt JA, Seelen HA, Vlaeyen JW, et al. Disuse and deconditioning in chronic low back pain: concepts and hypotheses on contributing mechanisms. Eur J Pain 2003; 7:9–21. 18. Young JZ. Effects of use and disuse on nerve and muscle. Lancet 1946; 109–113. 19. Nielens II, Plaghki L. Cardiorespiratory fitness, physical activity level, and chronic pain: are men more affected than women? Clin J Pain 2001; 17:129–137. 20. Protas EJ. Physical activity and low back pain. In: Mitchell M, et al., eds. Pain 1999 an updated review refresher course syllabus. 9th World Congress on Pain. Seattle: IASP Press; 1999:145–152. 21. Verbunt JA, Westerterp KR, Van der Heijden GJ, et al. Physical activity in daily life in patients with chronic low back pain. Arch Phys Med Rehabil 2001; 82: 726–730. 22. Nielens II, Plaghki L. Perception of pain and exertion during exercise on a cycle ergometer in chronic pain patients. Clin J Pain 1994; 10:204–209. 23. Nielens H, Plaghki L. Evaluation of physical adaptation to exercise of chronic pain patients by steptest procedure. Pain Clin 1991; 4:21–25. 24. Schmidt AJ. Persistence behaviour of chronic low back pain patients in treadmill test with false and adequate feedback. Thesis; 1986.
1219
Part 3: Specific Disorders 25. Kremer EF, Block A, Gaylor M. Behavioral approaches to treatment of chronic pain: the inaccuracy of patient self-report measures. Arch Phys Med Rehabil 1981; 62:188–191.
52. Neufer PD, Cistill DL, Fielding MG. Effect of reduced training on muscular strength and endurance in competitive swimmers. Med Sci Sports Exerc 1987; 19:486–490.
26. Brennan GP, Ruhling RO, Hood RS. Physical characteristics of patients with herniated intervertebral lumbar discs. Spine 1987; 12:699–702.
53. Houston ME, Froese EA, Green HA, et al. Muscle performance, morphology, and metabolic capacity during strength training and detraining: a one-leg model. Eur J Appl Physiol 1993; 51:25–35.
27. Schmidt AJ. Performance level of chronic low back pain in patients in different treadmill test conditions. J Psychosom Res 1985; 29:639–645. 28. Van der Velde G, Mierau D. The effect of exercise on percentile rank aerobic capacity, pain, and self-rated disability in patients with chronic low back pain: a retrospective chart review. Arch Phys Med Rehabil 2000; 81:1457–1463. 29. Wittink H, Hoskins MT, Wagner A, et al. Deconditioning in patients with chronic low back pain. Fact or fiction? Spine 2000; 25(17):2221–2228.
55. Mayer TG, Smith SS, Keeley J, et al. Quantification of lumbar function. Part 2: Sagittal plane trunk strength in chronic low-back pain patients. Spine 1985; 10(8):765–772.
30. Battie M, Bigos SJ, Fisher LD, et al. A prospective study of the role of cardiovascular risk factors and fitness in industrial back pain complaints. Spine 1989; 14:141–147.
56. Kishino ND, Mayer TG, Gatchel RJ, et al. Quantification of lumbar function. Part 4: Isometric and isokinetic lifting simulation in normal subjects and low-back dysfunction patients. Spine 1985; 10(10):921–927.
31. Kellett KM, Kellett DA, Nordholm LA. Effects of an exercise program on sick leave due to back pain. Phys Ther 1991; 71:283–290.
57. Coyle EF, Martin WH, Sinacore DR, et al. Time course of loss of adaptations after stopping prolonged intense endurance training. J Appl Physiol 1985; 57:1857–1864.
32. Hurri H, Mellin G, Korhonen O, et al. Aerobic capacity among chronic low back pain patients. J Spinal Disord 1991; 4:34–38. 33. Wittink H, Michel TH, Knich R, et al. Aerobic fitness testing in patients with chronic low back pain; which test is best? Spine 2000; 25:1704–1710.
58. Mujika I, Padilla S. Detraining: loss of training induced physiologic and performance adaptations. Part I: short term insufficient stimulus. Sports Med 2000; 30:79–87. 59. Mujika I, Padilla S. Muscular characteristics of detraining in humans. Med Sci Sports Exerc 2001; 33:1297–1303.
34. Wittink H, Michel TH, Sukiennik A, et al. The association of pain with aerobic fitness in patients with chronic low back pain. Arch Phys Med Rehabil 2002; 83:1467–1471.
60. Holloszy JO, Coyle EF. Adaptations of skeletal muscle to endurance, exercise and their metabolic consequences. J Appl Physiol 1984; 56:831–838.
35. Cady LD, Bischoff DP, O'Connell ER, et al. Strength and fitness and subsequent back injuries in firefighters. J Occup Med 1979; 21(4):269–272.
61. Booth F, Chakravarthy MV. Waging war on physical inactivity: using modern molecular ammunition against an ancient enemy. J Appl Physiol 2002; 93:3–30.
36. Hazard RG, Fenwick JW, Kalisch SM, et al. Functional restoration with behavioral support: a one-year prospective study of patients with chronic low back pain. Spine 1989; 14:157–165.
62. Luoto S, Taimela H, Hurri H, et al. Psychomotor speed and postural control in chronic low back pain patients. A controlled follow-up study. Spine 1996; 15:2621–2627.
37. Houston ME, Bentzen H, Larsen H. Irrelationships between muscle adaptations and performance as studied by training and detraining. Acta Physiol Scand 1979; 105:163–170.
63. Hodges P, Richardson C. Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominus. Spine 1996; 21:2640–2650.
38. Hortobagyi T, Houmard JA, Stevenson JR, et al. The effects of detraining on power athletes. Med Sci Sports Exerc 1993; 25:929–935.
64. Hodges P, Richardson C. Altered trunk muscle recruitment in people with low back pain and upper limb movement at different speeds. Arch Phys Med Rehabil 1999; 80:1005–1012.
39. Coyle EF. Detraining and retention of training-induced adaptations. Sports Sci Exchange 1990; 2:1–5. 40. Larsson L, Ansved T. Effects of long-term physical training and detraining on enzyme histochemistry and functional skeletal muscle characteristics in man. Muscle Nerve 1985; 714–722. 41. Staron RS, Hagerman FC, Hikida RS. The effects of detraining on elite power athletes: a case study. J Neurol Sci 1981; 51:247–257. 42. Hakkinen K, Alen M. Physiologic performance, serum hormones, enzymes and lipids of an elite power athlete during training with and without androgens during prolonged detraining: a case study. J Sports Med 1986; 26:92–100. 43. Hakkinen K, Alen M, Komi PV. Changes in isometric force and relaxation-time, electromyographic and muscle fiber characteristics of human skeletal muscle during strength training and detraining. Acta Physiol Scand 1985; 125:573–585. 44. Amigo N, Cadefau JA, Ferrer I, et al. Effect of summer intermission on skeletal muscle of adolescent soccer players. J Sports Med Phys Fitness 1998; 38:298–304. 45. Dahlstrom M, Esbjornsson M, Jansson E, et al. Muscle fiber characteristics in female dancers during active and an inactive period. Int J Sports Med 1987; 8:84–87. 46. Allen GD. Physiological and metabolic changes with six weeks detraining. Aust J Sci Med Sport 1981; 21:4–9.
65. Rudy TE, Boston JR, Lieber SJ, et al. Body motion patterns during repetitive wheel rotation task. A comparative study of healthy subjects and patients with low back pain. Spine 1995; 20(23):2547–2554. 66. Haines RJ. Effect of bed rest and exercise on body balance. J Appl Physiol 1974; 36:323–327. 67. Danneels LA, Coorevits PL, Cools AM, et al. Differences in electromyographic activity in the multifidis muscle and the iliocostalis lumborum between healthy subjects and patients with sub-acute and chronic low back pain. Eur Spine J 2002; 11:13–19. 68. Cassisi JE, Robinson ME, O'Conner P, et al. Trunk strength and lumbar paraspinal muscle activity during isometric exercise and chronic low-back pain patients and controls. Spine 1993; 18(2):245–251. 69. Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain: a motor control evaluation of transversus abdominis. Spine 1995; 21(22):2640–2650. 70. Sothmann MS, Hart B, Horn TS. Plasma catecholamine response to acute psychological stress in humans: relation to aerobic fitness and exercise training. Med Sci Sports Exerc 1991; 23:860–867. 71. Toda Y, Segal N, Toda T, et al. Lean body mass and body fat distribution in participants with chronic low back pain. Arch Intern Med 2000; 160:3265–3269.
47. Mayer TG, Vanharanta H, Gaetchel RJ, et al. Comparison of CT scan muscle measurements and isokinetic trunk strength in postoperative patients. Spine 1989; 14:33–36.
72. Lethem J, Slade PD, Troup JDG, et al. Outline of a fear-avoidance model of exaggerated pain perceptions. Behav Res Ther 1983; 21:401–408.
48. Gibbons LE, Videman T, Battie MC. Isokinetic and psychophysical lifting strength, static back muscle endurance, and magnetic resonance imaging of the paraspinal muscles as predictors of low back pain in men. Scand J Rehab Med 1997; 29:187–191.
73. Vlaeyen JWS, Kole-Snijders AMJ, Boeren RGB, et al. Fear of movement/(re)injury in chronic low back pain and its relation to behavioral performance. Pain 1995; 62:363–372.
49. Hultman G, Nordin M, Saraste H, et al. Body composition, endurance, strength, cross-sectional area and density of MM erector spinae in men with and without low back pain. J Spinal Disord 1993; 6:114–123.
74. Vlaeyen JWS, Kole-Snijders AMJ, Boeren RGB, et al. The role of fear of movement/(re)injury in pain disability. J Occup Rehabil 1995; 5:235–252.
50. Parkkola R, Rytokoski U, Kormano M. Magnetic resonance imaging of the discs and trunk muscles in patients with chronic low back pain and healthy control subjects. Spine 1993; 18:830–836. 51. Hakkinen K, Komi PV, Tesch PA. Effect of combined concentric and eccentric strength training and detraining on force-time, muscle fiber and metabolic characteristics of leg extensor muscles. Scand J Sports Sci 1981; 3:50–58.
1220
54. Cassisi Je, Robinson ME, O'Conner P, et al. Trunk strength and lumbar paraspinal muscle activity during isometric exercise in chronic low-back pain patients and controls. Spine 1993; 18:245–251.
75. Vlaeyen JWS, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain 2000; 85:317–332. 76. Romano JM, Turner JA. Chronic pain and depression. Does the evidence support relationship? Psychol Bull 1985; 97:311–318. 77. McQuade KJ, Turner JA, Buchner DM. Physical fitness and chronic low back pain. Clin Orthop Rel Res 1988; 233:198–204.
Section 5: Biomechanical Disorders of the Lumbar Spine 78. Harding VR, Williams AC. Activities training: integrating behavioural and cognitive methods with physiotherapy in pain management. J Occup Rehabil 1998; 8(1):47–61.
92. Burton AK, Tillotson KM, Main CJ, et al. Psychosocial predictors of outcome in acute and subchronic low back trouble. Spine 1995; 20:722–728.
79. Murphy D, Lindsay S, Williams A. Chronic low back pain: predictions of pain and relationship to anxiety and avoidance. Behav Res Ther 1997; 35:231–238.
93. Pincus T, Burton KA, Vogel S, et al. A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine 2002; 27(5):E109–E120.
80. McCracken LM, Zayfert C, Gross RT. The pain anxiety symptoms scale: development and validation of a scale to measure fear of pain. Pain 1992; 50:63–67.
94. Polatin PB, Kinney RK, Gatchel RJ. Psychiatric illness and chronic low back pain: the mind and the spine – which goes first? Spine 1993; 18:66–71.
81. Miller RP, Kori SH, Todd DD. The Tampa Scale. Unpublished report, Tampa, FL: 1991.
95. Fishbain DA, Cutler R, Rosomoff HL, et al. Chronic pain-associated depression: antecedent or consequence of chronic pain? A review. Clin J Pain 1997; 13: 116–137.
82. Crombez G, Vervaet L, Lysens R, et al. Avoidance and confrontation of painful, back straining movements in chronic back pain patients. Behav Modification 1998b; 22:62–77.
96. Crews DJ, Landers DM. A meta-analytic review of aerobic fitness and reactivity to psychosocial stressors. Med Sci Sports Exerc 1987; 19:S114–S120.
83. Crombez G, Vlaeyen JWS, Heuts PHTG, et al. Fear of pain is more disabling than pain itself. Evidence on the role of pain-related fear in chronic back pain disability. Pain 1999; 80:329–340.
97. Norris R, Carroll D, Cochrane R. The effects of aerobic and anaerobic training on fitness, blood pressure, and psychological stress and well-being. J Psychosom Res 1990; 34 4:367–375.
84. Wittink H, Rogers W, Gascon C, et al. Relative contribution of mental health and exercise-related pain increment to treadmill test intolerance in patients with chronic low back pain. Spine 2001; 26(21):2368–2374.
98. Thirlaway K, Benton D. Participation in physical activity and cardiovascular fitness have different effects on mental health and mood. J Psychol Res 1992; 36: 657–665.
85. Waddell G, Newton M, Henderson I, et al. A Fear-Avoidance Beliefs Questionnaire (FABQ) and the role of fear-avoidance beliefs in chronic low back pain and disability. Pain 1993; 52:157–168.
99. Petruzello SJ, Landers DM, Hatfield BD, et al. A meta-analysis on the anxiety-reducing effects of acute and chronic exercise. Sports Med 1991; 11: 143–182.
86. Linton SJ, Buer N. Working despite pain: factors associated with work attendance versus dysfunction. Int J Behav Med 1995; 2(3):252–262.
100. Vlaeyen JWS, de Jong J, Geilen, M, et al. The treatment of fear of movement/ (re)injury in chronic low back pain: further evidence on the effectiveness of exposure in vivo. Clin J Pain 2002; 18:251–261.
87. McCracken LM, Gross RT, Aikens J, et al. The assessment of anxiety and fear in persons with chronic pain: a comparison of instruments. Behav Res Ther 1996; 34:927–933. 88. Verbunt JA, Seelen HA, Vlaeyen JW, et al. Fear of injury and physical deconditioning in patients with chronic low back pain. Arch Phys Med Rehabil 2003; 84:1227–1232. 89. Klenerman L, Slad PD, Stanley IM, et al. The prediction of chronicity in patients with an acute attack of low back pain in a general practice setting. Spine 1995; 4:478–484. 90. Linton SJ, Buer N, Vlaeyen JWS, et al. Are fear-avoidance beliefs related to the inception of an episode of back pain? A prospective study. Psychol Health 1999 (in press). 91. Fritz JM, George SZ, Delitto A. The role of fear-avoidance beliefs in acute low back pain: relationships with current and future disability and work status. Pain 2001; 94:7–15.
101. Woby SR, Watson PJ, Roach NK, et al. Are changes in fear-avoidance beliefs, catastrophizing, and appraisals of control, predictive changes in chronic low back pain and disability? Eur J Pain 2004; 8:201–210. 102. Spinhoven P, ter Kuile M, Kole-Snijders AMJ, et al. Catastrophizing and internal pain control as mediators of outcome in the multidisciplinary treatment of chronic low back pain. Eur J Pain 2004; 8:211–219. 103. Klaber Moffett JA, Carr J, Howarth E. High fear-avoiders of physical activity benefit from an exercise program for patients with back pain. Spine 2004; 29(11):1167–1173. 104. George SZ, Fritz JM, Bialosky JE, et al. The effect of a fear-avoidance-based physical therapy intervention for patients with acute low back pain: results of a randomized clinical trial. Spine 2003; 28(23):2551–2560.
1221
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar ■ i: Functional Restoration
CHAPTER
112
Functional Restoration Program Characteristics in Chronic Pain Tertiary Rehabilitation Tom G. Mayer
INTRODUCTION After most surgical and nonoperative primary and secondary treatment approaches have been exhausted, the majority of patients with occupational musculoskeletal disorders have returned to work and decreased their health utilization. Depending on the US state or federal workers’ compensation venue and musculoskeletal area, an average of about 10% of patients persist with workers’ compensation disability 3–4 months postinjury. The range is about 5–25%, with a smaller (but growing) group of patients persisting in ‘perpetual limited duty’ (or partial disability) in conjunction with the recent advocacy for ‘keeping patients on the job.’ In time, unless such patients are unable to return to full duty or significantly modified jobs, they too go on to persistent work adjustment problems with employers and increasing disability behaviors. Certain musculoskeletal disorders have a predilection for becoming chronic disabling problems. Spinal disorders, particularly those affecting the low back, usually beginning as ‘sprains and strains,’ are more highly represented among chronic pain/disability workrelated injuries than other musculoskeletal areas. Upper extremity non-neurocompressive complaints, particularly those termed repetitive motion or cumulative trauma disorders (CTD) also have a higher rate of developing chronicity, and CTD claims are known to be 1.8 times more expensive than non-CTD claims.1–7 By contrast, lower extremity injuries, particularly if they involve fractures, tend to resolve more completely within a usual tissue healing period. In many ways, the more subjective the diagnosis and mechanism of injury, the greater the likelihood of symptom persistence. Chronic spinal disorder (CSD) pain is not merely a function of incomplete healing after injury. Traditional medical efforts to treat and rehabilitate chronic back pain have often been met with poor outcomes. Past failed efforts to identify the source of, or treat, CSDs have resulted in the identification of ‘psychogenic’ or ‘functional’ pain, terms attributed to pain for which no physical substrate could be found and, therefore, for which psychological or ‘nonorganic’ causes were suspected. Back pain has been found to be subject to diverse influences including psychological difficulties (e.g. anxiety, substance use, depression), and social losses (e.g. inability to work, family role changes, financial stresses). Turk and Rudy8 set forth the biopsychosocial model of pain asserting that pain is engendered not only by physical insult, but also by cognitive, affective, psychosocial, and behavioral influences. Based on this biopsychosocial theory, CSD treatment considerations now go beyond the physical source of the pain to consider psychological and socioeconomic variables as well. Much controversy exists regarding the development of chronic pain/disability syndromes after work-related musculoskeletal inju-
ries. A variety of psychosocial host factors, secondary gain and socioeconomic predictors have been variably reported in the literature. Clinicians tend to focus on the nonphysiological aspects of pain persistence, regardless of the diagnosis, because of the reasonable assumption that bones, joints, and soft tissues have healed completely, even if imperfectly, in a finite period of time. While there may be persistent bony malalignment, joint degenerative arthritis or soft tissue scar, these changes are deemed ‘set in stone.’ They may result in some degree of permanent impairment. However, while the majority of injured workers (and a perceived greater percentage of patients without compensation) seem to recover in a timely fashion, a disturbingly large and costly group of chronic disability patients remain disabled and refractory to treatment over a substantial period of time. These patients tend to demand a significant preponderance of indemnity and medical costs, and if followed in most federal social systems for 15–20 years, represent the largest number of patients in every industrialized country who become permanently disabled for the longest periods of time. This is because the average age of workrelated musculoskeletal injury developing permanent disability is in the mid-30s, much earlier than any other diagnostic entity producing such disability (with the possible exception of the much less common psychiatric disorders). For these chronic pain/disability patients, repeated passive therapy, manipulation, or surgical intervention has commonly been tried, but has failed to relieve symptoms and overcome disability. These patients tend to produce the most significant cost to society in terms of medical care, disability payments, and loss of productivity. As such, they provoke a great deal of concern and interest. It is this difficult group of patients, failures of ‘conservative care’ and/or surgery, for whom spinal functional restoration is intended. Economic globalization may create dislocations of local economies. In industrialized countries such as the US, these dislocations cause major shifts in demand for workers in different labor-intensive industries. There are pressures on workers to develop skills to shift jobs within the changing job markets. Industry is incentivized to reject those workers unable to make the transition. There are similar incentives to minimize the appearance of unemployment and job dislocations by ‘disappearing’ less flexible employees from the national economy. When chronic disabling musculoskeletal disorders lead to long-term re-employment problems, employers may find it more convenient to convert them to ‘throwaway workers.’ This creates pressure to compensate such patients with public, rather than private financing. Since the 1960s, Social Security Disability Insurance (SSDI), more recently linked to medical benefits through Medicare, has been provided to such individuals under certain circumstances. There has been a recent exponential growth in acceptance of younger and potentially more able-bodied workers onto this 1223
Part 3: Specific Disorders
national insurance scheme, which was initially intended for retirees. Although musculoskeletal problems have decreased as the reason for acceptance onto SSDI rolls, they remain above 35% of all accepted claims. The combination of musculoskeletal and mental health ‘stress claims,’ which are often intertwined, have become the majority of acceptances onto SSDI. Because of the young age (30–45 years) at which many of these workers are accepted for long-term payments, Social Security actuaries have referred to the problem as one of ‘early, early retirement.’ Current costs are US$100 billion/year for SSDI, up 150% since 1980. There are now nearly 9 million ‘disabled’ preretirement Americans on Social Security, more than double the number in 1980.9 There is huge variance from state to state, with twice as many claims accepted in the disability determination process, and three times as many after the administrative hearing process, in the high-acceptance states (New Hampshire, Maine) compared to lowacceptance states (District of Columbia, Texas). The younger the patient accepted, the more likely there is a musculoskeletal basis, and low back pain is the single largest cause of musculoskeletal disability. With disability payments currently representing 5% of the entire US budget, such payments are becoming an increasing drain on the Social Security funds that were initially intended solely for retirees. Failure of tertiary rehabilitation for chronic occupational spinal disorders leads inevitably to patients departing the employment statistics and transitioning to insurance schemes such as SSDI in ever-increasing numbers. Thus, tertiary rehabilitation becomes the leading prevention strategy against permanent loss of productivity and high social cost in US spinal disorder medical care. Because of the multifactorial and subjective nature of chronic pain, traditional therapy has been less than fully effective in treating and rehabilitating CSD patients. As a result, medical approaches have evolved to accommodate this costly and complex phenomenon. There are several risk factors that can be used to guide the treatment of spinal disorders and pain based on the levels of treatment described below. The severity of the dysfunction must be considered. The severity of a musculoskeletal dysfunction is related more to the patient’s chronicity and level of disability than to the presumed causative event. While diagnoses (e.g. degenerative disc disease, facet arthropathy, disc disruption, segmental instability) may be important in identifying surgically treatable pathology, their relevance fades in chronic pain conditions in which patients have generally failed to respond to invasive procedures, or have been deemed unsuitable for surgery. In addition to the psychological factors, inactivity and disuse may play a major role. They may lead to the deconditioning syndrome, in which the injured spinal region becomes a ‘weak link’ connecting the body’s functional units. Deficits of motion, strength, and endurance interfere with physical performance of otherwise unaffected joints and muscles.10–14 While the need for spine surgery is rarely so imminent that a trial of nonoperative therapy is not indicated, there is often a limited understanding of the levels and purposes of such care as a function of the severity of the problem. No one has yet managed to identify the unique structural ‘pain generator’ in the majority of CSD patients. Description of such a site has eluded basic scientists, surgeons, internists, and psychologists, and probably will continue to do so. The obvious reason for this is that pain is a subjective central experience of multifactorial origin. With the source of the pain deeply submerged and inaccessible to visual inspection (similar to headache and chronic abdominal pain) the spine is subject to diverse influences such as psychological difficulty, social losses, and financial uncertainties. These ‘secondary phenomena’ tend to be ignored by the health provider who has no mechanism available to deal with these problems. As a consequence, a critical part of our understanding of spinal disability is lost. Since interdisciplinary experience is not usually part of most physi1224
cian training, lack of conceptualization and resolution in the area of chronic spinal disability is to be anticipated.
Three levels of nonsurgical care The chronologic severity of a spinal disorder can be used as a guidepost in determining the appropriate level of nonsurgical care, which can be organized into three distinct levels. Primary treatment is intended to address acute cases of back and neck pain, usually encompassing treatment of acute pain from an initial or recurrent event to 8–12 weeks after an incident or pain onset. In the majority of individuals experiencing back pain, pain usually resolves spontaneously within this time frame, accompanied only by passive care directed toward symptom control. Treatment modalities include medication (often narcotics, nonsteroidal antiinflammatories, and muscle relaxants), short periods of bed rest, thermal modalities, electrical stimulation, and manipulation techniques. Primary treatment may be supplemented with low-intensity supervised range of motion (ROM) exercise and education. Secondary treatment applies to those individuals (approximately 20–30%) whose pain persists beyond 2–6 months after the initial pain onset (i.e. beyond a reasonable tissue healing period), and who have not responded to primary treatment. More precisely, patients in the postacute phase of injury (and some postoperative patients) are likely to qualify for secondary nonoperative treatment. The secondary level of treatment is geared mainly toward patient reactivation, providing treatment of medium intensity. This intensity level is based on prevention strategies for managing risk factors for developing disability, deconditioning, and chronicity. The secondary level of treatment includes reactivation therapies that involve exercise and education specifically designed to prevent physical deconditioning. The exercise therapy may be supplemented by spinal injections for nerve irritation not requiring surgical decompression (epidural steroids), trigger point injections, or sacroiliac joint injections.15–17 Facet injections may be provided either for pain of facet origin, known as the facet syndrome, or for segmental rigidity noted on physical examination.18–23 Pharmacologic agents may be useful, but trends are away from habituating medication, such as narcotics and benzodiazepine ‘muscle relaxants,’ towards antiinflammatory medications. Exercise and education is usually provided by physical and/or occupational therapists in treatments lasting 1–3 hours several times weekly. Such treatments may also be supplemented by consultative psychological, case management, and physician services in formal programs; such programs are currently termed work conditioning or work hardening, and may involve daily utilization of 4–8 hours/day. The 5–8% of patients whose CSD pain persists beyond 4–6 months after the initial occurrence, and for whom disability predominates, are considered for referral to the tertiary level of treatment. Tertiary treatment at its best is a physician-directed, intensive, interdisciplinary team approach aimed at overcoming chronic pain and disability. The main goal of tertiary treatment is to ameliorate the permanent impairments and prevent the costly permanent disabilities related to CSDs that are the number one causes of total disability payments to claimants under age 45 for federal (public) or long-term (private) disability insurance schemes. Functional restoration programs are typically organized in a fashion similar to the traditional pain rehabilitation clinic, but these are more diverse and eclectic. The Commission for Accreditation of Rehabilitation Facilities (CARF) has guidelines that can be used as a minimum standard for tertiary care programs, currently termed Interdisciplinary Pain Rehabilitation programs. Because of the wide international reach of CARF, such programs may represent functional restoration for occupational injuries (as discussed in this case), or run the gamut to programs that are
Section 5: Biomechanical Disorders of the Lumbar Spine
most involved in cancer care or are mainly an adjunct to pain physician injection therapies and other palliative procedures. Because tertiary care patients have been shown to have a history of psychosocial, as well as functional, disturbances (e.g. substance abuse, affective disorders, limited compliance), tertiary treatment programs address issues of both physical and psychosocial deterioration. Functional restoration is one mode of tertiary treatment that has arisen in response to the poor outcomes associated with the traditional pain clinic, particularly in occupation CSDs.
and guide treatment. In addition to psychosocial problems originating because of persistent pain and disability, latent psychopathology may also be activated by life disruption produced by pain/disability. As such, psychiatric interventions, including use of psychotropic drugs and detoxification from narcotic and tranquilizer habituation, are helpful. Primary and secondary treatment alone may be ineffective in dealing with these multifactorial chronic dysfunctions, so that programmatic care delivered by an interdisciplinary team is desirable, if available.
The site of the disorders: cervical and lumbar
QUANTIFICATION OF PHYSICAL DECONDITIONING
One further consideration in the provision and qualification of CSD treatment is the site of the pain problem or injury. The lumbar and cervical spine have been associated with 60–75% of all musculoskeletal disability cases, while the thoracic spine is a rare problem area. As a result, pondering the similarities and differences between these spinal areas is important. Both the cervical and lumbar spine are characterized by a 3-joint anatomic complex controlling motion, and serving to maximize mobility while protecting neurologic structures. Thoracic motion is limited by a barrel-like rib/spine complex. There is a similarity in the relative size and stabilization of the cervical and lumbar anatomic structures used to support the different loads of the head or trunk, respectively. Compared to the thoracic spine, the lumbar and cervical areas demonstrate lower stability, higher mobility and a greater reliance on soft tissue support. As a result, individuals with injuries in these two spinal areas seem more likely to develop facet and degenerative disc disease, and show a higher rate of developing disabling symptoms associated with disuse, inactivity, and progressive deconditioning. The cervical and lumbar spinal areas also demonstrate characteristic differences. First, cervical disorders occur less frequently than lumbar ones. This region is also associated with ‘whiplash’ injuries and catastrophic neurological injury not found in the lumbar spine. The injuries to the cervical spinal area pose more of an upper motor neuron risk and are affected by sedentary activities, static positioning (e.g. sitting, writing, driving) and upper extremity activities (e.g. reaching, lifting over shoulder height, etc.). Injuries to the lumbar spinal area are exacerbated by the transmission of heavy loads from the hands through the trunk (e.g. lifting from floor while bending or twisting). Cervical spinal motion occurs in three planes (sagittal/coronal/axial) with biomechanical links to the shoulder, whereas lumbar motion occurs primarily in two planes (sagittal/ coronal) with biomechanical links to hip/pelvis. Understanding of these similarities and differences is a key component in designing and implementing an appropriate rehabilitation strategy for specific spinal disorders. The greatest assessment error for most clinicians is the failure to recognize the critical importance of socioeconomic factors in patients with chronic pain. It has been well established over the years that patients being paid for remaining disabled and nonproductive will behave differently from patients who are uncompensated.24–27 Similarly, patients likely to receive a bonus settlement for permanent impairment, even if they are not receiving direct disability indemnity benefits, will likely demonstrate some illness behaviors. Major Axis I psychiatric diagnoses (DSM-IV), such as substance use (often preexisting or iatrogenically abetted), or major depression, may strongly affect treatment progress and ultimate outcomes.28–30 This is particularly true if the clinician fails to recognize, or ignores, these crucial issues, dealing ‘only with the body and not the mind.’ Various treatment interventions have been designed to cope with the psychosocial and socioeconomic factors involved in total or partial disability. Psychosocial assessment is often necessary to identify these factors
While a normal soft tissue, joint, or bony healing period will generally have occurred by the time a patient enters a period of chronic pain/disability, progressive deterioration of physical and functional capacity may still be in an early stage. Deconditioning occurs as a consequence of disuse and fear-related inhibition. The quantitative assessment of function is a vital aspect of developing an effective treatment program for disabling spinal disorders. In the extremities, there is relatively good visual feedback of physical capacity. Joints are easily seen and mobility subject to goniometric measurements, and the muscle bulk is subject to tape measurements. Right/left comparisons between a normal and abnormal side can frequently be made. In the spine, there is inadequate direct visual feedback of physical capacity. Yet, this deficiency has not been generally recognized by clinicians who often continue to rely on subjective self-report or physical measures that are either inaccurate or irrelevant. More accurate methods are necessary for objective quantification.31–34 This information is discussed in greater detail in another chapter. However, for the focuses of this chapter, the author wishes to illustrate several aspects of quantification of function. In Figure 112.1, one sees the dual inclinometer method being used to measure spinal sagittal motion. In Figure 112.2, sagittal spine strength is being tested. The measurements of localized mobility and strength in the injured spinal region is termed physical capacity as it documents the ‘weak link’ deconditioning of an injured or involved area. This is contrasted with the concept of functional capacity, representing whole-person measurements. For whole-person functional measurements, lifting is
Fig. 112.1 Subject being tested for sagittal flexion utilizing the dual inclinometer method. One inclinometer is placed over T12 while the other is placed over the sacrum. 1225
Part 3: Specific Disorders
Fig. 112.2 A trunk extension/flexion (TEF) testing device used to measure sagittal trunk strength isokinetically and isometrically. Computerized calculations from the measurement dynamometer of torques in foot-pounds are generalized, normalized for effective patient comparisons, by age, gender, and body weight.
a useful tool to assess lumbar (floor-to-waist) and cervical (waistto-shoulder) functional regions. The progressive isoinertial lifting evaluation (PILE) test is a simple and inexpensive way to accomplish such measurement as seen in Figure 112.3A.35–37 Figure 112.3B demonstrates isokinetic and isometric (National Institute of Occupational Safety and Health) lift testing being performed.
PSYCHOSOCIAL AND SOCIOECONOMIC ASSESSMENT In a work environment, when injury is associated with compensation for disability, physical problems are rarely the only factor to be con-
A
sidered in organizing a treatment program. Many psychosocial and socioeconomic problems may confront the patient recovering from a spinal disorder, particularly if inability to lead a productive lifestyle is associated with the industrial injury. The patient’s inability to see a ‘light at the end of the tunnel’ may produce a reactive depression, often associated with anxiety and agitation. The musculoskeletal injury itself may be associated with emotional distress as expressed by rebellion against authority or job dissatisfaction. Poor coping styles associated with reaction to stress or underlying personality disorders may be manifested in anger, hostility, and noncompliance directed at the therapeutic team. Organic brain dysfunction from age, alcohol, drugs, or a supposedly minor head injury, or limited intelligence may produce cognitive dysfunctions that make patients difficult to manage and refractory to education. Many CSDs exist within an occupational ‘disability system.’ Workers’ compensation laws were initially devised to protect workers’ income and provide timely medical benefits following industrial accidents. In return for providing these worker rights, employers were absolved of certain consequences of negligence, generally including cost-capped liability for any injury, no matter how severe, and set by state or federal statute. Unfortunately, certain disincentives to recovery may emerge. One outcome of a guaranteed paycheck, while Temporary Total Disability persists, is that there may be limited incentives for an early return to work. A casual approach to surgical decision-making and rehabilitation may lead to further deconditioning, both mental and physical, making getting well more problematic. Complicating matters even further is the observation that no group (other than the employer) has a verifiable financial incentive to rapidly return patients to productivity. In consequence, an assortment of health professionals, attorneys, insurance companies, and vocational rehabilitation specialists are involved with limited motivation to combat foot-dragging on the disability issue. Early efforts to distinguish between ‘functional’ (nonorganic) and ‘organic’ pain did not meet with success. The complex nature of chronic pain makes it difficult to categorize component factors as purely physical or psychological. Chronic pain must be understood as an interactive, psychophysiological behavior pattern wherein the physical and the psychological overlap. The focus of psychological
B
Fig. 112.3 (A) The progressive isoinertial lifting evaluation (PILE) test uses simple milk cartons, standard-height shelves, and inexpensive weights added to a box with a fixed protocol. (B) A cable lifting device with a dynamometer permitting isometric and isokinetic lift assessment to a full range of motion (or selected ranges) from floor to above shoulder. Again, age, gender, and body weight normalization is common. 1226
Section 5: Biomechanical Disorders of the Lumbar Spine
evaluation of the patient with pain must shift away from ‘functional’ versus ‘organic’ distinctions to the identification of psychological behavioral motivators for each patient. These characteristics impact a patient’s disability and his or her response to treatment efforts. Treatment planning and the prediction of favorable treatment outcome are facilitated by first identifying and then controlling these factors. The assessment goal is to obtain a DSM-IV psychiatric diagnosis, particularly Axis I or II, to assist the interdisciplinary treatment team in understanding and dealing with the preexisting and posttraumatic barriers to recovery. Depression, anxiety, substance use, and stress disorders (Axis I) frequently accompany CSDs, as do preexisting personality disorders (Axis II) and childhood abuse experiences. Socioeconomic factors related to compensation for the injury (or its premature cessation), may be factored in with the variety of problems associated with education, transferable skills or family distress. Multidisciplinary medical treatment may include psychiatric interventions to detoxify and stabilize on psychotropic medication before the interdisciplinary team becomes involved in a treatment approach that requires physical training, education, and counseling as a significant component. Individualizing pain management, stress controls, and education, as well as guidance towards future return to productivity, is a vital outgrowth of the psychosocial assessment.
TERTIARY INTERDISCIPLINARY FUNCTIONAL RESTORATION TREATMENT Sports medicine concepts and physical training The principles of sports medicine have come to be used generally to refer not merely to the rehabilitation of the competitive athlete. Instead, they have been modified to emerge as a conceptual and methodological framework for actively treating all individuals who wish to return to high levels of function. Its component parts are shown in Table 112.1. Much of the initial work was done with extremity injury, but these concepts now involve the spine as well. The physiologic approach to the deconditioning syndrome involves therapeutic exercise to address mobility, strength, endurance, cardiovascular fitness, and agility/coordination. The exercises must progress to involve simulation of customary physical activities to restore task-specific functions. Such exercises must be focused at the specific functional unit that has become deconditioned, and ultimately be generalized to whole-body functions.
Table 112.1: Components of a Functional Restoration Program 1. Quantification of physical capacity and functional capacity 2. Quantification of psychosocial function 3. Reactivation for restoration of fitness 4. Reconditioning of the injured functional unit (weak link) 5. Retraining in multiunit functional task performance 6. Work simulation in common generic tasks 7. Multimodal disability management program 8. Vocational/societal reintegration 9. Formalized outcome tracking 10. Post-treatment fitness maintenance program and monitoring
Dynamic muscle training, which has been shown to be the most efficient method of training, can be employed in CSDs. It involves three basic modes: isotonic, isokinetic, and psychophysical (free weights).38 Isotonic exercises are those in which the same force is applied throughout the dynamic range and is often inappropriately used for exercises in which a changing lever arm actually alters the applied torque. This type of exercise is most often associated with the variable resistance devices, utilizing a cam to equalize muscular demands throughout the dynamic range of motion. Secondary effects of a functional restoration program are also critically important. Physical training appears to have a specific beneficial effect on pain (possibly through increased synthesis of specific neurotransmitters) and has been demonstrated to prevent scarring and adhesions while improving cartilage nutrition. Mobility appears to be the key, which can be done initially through passive and then subsequently through active means. Development of normal to supernormal strength and endurance in muscles acting around a joint may be of benefit in protecting a joint having sustained cartilage damage or instability due to ligamentous incompetence. This development of protective muscular mechanisms is particularly important when a complete return to normal joint architecture can no longer be anticipated. In the early stages of the program, mobility exercise is the most important aspect of physical training. Muscle training requires putting the affected joint (or spinal segment) through a full range of motion to be effective. Endurance training generally accompanies or follows strength training. Stretching of joints as much as possible, sometimes accompanied by use of antiinflammatory medication and/ or corticosteroid injections, is an important first step in the physical rehabilitation process. Yoga-type exercises, with the holding of postures at greater length than many patients are used to, including use of breathing to encourage relaxation, can be an effective tool. It is always a part of lifelong learning as a component of the fitness maintenance program. Strength training is generally done with weight machines. In the functional restoration program at PRIDE (Productive Rehabilitation Institute of Dallas for Ergonomics) the quantification of function using tests described in the previous chapter develops data that are fed into a computer system, which calculates suggested levels of training based on age, gender, body weight, and anticipated activity levels. A stepwise program to increase from the test-determined starting levels, checked periodically with repeat testing, is utilized. In Figure 112.4A, a torso rotation device to strengthen oblique spinal and abdominal musculature is utilized. Figure 112.4B shows a pulldown device for shoulder strength that also affects musculature in the cervical area (paraspinal muscles, trapezii, and scalene muscles). When a fitness maintenance program is developed for patients to continue with what they have learned during their rehabilitation, a Roman chair (Figure 112.4C) may be useful for extensor strengthening of all of the spine muscles from cervical to lumbar area, including the gluteal/hip muscles. In the physical therapy areas, patients train the injured ‘weak link’ area of the spine. This area must be isolated and focused on by the therapists in a supervised environment, because patients are generally inhibited by fear-avoidance or prolonged disuse. Most training devices are therefore specific to a certain injured part of the body (e.g. cervical spine, lumbar spine, knees, etc.). In the occupational therapy area, patients focus on coordinating the injured ‘weak link’ with other body parts to achieve full-person functional activities. The performance of such functional activities predominates, encouraging such capabilities as lifting, bending, reaching, climbing, or twisting. An obstacle course of multiple devices used to demand patient agility in performing functional tasks can be very useful. Figure 112.5A 1227
Part 3: Specific Disorders
B
A
Fig. 112.4 (A) A torso rotation strength device using weight stacks with training levels individualized by patient testing scores, age, gender, and body weight. (B) A shoulder pull-down device is used to help strengthen the neck and shoulder girdle musculature. (C) A Roman chair device can be used at home or in a fitness center to help maintain strength of the spinal extensors and gluteal/hip musculature.
C
A
1228
B
Fig. 112.5 (A) Shows a patient engaged in functional tasks in the occupational therapy gym, combining carrying, lifting, and climbing tasks. (B) Shows patients engaged in upper extremity functional tasks.
Section 5: Biomechanical Disorders of the Lumbar Spine
demonstrates a patient who combines functional tasks, including lifting, carrying, and climbing, with a relatively simple stair device. Figure 112.5B shows wall-mounted devices that can be used to enhance upper extremity motion for patients with cervical CSDs with radicular problems, or associated upper extremity disorders. In the later stages of functional restoration, the occupational therapists supervise a ‘ready room’ allowing actual simulation of work tasks, such as truck driving, clerical work, construction work (carpentry, electrical, plumbing, etc.) and other manual tasks.
patients generally achieve a much higher level of physical and functional capacities, which must be continued in a fitness maintenance program (FMP). The patient is educated on an individualized FMP, based on the training level they have achieved by the program’s conclusion. Follow-up objective physical quantification leads to feedback to the patient on maintenance of physical capacity, which can be correlated with job demands. Relevant pieces of durable medical equipment (DME) (see Fig. 112.4C) or memberships in appropriately equipped fitness centers, may be suggested.
Psychosocial interventions in functional restoration
SUMMARY
The patient undergoing CSD rehabilitation is customarily one who has issues of prolonged disability, associated with longstanding pain. Traditional approaches have focused on ‘pain management’ which is intended to teach patients about coping with pain and modifying self-defeating behaviors. The essential flaw in solely utilizing this approach has been the continued focus on the patient’s self-report of pain, which is ultimately self-serving and unmeasurable. In functional restoration, the physician emphasizes the return to function and the setting of specific goals to achieve this return, recognizing that improved physical capacity, decreased stress and tension, and return of self-esteem and self-confidence will probably reduce the patient’s pain perception. The rehabilitation process itself may be a stressful and physically painful ‘spring training’ experience for the physically and psychologically deconditioned individual. One-half of the program is devoted to education and counseling, and incorporates supportive and inspirational interventions to help the patient to successfully complete rehabilitation.
Individual and group counseling Patients are typically defensive in initial psychological counseling, and resist any interpretation of behavior that does not first acknowledge the validity of their physical complaints. Frustration regarding the pace of training inevitably occurs, making support during the difficult physical and psychological tasks essential, and often takes place on one-on-one individual sessions. In group settings, discussion of difficulties with the process of rehabilitation is encouraged. The use of a ‘buddy system,’ pairing an advanced patient with one who is just getting started, can be helpful. There are group discussions of subjects such as psychological testing, confidentiality, personal responsibility, the work ethic, concerns about returning to work, litigation, fear of pain, and medication/drug use. Depression is presented as a frequent component of chronic pain. Patients are encouraged to discuss their reactions with treatment staff, and are given feedback about their behavior.
Behavioral stress management training Anxiety and accompanying physical tension clearly accentuate the psychophysiological experience of pain. Behavioral stress management is an important component of the treatment program. Biofeedback improves the patient’s ability to relax physically and to gain better self-control over tight and painful muscles. Cognitive behavioral training enables him to relax by gaining control over unwanted thoughts directing his attention away from stressors. Education in stress management teaches him to modulate stress by properly controlled breathing. Group sessions provide discussion of the role of stress in sleep disturbance, stiff joints, tight muscles, and emotional distress, so that patients more clearly understand the importance of a relaxation response when pain and tension increase. The patient’s ultimate socioeconomic outcomes depend on the maintenance of treatment goals. Under treatment supervision,
Chronic spinal disorder pain/disability is a very costly and serious phenomenon in most industrialized countries. Although the majority of individuals will experience back pain in their lifetime, most will see their symptoms remit within a short time. A minority will experience ongoing pain and physical disability well beyond the expected healing time. This minority generates 90% of the cost associated with treating spinal disorders when measured over more than 1–2 decades. Our understanding of CSDs has evolved over the years from a binary classification of pain as either psychogenic or physically based, to a multifactorial model of interlaced phenomena contributing to the pain experience, including biological, social, and psychological influences. As a result of the evolution in our understanding of chronic pain, applicable treatments have also evolved, culminating in the genesis of an eclectic mix of pain clinics across the United States, with treatments geared toward treating the physical substrate of pain as well as addressing psychological and socioeconomic factors. Tertiary treatment is indicated for patients experiencing chronic disability. This level of care involves an intense, interdisciplinary treatment team approach focusing on reestablishing physical function and helping the patient manage the psychological and socioeconomic barriers to recovery. Functional restoration is a form of tertiary treatment which uses objective evaluations of a patient’s physical, functional, and emotional capacity to organize a physician-directed interdisciplinary team-treatment approach whose primary goal is to improve functional status. The functional restoration approach differs from other tertiary chronic pain treatment modalities through an emphasis on physical reconditioning and improved function over the goal of pain relief alone. Traditional chronic pain management programs, however, place pain relief as a primary goal regardless of a patient’s activity level or medication regimen. Patients who fail to respond to both surgical and less invasive levels of nonoperative treatments for CSDs may be referred to functional restoration rehabilitation. In most cases, this is the final level of care before patients reach a medical treatment endpoint, known in most workers’ compensation venues as maximum medical improvement (MMI). This is the point at which all reasonable medical treatments designed to improve or cure the condition have been offered or provided. At this point, it is the patient’s decision whether to return to productivity and decrease health utilization, or to pursue efforts at obtaining compensation for permanent disability through one of the public (SSDI or SSI) or private (LTD) insurance schemes that they may be eligible for. The complex interaction of financial, psychosocial, and physical factors affect the individual’s ultimate decision, and determine the socioeconomic outcomes of a functional restoration program.
References 1. Mayer T, Gatchel R, Polatin P, et al. Outcomes comparison of treatment for chronic disabling work-related upper extremity disorders and spinal disorders. J Occup Environ Med 1999; 41:761–770. 2. Vender M, Kasdan M, Truppa K. Upper extremity disorders: A literature review to determine work-relatedness. J Hand Surg 1995; 20A(4):534–541.
1229
Part 3: Specific Disorders 3. Association of Schools of Public Health/National Institutes for Occupational Safety and Health. Proposed national strategies for the prevention of leading work-related diseases and injures. Part 1 Washington, DC: Association of Schools of Public Health; 1986:19. 4. Bureau of Labor Statistics. Workplace injuries and illnesses in 1994 (USDL Publication No. 95–508). Washington DC: US Department of Labor; 1995. Available: osh/osnr0001.txt 5. Bureau of Labor Statistics. Workplace injuries and illnesses in 1996 (USDL Publication No. 97–453). Washington, DC: US Department of Labor; 1997. Available: osh/osnr0005.txt 6. Brogmus G, Sorock G, Webster B. Recent trends in work-related cumulative trauma disorders of the upper extremities in the United States: An evaluation of possible reasons. J Occup Environ Med 1996; 38(4):401–411. 7. Webster B, Snook S. The cost of compensable upper extremity cumulative trauma disorders. J Occup Med 1994; 36(7):713–727. 8. Turk D, Rudy T. Toward a comprehensive assessment of chronic pain patients. Behavioral Res Ther 1987; 25:237–249. 9. Charting the future of Social Security Disability Programs: the need for fundamental change, Social Security Advisory Board Report. Washington, DC: Congressional Printing Office; January 2001. 10. Beals R. Compensation and recovery from injury. West J Med 1994; 140: 233–237. 11. Keeley J, Mayer T, Cox R, et al. Quantification of lumbar function, part 5: reliability of range of motion measures in the sagittal plane and an in vivo torso rotation measurement technique. Spine 1986; 11:31–35. 12. Kishino N, Mayer T, Gatchel R, et al. Quantification of lumbar function, part 4: isometric and isokinetic lifting simulation in normal subjects and low back dysfunction patients. Spine 1985; 10:921–927. 13. Mayer T, Smith S, Keeley J, et al. Quantification of lumbar function, part 2: sagittal plane trunk strength in chronic low back pain patients. Spine 1985; 10:765–772. 14. Mayer T, Tencer A, Kristoferson S, et al. Use of noninvasive techniques for quantification of spinal range-of-motion in normal subjects and chronic low-back dysfunction patients. Spine 1984; 9:588–595.
21. Mayer T, Gatchel R, Keeley J, et al. A randomized clinical trial of treatment for lumbar segmental rigidity. Spine; In press. 22. Mooney V, Robertson J. The facet syndrome. Clin Orthop 1976; 115:149–156. 23. Schwarzer A, Aprill C, Derby R, et al. Clinical features of patients with pain stemming from the lumbar zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994; 19:1132–1137. 24. Rainville J, Hartigan C, Wright A. The effect of compensation involvement on the reporting of pain and disability by patients referred for rehabilitation of chronic low back pain. Spine 1997; 22:2016–2024. 25. Greenough C, Fraser R. The effects of compensation on recovery from low back injury. Spine 1989; 14:947–955. 26. Hadler N, Carey T, Garrett J. The influence of indemnification by workers’ compensation insurance on recovery from acute backache. Spine 1995; 20:2710–2715. 27. Sanderson P, Todd B, Holt G, et al. Compensation, work status, and disability in low back pain patients. Spine 1995; 20:554–556. 28. Polatin P, Kinney R, Gatchel R, et al. Psychiatric illness and chronic low back pain: The mind and the spine – Which goes first? Spine 1993; 18:66–71. 29. Dersh J, Gatchel R, Polatin P. Chronic spinal disorders and psychopathology: research findings and theoretical considerations. Spine J 2001; 1:88–94. 30. Dersh J, Gatchel R, Polatin P, et al. Prevalence of psychiatric disorders in patients with chronic work-related musculoskeletal pain disability. J Occup Environ Med 2002; 44:459–468. 31. Gatchel R, Mayer T, Hazard R, et al. Functional restoration: Pitfalls in evaluating efficacy [editorial]. Spine 1992; 17:988–995. 32. Hazard R. Spine update: Functional restoration. Spine 1995; 20:2345–2348. 33. Hazard R, Fenwick J, Kalish S, et al. Functional restoration with behavioral support: A one-year prospective study of chronic low back pain patients. Spine 1989; 14:157–165.
15. Benzon H. Epidural steroid injections for low back pain and lumbosacral radiculopathy. Pain 1986; 24:277–295.
34. Mayer T, Gatchel R, Mayer H, et al. A prospective two-year study of functional restoration in industrial low back injury: An objective assessment procedure. JAMA 1987; 258:1763–1767.
16. Dilkem T, Burry H, Grahame R. Extradural corticosteroid injection in management of lumbar nerve root compression. Br Med J 1973; 16:635–637.
35. Mayer T, Barnes D, Nichols G, et al. Progressive isoinertial lifting evaluation, Part I: A standardized protocol and normative database. Spine 1988; 13:993–997.
17. Weinstein SM, Herring SA, Derby R. Epidural steroid injections. Spine 1995; 20:1842–1846.
36. Mayer T, Barnes D, Nichols G, et al. Progressive isoinertial lifting evaluation, Part II: A comparison with isokinetic in a disabled chronic low back pain industrial population. Spine 1988; 13:998–1002.
18. Dreyfuss P, Dreyer S, Herring S. Lumbar zygapophyseal (facet) joint injections. Spine 1995; 20:2040–2047. 19. Jackson R, Jacobs R, Montesano P. Facet injection in low back pain: a prospective statistical study. Spine 1998; 13:966–971.
1230
20. Mayer T, Robinson R, Pegues P, et al. Lumbar segmental rigidity: can its identification with facet injections and stretching exercises be useful? Arch Phys Med Rehabil 2000; 81:1143–1150.
37. Mayer T, Gatchel R, Barnes et al. Progressive isoinertial lifting evaluation: an erratum notice. Spine 1990; 15:5. 38. Eriksson E. Sports injuries of knee ligaments. their diagnosis, treatment, rehabilitation and prevention. Med Sci Sports 1976; 8:133–144.
PART 3
SPECIFIC DISORDERS
Section 5
Biomechanical Disorders of the Lumbar Spine ■ iv: FBSS-Cervical, Thoracic, and Lumbar ■ i: Functional Restoration
CHAPTER
113
Tertiary Rehabilitation Program Outcomes Robert J. Gatchel and Tom G. Mayer
Pain is usually broadly defined as either acute, chronic, or recurrent, depending on its time course.1 Acute pain is often indicative of tissue damage, and it is characterized by momentary intense noxious sensations (i.e. nociception). It serves as an important biological signal of potential tissue/physical harm. Some anxiety may initially be precipitated, but prolonged physical and emotional distress usually is not. Indeed, anxiety, if mild, can be quite adaptive in that it stimulates behaviors needed for recovery, such as the seeking of medical attention, rest, and removal from the potentially harmful situation. As the nociception decreases, acute pain usually subsides. Chronic pain is defined as pain that lasts 6 months or longer, well past the normal healing period one would expect for its protective biological function. Arthritis, back injuries, and cancer can produce chronic pain syndromes and, as the pain persists, it is often accompanied by emotional distress such as depression, anger, and frustration. Such pain can also often significantly interfere with activities of daily living. Recurrent pain refers to intense, episodic pain, reoccurring for more than 3 months. Recurrent pain episodes are usually brief (as are acute pain episodes); however, the reoccurring nature of this type of pain makes it similar to chronic pain in that it is very distressing to patients. Such episodes may develop without a well-defined cause, and then may begin to generate an array of emotional reactions, such as anxiety, stress, and depression/helplessness. Often, pain medication is used to control the intensity of the recurrent pain, but it is not usually helpful in reducing the frequency of the episodes that a person experiences. It should also be noted that, many times, patients find it difficult to distinguish between chronic and recurrent pain. Patients will often present with ‘chronic-like’ symptoms from prolonged episodes of, say, headache or back pain. These do not always fit the description of chronic pain, but are usually persistent and can be as disabling. Of course, the above types of pain require different treatment approaches.2 In discussing back pain rehabilitation, for example, primary care is applied usually to acute cases of pain of limited severity. Basic symptom control methods are utilized in relieving pain during the normal early healing period. Frequently, some basic psychological reassurance that the acute pain episode is temporary, and will soon be resolved, is quite effective. There is now evidence for safety, treatment- and cost-effectiveness of evidence-based guidelines for the management of acute low back pain in primary care.3 Secondary care represents ‘reactivation’ treatment administered to those patients who do not improve simply through the normal healing process. It is administered during the transition from acute (primary) care to the eventual return to work. Such treatment has been designed in order to promote return to productivity before advanced physical
deconditioning and significant psychosocial barriers to returning to work occur. At this phase, more active psychosocial intervention may need to be administered to those patients who do not appear to be progressing. Finally, tertiary care requires an interdisciplinary and intensive treatment approach. It is intended for those patients suffering the effects of physical deconditioning and chronic disability. In general, it differs from secondary treatment in regard to the intensity of rehabilitation services required, including psychosocial and disability management.
THE BIOPSYCHOSOCIAL MODEL OF PAIN Before discussing tertiary care, which is a topic of the present chapter, it is important to first review the underlying theoretical model of pain upon which tertiary rehabilitation is based – the biopsychosocial model of pain. Today, this biopsychosocial model is accepted as the most heuristic perspective to the understanding and treatment of chronic pain disorders.4,5 This model views physical disorders such as pain as the result of a complex and dynamic interaction among physiologic, psychologic, and social factors that perpetuate and may even worsen the clinical presentation. Each individual experiences pain uniquely, as the result of the range of psychologic, social, and economic factors that can interact with physical pathology to modulate that individual’s report of symptoms and subsequent disability. The development of this biopsychosocial approach has grown rapidly during the past decade, and a great deal of scientific knowledge has been produced in this short period of time concerning the best care of individuals with complex pain problems, as well as pain prevention and coping techniques. As Turk and Monarch5 and Gatchel and Maddrey6 have discussed in their comprehensive reviews of the biopsychosocial perspective on chronic pain, people differ significantly in how frequently they report physical symptoms, in their tendency to visit physicians when experiencing identical symptoms, and in their responses to the same treatments. Often, the nature of a patient’s response to treatment has little to do with his or her objective physical condition. For example, White and colleagues7 have noted that less than one-third of all individuals with clinically significant symptoms consult a physician. On the other hand, 30–50% of patients who seek treatment in primary care do not have specific diagnosable disorders!8 Turk and Monarch5 also make the distinction between disease and illness in better understanding chronic pain. The term disease is basically used to define ‘an objective biological event’ that involves the disruption of specific body structures or organ systems caused by either anatomical, pathological, or physiological changes. Illness, in contrast, is generally defined as a ‘subjective experience or self-attribution’ that a disease is present. An illness will produce physical discomfort, 1231
Part 3: Specific Disorders
behavioral limitations, and psychosocial distress. Thus, illness refers to how a sick individual and members of his or her family live with, and respond to, symptoms and disability. This distinction between disease and illness is analogous to the distinction made between pain and nociception. Nociception involves the stimulation of nerves that convey information about tissue damage to the brain. Pain, on the other hand, is a more subjective perception that is the result of the transduction, transmission, and modulation of sensory input. This input may be filtered through a person’s genetic composition, prior learning history, current physiological status, and sociocultural influences. Pain, therefore, cannot be comprehensively assessed without a full understanding of the individual who is exposed to the nociception. The biopsychosocial model focuses on illness, which is the result of the complex interaction of biological, psychological, and social factors. With this perspective, a diversity in pain or illness expression (including its severity, duration, and psychosocial consequences) can be expected. The interrelationships among biological changes, psychological status, and the sociocultural context all need to be taken into account in fully understanding the pain patient’s perception and response to illness. A model or treatment approach that focuses on only one of these core sets of factors will be incomplete. Indeed, the treatment efficacy of a biopsychosocial approach to pain has consistently demonstrated the heuristic value of this model.5
THE BIOPSYCHOSOCIAL APPROACH TO TERTIARY PAIN MANAGEMENT Thus, the biopsychosocial approach to tertiary pain management appropriately conceptualizes pain as a complex and dynamic interaction among physiologic, psychologic, and social factors that often results in, or at least maintains, pain. It cannot be broken down into distinct, independent psychosocial or physical components. Each person also experiences pain uniquely. The complexity of pain is especially evident when it persists over time, as a range of psychological, social, and economic factors can interact with pathophysiology to modulate a patient’s report of pain and subsequent disability. The model utilizes physiologic, biologic, cognitive, affective, behavioral, and social factors, as well as their interplay, when explaining a patient’s report of pain. As will be discussed, there have been a number of reviews that have documented the clinical effectiveness of such interdisciplinary treatment of patients with chronic pain.9–12 Interdisciplinary programs are needed for patients with chronic pain who have complex needs and requirements. One variant of interdisciplinary tertiary pain management programs – functional restoration (FR) – has been comprehensively presented in Chapter 112. It has also been described in detail in a number of publications.13–19 The primary goal of this rehabilitation process is to improve function and deal with any potential psychosocial and economic barriers to attaining this goal. As will be noted, these components are amenable to systematic outcome quantification. Indeed, this FR approach to the treatment of low back pain disability has received increasing attention in recent years because of its documented clinical effectiveness. Research has shown that the FR program, when fully implemented, is associated with substantive improvement in various important societal outcome measures (e.g. return to work and resolution of outstanding legal and medical issues) in chronically disabled patients with spinal disorders in a 6-month follow-up study,20 1-year followup studies,21–26 as well as a 2-year follow-up study.27 For example, in the 2-year follow-up study by Mayer et al.,27 87% of the FR treatment group was actively working at 2 years as compared to only 41% of a nontreatment comparison group. Moreover, about twice as many of the comparison group of patients had both additional spine surgery and unsettled workers’ compensation litigation relative to the treat1232
ment group. The comparison group continued with approximately a fivefold higher rate of patient visits to health professionals and had higher rates of recurrence or reinjury. Thus, the results demonstrate the striking impact that an FR program can have on these important outcome measures in a chronic group consisting primarily of workers’ compensation cases (traditionally the most difficult cases to treat successfully). Finally, it should be noted that the original FR program was independently replicated by Hazard et al.23 in this country, as well as Bendix and Bendix24 and Bendix et al.25 in Denmark, Jousset et al. in France,20 Hildebrandt et al.26 in Germany, and Corey et al.28 in Canada. The fact that different clinical treatment teams, functioning in different states (Texas and Vermont) and different countries, with markedly different economic/social conditions and workers’ compensation systems, produced comparable outcome results speaks highly for the robustness of the research findings and utility, as well as the fidelity, of the FR approach. In addition, Burke et al.29 have demonstrated its efficacy in 11 different rehabilitation centers across 7 states. Hazard30 has also reviewed the overall effectiveness of FR. Thus, the clinical effectiveness of FR has been well documented. Indeed, Gatchel and Turk31 and Turk32 have reviewed both the therapeutic- and cost-effectiveness of interdisciplinary programs, such as functional restoration, for the wide range of chronic pain conditions. One of the hallmarks of FR since its development by Mayer and Gatchel16 has been the objective documentation of outcomes, even before it became a requirement in today’s evidence-based medicine environment.
THE IMPORTANCE OF TREATMENT OUTCOMES EVALUATION As Mayer et al.33 have noted, healthcare costs are continuing to increase at an alarming rate in the United States. Therefore, changes in healthcare policy and demands for improved allocations of health resources have recently placed great pressure on healthcare professionals to provide the most cost-effective treatment for pain syndromes and to validate treatment efficacy. As a result, treatment-outcome monitoring has gained new importance in healthcare. Indeed, as highlighted in an Outcomes Symposium sponsored by the American Orthopedic Association, the current outcomes movement has begun to revolutionize clinical research, with the concomitant increased emphasis on the use of well-validated outcome measures.34 Healthcare professionals are now themselves being monitored to determine the effectiveness of the treatments they provide, as well as patient satisfaction with their treatment. Often, a ‘scorecard’ is maintained by third-party payers to monitor practitioners’ efficacy.1 Healthcare professionals also need to monitor such outcomes for quality assurance purposes. In addition, data are also needed that can provide third-party payers with demonstrations of treatment efficacy. This can be an important marketing strategy to highlight the effectiveness of one’s pain management program. Unfortunately, many healthcare professionals do not have a background in conducting program or treatment evaluations because of the requisite experimental methodology and statistical tools needed for such evaluations. One needs to set up a database with appropriate psychometrically sound measures to use at baseline and follow-up evaluations. Such data then need to be statistically analyzed. Fortunately, there are now templates and reviews available for conducting such evaluations. Flores et al.,35 Gatchel,36 and Mayer et al.37 have provided such overviews. These will be discussed below. Morley and Williams38 have also presented a comprehensive review of how to conduct and evaluate treatment outcome studies.
Section 5: Biomechanical Disorders of the Lumbar Spine
It should also be noted that, at an early point in time, Blanchard39 highlighted six important dimensions that one should consider in evaluating clinical applications and effectiveness of therapeutic modalities, using biofeedback as an example. These same six dimensions would similarly be appropriate for the evaluation of various pain management procedures. These dimensions consist of the following: ● ● ● ● ● ●
The percentage or fraction of the treated patient sample that demonstrated significant therapeutic improvement. The degree of clinical meaningfulness of the therapeutic changes that were obtained. The degree of transfer of changes that were obtained in the clinical setting to the patient’s natural environment. The degree of change in the biopsychosocial response for which the treatment was prescribed. The degree of replicability of the results by different clinicians and clinical sites. The extent and thoroughness of the follow-up data for pain.
Each of these dimensions is important, and should be considered when evaluating the therapeutic effectiveness of any pain management intervention. Finally, in any discussion of treatment outcomes monitoring, clinicians now need to be aware of the HIPAA Privacy Rules. These rules establish patients’ rights concerning the use and disclosure of their healthcare information (including when it is being used for research outcomes purposes). Besides the usual informed consent obtained according to each institution’s review board monitoring the safety of subjects involved in any clinical research trial, an additional HIPAA consent form must also be obtained. Healthcare professionals may order HIPAA Privacy Rules from their specialty organizations. For example, HIPAA for Psychologists can be ordered by going to www.apapractice.org.
REVIEW OF OUTCOME MEASURES The article by Flores and colleagues35 reviewed the three broad categories of measures that have been used to objectively evaluate functional improvement in patients with spinal pain disability: physical, psychological and socioeconomic. Moreover, within each of these three categories, some of the major measures utilized were discussed. This review started with the following folk tale: It was six men of Indostan to learning much inclined Who went to see the Elephant (though all of them were blind) That each by observation Might satisfy his mind. The First approached the Elephant And happening to fall against his broad and sturdy side At once began to bawl: ‘Bless me! but the Elephant is very like a wall!’ The Second, feeling of the tusk, cried, ‘Ho! what have we here, so very round and smooth and sharp? To me ‘tis mighty clear This wonder of an Elephant is very like a spear!’ The Third approached the animal, and happening to take the squirming trunk within his hands Thus boldly up and spake: ‘I see,’ quoth he, ‘the Elephant is very like a snake!’ And so these men of Indostan disputed loud and long Each in his own opinion exceeding stiff and strong Though each was partly in the right, and all were in the wrong”! The Blind Men and the Elephant: An Old Indian Folk Tale, version written by John Godfrey Saxe
Just as the blind men in this folk tale viewed and described the ‘whole,’ or the elephant, in quite different terms, depending on what part of it each measured or touched, so too, may functional measures of improvement might be described quite differently depending on what referent or measure of function one decides to touch or quantify. Indeed, when trying to quantify functional change in spinal disorders, there are three broad categories of measures that have been used – physical, psychological and overt behavior (i.e. observable behaviors such as activities of daily living, return-to-work, etc.). Of course, at first blush, they may not appear to be closely related in describing the ‘whole.’ However, upon more careful scrutiny and analysis, they are merely measuring different parts of a whole person’s functional performance. At the outset, though, it should be clearly noted that these three different categories of measures may not always display high concordance with one another in all situations. Such less than perfect concordance among these behavioral referents of a construct such as function or functional improvement is not, however, unique to the area of spinal disorders or rehabilitation medicine in general. For example, it has long been noted in the psychology literature that self-report, overt behavior, and physiological indices of behavior sometimes show low correlations among one another. Thus, if one uses a self-report measure as a primary index of a construct and compares it to the overt behavior or physiologic index of the same construct, direct overlap cannot automatically be assumed. Moreover, two different self-report indices or physiological indices of the same construct may not be as highly correlated as one would desire (Fig. 113.1). In general, what has often plagued the evaluation arena has been the lack of agreement on the wide variation of measures used to document a construct and changes in that construct. Thus, the literature is full with many different measurement techniques and tests of a construct such as function. Recently, though, the literature has begun to demonstrate which measures of function and functional improvement appear to be most reliable and valid. For example, Mayer et al.40 have reviewed the evaluation process of outcomes associated with FR. Because of the emphasis on the return to productivity inherent in FR, socioeconomic outcomes should be evaluated. Some of these outcomes include work status, healthcare utilization, recurrent injury, etc. Such socioeconomic outcomes will be reviewed in greater detail below. Other less objective outcomes that are used, such as validated psychosocial questionnaires, will also be subsequently discussed.
Fig. 113.1 The often low concordance among and within physical, psychosocial, and overt behavior measures.85 From Gatchel 1998,52 with permission of American Pain Society. 1233
Part 3: Specific Disorders
Table 113.1: Major Categories of Measures that can be used to Document Functional Improvement PHYSICAL MEASURES Range of motion Spine strength Lifting capacity Other tests of human performance capability PSYCHOLOGICAL MEASURES Psychological test measures Self-report measures of pain and disability The clinical interview Clinician rating of overt pain behavior SOCIOECONOMIC MEASURES Work status New health utilization Recurrent injury claim Financial claim resolution
Finally, physical assessment as used by the Productive Rehabilitation Institute of Dallas for Ergonomics (PRIDE) involves the evaluation of many variables (such as range-of-motion, strength lifting, and aerobic capacity), normalized to age, gender, or body mass. Once all of these variables are collected, then pre- to postrehabilitation change can be prospectively monitored in order to document improvement. Flores and colleagues also pointed out two major ‘assumption traps’ that clinicians and researchers need to avoid when considering the best measure of function or functional improvement. First, one cannot assume on an a priori basis that one measure will necessarily be more valid or reliable than another measure. In general, the more objectively quantified the measure, the more likely it can be empirically established as a reliable and valid referent or marker. Second, one cannot assume that a physical measure will always be more objective than self-report or psychological measures. As Rudy and Stacey41 had earlier noted, no matter what the level of accuracy or sophistication of a mechanical device used to collect physiological measures, human interpretation must ultimately be used in the understanding of these findings. Moreover, a patient’s performance during a physical assessment protocol may be greatly influenced by fear of pain or injury, instructional set, motivation, etc. With these caveats in mind, Flores and colleagues provided a comprehensive review of the three broad classes of functional measures, which are presented in Table 113.1.
NORTH AMERICAN SPINE SOCIETY’S COMPENDIUM OF OUTCOME INSTRUMENTS FOR ASSESSMENT AND RESEARCH OF SPINAL DISORDERS With the increased scrutiny of healthcare utilization costs and effectiveness by the Federal government and third-party payers, the North American Spine Society42 felt it important to develop a resource for its membership that provided the most reliable and valid measures to utilize for assessment and research purposes. A guiding principle used in selecting the best measures to include in the Compendium was the following quote by Tukey:43 1234
When the right thing can only be measured poorly, it tends to cause the wrong to be measured well. And it is often much worse to have a good measurement of the wrong thing – especially when, as is so often the case, the wrong thing will IN FACT be used as an indicator of the right thing – than to have a poor measurement of the right thing. With this quotation in mind, the Compendium was developed to avoid the many pitfalls often encountered when attempting to measure the right thing (e.g. functional improvement) with good measurements, those that have been reviewed in the Compendium. Table 113.2 presents a summary of the various measures included in this Compendium. It should also be noted that for more comprehensive reviews of the various measures included in the Compendium, as well as other important works, the following are highly recommended: ACC and the National Health Committee,44 Beurskens et al.,45 Deyo et al.,46 Kopec and Esdaile,47 and Turk and Melzack.48 Some of the questionnaires more commonly used to evaluate pain and disability will be briefly reviewed next.
The Oswestry Low Back Pain Disability Questionnaire The Oswestry Low Back Pain Disability Questionnaire49 is the oldest and most thoroughly researched instrument designed to assess functional status and disability.45,50,51 A strength of the Oswestry is that it possesses strong psychometric properties and has been thoroughly investigated.49,52–60 Moreover, a number of studies have shown the Oswestry to be a very responsive self-report instrument in detecting clinically meaningful change.50,61–66 A possible weakness of the Oswestry, though, are studies suggesting a possible floor effect, such that extremely low scores may not be as accurate as more moderate or high scores.50,52,67 Also, as noted by Kopec,52 the majority of currently available disability indices (including the Oswestry) focus primarily on the physical activities of daily living, with only minimal attention given to psychosocial concerns. In fact, no items on the Oswestry directly inquire about one’s emotional or psychological state, despite the fact that research has indicated that psychological factors play an integral role in the development and maintenance of disability.68,69
The Roland-Morris Disability Questionnaire This questionnaire primarily evaluates a person’s physical abilities, such as dressing, walking, and lifting. The Roland-Morris70 was originally intended to be used for research purposes, but it subsequently was found useful in clinical practice.50 The Roland-Morris was derived from the 136-item Sickness Impact Profile,71 which was developed as a generic health status indicator for use in a variety of chronic diseases, but not specifically for back or musculoskeletal injury.72 While the validity and reliability of the Roland-Morris have been proven over time, the responsiveness of the instrument has been the subject of some scrutiny. In fact, it has been shown to be the least responsive measure to clinically meaningful change when compared to other prominent indices of functional status.47,73 In addition, the Roland-Morris is less sensitive at detecting change when disability is classified as severe, likely a shortcoming that can be attributed to the two-level response format of the questionnaire.47,50
The Million Visual Analog Scale This is a 15-item measure designed to assess disability and physical functioning useful primarily in chronic low back pain disorders. Its visual analog scale provides a simple, easy to understand format that causes little difficulty for patients.74 The instrument has been the
Section 5: Biomechanical Disorders of the Lumbar Spine
Table 113.2: Summary of Outcome Measures Included in the Compendium of Outcome Instruments for Assessment and Research of Spinal Disorders MAJOR BIOPSYCHOSOCIAL MEASURES Range of motion Spine strength Lifting capacity (functional measure) Other tests of human performance capacity Psychological test measures Self-reported measures of pain and disability Clinical interview Clinician rating of overt pain behavior PRETREATMENT TO POST-TREATMENT EFFICACY/OUTCOME MEASURES Range of motion, spine strength, lifting capacity and other tests of human performance capacity Self-report measures of pain and disability Psychological measures monitoring functional improvement Socioeconomic measures Treatment helpfulness Gatchel RJ. 2001.42
focus of few studies since its development and, as a result, very little is known about the Million’s psychometric properties outside of the original validation study.53
The SF-36 This is a multipurpose health survey with 36 questions, but was not initially developed with a musculoskeletal pain disability population in mind.75 While it is generally not considered to be a traditional functional status or disability instrument, the SF-36 has been employed as an outcome measure in numerous studies investigating low back pain.62,76,77 Despite the psychometric strengths of the SF-36, its clinical utility as a valuable outcome instrument within the musculoskeletal patient population is uncertain.77 Gatchel and colleagues,77 in an investigation of the SF-36 with a chronically disabled back pain population, found that SF-36 scores demonstrated its utility in documenting group changes over time, but evidenced inadequacies when the instrument was used for individual patient assessment. Furthermore, it was reported that other instruments, such as the Oswestry and the Million Visual Analog Scale, were more useful in providing clinical data on an individual basis. Other studies confirmed these findings.76
Other studies Other less studied indices, such as the Waddell Disability Index78 the Low Back Outcome Score,79 the Quebec Back Pain Disability Scale,52 or the Functional Rating Index,51 show promising beginnings, but have a small research literature relative to the Oswestry and Roland-Morris.45 Furthermore, each primarily assesses activities of daily living, while placing little emphasis on psychosocial factors. Due to the lack of studies investigating these measures, or describing their psychometric properties, an unequivocal statement regarding their utility cannot be made at this point in time.
Pain Disability Questionnaire Finally, one measure developed subsequent to the publication of the Compendium that shows great promise for monitoring change in chronic musculoskeletal disorders is the Pain Disability Questionnaire (PDQ) developed by Anagnostis, Gatchel and Mayer.80 The PDQ was developed as a new measure of functional status. As noted by Anagnostis et al.,80 the measurement of clinical outcomes is an essential element of any musculoskeletal treatment. The PDQ was developed for this purpose, and it yields a total functional disability score ranging from 0 to 150. The focus of the PDQ, much like other health inventories, is primarily on disability and function. Unlike most other measures, however, the PDQ is also designed for the full array of chronic disabling musculoskeletal disorders, rather than purely low back pain alone. Moreover, psychosocial variables, which recent studies have shown to play an integral role in the develop and maintenance of chronic pain disability, formed an important core of the PDQ. The psychometric properties of the PDQ have been found to be excellent, demonstrating stronger reliability, responsiveness, and validity relative to many other existing measures of functional status, such as the Oswestry, Million Visual Analog Scale and SF-36 instruments. In addition, a factor analysis of the PDQ revealed two independent factors that can be evaluated: a functional status component and a psychosocial component. Analyses demonstrated each of these two components to be valid in assessing their theorized constructs.
REVIEW OF OBJECTIVE OUTCOME EVALUATION METHODS Since the development of FR by Mayer and Gatchel,16 its authors have steadfastly held to the belief that the systematic tracking of socioeconomic outcomes was the best approach to documenting the effectiveness of their program. As the approach of FR began to 1235
Part 3: Specific Disorders
receive national and international attention, its authors were routinely approached by other clinical researchers to help in their attempts to objectively evaluate treatment outcomes. In response to these many requests, Mayer and Gatchel published a concise description of their method used at PRIDE.37 Table 113.3 presents the basic dimensions and elements of the objective monitoring of socioeconomic outcomes used in the FR program. In this publication, the ‘nuts and bolts’ of the data collection system are provided, ranging from the actual data coding sheet utilized, to more specific details such as the required structured clinical interviewing skills needed for follow-up evaluations, as well as the best method for tracking patients over a long period of time.
COST-EFFECTIVENESS OF PAIN MANAGEMENT Intimately related to the above reviewed topic of treatment outcomes evaluation is the issue of cost-effectiveness. For example, chronic pain alone is a very expensive healthcare item, with estimates as high as US$125 million annually for healthcare and indemnity costs. Specialized pain management programs are usually expensive, averaging US$8100 for comprehensive treatment programs.81 Thus, if interdisciplinary pain programs are to survive in today’s managed care environment, they will need to demonstrate that they are both clinically effective and cost-effective. Fortunately, there has been systematic evaluations of outcomes related to the issue of cost-effectiveness of interdisciplinary pain management program. For example, Turk and Okifuji82 reported the cost-effectiveness of such programs by calculating differences in pain medication, healthcare utilization, and disability payments. They then compared the outcome of these financial parameters to the most frequently used treatment modalities. Overall, their results demonstrated that pain rehabilitation programs were up to 21 times more cost-effective than alternative treatments such as
surgery. Other publications have also reported such savings.32 It is very worthwhile to provide such scientific data to third-party payers in order to justify the clinical and cost-effectiveness of comprehensive pain management programs. It should also be kept in mind that many treatments for pain involve a wide variety of components delivered in potentially different ways (e.g. individual versus group, inpatient versus outpatient, daily versus weekly), and may also include different healthcare providers. To date, there has been very little research conducted to isolate what features are vitally necessary and sufficient to produce the optimal outcomes. Apparently, third-party payers are insisting that healthcare providers consider cost-effectiveness. The trend for evidence-based medicine requires that we begin to demonstrate the clinical and costeffectiveness of the treatments that are provided.83 In the future, we need to pay better attention to the issue of both what is necessary and also sufficient to produce the best outcomes with specific pain syndromes. As Gatchel and Herring have noted,84 the reasons for monitoring evidence-based outcomes include the following: ●
●
●
To provide objective data to third-party payers in order to document treatment effectiveness. These data can also be used to market the clinical effectiveness of a practice. In order to monitor the quality assurance in one’s own practice. Regular evaluation of treatment outcomes allows the practitioners to ascertain whether there is any ‘slippage’ in the quality of care being provided. For those interested in contributing to the scientific literature, such evidence-based outcomes serve as a foundation for publication or presentation of data at professional meetings.
SUMMARY AND CONCLUSIONS There is now a mandate in today’s evidence-based medicine environment to objectively and reliably monitor treatment outcomes. Fortunately, since its development by Mayer and Gatchel,16 a major
Table 113.3: Major Socioeconomic Outcome Measures used to Evaluate Effectiveness of Functional Restoration RETURN-TO-WORK Work return Work retention (at 1 year) HEALTHCARE UTILIZATION Surgery to injured musculoskeletal area Percentage of patients visiting a new healthcare provider (continued care-and-documentation-seeking behaviors) Number of visits to new healthcare providers RECURRENT (SAME MUSCULOSKELETAL AREA) OR NEW (DIFFERENT AREA) INJURY CLAIMS Percentage with recurrent or new injury claims Percentage with injury claims involving work absence (lost time) CASE CLOSURE Resolution of legal/administrative disputes over permanent partial/total impairment or disability resulting from occupational injury Resolution of related disputes (third-party personal injury or product liability claims) Resolution of financial claims arising from perceived permanent disability (long-term disability, social security disability income, etc.) Mayer TG, Prescott M, Gatchel RJ. 2000.37
1236
Section 5: Biomechanical Disorders of the Lumbar Spine
hallmark of FR has always been objective quantification of psychological and socioeconomic outcomes. This chapter reviewed these data, as well as the actual process through which such monitoring can be achieved. As a preamble to that review, the biopsychosocial perspective of chronic pain was presented, which serves as the cornerstone of interdisciplinary, tertiary rehabilitation programs such as FR. The distinction was made between disease and illness, with the emphasis that, when dealing with chronic pain conditions, a focus should be on the complex interaction of biological, psychosocial, and social factors in order to fully understand the chronic low back pain patient’s perception and response to illness. A model or treatment that focuses on only one of these core sets of factors will be incomplete. The treatment- and cost-effectiveness of the alternative – interdisciplinary FR – has been consistently demonstrated in the scientific literature. Finally, this chapter reviewed the measures that can be used in documenting outcomes.
Acknowledgments The writing of this chapter was supported in part by Grants No. 5R01 MH046452, K05 MH1107 and 5R01 DE010713 (from the National Institutes of Health) and Grant No. DAMD17-03–1-0055 (from the Department of Defense).
References 1. Gatchel RJ, Oordt MS. Clinical health psychology and primary care: practical advice and clinical guidance for successful collaboration. Washington, DC: American Psychological Association; 2003. 2. Gatchel RJ. Psychological disorders and chronic pain: Cause and effect relationships. In: Gatchel RJ, Turk DC, eds. Psychological approaches to pain management: a practitioner’s handbook. New York: Guilford; 1996:33–52. 3. McGuirk B, King W, Govind J, et al. Safety, efficacy and cost-effectiveness of evidence-based guidelines for the management of acute low back pain in primary care. Spine 2001; 26:2615–2622. 4. Gatchel RJ. Clinical essentials of pain management. Washington, DC: American Psychological Association; In press. 5. Turk DC, Monarch ES. Biopsychosocial perspective on chronic pain. In: Turk DC, Gatchel RJ, eds. Psychological approaches to pain management: a practitioner’s handbook. 2nd edn. New York: Guilford; 2002.
16. Mayer TG, Gatchel RJ. Functional restoration for spinal disorders: the sports medicine approach. Philadelphia: Lea & Febiger; 1988. 17. Mayer TG, Gatchel RJ. Functional restoration for chronic low back pain. Part I: quantifying physical function. Pain Manage 1989; 2:67–75. 18. Mayer TG, Mooney V, Gatchel RJ, et al. Quantifying postoperative deficits of physical function following spinal surgery. Clin Orthopaed Related Res 1989; 244: 147–157. 19. Mayer TG, Polatin PB. Tertiary nonoperative interdisciplinary programs: The functional restoration variant of the outpatient chronic pain management program. In: Mayer TG, Gatchel RJ, Polatin PB, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott, Williams & Wilkins; 2000:639–649. 20. Jousset N, Fanello S, Bontoux L, et al. Effects of functional restoration versus 3 hours per week physical therapy: A randomized controlled study. Spine 2004; 29(5):487–493. 21. Mayer TG, Gatchel RJ, Kishino N, et al. Objective assessment of spine function following industrial injury: A prospective study with comparison group and one-year follow-up. Spine 1985; 10:482–493. 22. Mayer TG, Gatchel RJ, Kishino N, et al. A prospective short-term study of chronic low back pain patients utilizing novel objective functional measurement. Pain 1986; 25(1):53–68. 23. Hazard RG, Fenwick JW, Kalisch SM, et al. Functional restoration with behavioral support: A one-year prospective study of patients with chronic low-back pain. Spine 1989; 14:157–161. 24. Bendix T, Bendix A. Different training programs for chronic low back pain – a randomized, blinded one-year follow-up study. Seattle: International Society for the Study of the Lumbar Spine; 1994. 25. Bendix AE, Bendix T, Vaegter K, et al. Multidisciplinary intensive treatment for chronic low back pain: A randomized, prospective study. Cleveland Clin J Med 1996; 63:62–69. 26. Hildebrandt J, Pfingsten M, Saur P, et al. Prediction of success from a multidisciplinary treatment program for chronic low back pain. Spine 1997; 22:990–1001. 27. Mayer TG, Gatchel RJ, Mayer H, et al. A prospective two-year study of functional restoration in industrial low back injury. An objective assessment procedure [published erratum appears in JAMA 1988; 259(2):220]. JAMA 1987; 258(13): 1763–1767. 28. Corey DT, Koepfler LE, Etlin D, et al. A limited functional restoration program for injured workers: A randomized trial. J Occup Rehabil 1996; 6:239–249. 29. Burke S, Harms-Constas C, Aden P. Return to work/work retention outcomes of a functional restoration program: A multi-center, prospective study with a comparison group. Spine 1994; 19:1880–1886. 30. Hazard RG. Spine update: Functional restoration. Spine 1995; 20:2345–2348.
6. Gatchel RJ, Maddrey AM. The biopsychosocial perspective of pain. In: Raczynski J, Leviton L, eds. Healthcare psychology handbook. Washington, DC: American Psychological Association Press; 2004.
31. Gatchel RJ, Turk DC. Interdisciplinary treatment of chronic pain patients. In: Gatchel RJ, Turk DC, eds. Psychosocial factors in pain: critical perspectives. New York: Guilford; 1999:435–444.
7. White KL, Williams F, Greenberg BG. The etiology of medical care. N Engl J Med 1961; 265:885–886.
32. Turk DC. Clinical effectiveness and cost effectiveness of treatment for patients with chronic pain. Clin J Pain 2002; 18:355–365.
8. Dworkin SF, Massoth DL. Temporomandibular disorders and chronic pain: Disease or illness? J Prosthet Dentist 1994; 72(1):29–38.
33. Mayer TG, Gatchel RJ, Polatin PB, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott Williams & Wilkins; 2000.
9. Gatchel RJ. Perspectives on pain: a historical overview. In: Gatchel RJ, Turk DC, eds. Psychosocial factors in pain: critical perspectives. New York: Guilford; 1999: 3–17.
34. Bourne RB, Maloney WJ, Wright JG. An AOA critical issue: The outcome of the outcomes movement. J Bone Joint Surg 2004; 86(A):633–640.
10. Deschner M, Polatin PB. Interdisciplinary programs: chronic pain management. In: Mayer TG, Gatchel RJ, Polatin PB, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott, Williams & Wilkins; 2000:629–637.
35. Flores L, Gatchel RJ, Polatin PB. Objectification of functional improvement after nonoperative care. Spine 1997; 22(14):1622–1633.
11. Wright AR, Gatchel RJ. Occupational musculoskeletal pain and disability. In: Turk DC, Gatchel RJ, eds. Psychological approaches to pain management: a practitioner’s handbook. 2nd edn. New York: Guilford; 2002:349–364.
37. Mayer TG, Prescott M, Gatchel RJ. Objective outcomes evaluation: Methods and evidence. In: Mayer TG, Polatin PB, Gatchel RJ, eds. Occupational musculoskeletal disorders: function, outcomes and evidence. Philadelphia: Lippincott Williams & Wilkins; 2000.
12. Okifuji A. Interdisciplinary pain management with pain patients: Evidence for its effectiveness. Sem Pain Manage 2003; 1:110–119. 13. Gatchel RJ, Mayer TG. Functional restoration for chronic low back pain, part II: Multimodal disability management. Pain Manag 1989; 2:136–140. 14. Gatchel RJ, Mayer TG, Hazard RG, et al. Functional restoration. Pitfalls in evaluating efficacy [editorial] [see comments]. Spine 1992; 17(8):988–995. 15. Kermond W, Gatchel RJ, Mayer TG. Functional restoration for chronic spinal disorders or failed back surgery. In: Mayer TG, Mooney V, Gatchel RJ, eds. Contemporary conservative care for painful spinal disorders. Philadelphia: Lea & Febiger; 1991:473–481.
36. Gatchel RJ. A biopsychosocial overview of pre-treatment screening of patients with pain. Clin J Pain 2001; 17:192–199.
38. Morley S, Williams AdC. Conducting and evaluating treatment outcome studies. In: Turk DC, Gatchel RJ, eds. Psychological approaches to pain management: a practitioner’s handbook. 2nd edn. New York: Guilford; 2002. 39. Blanchard EB. Biofeedback and the modification of cardiovascular dysfunctions. In: Gatchel RJ, Price KP, eds. Clinical applications of biofeedback: appraisal and status. New York: Pergamon Press; 1979. 40. Mayer TG, McGeary D, Gatchel RJ. Chronic pain management through functional restoration for spinal disorders. In: Frymoyer JF, Wiesel S, eds. Adult and pediatric spine. 3rd edn. Philadelphia: Lippincott Williams & Wilkins; 2004.
1237
Part 3: Specific Disorders 41. Rudy TE, Stacey BR. The futility of neglecting physical aspects of disability. Am Pain Soc J 1994; 3:200–203. 42. Gatchel RJ. A compendium of outcome instruments for assessment and research of spinal disorders. LaGrange, IL: North American Spine Society; 2001. 43. Tukey JW. Methodology and the statistician’s responsibility for both accuracy and relevance. J Am Statistical Assoc 1979; 74:786–793. 44. ACC and the National Health Committee. New Zealand Acute Low Back Guide. Wellington, New Zealand: 1997. 45. Beurskens AJ, deVet HC, Koke AJ, et al. Measuring the functional status of patients with low back pain: Assessment of the quality of four disease-specific questionnaires. Spine 1995; 20:1017–1028.
65. Burchiel KJ, Anderson VC, Brown FD. Prospective, multicenter study of spinal cord stimulation for relief of chronic back and extremity pain. Spine 1996; 21: 2786–2794. 66. Tandon V, Campbell F, Ross ERS. Posterior lumbar interbody fusion: association between disability and psychological disturbance in noncompensation patients. Spine 1999; 24:1833–1838. 67. Kopec JA, Esdaile JM, Abrahamowicz M, et al. The Quebec Back Pain Disability Scale: measurement properties. Spine 1995; 20:341–352.
46. Deyo RA, Andersson G, Bombardier C, et al. Outcome measures for studying patients with low back pain. Spine 1994; 19:2032S–2036S.
68. Fordyce WE, Roberts AH, Sternbach RA. The behavioral management of chronic pain: A response to critics. Pain 1985; 22:112–125.
47. Kopec JA, Esdaile JM. Functional disability scales for back pain. Spine 1995; 20(17):1943–1949.
69. Turk DC. Assessment of patients reporting pain: An integrated perspective. Lancet 1999; 353:1784–1788.
48. Turk DC, Melzack R. Handbook of pain assessment. 2nd edn. New York: Guilford; 2001.
70. Roland M, Morris R. A study of the natural history of back pain. Part I: Development of a reliable and sensitive measure of disability and low back pain. Spine 1983; 8:141–144.
49. Fairbanks JC, Couper J, Davies JB, et al. The Oswestry low back pain disability questionnaire. Physiotherapy 1980; 66:271–273. 50. Roland M, Fairbank J. The Roland-Morris disability questionnaire and the Oswestry Disability Questionnaire. Spine 2000; 25:3115–3124. 51. Feise RJ, Menke JM. A new valid and reliable instrument to measure the magnitude of clinical change in spinal conditions. Spine 2001; 26:78–87. 52. Kopec JA. Measuring functional outcomes in persons with back pain. Spine 2000; 25:3110–3114. 53. Ohnmeiss DD. Oswestry back pain disability questionnaire. In: Gatchel RJ, ed. Compendium of outcome instruments for assessment and research of spinal disorders. LaGrange, IL: North American Spine Society; 2000. 54. Triano JJ, McGregor M, Cramer GD. A comparison of outcome measures for use with back pain patients: Results of a feasibility study. J Manip Physiolog Ther 1993; 16:67–73. 55. Gronblad M, Hupli M, Wennerstrand P. Intercorrelation and test–retest reliability of the Pain Disability Index and the Oswestry Disability Questionnaire and their correlation with pain intensity in low back pain patients. Clin J Pain 1993; 9: 189–195.
71. Bergner M, Bobbitt RA, Pollard WE, et al. The Sickness Impact Profile: validation of a health status measure. Med Care 1976; 14:57–67. 72. Deyo RA. Measuring the functional status of patients with low back pain. Arch Phys Med Rehabil 1988; 69:1044–1053. 73. Heijden GJ, Beurskens AJ, Koes BW, et al. Traction for back and neck pain: A randomized clinical trial. Design and results of a pilot study. Physiotherapy 1995; 81:29–35. 74. Von Korff M, Jensen MP, Karoly P. Assessing global pain severity by self-report in clinical and health services research. Spine 2000; 25:3140–3153. 75. Ware JE, Sherbourne CD. The MOS 36-Item Short-Form Health Survey (SF-36). I. Conceptual framework and item selection. Med Care 1992; 30:473–483. 76. Gatchel RJ, Mayer TG, Dersh J, et al. The association of the SF-36 Health Status Survey with one-year socioeconomic outcomes in a chronically disabled spinal disorder population. Spine 1999; 24:2162–2170. 77. Gatchel RJ, Polatin PB, Mayer TG, et al. Use of the SF-36 health status survey with a chronically disabled back pain population: Strengths and limitations. J Occup Rehabil 1998; 8:237–246.
56. Fisher K, Johnson M. Validation of the Oswestry low back pain disability questionnaire, its sensitivity as a measure of change following treatment and its relationship with other aspects of the chronic pain experience. Physiother Theory Pract 1997; 13:67–80.
78. Waddell G, Main CJ. Assessment of severity in low back disorders. Spine 1984; 9:204–208.
57. Leclaire R, Blier F, Fortin L, et al. A cross-sectional study comparing the Oswestry and Roland-Morris Functional Disability Scales in two populations of patients with low back pain of different levels of severity. Spine 1997; 22:68–71.
80. Anagnostis C, Gatchel R, Mayer T. The development of a comprehensive biopsychosocial measure of disability for chronic musculoskeletal disorders: The Pain Dysfunction Questionnaire. Spine; In press.
58. Kaplan GM, Wurtele SK, Gillis D. Maximal effort during functional capacity evaluations; An examination of psychological factors. Arch Phys Med Rehabil 1996; 77:161–164.
81. Marketdata Enterprises I. Chronic Pain Management Programs: A Market Analysis. Valley Stream, NY: Marketdata Enterprises; 1995.
59. Ohnmeiss DD, Vanhanaranta H, Estlander AM, et al. The relationship of disability (Oswestry) and pain drawings to functional testing. Eur Spine J 2000; 9:208–212. 60. Gronblad M, Jarvinen E, Hurri H. Relationship of the Pain Disability Index (PDI) and the Oswestry Disability Questionnaire (ODQ) with three dynamic physical tests in a group of patients with chronic low-back pain and leg pain. Clin J Pain 1994; 10:197–203. 61. Beurskens AJ, deVet HC, Koke AJ. Responsiveness of functional status in low back pain: A comparison of different instruments. Pain 1996; 65:71–76. 62. Taylor SJ, Taylor AE, Foy MA, et al. Responsiveness of common outcome measures for patients with low back pain. Spine 1999; 24:1805–1812. 63. Hazard RG, Bendix A, Fenwick JW. Disability exaggeration as a predictor of functional restoration outcomes for patients with chronic low back pain. Spine 1991; 16:1062–1067.
1238
64. Frost H, Moffett JA, Moser JS, et al. Randomized controlled trial for evaluation of fitness programme for patients with chronic low back pain. Br Med J 1995; 310:151–154.
79. Greenough CG, Fraser RD. Assessment of outcome in patients with low back pain. Spine 1992; 17:36–41.
82. Turk DC, Okifuji A. Treatment of chronic pain patients: Clinical outcomes, costeffectiveness, and cost-benefits of multidisciplinary pain centers. Crit Rev Phys Rehabil Med 1998; 10:181–208. 83. Turk DC, Gatchel RJ. Multidisciplinary programs for rehabilitation of chronic low back pain patients. In: Kirkaldy-Willis WH, Bernard TN Jr, eds. Managing low back pain. 4th edn. New York: Churchill Livingstone; 1999:299–311. 84. Gatchel RJ, Herring SA. Evidenced-based medicine. In: Cole AJ, Herring SA, eds. The low back pain handbook. 2nd edn. Philadelphia: Hanley & Belfus; 2002. 85. Gatchel RJ. Research alert: The need for relevant treatment outcomes. American Pain Society Bulletin 1998; 8:8–11.
PART 4
EXTRA-SPINAL DISORDERS
Section 1
Sacroiliac Joint Syndrome
CHAPTER
Epidemiology and Examination
114
Philip Tasca and Curtis W. Slipman
INTRODUCTION The most current paradigm of interventional spine care admits a multiplicity of potential spine-related sources of axial and appendicular pain. There are 183 anatomic potential sites of spinal pain, including the 23 intervertebral discs, the 50 paired facet joints and most cephalad intervertebral articulations, the 60 paired nerve roots, the 48 paired costovertebral articulations, and the paired sacroiliac joints. The remainder of a myriad of possible symptom generators includes the various ligamentous, tendinous, and supporting structures; the muscles; the various neural elements; and various other interstitial elements. The sacroiliac joints proper represent a solitary pair within this virtual infinitude of potential areas of interest for the interventional spine clinician; moreover, the very fact of their clinical relevance remains controversial. Yet the potential significance of these two structures has been verified by the amount of attention they have received from interested clinicians since they were first ascribed potential clinical importance over a century ago in 1905.1 Confounding factors in the development of rigorous diagnostic and therapeutic guidelines regarding the sacroiliac joints stem not only from the relative numerical minority represented by these articulations and their supporting structures among the spine clinician's vast list of potential painful sites. Variability in epidemiologic and clinically obtainable data also hinders the construction of universally agreed upon clinical pathways and gold standard comparitors. Nevertheless, increasingly detailed anatomic and physiologic data are providing the theoretical foundation for the increasing number of objective clinical observations being made regarding the sacroiliac joints. Armed with these anatomic, physiologic, and clinical facts, the spine clinician may begin to make meaningful assessments and decisions regarding these structures. The validity of such assessments and decisions is the source from which a clinical algorithm draws its success.
EPIDEMIOLOGY Anatomy The anatomic properties of the sacroiliac joints have been well studied, both at the gross and histologic scales. Grossly, the sacroiliac joint is an articulation between the ilium and the sacrum – usually S1–S4 but including the fifth lumbar vertebra up to 5% of the time.2,3 The joint's shape is commonly described as auricular, or L-shaped, with two arms of usually unequal length: the longer arm is dorsocaudally directed, and the shorter arm is dorsocranially oriented.4 The embryologic development of the sacroiliac joint begins in the tenth week and obtains a definitive form by the four month.5 Flat until at least the time of puberty, the articular surfaces eventually become roughened, with numerous and highly variable grooves and protu-
berances on each opposing face.6 In the adult, there is commonly a longitudinal sacral groove at S2 which admits an iliac ridge, although this arrangement may be reversed.4 Gross supporting structures exist anteriorly and posteriorly. Stabilization against anterior motion of the sacral promontory may be aided by the anterior sacroiliac ligament7,8 and the sacrotuberous and sacrospinous ligaments.9,10 Resistance against downward translation of the sacrum may be aided by a posterior structure, the posterior sacroiliac ligament.9 The interosseous ligament, another posterior structure, is thought to be a primary joint stabilizer.10 Anterior and posterior fibrous joint capsule fibers mesh with these structures. In keeping with the somewhat controversial nature of the sacroiliac joint, the histologic characteristics of this structure render strict definitions difficult. The cartilaginous architecture of the sacral and iliac aspects of this joint differ, the sacral face being hyaline with an overall thickness of 1–3 mm, the iliac face composed of columns of fibrocartilage oriented perpendicular to the joint surface and interposed with islands of hyaline cartilage, with a thickness of less than 1 mm.4 The overall histologic architecture of the joint has been postulated to change throughout life, beginning as a diarthrodial joint and progressively losing mobility.6 Further variation is provided by gender: a cadaveric study of 47 specimens by Vleeming found that articular interdigitation was greater in males than in females.11 Thus, the sacroiliac joints have been described as diarthrotic, synarthrotic, and amphiarthrotic.3
Physiology Of physiologic concern is the innervation of the sacroiliac joint, although definitive understanding of this has been elusive. The anterior aspect of the joint is likely innervated by the posterior rami of the L2 through S2 roots, while the posterior portion is likely innervated by the posterior rami of L4 through S3. Innervation is thought to be highly variable, even between two joints in a given individual.12–14 Anterior joint innervation may be further subserved by the obturator nerve, superior gluteal nerve, or the lumbosacral trunk.15,16 Physiologic characterization of the sacroiliac joint, as with all joints, falls under two broad categories: kinetic and kinematic evaluation. The primary kinetic and kinematic considerations of the sacroiliac joints, by definition, involve sacroiliac force transmission and subsequent sacral motion relative to the ilia. In the standing position, superincumbent body weight is associated with an inferiorly directed translatory force acting upon the sacrum.17 An equally important induction of an anteriorly directed rotary force upon the sacral prominence relative to the ilia has been understood since the nineteenth century;18 the axis of this rotary force has been theorized to coincide with the horizontal line connecting the paired iliac tuberosities,2 although other axes of rotation have been postulated, and more than one may exist.19,20 In the standing position these two 1239
Part 4: Extra-Spinal Disorders
forces – one linear and the other rotatory and thus properly termed a torque – should by Newton's first law induce a respective inferior translation and anterior rotation (or flexion, termed nutation) of the sacrum relative to the ilia, unless sacroiliac motion were completely restrained. Likewise, changing positions from standing is accompanied by changes in translatory forces and torques acting on the sacrum, and should therefore induce differing sacral translations and rotations relative to the ilia. The physical parameter that couples the above forces acting on the sacroiliac joint with resultant sacroiliac motion is none other than joint mobility. As sacroiliac mobility has not been well quantified, the effect of sacroiliac kinetics on sacroiliac kinematics has not been well established. The presence of sacroiliac mobility in the pregnant female was suspected by Hippocrates and later by other researchers.2,19 In pregnant women, sacroiliac joint laxity has been quantified using Doppler ultrasound; side-to-side asymmetries in such laxity have been postulated to be associated with pregnancy-related pelvic pain and predictive of postpartum pelvic pain.21 In the nonpregnant patient, however, reported joint range of motion in both the normal and pathologic states varies widely. An early analysis was performed by Mennell, who noted that with a change in position from prone to sitting, the posterior superior iliac spines were displaced apart from each other by 0.5 inch.22 Attempting to verify such sacroiliac motion in normal subjects, Colachis et al. used Kirschner wires to mark bilateral iliac landmarks, and interwire distances were noted in nine different subject positions. Maximal iliac motion was found with trunk flexion from the standing position. The interiliac relationship previously described by Mennell was reversed, however, with greater posterior superior iliac spine approximation found with sitting versus the prone position.19 Subsequent research, in order to maximize sensitivity of detecting sacroiliac motion, has evaluated the extremes of motion about the sacroiliac joint, such as the reciprocal straddle position and other extremes of hip motion. Smidt et al.23 found interinnominate rotation to average 9° around an oblique sagittal axis and 5° around the transverse axis. Similar analyses by Barakatt et al.24 recorded interinnominate motions of up to 36°. Increased detail has been allowed with the use of radiologic studies. In a follow-up cadaveric study utilizing computed tomography, Smidt25 found sagittal sacroiliac motion of up to 17° with hips placed at end-ranges of motion. In contrast to such large values, Sturesson et al., in a roentgen stereophotogrammetric study of 25 individuals diagnosed with sacroiliac disorders, simulated typical motions about the joints and found mean sacral translation of 0.5 mm and usual sacral rotation of less than 3.6°.26 Such minimal amounts of rotation – less than 1.6° – were confirmed by this author in a second study involving six women, five of whom experienced postpregnancy posterior pelvic pain.27 This order of magnitude of rotation echoed similar radiostereometric results obtained by Egund et al.20 The minimal amount of sacroiliac joint mobility described in these latter studies not only contrasts the results of previously noted investigations but also tends to cast doubt on the clinician's ability to detect any related change in joint alignment by physical examination alone. Yet the clinical detectability of sacroiliac joint misalignment has been proposed.28,29
Joint pain Unresolved issues in the anatomic and physiologic characterization of the sacroiliac joint foreshadow the controversy surrounding clinical features associated with putative derangement of this structure. In both historical/epidemiological and clinically observable data, high degrees of variability confound the clinician's ability to reliably diagnose, much less qualify, dysfunction of the sacroiliac joint. The very presence of pain emanating from the sacroiliac joint, the pathologic 1240
factors that cause such pain, the subjective location of such pain, as well as aggravating and alleviating factors, have all been studied to a limited degree, and with limited agreement as to outcome. Pain emanating from the sacroiliac joint may stem from multiple primary and relatively well-defined causes: a list drawing from familiar pathologic categories, such as trauma, infection, tumor, and systemic illness. In the particular case of the sacroiliac joint, these broad categories have been reported specifically as traumatic pelvic ring fracture, intrapartum diastasis, pyarthrosis, metastatic adenocarcinoma, and spondyloarthropathy.12,30,31 Even well-understood pathologies within the sacroiliac joint present with cryptic clinical findings: Bohay reported that in sacroiliac joint pyarthroses the most common symptom and sign was fever. Other common symptoms were also non-specific, including ipsilateral hip, leg, or buttock pain or low back pain. Physical examination focused on the joint is thought to be helpful in timely diagnosis of a suppurative process, and serial Patrick's and Gaenslen's tests and sacroiliac joint compression (described below) are recommended.31 A separate cause of sacroiliac joint pain, intrinsic to and emanating from the joint itself, has been termed sacroiliac joint dysfunction,12,32 and is postulated to stem from an anatomic derangement of the joint. Attempts have been made to characterize this entity,28,29,33–35 although its existence has not been universally accepted in the allopathic medical literature. Within this same body of literature, further clinical analyses have been undertaken, with tacit understanding of the uncertain nature of the underlying pathology of sacroiliac joint dysfunction. These analyses, which are few in number, range from the direct testing of the most basic clinical hypotheses to more advanced, multivariate evaluations. Borrowing from the model set forth by Dwyer and Aprill,36,37 Fortin et al. attempted to derive sacroiliac joint pain referral maps from asymptomatic volunteers. Ten subjects with no history of prior back pain underwent unilateral contrast injection into the sacroiliac joint. This was followed by analyses of the distribution of subsequently produced pain and hypoesthesia. Delineation of area of hypoesthesia was repeated after infusion of Xylocaine into the joint. Hypoesthesia after instillation of an average of 1.6 mL of contrast was noted to comprise one of three patterns: medial buttock inferior to the posterosuperior iliac spine, this area plus the superior greater trochanter, and this last area plus the superior lateral thigh. Areas of provoked pain were found to coincide with these areas of hypoesthesia. Given that the approach used was believed to minimize needle penetration of adjacent potential pain generators, including ligaments and muscle, it was inferred that these referral patterns were derived solely from the sacroiliac joint itself.38 In a follow-up study, Fortin et al. tested the clinical significance of one of the previously derived pain referral zones. Of 54 consecutive patients referred for treatment of lumbar discogenic or facet pain, 16 were tentatively diagnosed with sacroiliac joint-mediated pain based on pain diagrams that indicated maximal discomfort within a region inferior to the posterosuperior iliac spine. All of these patients subsequently demonstrated concordant pain and sensory changes after provocative instillation of contrast into the sacroiliac joint, confirming the diagnosis. Ten of these patients underwent diagnostic evaluation of the lowest two intervertebral discs and lowest two facet joints ipsilateral to their initial pain, and in all cases these structures were deemed not to be pain generators.39 However, subsequent investigation of 100 subjects with and without sacroiliac joint pain, by Schwarzer et al.,40 called into question the clinical validity of sacroiliac pain reproduction by intra-articular contrast injection. Failure to reproduce pain was noted to have some negative predictive value, while pain reproduction was noted to have little positive predictive value. The gold standard here was
Section 1: Sacroiliac Joint Syndrome
pain reduction with subsequent anesthetic injection into the joint. Comparison of historical features of sacroiliac joint versus nonsacroiliac joint-mediated pain yielded only a single statistically significant distinguishing factor: the presence of groin pain with sacroiliac jointmediated pain. No potentially exacerbating or mitigating factors, such as sitting, standing, walking, flexion, or extension, were found to correlate with the presence or absence of sacroiliac joint pain. Following Schwarzer's use of anesthetic instillation into the joint as the diagnostic gold standard for sacroiliac pain, Dreyfuss et al.12 used this injection technique to compare historical features and physical examination findings in patients with and without sacroiliac joint pain. In a group of 85 patients who had been referred for sacroiliac injection, composite preinjection pain diagrams revealed a solitary factor that distinguished sacroiliac joint mediated pain from nonsacroiliac joint pain: the presence of pain above the L5 dermatome in patients without sacroiliac joint pain. Schwarzer's analysis of potentially exacerbating or mitigating factors was modified slightly and extended greatly to include sitting, standing, walking, lying down, coughing/sneezing, defecation, use of heeled footwear, and job activities. Symptom relief with standing was found to be possibly specific for sacroiliac joint pain, although the statistical significance of this finding was not certain. None of the other factors was found to correlate with the presence or absence of sacroiliac joint pain. A similar lack of predictive value was found on analysis of previous response to a variety of therapeutic modalities, including certain classes of oral medication, physical therapy, manipulation, and certain modalities. In a more focused analysis of pain referral zones, Slipman et al.41 studied 50 patients with sacroiliac pain whose diagnosis was tentatively made by means of physical examination maneuvers and confirmed by fluoroscopically guided sacroiliac joint block. Pretreatment interviews were utilized to localize the patients' pain: buttock pain was found to be the most prevalent area of referred pain, occurring in 94% of patients, followed by lower lumbar (72%), thigh (48%), and lower leg pain (28%). Other painful areas included the foot and ankle as well as the groin, upper lumbar region, and abdomen. The greatest prevalence of buttock pain, followed by a descending prevalence of progressively distal lower extremity pain referral, is reminiscent of the previous results of Fortin et al.38,39 Slipman et al. further noted a statistically significant inverse relationship between patient age and the presence of referred pain distal to the knee. The literature thus far, although rather scant, has already yielded some clinical insight into the nature of sacroiliac joint-mediated pain. Firstly, Schwarzer was able to confirm the very presence of such pain by alleviating this symptom with injection of anesthetic into that joint in patients whose symptoms were not relieved by similar injections into neighboring structures.40 The works of Schwarzer, Fortin, and Slipman served to establish and later validate the use of fluoroscopically guided anesthetic injection as the diagnostic gold standard for sacroiliac joint-mediated pain. Although by no means a gold standard, the pain referral zones presented first by Fortin et al. and later by Slipman et al. are at least foundations on which further clinical analyses may be conducted. Assessing possible reasons for the limited clinical usefulness of pain referral zones in the diagnosis of sacroiliac joint pain, Slipman has noted the complexity and variability of this joint's innervation, possible sclerotomal referral patterns, and the proximity of other potential secondary pain generators activated by primary sacroiliac joint pathology. The sacroiliac joint's complex and incompletely understood innervation, described above, may lead to referred pain in the L2–S3 distribution. Sclerotomal referral indicates pain generated in a structure originating from a given embryonic somite being referred to another structure originating from that same somite. As the osseous structures of the spinal column originate from the ventromedial portion of
their respective somites, and the muscles of the trunk and extremity originate from the corresponding posterolateral portions, sclerotomal, or somatic, referral may include a broad swath of the low back, buttock, and lower extremity. A further confounding factor is the proximity of other potential pain generators that may be directly irritated by a putative derangement in the anatomy or mechanics of the sacroiliac joint. An early study by Yeoman, involving sciatica, hints at such a pathologic mechanism,42 which has been further reported more recently.43 In spite of these inherent obstacles, the current literature points undeniably towards continued refinements in the ability to diagnose sacroiliac joint-mediated symptomatology based on historical and epidemiological factors, even if such refinements include further insight into which factors are not clinically useful. In the authors' experience, the above-cited literature has proved useful in helping to determine whether sacroiliac joint syndrome should be present in the differential diagnosis and the relative rank of this syndrome as a possible diagnosis among others. It has been our clinical experience, however, that not only pain location but other qualitative factors are useful as well. One seemingly specific sign is a history of a ‘clunking’ sound emanating from the sacroiliac region. This sound, which is deep, almost resonant, and reminiscent of crepitus, may be experienced audibly by the patient as well as being felt as a ‘clunking’ sensation emanating from deep within the posterior pelvic area. It is to be distinguished from the higher-pitched ‘clicking’ or ‘popping’ sounds and sensations that commonly emanate from other arthritis joints, including the intervertebral disc. It has been our experience that when asked specifically about this ‘clunking’ sound and sensation, with a minimum of explanation and distinction from other sounds on the part of the examiner, patients with sacroiliac syndrome often admit to such a symptom. We have noted that perhaps an even more specific finding associated with sacroiliac joint syndrome is when the patient describes such ‘clunking’ in detail without first being asked specifically about this symptom. Similarly, patients may note a feeling of ‘instability’ in the pelvis, or note frequent occurrences of a sudden pelvic ‘shifting’ sensation. It has been the author' working hypothesis that ‘clunking,’ ‘instability,’ and ‘shifting’ are all manifestations of minute but abnormal sacroiliac joint motions that can be associated with sacroiliac joint syndrome. All three symptoms, which almost always are noted by the patient to occur unilaterally, are almost invariably associated with ipsilateral pain. Yeoman's implication that secondary pain-generating structures may be activated by primary sacroiliac pathology brings to mind a second class of confounding factors in the historical picture of sacroiliac joint dysfunction: other proximate pain generators, unrelated to the sacroiliac joint, which may be the source of symptoms. Each of these extrinsic sources of symptoms has their own associated pain referral pattern; these often overlap the referral zones of the sacroiliac joint. Theoretically, even the most sensitive historical/epidemiologic data set for detecting sacroiliac pain would be of diminished clinical value if specificity were confounded by such external factors. This problem may be mitigated by the standard next step in the clinical algorithm: the physical examination.
PHYSICAL EXAMINATION It is perhaps the increased potential specificity of the physical examination that has led to the greater amount of published research being directed towards this subject rather than towards historical/ epidemiologic data. Such research typically falls under one of two categories: physical findings in sacroiliac joint dysfunction, and provocative maneuvers in sacroiliac joint dysfunction. Along a different axis, studies evaluating physical findings or provocative maneuvers 1241
Part 4: Extra-Spinal Disorders
in sacroiliac joint dysfunction may also be divided another way: those that aim to determine the predictive value of specific clinical tests and those that aim to determine intertester reliability of such tests.
Physical findings The current peer-reviewed literature contains a relative paucity of inquiry into physical findings associated with sacroiliac joint dysfunction. Excluding by definition provocative maneuvers, such findings are limited to findings obtained by pure patient observation, either through visualization or palpation. Visible signs discussed in the extant literature focus mainly on leg length discrepancy theorized to be secondary to asymmetric innominate tilt, as well as asymmetric hip range of motion. Palpable signs are theorized to detect asymmetry of the bony structures about the sacroiliac joint or abnormal sacral–innominate motion with certain patient movements. Table 114.1 summarizes some physical findings that have been reported to be associated with sacroiliac joint dysfunction.
Study of visible and palpable signs has been performed by Potter and Rothstein,44 in which eight physical therapists – medical professionals whose training specifically addresses the palpation of bony structures – examined 17 patients for whom sacroiliac joint dysfunction was in the differential diagnosis. The methodologies of all 13 tests are well known and had been previously published.45 Eleven of the 13 studied were based on palpation of body landmarks of the sacrum and innominate bones plus or minus evaluation of subsequent changes in these landmarks' relationship to each other with positional changes. These evaluations included the standing flexion test (Fig. 114.1), the sitting flexion test (Fig. 114.2), and the Gillet test (Fig. 114.3), described in Table 114.1. Two of the 13 tests were based on symptom provocation (Table 114.2): the supine iliac gapping test attempts to reproduce pain essentially through the examiner pushing the anterior ilia apart while the patient lies supine (Fig. 114.4), and the side-lying iliac compression test would reproduce pain through the examiner pushing the upward-facing ilium medially in the side-lying patient (Fig. 114.5).
Table 114.1: Visible and palpable physical findings in sacroiliac joint syndrome Visible findings Test name
Procedure
Positive when…
External rotation sign – lying*
Patient is asked to lie supine as comfortably as possible.
Most comfortable position attained includes obvious external rotation of the ipsilateral hip. Passive internal rotation diminishes patient comfort.
External rotation sign – standing*
Patient is asked to stand at rest as comfortably as possible.
Most comfortable position attained includes external rotation and flexion of the ipsilateral hip – often supported by a plantarflexed foot.
Prone knee flexion test
Patient lies prone with hips and knees extended, knees are passively flexed to 90°.
One leg is initially shorter, indicating ipsilateral sacroiliac joint dysfunction. Apparent leg lengthening with knee flexion indicates ipsilateral posterior innominate rotation; shortening indicates anterior rotation.
Supine long sitting test
Patient lies supine with legs fully extended; examiner compares relative locations of both medial malleoli. Patient sits up, flexing hips but leaving knees extended.
Relative position of medial malleoli change with sitting up. Apparent leg length increase is due ipsilateral posterior innominate rotation or contralateral anterior innominate rotation. Apparent leg length decrease is due to opposite rotations.
Palpable findings Gillet test
Patient stands at rest; examiner places one thumb under the PSIS and the other thumb on the adjacent S2 tubercle. The patient maximally flexes the ipsilateral hip and knee.
The PSIS under the examiner's thumb does not migrate inferiorly relative to the adjacent S2 tubercle.
Sitting flexion test
Patient sits at rest; examiner palpates bilateral posterior superior iliac spines. Patient bends trunk forward.
There is asymmetry in the motion of the posterosuperior iliac spines, with increased PSIS motion on the side of joint restriction.
Spring test
Patient supine; examiner repeatedly applies downward pressure to the superior sacrum.
Palpably decreased resistance to motion is noted.
Standing flexion test
Patient stands at rest; examiner palpates bilateral posterior superior iliac spines. Patient bends trunk forward.
There is asymmetry in the motion of the posterosuperior iliac spines, with increased PSIS motion on the side of joint restriction.
Standing/sitting iliac crest palpation
Patient stands/sits at rest; examiner palpates bilateral iliac crests.
The iliac crests are of asymmetric heights.
Standing/sitting posterior superior iliac spine palpation
Patient stands/sits at rest; examiner palpates bilateral posterior superior iliac spines.
The posterior superior iliac spines are of asymmetric heights.
*
1242
Denotes findings noted by the authors.
Section 1: Sacroiliac Joint Syndrome
B
A Fig. 114.1 These evaluations included the standing flexion test.
A
B
Fig. 114.2 The sitting flexion test.
A
B
Fig. 114.3 The Gillet test. 1243
Part 4: Extra-Spinal Disorders
Table 114.2: Provocative tests for sacroiliac joint syndrome
1244
Test name
Procedure
Positive with pain in…
Gaenslen's test
Patient supine, one leg with hip and knee maximally flexed, the opposite innominate bone and leg is off of side of examination table with hip extended.
Joint on side off of table.
Patrick's test (FABER test)
Patient prone; examiner passively simultaneously flexes, abducts, and externally rotates hip.
Ipsilateral joint.
Posterior shear test
Patient supine, one leg flexed at hip and knee. Examiner exerts downwards pressure on femur of flexed leg.
Joint on side of flexed hip and knee.
Sacral sulcus pressure
Patient prone; examiner exerts pressure just medial to posterior superior iliac spine.
Ipsilateral joint, namely area of palpation.
Sacral thrust
Patient prone; examiner exerts pressure on sacrum.
Ipsilateral joint.
Side-lying iliac compression test
Patient in lateral decubitus position; examiner applies downward pressure to iliac crest.
Topmost joint.
Supine iliac gapping test
Patient supine; examiner pushes anterior superior iliac spines laterally.
Ipsilateral joint.
Fig. 114.4 The examiner pushing the anterior ilia apart while the patient lies supine.
Fig. 114.5 The side-lying iliac compression test would reproduce pain through the examiner pushing the upward-facing ilium medially in the side-lying patient.
It was theorized that anatomic derangement of either or both sacroiliac joints would be accompanied by palpable static or dynamic changes in the relative positioning of the sacrum and the innominate bones, given the ranges of joint motion described previously. The reproducibility of such measurable changes in position was tested by each patient being evaluated in a blinded fashion by two therapists from a pool of eight, who performed all 13 tests on each patient. It was revealed that none of the testing maneuvers that were based on palpating abnormalities in sacroiliac joint positioning achieved intertester reliability of greater than 50%; all of these tests were thus deemed clinically unreliable by the authors. The two provocative maneuvers, supine iliac gapping and side-lying iliac compression tests, in contrast, achieved 94% and 76% intertester agreement, respectively. Of import, however, is the fact that in this study the intertester reliability was evaluated for each test applied in isolation.
Recognizing that no single physical examination finding or maneuver may be diagnostic of sacroiliac joint dysfunction, Cibulka et al.28 utilized the standing flexion test, the prone knee flexion test, the supine long sitting test, and palpation of the posterior superior iliac spine as a single test battery. Twenty-six patients with non-specific low back pain were evaluated by two examiners, and positive results with three of the four maneuvers was deemed sufficient for diagnosis of sacroiliac joint dysfunction. Intertester agreement analysis revealed a Cohen's kappa value of 0.88, considered to represent excellent clinical agreement.46 A pool of only two examiners, who may have been very familiar with each other's technique, effectively diminishes the clinical utility of this study as it applies to the examination maneuvers themselves, potentially as performed by one or more of a pool of many examiners. More recent analysis of the intertester reliability of four testing maneuvers was performed by Riddle and Freburger47 in which paired
Section 1: Sacroiliac Joint Syndrome
examiners were chosen from a pool of 34. Since the ‘subjects’ in this study are not only the patients but also the examiners with their yield of examination data, this larger number of examiners is theorized to better approximate true clinical circumstances by taking into account real-world variations in examination technique. Sixty-five patients with low back pain were examined via the same four tests used by Cibulka.28 It was found that percentage single-test agreement between the paired examiners was between 44% and 63% depending on which test was used. Agreement that three of four tests were positive was between 60% and 69%. This study's usefulness is bolstered by the larger number of included examiners; however, the quality of the patient population perhaps subtracts from the study's utility, as a possibly low prevalence of sacroiliac joint dysfunction in this population is noted by the authors. Turning attention from intertester reliability and towards test specificity, Dreyfuss et al. evaluated the positivity of sacroiliac joint physical findings in 101 asymptomatic subjects. In this blinded study, in which examiners did not know whether or not subjects were symptomatic, the standing flexion test, seated flexion test, and Gillet test were scrutinized. Overall, 20% of asymptomatic subjects had at least one test maneuver that was positive, with single-test false-positive rates of 13% for the standing flexion test, 8% for the seated flexion test, and 16% for the Gillet test. Overall, female subjects demonstrated more such false-positive results than males.32 Other research has focused on hip range of motion as related to sacroiliac joint dysfunction, instead of specific testing maneuvers. Early work by LaBan noted unilateral limitation in hip abduction and external rotation in the presence of sacroiliac joint inflammation.48 Basing itself on the above-mentioned studies, later work by Cibulka et al.49 noted that in subjects with low back pain not attributable to sacroiliac joint dysfunction passive hip range of motion is generally greater for external rotation than for internal rotation. This disparity was found to be increased in a hip joint ipsilateral to a posteriorly rotated innominate bone. In this research, one examiner performed the four sacroiliac joint examination maneuvers used previously by Cibulka28 and designated three of four positive results to be diagnostic of sacroiliac joint dysfunction. Intratester reliability was measured by repeat assessment with these four tests on a different day – with a kappa value of 0.86. A second examiner obtained goniometric measurements of passive hip external and internal rotation and came to the above-mentioned conclusion. If asymmetry in muscle tone is postulated as the intermediary between sacroiliac joint pathology and asymmetry in hip range of motion, it is debatable whether the asymmetry in muscle tone is the cause or the effect of the sacroiliac joint pathology. On the whole, the existing literature on visible and palpable signs of static or dynamic sacroiliac joint derangement seems to indicate that no single test is very reliable, but that certain batteries of tests may be. Technical limitations of such tests are easily imagined given laboratory literature that reports sacroiliac joint ranges of motion on the order of millimeters of translation and less than 5° of rotation and noting that such small motions are to be palpated through skin, fat, and muscle, or observed in the distal lower extremity where such minute changes in configuration may be easily masked by a myriad of other asymmetries. Perhaps more importantly, demonstration of a test's reliability does not imply the validity of that test for the detection of a particular pathology. Lack of proof of validity represents the primary deficiency in the extant peer-reviewed literature on nonprovocative sacroiliac joint examination maneuvers. This lack of evidence-based visible and palpable signs of sacroiliac joint dysfunction has not discouraged many spine care specialists from, as it were, keeping their eyes open in the hopes of discovering some sign that may prove useful.
One such sign that the authors have noted is the presence of seemingly acute, severe pain, attended by obvious discomfort on the part of the patient. Often the patient will grimace with pain, change from sitting to standing frequently, or shift body weight while sitting or standing. Such an appearance of acute pain is all the more impressive when a history is related of longstanding, or chronic, symptomatology. When asked specifically, the sacroiliac joint syndrome patient will frequently admit to being as acutely uncomfortable as presently for months or even years. It has been the authors' further experience that patients with sacroiliac joint syndrome, on standing, tend to place the majority of their body weight on the contralateral lower limb. More specifically, a stereotypical posture is adopted whereby the ipsilateral limb is externally rotated and the hip flexed, this flexion being maintained and assisted by a plantarflexed foot contacting the floor solely distal to the metatarsal heads (Fig. 114.6). Such a posture is assessed when the patient first stands at rest during the initial phase of our physical examination. If the patient does not stand still on his or her own, perhaps due to discomfort alleviated by constantly shifting weight, he or she is asked to stand still in a way that provides maximal comfort. If the above posture is assumed, it is taken as a relatively specific sign of sacroiliac joint syndrome. A relatively less-specific sign can present if the patient does not assume the above posture when asked to stand comfortably: his or her leg is positioned by the examiner as described above, and the patient is then asked if this provides more or less comfort than had been present when initially standing at rest. If the patient states that standing with the ipsilateral hip flexed and externally rotated does indeed provide some relief, we consider it a sign of relief from sacroiliac joint-mediated pain. To be certain, we often adjust the leg into other positions, such as internally rotated, and query the patient as to any pain relief, which in this latter case should not occur. On sitting, the sacroiliac joint syndrome patient often reduces weight bearing on the side of the lesion, sitting in a contralaterally side-leaning position, sometimes with the ipsilateral buttock entirely off of the chair or examination table. A fourth sign that the authors have noted occurs when the patient lies on the examination table at rest in the supine position with both knees fully extended: the ipsilateral leg is externally rotated when the contralateral hip is in neutral rotation This rotation is more than a few degrees – it is obvious even from a distance (Fig. 114.7). On
Fig. 114.6 The flexion being maintained and assisted by a plantarflexed foot contacting the floor solely distal to the metatarsal heads. 1245
Part 4: Extra-Spinal Disorders
Fig. 114.7 The ipsilateral leg is externally rotated when the contralateral hip is in neutral rotation.
questioning, the patient sometimes will admit to the fact that such external rotation is the usual positioning when lying supine. If the limb is rotated to the neutral position, the patient will admit that this is less comfortable, and may even axially rotate the pelvis contralaterally such that the contralateral leg externally rotates. Conversely and perhaps less specifically, a patient for whom sacroiliac joint syndrome is in the differential diagnosis, if lying supine with both lower limbs neutrally rotated, will often admit to more comfort if the examiner externally rotates the ipsilateral lower limb.
Provocative maneuvers Given the inherent technical limitations of visible and palpable signs of sacroiliac joint dysfunction, another broad category of clinical signs has been described, one that perhaps makes use of the increased subjective sensitivity of the patient to minute internal anatomic derangements that would otherwise go unnoticed by the measurements-from-without described above. These are the provocative maneuvers, designed to reproduce or increase pain emanating from putative pathology within the sacroiliac joint. Like the aforementioned visible and palpable signs of static or dynamic anatomic derangement, these provocative tests have been evaluated with respect to intertester reliability. Moreover, this category of test has found itself being compared to different test methodologies in an attempt to glean not just repeatability but overall validity. More recently, the provocative maneuvers have become the subject of comparison to a newly emerging gold standard: the diagnostic sacroiliac joint injection. Lacking a definitively more accurate method of determining the presence of sacroiliac joint pathology per se, earlier evaluations of provocative maneuvers utilized as a gold standard the more readily diagnosable presence of ankylosing spondylitis. Russell et al.50 prospectively studied just over 100 subjects with low back pain, almost half of whom carried the diagnosis of ankylosing spondylitis based on definite radiologic abnormalities. Provocative maneuvers, in the form of ‘stress tests’ and ‘direct pressure’ tests, were performed. The former category includes Gaenslen's test, in which the supine patient's contralateral hip and knee are flexed and the ipsilateral innominate bone and lower limb hang off the examination table (Fig. 114.8); the sidelying iliac compression test described above; and another test where downward pressure is applied to both ilia in the supine patient. The ‘direct pressure’ tests include direct and forceful palpation over the 1246
Fig. 114.8 Gaenslen's test, in which the supine patient's contralateral hip and knee are flexed and the ipsilateral innominate bone and lower limb hang off the examination table.
sacroiliac joints, the sacrum, or the lower lumbar interspinous areas. Poor correlation was noted between the presence of ankylosing spondylitis and positive examination maneuver results. Along these lines, Blower and Griffin found in a study of 66 low back pain patients that two provocative tests, namely downward bilateral iliac pressure in the supine patient and downward pressure over the inferior sacrum in the prone patient, were each specific for ankylosing spondylitis. More impressive to these authors was the fact that these maneuvers correlated better with the presence of HLA B-27 than with radiologic evidence of ankylosing spondylitis, implying to them that these tests could detect ‘presumptive ankylosing spondylitis’ which does not meet the standard criteria for definitive diagnosis due to insufficient radiologic evidence.51 Assessment of intertester reliability of seven provocative tests was performed by Laslett et al. on 51 patients with low back pain. Tests included the previously described supine iliac gapping test, the sidelying iliac compression test, and Gaenslen's test. Three other tests were assessed as well (see Table 114.2). One was the posterior shear test, in which pressure is transmitted from the examiner through the femur through the flexed hip and into the innominate bone in the supine patient (Fig. 114.9). The sacral thrust test entails direct downward pressure to the sacrum in the prone patient (Fig. 114.10). The cranial shear test involves cranial pressure directed on the sacrum from below the coccyx while the ipsilateral lower limb is pulled in a caudal direction, thus stabilizing the ilium. All examinations were performed by one fixed examiner and another drawn from a pool of five. Paired examinations for all tests demonstrated intertester agreement of at least 78%. Kappa values were lowest for sacral thrust at 0.52 and highest for posterior shear at 0.88. The late 1990s saw the more widespread use in the referred literature of the diagnostic sacroiliac joint block, involving fluoroscopically guided instillation of anesthetic into the joint with subsequent transient symptom relief, become the gold standard for assessing the validity of physical examination provocative maneuvers. Maximizing the presumed ‘gold standard’ status of the diagnostic sacroiliac joint block, Maigne et al. used a double diagnostic block paradigm to more confidently diagnose low back pain as being of sacroiliac origin: 54 patients with symptoms suspicious for sacroiliac joint pathology underwent a fluoroscopically guided
Section 1: Sacroiliac Joint Syndrome
Fig. 114.9 The posterior shear test, in which pressure is transmitted from the examiner through the femur through the flexed hip and into the innominate bone in the supine patient.
Fig. 114.10 The sacral thrust test entails direct downward pressure to the sacrum in the prone patient.
‘screening block’ with instillation into the joint of 2 cc of 2% lidocaine.52 The 19 patients who responded to this injection returned a week later for instillation of 0.5% bupivacaine, a longer-lasting agent that allowed assessment of pain reduction during activities of daily living. Greater than 75% pain relief for at least 2 hours constituted a positive response, present in 10 patients. The following tests were studied: supine iliac gapping, side-lying iliac compression, Gaenslen's, sacral pressure, and Patrick's test. Two other tests included pain provocation with resisted external hip rotation in the prone patient and pressure applied to the pubic symphysis. Unfortunately, this group's emphasis on the assumed value of the diagnostic block was counteracted by their minimal evaluation of the testing maneuvers of interest – response to the double block protocol was compared only to responses to individual tests, a proposition essentially invalidated by Potter and Rothstein.44 Furthermore, the number of examiners is not given; it
is possible that there was only one examiner. Given that the tests themselves are the subject of study, a large number of patients should be accompanied by a large number of examiners to prevent idiosyncratic features of one clinician's examination from skewing the entire data set. A more sophisticated analysis was performed in the previously cited study by Dreyfuss et al.12 Here, 85 patients with low back pain were evaluated in terms of historical features of their symptoms as well as seven provocative maneuvers. These included the Gillet test, the posterior shear test, Gaenslen's maneuver, sacral thrust, and palpation of the sacral sulcus. Another test utilized was Patrick's test, also known as the ‘FABER’ test, in which the ipsilateral hip is passively flexed, abducted, and externally rotated (‘FABER’ is an acronym derived from these three motions). The seventh test, the spring test, involves palpation of motion play at the superior sacrum while the sacrum is pushed in a posteroanterior direction with the patient lying prone. Test results were studied individually and in groups; sacroiliac joint dysfunction was diagnosed based on a stringent 90% symptom reduction with instillation of 1.5 cc lidocaine and 0.5 cc Celestone Soluspan. Intertester reliability was measured between two examiners, a physician and a chiropractor. This was highest, at 87%, for sacral sulcus tenderness, but with a modest associated kappa value of 0.41. The highest kappa value was achieved by the posterior shear test: 0.64, with an associated intertester agreement of 82%. Sacral sulcus tenderness showed the highest individual sensitivity: 0.93 for the physician, 0.84 for the chiropractor. No other test had a sensitivity greater than 0.71 in either clinician's hands. Single-test specificity was even less impressive, never exceeding 0.64 and reaching as low as 0.10 for sacral sulcus tenderness as performed by the physician. Further grouping of tests which were positive for either or both examiners failed to find any particular set of tests that attained clinically useful sensitivity, specificity, or likelihood ratios. The validity of all of the tests was thus called into question, even if intertester reliability was otherwise proven to be good. Slipman et al.41 utilized fluoroscopically guided sacroiliac joint blocks to determine the presence of sacroiliac joint pathology in 50 consecutive patients. Provocative tests studied included Gaenslen's, Patrick's, and Yeoman's tests, pressure application to the sacral sulcus, bilateral pressure to the ilia in the supine patient, side-lying compression, and standing hyperextension. This group concluded that in patients with complaints consistent with sacroiliac joint pathology, including pain over the sacral sulcus, a positive Patrick's test, sacral sulcus pressure test, and at least one more of the other aforementioned provocative tests provided a 60% likelihood of greater that 80% pain relief following a diagnostic sacroiliac joint block with Celestone Soluspan and lidocaine. A positive Patrick's test has been noted by Slipman to include not only ipsilateral pain reproduction but also diminished ipsilateral hip external rotation following flexion and abduction, possibly due to bony block at the sacroiliac joint. These results are in accord with the previous literature utilizing diagnostic blocks to make the definitive diagnosis of sacroiliac joint-mediated pain.
CONCLUSION The peer-reviewed literature of the last two decades bears witness to the conceptual evolution regarding the physical examination of the patient with possible sacroiliac joint-mediated pain. Parameters that were once confidently associated with sacroiliac joint pathology were found to have poor intertester reliability and were discarded. More reproducible tests were sought, and following critical analysis it was found that sets of these tests, not solitary maneuvers, were required to achieve reliability. With the advent of the widespread use 1247
Part 4: Extra-Spinal Disorders
of the diagnostic sacroiliac injection, the question of external validity was brought to the fore. The validity of single tests was again replaced by the validity of test batteries. Finally, the certainty, bordering on hubris, that characterized the initial, misguided ‘common sense approach’50 to the physical examination in putative sacroiliac joint syndrome was slowly replaced by a mood and clinical tenor far more useful to the spine clinician than certainty: humility. And it is because of this humility, not in spite of it, that it is probable that the clinical assessment of sacroiliac joint syndrome will likely continue to make slow but steady progress. Such humility and caution become the spine clinician in almost all endeavors, as our field is still young and much is left to be learned, uncovered, and understood. For now, the sacroiliac joints, though just a pair out of the multitude of structures of interest, still seem to hold a disproportionate amount of mystery and undiscovered secrets within their appropriately gnarled and crevassed walls.
References 1. Goldwaith JH, Osgood RB. A consideration of the pelvic articulations from an anatomical pathological and clinical standpoint. Boston Med Surg J 1905; 152:593–601. 2. Brunner C, Kissling R, Jacob HAC. The effects of morphology and histopathologic findings on the mobility of the sacroiliac joint. Spine 1991; 16:1111–1117. 3. Solonen KA. The sacroiliac joint in the light of anatomical, roentgenological, and clinical studies. Acta Orthop Scand 1957; 27:1–115. 4. Schunke GB. The anatomy and development of the sacro-iliac joint in man. Anat Rec 1938; 72:313–331. 5. Pilatte R, Vignes H. Articulation sacro-iliague (anatomique et physiologie). Le Progrès Medical [Paris] 1919; 34:479–483. 6. Sashin D. A critical analysis of the anatomy and the pathologic changes of the sacroiliac joints. J Bone Joint Surg 1930; 28:891–910. 7. Kirkaldy-Willis WH, Hill RJ. A more precise diagnosis for low back pain. Spine 1979; 4:102–108. 8. Alderink GJ. The sacroiliac joint: review of anatomy, mechanics, and function. J Orthop Sports Phys Ther 1991; 13:71–84. 9. Kapandji IA. The physiology of the joints, vol. 3. New York; Churchill Livingstone: 1974:54–71. 10. Williams PL. In: Warwick R, ed. Grays Anatomy, 36th edn. Philadelphia: WB Saunders; 1980:473–477. 11. Vleeming A, Stoeckart R, Volers ACW, et al. Relation between form and function in the sacroiliac joint, part I: clinical anatomic aspects. Spine 1990; 15:130–136. 12. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in diagnosing sacroiliac joint pain. Spine 1996; 21:2594–2602. 13. Bogduk N. The sacroiliac joint. In: Bogduk N, ed. Clinical anatomy of the lumbar spine and sacrum, 3rd edn. New York: Churchill Livingstone; 1997:177–186. 14. Bernard TN Jr, Cassidy JD. The sacroiliac joint syndrome: pathophysiology, diagnosis, and management. In: Frymoyer JW, ed. The adult spine - principles and practice, 2nd edn. New York: Raven Press; 1997:2343–2366. 15. Russell A, Maksymowych W, LeClerq S. Clinical examination of the sacroiliac joint: a prospective study. Arthritis Rheum 1981; 12:1575–1577. 16. Slipman CW, Sterenfeld EB, Pauza K, et al. Sacroiliac joint syndrome: The diagnostic value of single photon emission computed tomography. ISIS Newsletter 1994; 2:2–20. 17. Hollinshead WH, Jenkins DB. The bony pervis, femur, and hip joint. In: Hollinshead WH, ed. Functional anatomy of the limbs and back, 5th edn. Philadelphia: WB Saunders; 1981:231–240. 18. Slocumb L, Terry RJ. Influence of the sacrotuberous and sacrospinous ligaments in limiting movements at the sacroiliac joint. JAMA 1926; 87:307–309. 19. Colachis SC, Worden RE, Bechtal CO, et al. Movement of the sacroiliac joint in the adult male: a preliminary report. Arch Phys Med Rehabil 1963; 44:490–498. 20. Egund N, Olsson TH, Schmid H, et al. Movements in the sacroiliac joints demonstrated with roentgen sterophotogrammetry. Acta Radiol Diagn 1978; 19:833–846. 21. Damen L, Buyruk HM, Güler-Uysal F, et al. The prognostic value of asymmetric laxity of the sacroiliac joints in pregnancy-related pelvic pain. Spine 2002; 27:2820–2824. 22. Mennell JB. The science and art of joint manipulation, vol. 2. New York: Blakiston; 1952:24–31.
1248
23. Smidt GL, McQuade K, Wei S-H, et al. Sacroiliac kenimatics for reciprocal straddle positions. Spine 1995; 20:1047–1054. 24. Barakatt E, Smidt GL, Dawson JD, et al. Interinnominate motion and symmetry: comparison between gymnasts and nongymnasts. J Orthop Sports Phys Ther 1996; 23:309–319. 25. Smidt GL, Wei S-H, McQuade K, et al. Sacroiliac motion for extreme hip positions. Spine 1997; 22:2073–2082. 26. Sturesson B, Selvik G, Udén A. Movements of the sacroiliac joints – a roentgen sterophotogrammetric analysis. Spine 1989; 14:162–165. 27. Sturesson B, Uden A, Vleeming A. A radiostereometric analysis of the movements of the sacroiliac joints in the reciprocal straddle position. Spine 2000; 25:214–217. 28. Cibulka MT, Delitto A, Koldehoff RM. Changes in innominate tilt after manipulation of the sacroiliac joint in patients with low back pain: an experimental study. Phys Ther 1988; 68:1359–1363. 29. Cibulka MT, Delitto A. A comparison of two different methods to treat hip pain in runners. J Orthop Sports Phys Ther 1993; 17:172–176. 30. Humphrey SM, Inman RD. Metastatic adenocarcinoma mimicking unilateral sacroiliitis. J Rheumatol 1995; 2:970–972. 31. Bohay DR, Gray JM. Sacroiliac joint pyarthrosis. Orthop Review 1993; 22(7):817–823. 32. Dreyfuss P, Dreyer S, Griffin J, et al. Positive sacroiliac screening tests in asymptomatic adults. Spine 1994; 19:1138–1143. 33. Beal MC. The sacroiliac problem: review of anatomy, mechanics, and diagnosis. J Am Osteopath Assoc 1982; 81:667–678. 34. Greenman PE. Sacroiliac dysfunction in the failed low back pain syndrome. In: Vleeming A, Mooney V, Snijders C, et al., eds. Proceedings from the First Interdisciplinary World Congress on Low Back Pain and its Relation to the Sacroiliac Joint. San Diego, CA. 1992; 329–343. 35. Cibulka MT, Koldehoff R. Clinical usefulness of a cluster of sacroiliac joint tests in patients with and without low back pain. J Orthop Sports Phys Ther 1999; 29:83–92. 36. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal joint pain patterns I: a study in normal volunteers. Spine 1990; 15:453–457. 37. Aprill C, Dwyer A, Bogduk N. Cervical zygapophyseal joint pain patterns II: A clinical evaluation. Spine 1990; 15:458–461. 38. Fortin JD, Dwyer AP, West S, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique, part I: asymptomatic volunteers. Spine 1994; 19:1475–1482. 39. Fortin JD, Aprill CN, Ponthieux RT, et al. Sacroiliac joint: pain referral maps upon applying a new injection/arthrography technique, part II: Clinical evaluation. Spine 1994; 19:1483–1489. 40. Schwarzer AC, Aprill CN, Bogduk N. The sacroiliac joint in chronic low back pain. Spine 1995; 20:31–37. 41. Slipman CW, Jackson HB, Lipetz JS, et al. Sacroiliac joint pain referral zones. Arch Phys Med Rehab 2000; 81:334–337. 42. Yeoman W. The relation of arthritis of the sacroiliac joint to sciatica, with an analysis of 100 cases. Lancet 1928; 2:1119–1122. 43. Hiltz DL. The sacroiliac joint as a source of sciatica. Phys Ther 1976; 15:1373. 44. Potter NA, Rothstein JM. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1985; 65:1671–1675. 45. Erhard R, Bowling R. The recognition and management of the pelvic component of low back and sciatic pain. Bulletin of the Orthopaedic Section, American Phys Ther Assoc 1977; 2:4–15. 46. Feinstein AR. Clinical epidemiology: the architecture of clinical research. Philadelphia: WB Saunders; 1985:86. 47. Riddle DL, Freburger JK. Evaluation of the presence of sacroiliac joint region dysfunction using a combination of tests: a multicenter intertester reliability study. Phys Ther 2002; 82:772–781. 48. LaBan MM, Meerschaert JR, Taylor RS, et al. Symphyseal and sacroiliac joint pain associated with pubic symphysis instability. Arch Phys Med Rehabil 1978; 59:470–472. 49. Cibulka MT, Sinacore DR, Cromer GS, et al. Unilateral hip rotation range of motion asymmetry in patients with sacroiliac joint regional pain. Spine 1998; 23:1009–1015. 50. Russell AS, Maksymowych W, LeClercq S. Clinical examination of the sacroiliac joints: a prospective study. Arthritis Rheum 1981; 24:1575–1577. 51. Blower PW, Griffin AJ. Clinical sacroiliac joint tests in ankylosing spondylitis and other causes of low back pain – 2 studies. Ann Rheum Dis 1984; 43:192–195. 52. Maigne J-Y, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892.
PART 4
EXTRA-SPINAL DISORDERS
Section 1
Sacroiliac Joint Syndrome
CHAPTER
Sacroiliac Joint Rehabilitation and Manipulation
115
Heidi Prather and Clayton Skaggs
INTRODUCTION The path taken to diagnose sacroiliac joint (SIJ) pain may not be a straight or clearly marked one. Although several studies point to a battery of tests for diagnosing SIJ problems, a standardized protocol has yet to be devised. As a result, the treatment of SIJ pain can be difficult. Similar to many musculoskeletal problems, treatment success with SIJ pain is often varied due to cofactors surrounding each patient. Accordingly, one uniform approach is not likely. Instead, a combination of treatment options that can be applied to varied patient classifications will be more effective. A sacroiliac joint belt with manual therapy may be very successful in one individual and merely provoke pain in another. The treatment must be tailored to the individual. The patient’s history regarding the circumstances around when the pain began is often paramount in selecting treatment and management. For the sake of consistency in this chapter, the authors will use the term posterior pelvic pain to be inclusive of pain related to the sacroiliac joint, but not exclusive to only intra-articular pain. Posterior pelvic pain includes reference to periarticular pain including muscle, fascia, and ligaments around the sacroiliac joint. Patients with pain in the posterior pelvis after a direct fall or trauma to the joint will require management that will resemble treatment of other acute joint injuries. Treatment for a patient with an insidious onset of pain in the posterior pelvis may be directed more towards the spine or hip, depending on where the weak link in the system is thought to occur. Therapeutic intervention should be directed towards reducing tension in pain-generating structures and restoring the mechanics and function of the system complex involving the spine, pelvis, and hip. Limiting treatment only to the site of pain will have limited success.
TREATMENT Initiating treatment often includes testing the healthcare provider’s hypothesis for what caused the breakdown in the system leading to pain. For example, if the posterior pelvic pain began after an episode of lumbar discogenic pain, correcting the motion, loading, and unloading inadequacies in the lumbar spine must be accomplished in order to affect the mechanics at the pelvis and decrease symptoms. In the same fashion, an injury to the ankle may cause a change in gait pattern, giving rise to secondary adaptive changes such as shortening of the hip external rotators. After the ankle injury resolves, this loading and unloading through the hip joint and/or sacroiliac joint may result in posterior pelvic pain. Correcting the muscle imbalances around the hip may be dependent on soft tissue and propriosensory rehabilitation of the lower limb. Determining the site of breakdown in function is important, but recognizing that pain must be diminished first in order to accomplish improved function is essential. For example, if the patient with discogenic low back pain and positive neural tension
signs does not receive medications and education on how to reduce neural symptoms, the appropriate muscle strengthening cannot be accomplished. Neurogenic symptoms can inhibit muscle function. As the pain is reduced, the muscle flexibility and strengthening program can progress. Additionally, the patient should be screened for pain behavior or fear–avoidance behavior that could be perpetuating the neurogenic symptoms. Common examples include self-manipulation or stretching of the joints and soft tissues in the area of pain.
Medication Medications can be very helpful in modifying pain. Choosing a medication involves selecting a medication specific for the problem. For example, the patient with recent trauma that appears to involve the intra-articular and/or periarticular sacroiliac joint related will likely respond well to consistent antiinflammatory medication usage for a set period of time. Conversely, the patient with insidious onset of posterior pelvic pain present for several months may not respond to the same medication. Therefore, the medication should be tailored to the presumed type of pain. Myofascial pain often responds well to tricyclic antidepressants or similar agents such as trazodone and cyclobenzaprine. Antiinflammatories may be helpful and should be tried, but should likewise be discontinued if no added benefit is achieved. Pain that appears to have a neurogenic component can be treated with antiinflammatories in the acute and subacute phases of treatment. Other medications specific for neurogenic pain again include the tricyclic antidepressants, and similar agents including trazodone and cyclobenzaprine. A variety of adjuvant analgesics such as an antiepileptic medication be helpful. These agents have various side effects such as dizziness and sedation that can impair function. Also, some of these medications require monitoring. The complexity of risk–benefit issues need to be taken into consideration when choosing the agent to prescribe. Narcotics and related medications such as tramadol can be helpful in reducing moderate to severe pain, but again, only for a defined duration. The physician should keep in mind that pain not responding well to a narcotic may not need more narcotic, but another agent to address the type of pain. Neurogenic pain commonly does not respond entirely to narcotic medication and an agent that addresses neurogenic pain used with the narcotic may produce more satisfactory pain reduction.
Manual therapy Manual therapies can be used separately or in combination with other pain-reducing modalities. In fact, evidence suggests that decreasing musculoskeletal pain may be one of the most important roles for manual therapy.1,2 In several studies, manual therapy has been shown to be superior to traditional modalities in reducing pain, sometimes even in the absence of change to objective variables, such as range of 1249
Part 4: Extra-Spinal Disorders
motion.3,4 Accordingly, the authors believe it is important to consider manual therapy as a tool to reduce pain, and to pair it with rehabilitative strategies, such as stabilization exercise, to restore function. Unfortunately, there is a paucity of studies substantiating this position; however, the authors’ collective experiences suggest that this form of treatment can be beneficial. Due to the range of treatments that may be necessary for complete resolution of symptoms, the authors recommend a collaborative approach to care. It is currently recognized that a chiropractor or osteopath will have a better background in manual therapy and a physical therapist or athletic trainer will be more qualified in exercise. However, it is important to recruit and work with practitioners based on their knowledge and skill, and not merely their degrees. Obviously, a practitioner who has abilities and knowledge across a broad range of modalities and therapeutic interventions can be very beneficial.
Therapeutic rehabilitation Once pain has been reduced, participation in a therapeutic rehabilitation program will be more successful. There are many different approaches to a therapeutic program. The authors recommend considering multiple treatment theories and combining types of care according to the individual patient’s needs. This type of comprehensive approach is becoming more popular and will compress the timeline to return to function. There is a vast array of physical therapy approaches to treatment of posterior pelvic pain. One theory proposed by Sahrmann5,6 seeks resolution in symptoms by correcting muscle and joint dysfunction based on specific muscle(s) activation. This theory relies on conscious correction of motor patterns and avoiding activities that promote pain and/or poor movement patterns. A person treated for acute posterior pelvic pain utilizing this treatment method might be instructed to use crutches so as to not develop or enhance a poor gait pattern. In contrast, other theories of treatment develop recommendations based on gross movement patterns. An example is McKenzie’s theory
of systematic treatment for spine dysfunctions.7 Treatment applied is based on specific movement patterns related to spine pathology. A spine stabilization program attempts to combine therapeutic exercises based on deficiencies in spine, abdominal, and hip muscle length and strength. This method also relies on conscious overriding of poor movement patterns. At times, deciding what is acceptable and unacceptable pain while performing exercises in the latter two treatment groups can be difficult for the patient. Another theory proposed by Gray8 recommends using multiple joint movement patterns to improve function but relies on unconscious retraining of movement. The movement patterns are directed either into the restrictive range of movement or away from the restriction. Movement pattern direction is determined by the patient’s pain tolerance. If moving towards the restrictive movement is too painful, applying joint motion, loading, and unloading in the movement pattern and plane tolerated is suggested. As the motion and pain improves, the direction and combination of planes of motion advances. Gray’s approach also incorporates the pelvic floor musculature, an area often omitted from traditional programs. The pelvic floor and diaphragm are thought to play an important role in core or trunk stability. This theory is somewhat ahead of current research validation, but is a growing area of interest in some centers. In general, Gray’s approach to treatment focuses on developing a therapeutic exercise program to resemble the patient’s functional activity requirements. Regardless of what method or combination of methods are used, rehabilitation for posterior pelvic pain must incorporate spine, hip, and pelvic structures and mechanics. Pool-Goudzwaard et al.9 and Vleeming et al.10 have described the importance of the muscle and connective tissue network that assists in the stability of the lumbopelvis and specifically the sacroiliac joint. They have demonstrated through dissection and biomechanical modeling that there is a direct relationship between the tensioning of the dorsal sacral ligament, sacrotuberous ligament, erector spinae muscles, hamstrings, and the movement of the SIJ.11 Additionally, the iliopsoas commonly works in a shortened position. This shortened position can enhance the development of an anteriorly rotated ilium (Fig. 115.1). Hamstring
R
Neutral
L
R
Anteriorly rotated
L
R
Posteriorly rotated
L
L
Neutral
R
L
Anteriorly rotated
R
L
Posteriorly rotated
R
A
B
1250
Fig. 115.1 (A) An anterior view of an anteriorly and (B) posteriorly rotated ilium. This view illustrates the changes that occur at the pubic symphysis and the hip as a result of a change in position of the ilium.
Section 1: Sacroiliac Joint Syndrome
strengthening cannot be accomplished until the iliopsoas is restored to activating in a biomechanically efficient length. An anterior pelvic tilt forces the hamstring to work in a lengthened position. The hamstring is a key muscle in providing stability to the sacroiliac joint because of its direct attachment and/or fascial connections to the sacrotuberous ligament. Other muscles commonly found to be working in a shortened position include the rectus femoris, tensor fascia lata, adductors, quadratus lumborum, latissimus dorsi,12 and obturator internus. Achieving appropriate muscle flexibility may take weeks to achieve. The authors advocate utilizing a stretching program that encompasses all three planes of motion. As muscle length is restored and stiffness reduced, strengthening of muscles inhibited by the biomechanical deficit can be completed. Neuromuscular re-education and facilitation techniques are helpful with this process. Closed kinetic chain strengthening should be attempted first and can then be incorporated into the lumbopelvic stabilization exercises. As trunk strengthening improves, adding multiplanar strengthening exercises will facilitate return to functional activities. Muscles commonly found to be weak include the gluteus medius, gluteus maximus, lower abdominals, and hamstrings. These are merely suggestions that are based on the authors’ experience with respect to muscle patterns of movement proposed by Janda,13,14 and Norris.15,16 As Norris points out,16 these ‘muscle imbalance categorization can usefully assist the astute practitioner, they are not cast in stone.’ Each patient presents with a unique set of circumstances with regards to pain, muscle imbalance, and joint mechanics. The healthcare practitioner must take the patient’s individual set of problems, strengths, and goals into account when creating a treatment program. Manipulation is commonly used to treat posterior pelvic pain related to the sacroiliac joint. Manipulation is a term that may have several definitions. For the sake of discussion in this chapter it will refer to manipulation as treatment that involves manual techniques that restore joint motion. An explanation of the barrier systems utilized to direct manual therapy is useful in understanding the different approaches of manual medicine. The absolute end range of motion within any single plane of motion is referred to as the anatomic barrier (Fig. 115.2). Motion that goes beyond this barrier results in fracture, dislocation, or ligamentous or tendon tear. Within the total range of motion of any joint there are different limits to active and passive range. Active range of motion is limited by a physiological barrier. This barrier is maintained by muscle, ligament, tendon, and capsule. With passive range of motion, increased motion is obtained to the elastic barrier. Again, this barrier is maintained by the previously mentioned soft tissue structures, but at their endpoint of elasticity or length. A restrictive barrier forms as a result of a biome-
Bind
Bind
Ease
Ease
Physiologic barrier Elastic barrier Anatomic barrier
Restrictive barrier Midline neutral Pathologic neutral
Fig. 115.2 Illustration of barriers enhances understanding of the basis of the theory of manipulation.
chanical dysfunction. This barrier reduces the active range of motion and increases the space between available active range of motion and the elastic barrier. A restrictive barrier is created by skin, fascia, long and short muscles, ligament, tendon, and joint capsules. Regardless of the specific type of manipulation used, the goal is to move the restrictive barrier back toward the elastic barrier. There are many techniques that can be used to achieve this goal. The choice of technique is examiner dependent as well as dependent on what is thought to be causing the restriction(s). There are many different techniques used to manipulate a joint to restore motion. Strain–counterstrain developed by Jones,17 an osteopathic physician, is a technique where the healthcare provider palpates for tender points within the restricted area. There are many theories regarding the location and significance of trigger points. Overlap in location is noted in the trigger points identified as Travell’s myofascial trigger points,18 Chapman’s reflex points,17 and acupuncture. Strain–counterstrain utilizes any or all of these identified trigger points to assess and treat the patient. The treatment consists of the examiner monitoring the trigger point while passively positioning the patient until the pain is relieved at the trigger point. Once this position of relief is determined, it is maintained for 90 seconds. The examiner then passively repositions the patient back to a neutral position. In general, the position of comfort is found in the direction away from the restrictive barrier. Pain relief is thought to occur by reducing the inappropriate proprioceptor activity. The inappropriate strain reflex in the painful muscle is inhibited by stretching (counterstrain) the antagonist muscle. This technique is especially helpful to reduce pain related to muscle tone when more active intervention is painful. Muscle energy techniques were first described in osteopathic medicine in the 1960s by physicians T.J. Ruddy and Fred Mitchell, Snr.19 More recently, further expansion has been made by Karel Lewitt and Vladimir Janda. The basic principle involves the healthcare provider passively placing a joint in the position away form the restrictive barrier and the patient then performs an isometric contraction against the force of the healthcare provider. After completing the contraction, the healthcare provider stretches the soft tissues to allow the joint to move through the restrictive barrier. This method of treatment applies both passive positioning and muscle activation to move through a barrier. Lewitt20 has modified this approach and termed it postisometric relaxation (PIR). Importantly, PIR emphasizes a light contraction of the muscle and does not engage the stretch reflex. The procedure is very gentle and usually very comfortable. The doctor identifies the muscle that is overactive and takes the muscle to pathological barrier of functional resistance. The doctor will then ask the patient to lightly contract the muscle being lengthened for approximately 3–5 seconds. After the light contraction, the patient is asked to relax. With relaxation the doctor lengthens the muscle to a comfortable, improved length. This is typically repeated 3–4 times. This approach is particularly beneficial for the acute and subacute patient. The contract relax method of treatment is commonly used by physical therapists and is similar to muscle energy. Patient positioning and isometric contraction are the same, but the examiner’s goal is to improve range of motion to the restrictive barrier while muscle energy attempts to obtain range through the restrictive barrier. Active release therapy (ART) is a (patented) technique used to treat soft tissue problems involving muscles, tendons, ligaments, and nerves. ART is a method of soft tissue mobilization which lengthens hypertrophied or shortened muscles, tendons, ligaments, and connective tissue.21 Preliminary studies with ART have produced encouraging results with a variety of musculoskeletal conditions.22 Once the practitioner has identified the area of tension or adhesion of tissue, a firm manual contact is applied with the thumb or finger to the area 1251
Part 4: Extra-Spinal Disorders
of soft tissue pathology. The practitioner will then shorten the muscle or tissues being treated. While maintaining specific opposition on the area of identified tension or fibrosis, the practitioner will ask the patient to lengthen the muscle and release and/or break up the restrictive tissue. This often promotes better inter- and intramuscular gliding and can improve muscle activation. In cases of posterior pelvic pain, ART can help restore movement for the pelvis by addressing dorsal sacral ligament, sacrotuberous ligament, and hamstrings. This may also be applied to conditions of nerve entrapment by muscles or fascia. Common entrapment sites for posterior pelvic pain include sciatic, gluteal, or lateral femoral cutaneous nerve locations. High-velocity low-amplitude (HVLA) manipulation is the technique often associated with the term ‘manipulation.’ Evidence and international guidelines identifying the efficacy of this type of manipulation for low back pain have flourished since 1986.23–27 This type of manipulation is the form most commonly used by chiropractors. With this technique the patient is moved passively to the restrictive barrier and the examiner then applies an extrinsic force (quick thrust) to move the joint through the restrictive barrier.28 Optimally, one joint is mobilized at a time and restoration of motion at that joint is achieved. The thrust is thought to gap the joint and the gapping is thought to cause the audible pop. While the effects of thrust manipulation remain poorly understood, evidence suggests that the impact is largely a central neurological mechanism.29 Zhu et al.30 demonstrated that decreased pain response after lumbar manipulation was associated with abnormal somatosensory-evoked potentials from paraspinal patients with low back pain. Lehman and McGill,31 in their preliminary investigation, suggested that manipulation could attenuate the muscular response that directly inhibits pain. Suter et al.32 studied the effects of SIJ manipulation on the inhibitory effect of the quadriceps muscle in knee joint pathology. They showed an interaction between manipulation and inhibition of voluntary activity produced by pain. Joint mobilization is a general term coined by physical therapy which is similar in theory to HVLA with one exception. While the goal of HVLA is to move through the restrictive barrier, joint mobilization involves applying grades of pressure to improve motion up to the restrictive barrier but not through it. Lewitt,20 a Czech neurologist, describes several approaches to this type of mobilization for the SIJ. This can include engaging the barrier of resistance and holding or rhythmically springing the barrier. The risk surrounding HVLA for the lower back is often perceived high although it is actually relatively low. Shelkelle33 estimated the serious complication rate for lumbar manipulation at 1 in 100 million manipulations. Haldeman34 revealed that 16 of the 26 cases reported to have complications between 1911 and 1989 had been performed with anesthesia. Therefore, manipulation under anesthesia should be applied with caution. Absolute contraindications to use of manipulation include joint hypermobility and instability, and the presence of inflammatory joint disease, or cauda equina syndrome. Relative contraindications include bone tumors, metabolic bone disease, primary joint disease, congenital or acquired fixed deformities, and vertebral basilar artery insufficiency. Disc herniation and severe spondylosis would also fall in the category of relative contraindications. In these cases with stable neurological findings, manipulation can often facilitate a window of recovery and restoration. Manipulation used for posterior pelvic pain may include any one or combination of the aforementioned techniques. Choosing which to use is usually determined by the practitioner’s skill, experience, and training. When addressing asymmetries in the pelvis, a technique using muscle activation (ART, muscle energy, contract–relax) is often helpful. Utilizing the muscle activation is helpful as the muscles around the hip and pelvis are large, powerful, and have different functions 1252
Fig. 115.3 Example of an iliopsoas stretch that includes three planes of motion: sagittal (hip lunge), frontal (sidebending lumbar spine), and transverse (rotation of the hip) planes.
depending on positioning of the hip. Repositioning can continue until all planes of motion have been addressed. The natural follow-up to the muscle activation treatment is a muscle flexibility and strengthening home exercise program that mimics the manipulation. For example, after a muscle energy technique is applied to reverse a unilateral anterior iliac rotation, the patient should be educated how to perform an iliopsoas stretch encompassing three planes (frontal, sagittal, transverse) of motion (Fig. 115.3). The home exercise program can then facilitate maintaining the improvements made with manipulation. A HVLA treatment might be chosen when muscle activation techniques have failed to provide consistent improvement. There are several sacral thrust maneuvers (Fig. 115.4). In general, a thrust is
Fig. 115.4 One example of a HVLA sacral thrust performed for a diagnosed posterior sacral base dysfunction. The patient extends in a prone position by rising up on elbows. The practitioner places the heel of one hand on lumbosacral junction. The other hand is placed on the lower extremity to stabilize. Pressure is applied on the sacral base until the restrictive barrier is felt. As the patient exhales, the practitioner applies a short thrust anterior.
Section 1: Sacroiliac Joint Syndrome
applied to the sacrum, but is directed in the plane of restriction. The theory is that the applied force will allow a return of improved motion to the joint. Again, the home exercise program should be created to enhance the benefits of the manipulation. For example, the patient who benefits from a sacral thrust performed distally, thereby freeing a unilateral posterior iliac rotation, will likely benefit from a hamstring stretch as part of the home exercise program. Commonly, a practitioner will combine a variety of types of manipulative treatment. Strain–counterstrain or myofascial release might first be used to reduce pain and improve soft tissue elasticity prior to performing a technique involving muscle activation or a thrust. Some practitioner’s skills may lie predominantly with HVLA treatments while others might only use muscle activation treatments. The right combination is the one the practitioner is most skilled at using and allows for maximal patient safety.
Adjunct therapy SIJ belts are often offered as part of the treatment plan for posterior pelvic pain. The belts are used to provide compression to the pelvis (Fig. 115.5). This is particularly helpful in patients with hypermobility at the joint and/or significant muscle weakness. In addition to compression, proprioceptive feedback to the gluteal muscles can assist with neuromuscular re-education. Vleeming35 reported that SIJ belts applied to cadaver models reduced SIJ rotation by 30%. In the clinical setting, Vleeming demonstrated that by stabilizing the ilium, the belts assist with improving hip flexion active range of motion. The healthcare provider must insure that the patient is able to apply the belt appropriately. The SIJ belt should be secured posteriorly across the sacral base and anteriorly, inferior to the anterior superior iliac spines. SIJ belts can dramatically reduce symptoms during walking and standing activities. However, patients with significant pain and weakness may find the belt helpful in reducing symptoms when worn during sedentary activities as well. Recommendations regarding the use of SIJ belts should be individualized, based on the patient’s history and activity goals. Other adjunct treatment considerations include orthotics and shoe modifications. If a leg length discrepancy is noted on physical examination, the examiner should determine if it is a functional or anatomical discrepancy. A shoe lift to correct a functional leg length
Fig. 115.5 Sacroiliac joint belt is worn just below the anterior superior iliac spine.
discrepancy can be helpful in the acute setting to manage pain with weight bearing or ambulating. After the pain with weight bearing has improved, the healthcare provider should determine if the shoe lift should continue to be used. The goal should be to reduce or resolve the functional leg length discrepancy via the therapeutic rehabilitation program. There is some recent evidence that footwear modifications can have systemic effects.36 An inappropriate shoe lift can promote adaptive muscle imbalances, which may initially be asymptomatic. Over time, these changes in force transmission and absorption across the pelvis may become symptomatic. Anatomical leg length discrepancies should be determined as early in treatment as possible so that the appropriate modifications can be completed. SIJ injections can be used as an adjunct to a physical therapy program if the patient’s progress plateaus or the program cannot be advanced because of pain provocation. The injections can also be used diagnostically if done under fluoroscopic guidance. Maigne37 reported 18.5% of 54 patients diagnosed with SIJ pain responded to double SIJ block under fluoroscopic guidance. This study did not control for other treatments given and therefore accurately reports only what an injection alone can improve. Slipman et al. analyzed a cohort of 31 patients who underwent therapeutic SIJ intra-articular injection.38 A minimum follow-up interval of 12 months was used. They found statistically and clinically significant improvement in visual analog scale (VAS) ratings and Oswestry scores. The average VAS rating reduction was in excess of 30 (out of 100). Luukkainen and colleagues39 reported improved visual analog scale and pain index scores at 1 month after a periarticular SIJ steroid injection. This study included 13 patients who received steroid compared to 11 who received saline and lidocaine. The injections were performed by palpation over the painful site at the SIJ region and no control was made for other treatments. In another study, 10 of 12 patients who underwent SIJ steroid injection via MRI guidance reported an improved VAS at 3-month follow-up.40 Again, no control or standardization of other conservative treatment was completed. Though study numbers at this time are small, there is evidence to suggest that SIJ injections should be used as an adjunct treatment in pain management. Recently, studies have reported improvement in chronic SIJ pain treated with radiofrequency ablation (RFA). Ferrante and associates41 reported a 50% reduction in VAS reports for at least 6 months in 33 patients. The authors noted that a positive response to treatment was associated with an atraumatic inciting event, reduction in the area of referred pain on the pain diagram, normalization of SIJ pain provocation tests, and reduction in opioid use with radiofrequency denervations. Although the Ferrante study suggests that RFA was achieved, this conclusion is suspect. The technique used simply entailed placing three probes into the joint. It is more likely that osseous and/or cartilaginous injury resulted from the local heating effect rather than a denervation procedure. Yin and colleagues42 reported a retrospective review of 14 patients who underwent sensory stimulation-guided sacral lateral branch radiofrequency neurotomy for treatment of chronic SIJ pain. Sixty-four percent experienced consistent relief in pain with a 50% reduction in visual integer pain score 6 months after the procedure. Included in these successful outcomes were 36% who had complete relief in their symptoms. In another study, Cohen43 reported choosing radiofrequency ablation candidates for chronic SIJ pain by performing diagnostic blocks at the levels innervating the SIJ (L4–5 dorsal rami and S1–3 lateral branches). Thirteen of 18 patients reported significant relief with nine reporting greater than 50% relief at follow-up. These nine underwent radiofrequency ablation of all branches previously blocked. Eight out of nine (89%) obtained 50% or greater pain relief that continued at 9-month follow-up. Using the same basic theories behind radiofrequency ablation, Calvillo et al.44 reported two cases of chronic SIJ pain treated by 1253
Part 4: Extra-Spinal Disorders
implanting a neuroprosthesis at the third sacral root. The authors reported that the patients continued to use analgesics before and after the procedure, but the patients reported that their activities of daily living were ‘more tolerable.’ These procedures appear to have some promise in the treatment of chronic SIJ pain. More studies are needed to determine long-term outcomes and determine which patients might be good candidates. SIJ hypermobility unresponsive to the above-outlined program is a difficult problem. SIJ arthrodesis45 and percutaneous fixation46 have been utilized for instability. Long-term outcome studies thus far have not been completed and it is unknown what happens to surrounding articulations with the lumbar spine, contralateral SIJ, and hip years after SIJ fusion. Other therapies such as prolotherapy have been proposed as an invasive but less permanent option. Prolotherapy is described as the provocation of the laying down of an increased volume of normal collagen material in ligament, tendon, or fascia in order to restore function of the tissue at a specific site.47 Provocation is achieved by provoking an inflammatory response at the location. A wide variety of agents have been used to provoke local inflammation, including high-concentration glucose solutions to phenol alcohol. Often it is a combination of agents. Though the safety48 and clinical outcomes have been reported,49 no prospective, controlled studies exist to date on the specific use of prolotherapy and SIJ dysfunction.
TREATMENT SCENARIOS Acute phase of treatment for a traumatic injury (1–3 days) Acute injury is often associated with a direct trauma such as a fall or marked increase in intensity, frequency, or duration of a specific activity. Often, sacroiliac joint pain presents as a progressive problem with fluctuations in symptoms. The patient may only experience symptoms during certain activities, including sports or exercise. In the acute setting, antiinflammatory medications and icing are helpful. Relative rest after an acute injury assists with pain management. This includes restricting running or excessive walking as these activities often provoke sacroiliac joint pain. Identifying the activity that may aggravate symptoms is important, especially in those with a progressive onset of symptoms. In general, avoiding activities that require a single-leg stance (activities such as bowling, skating, running, elliptical trainer, and stair stepper) is helpful in alleviating symptoms. In the acute setting, a shoe lift might be used temporarily to help reduce pain associated with weight bearing when a functional leg length discrepancy is present. As pain improves and the leg length discrepancy resolves, the lift can be removed. An SIJ belt may be helpful, especially in patients who complain of clicking or the sense of instability. Many patients find that the belts help reduce pain, especially with walking and standing. Correcting asymmetries in muscle length or stiffness should start as soon as possible and progressed within pain-free limits. Muscle energy techniques are particularly helpful as they require patient activation of muscle groups, and therefore pain tolerance is easily monitored. Joint mobilization and HVLA can be very effective at this stage. Importantly, the ilium or sacroiliac joint opposite the site of pain and inflammation is most commonly the restricted complex. Therefore, joint mobilization and/or manipulation to the side opposite to the pain is indicated and a general guideline for manual therapy. A home stretching and/or self-mobilization program should reinforce the manual techniques used to correct the SIJ dysfunction.
Recovery phase (3 days to 8 weeks) Once pain has been controlled and the injured area has been rested, correction of the functional biomechanical deficit and tissue over1254
load complex50 becomes the focus of rehabilitation. Balancing lower extremity muscle length and strength is important because of direct and indirect force transmission across the ilium and sacrum. Muscle length must be restored to facilitate appropriate joint mechanics at the hip, SIJ, and spine. Again, in this phase of treatment muscle energy and active release techniques are often successful in reducing pain as well as restoring functional motion. In cases where the above techniques have been partially successful or unsuccessful at relieving pain and improving motion, HVLA or mobilization techniques may be helpful. The home exercise program should include selfmobilization exercises to insure carry-over of the manually applied treatment. Once the mobilization has been successful the focus of treatment should turn to maintaining muscle length while improving muscle strength and endurance. Maintaining muscle flexibility with exercises that address all three planes of motion will also reinforce improvements made with the manual techniques. Medications during this time should include nonsteroidal antiinflammatory medications. These medications should be initiated with consistent daily dosage and then weaned as needed and eventually discontinued. If sleep is a problem due to pain, taking advantage of the sedating side effect of muscle relaxers may be helpful by prescribing them for nighttime use. Narcotics and medicines such as tramadol, may be useful but in a limited setting. The goal is to minimize their use. If improvements are plateauing or limited by pain, a therapeutic SIJ steroid injection may be useful with regard to treatment, and a positive response makes one feel more comfortable about the diagnosis. The authors recommend these injections be performed with fluoroscopic guidance to insure accuracy of placement and reduce complications caused by misplacement. The patient should be made aware that the injection is an adjunct treatment utilized to facilitate the progress of physical therapy. As pain improves, the exercise prescription should advance. Muscle flexibility and strengthening exercises should progress to weight bearing, utilizing all three planes of motion. As this improves, the home program should start to incorporate or mimic functional, exercise, or sport-specific activities. Return to unrestricted activities or exercise occurs once the patient is pain free, range of motion and strength have been restored, the patient has demonstrated good technique with activities, and has returned to or initiated an aerobic training program. Education with regards to the importance of a maintenance program should be completed prior to discharge.
Treatment for a nontraumatic injury (1–3 days) The treatment course of a nontraumatic injury should progress similarly to that of a traumatic injury. Initially, the etiology of the problem may not be clear or identified and, as a result, a period of trial and error can often ensue. For example, if the patient began with a segmental restriction at L5–S1 and continues to have posterior pelvic pain that is responding only in part to therapy directed at the SIJ, the restriction at L5–S1 may need to be addressed before further progress can be made. Again, the L5–S1 restriction can be treated with a variety of therapeutic interventions including joint mobilization, manipulation, muscle energy, and contract–relax. Care must be taken to resolve neurogenic pain symptoms. This can be addressed via medications, neuromobilization, and injections. Recurrent or continuous neurogenic pain can inhibit progress being made with muscle flexibility and strength. Clearing hip dysfunction can also be a key factor in progressing a treatment program for posterior pelvic pain. Godges and colleagues51 described this scenario in a case report of a 74-year-old female with posterior pelvic pain thought to be related to the SIJ. They presented a detailed description of successive physical examinations and physical therapy sessions. The iliac and sacral
Section 1: Sacroiliac Joint Syndrome
restrictions resolved within a few sessions of combined manual techniques, neuromuscular re-education, and muscle flexibility and strengthening exercises. Despite these improvements, the patient continued to have pain and activity limitations. Further progress was made once the range of motion (ROM) of the hip on the symptomatic side improved to becoming more symmetrical with the ROM on the asymptomatic side. Adjunct treatments should be instituted in the nontraumatic patient in similar fashion as the traumatic patient. Again, care should be taken to look for areas of dysfunction away from the SIJ if the patient requires prolonged use of medications, or repeated injections. Repetitive manipulation to the SIJ can have long-term side effects of joint hypermobility. Freeing restrictions at the spine and pelvis can be vital in making SIJ manual therapy successful.
Special populations Pregnancy Studies have suggested that between 50–80% of women suffer from low back pain and/or posterior pelvic pain (LBP/PPP) during pregnancy.52–61 Ostgaard and Roos-Hansson62 demonstrated that during pregnancy pain is more commonly attributed to posterior pelvic pain and postpartum is more commonly occurring from dysfunctions within the lumbar spine.63 Of 119 women with pain for more than 2 months postpartum, 27% were thought to have posterior pelvic pain, 18% lumbar spine pain, 39% posterior pelvic and lumbar pain, and in 16% no pain could be provoked on physical examination. Understanding these different etiologies can better direct treatment plans. Treatment for posterior pelvic pain during pregnancy should progress similar to that in the nonpregnant population. Exceptions include the care that should be taken in both examining and applying manual therapy treatments in the pregnant population. Ligamentous laxity promotes joint hypermobility. Overzealous ROM or manipulation can provoke both further pain and dysfunction in this population. On the other hand, SIJ belts can be exceptionally helpful in reducing pain by providing proprioceptive feedback and compression to the gluteal muscles that help provide joint stability. Stabilization exercises should be promoted with care and not all activities should
A
be performed in the supine position. The home exercise program will need to be adjusted as the abdominal girth increases. Instead of lengthening the lever arm with strengthening exercises, it may need to be reduced to adjust for biomechanical inefficiencies. Education is key with regards to activities of daily living, ergonomics of lifting (Fig. 115.6), and position choices during labor when possible. For example, laboring in a side-lying position with the hip in full flexion, abduction and external rotation may further provoke posterior pelvic pain that began during pregnancy. Noren et al.,64 in their study using an education and physiotherapy intervention, calculated a cost savings of US$53 000 for reducing LBP/PPP in pregnancy in 30 women. Education for LBP/PPP in pregnancy has also been studied and proven helpful in reducing the common chronicity seen with these patients.35,61,62,65 These studies all suggest early advice for best results. The authors’ preliminary studies also suggest an important role for assessing and treating the muscles and ligaments of the spine and pelvis in pregnancy-related LBP/PPP.68 While several exercise-directed interventions have been proposed for soft tissue dysfunction in pregnancy-related LBP/PPP,67–72 very little has been studied regarding manual soft tissue intervention.73,74 The procedures the authors utilize most are the muscle energy and ART. While both address muscles, ligaments, tendons, and connective tissue, they are clinically different from traditional massage. PIR is a method of soft tissue mobilization which lengthens shortened muscles that are hypertonic or contain trigger points.20 A few studies on LBP in pregnancy have included manipulation and mobilization in their treatment protocols with encouraging preliminary results.60,75–77 McIntyre and Broadhurst75 and Daly and Rapoza76 showed a 90% success rate in reducing pain in women with pregnancy-related LBP by using thrust manipulation for sacroiliac dysfunction. Berg et al.60 found 70% improvement in women with severe LBP in pregnancy who received specific SIJ mobilization. In a retrospective review, Daikow provided evidence of an 84% success rate in reducing back pain during pregnancy and back labor through manipulation.76 The goal with these procedures is to reduce tension or restricted movement in the pain-generating structures, thereby decreasing the patient’s pain and assisting self-care strategies of activity modification, stretching, and exercise.
B
Fig. 115.6 Review of lifting techniques is important in treating women with low back pain during pregnancy and postpartum. (A) The mother is demonstrating an inappropriate technique of lifting that increases forces to the lumbar spine. (B) The mother demonstrates an appropriate technique to maximize utilization of hip musculature during lifting, allowing the abdominal and gluteal muscles to brace and thereby reduce the risk of sheer forces applied to the lumbar spine. 1255
Part 4: Extra-Spinal Disorders
CONCLUSION Treatment for posterior pelvic pain thought to be related to the SIJ must be approached with the idea that it is likely a variety of therapeutic activities may be required to resolve pain and dysfunction. Care should be taken to determine if coexisting or preexisting dysfunctions in the hip or spine are contributing to the current problem. All must be addressed. Manual therapies can be particularly beneficial in this patient population but should be applied for a specific problem. A home exercise program should then reinforce the manual techniques applied. If multiple manipulations continue to be needed, the practitioner should reevaluate and determine if restrictions outside the SIJ exist and treat them accordingly.
References
24. Aure OF, Nilsen JH, Vasseljen O. Manual therapy and exercise therapy in patients with chronic low back pain: a randomized, controlled trial with 1 year follow up. Spine 2003; 28(6):525–531. 25. Van den Hout JH, Vlaeyen JW, Houben RM, et al. The effects of failure feedback and pain-related fear on pain report, pain tolerance, and pain avoidance in chronic low back pain patients. Pain 2001; 92(1–2):247–257. 26. Manniche C, Jordan A. Evidence based medicine. Spine 2001; 26(7):842–844. 27. Royal College of General Practitioners. Clinical guidelines for the management of acute low back pain. London: Royal College of General Practitioners; 1999. (www. rcgp.org.uk) 28. Mein EA. Overview of techniques and system approaches to manipulation. Phys Med Rehabil Clin N Am 1996; 7(4):731–747. 29. Haldeman S. Neurologic effects of the adjustment. J Manip Physiol Ther 2000; 23:112–114.
1. Anderson R, Meeker WC, Wirick BE, et al. A meta-analysis of clinical trials of spinal manipulation. J Manip Physiol Ther 1992; 15:181–194.
30. Zhu Y, Starr A, Seffinger MA, et al. Paraspinal muscle evoked cerebral potentials in patients with unilateral low back pain. Spine 1993; 18:1096–1102.
2. Nilsson N, Christensen HW, Hartvigsen J. Lasting changes in passive range motion after spinal manipulation: a randomized, blind, controlled trial. J Manip Phys Ther 1996; 19(3):165–168.
31. Lehman GJ, McGill SM. Effects of a mechanical pain stimulus on erector spinae activity before and after a spinal manipulation in patients with back pain: a preliminary investigation. J Manip Phys Ther 2001; 24(6):402–406.
3. Koes BW, Bouter LM, Van Mameren H, et al. The effectiveness of manual therapy, physiotherapy, and treatment by the general practitioner for nonspecific back and neck complaints: A randomized clinical trial. Spine 1992; 17:28–35.
32. Suter E, Herzog W, Bray R. Conservative lower back treatment reduces inhibition in knee-extensor muscles: A randomized controlled trial. J Manip Physiol Ther 2000; 23:76–80.
4. Koes BW, Bouter LM, Van Mameren H, et al. Randomized clinical trial of manipulative therapy and physiotherapy for persistent back and neck complaints: Results of one year follow up. Br Med J 1992; 304:601–605.
33. Shelkelle PG, Chassin MR, Surwitz EL, et al. Spinal manipulation for low back pain. Ann Intern Med 1992; 117:590–598.
5. Sahrmann SA. Diagnosis and treatment of movement impairment syndromes. Chicago: Mosby; 2001. 6. Maluf KS, Sahrmann SA, Van Dillen LR. Use of a classification system to guide nonsurgical management of a patient with chronic low back pain. Phys Ther 2000; 80(11):1097–1111. 7. McKenzie RA. Mechanical diagnosis and therapy for low back pain. In: Physical therapy of low back pain. Edinburgh: Churchill Livingstone; 1987. 8. Gray GW. Total body functional profile. In: Gray GW, ed. Total body functional profile. Adrian, Michigan: Wynn Marketing, Inc and Gary Gray Physical Therapy Clinic, Inc; 2001:7–9. 9. Pool-Goudzwaard AL, Bleeming A, Stoeckart R, et al. Insufficient lumbopelvic stability: a clinical, anatomical and biomechanical approach to ‘a-specific’ low back pain. Man Ther 1998; 3(1):12–20. 10. Vleeming A, Pool-Goudzwaard AL, Stoeckart R, et al. The posterior layer of the thorocolumbar fascia. Spine 1995; 20:753–758. 11. Vleeming A, Hammudoghlu D, Stoeckart R, et al. The function of the long dorsal sacroiliac ligament. Spine 1996; 21:556–562. 12. Geraci MC. Rehabilitation of the hip and pelvis. In: Kibler WB, Herring SA, Press JM, eds. Functional rehabilitation of sports and musculoskeletal medicine. Maryland: Aspen Publishers; 1998:216–243.
34. Haldeman S, Rubenstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1992; 17:1469–1473. 35. Vleeming A, Buyruk HM, Stoeckart R, et al. Towards an integrated therapy for peripartum pelvic instability: A study of the biomechanical effects of pelvic belts. Am J Obs Gynecol 1992; 166:1243–1247. 36. Mundermann A, Nigg BM, Humble RN, et al. Foot orthotics affect lower extremity kinematics and kinetics during running. Clin Biomech 2003; 18(3):254–262. 37. Maigne JY, Aivaliklis A, Pfefer F. Results of sacroiliac joint double block and value of sacroiliac pain provocation tests in 54 patients with low back pain. Spine 1996; 21:1889–1892. 38. Slipman CW, Lipetz JS, Vresilovic EJ, et al. Fluoroscopically guided therapeutic sacroiliac joint injections for sacroiliac joint syndrome. Am J Phys Med Rehabil 2001; 80(6):425–432. 39. Luukkainen RK, Wennerstrand PV, Kautiainen HH, et al. Efficacy of periarticular corticosteroid treatment of the sacroiliac joint in non-spondyloarthropathic patients with chronic low back pain in the region of the sacroiliac joint. Clin Exp Rheumatol 2002; 20:52–54. 40. Pereira PL, Gunaydin I, Duda SH, et al. MR-guided steroid injection of the sacroiliac joints: preliminary results. J de Radiolgie 2000; 81:223–226. 41. Ferrante FM, King LF, Roche EA, et al. Radiofrequency sacroiliac joint denervations for sacroiliac syndrome. Reg Anesth Pain Med 2001; 26(6):592–593.
13. Janda V. Muscle weakness and inhibition in back pain syndromes. In: Grieve G, ed. Modern manual therapy of the vertebral column. Edinburgh; Churchill Livingstone: 1986.
42. Yin W, Willard F, Carreiro J, et al. Sensory stimulation-guided sacroiliac joint radiofrequency neurotomy: techniques based on neuroanatomy of the dorsal sacral plexus. Spine 2003; 28(20):2419–2425.
14. Janda V. Muscle spasm – a proposed procedure for the differential diagnosis. Manual Med 1991; 1001:6136–6139.
43. Cohen SP, Abdi S. Lateral branch blocks as treatment for sacroiliac joint pain: A pilot study. Reg Anesth Pain Med 2003; 28(2):113–119.
15. Norris CM. Spine stabilization. Muscle imbalance and the low back. Physiotherapy 1995; 81(3):127–138.
44. Calvillo O, Esses SI, Ponder C, et al. Spine 1998; 23(9) :1069–1072.
16. Norris CM. The designation debate. J Bodywork Movement Ther 2000; 4(4):225– 241. 17. Jones LH. Strain and counterstrain. In: Jones LH, ed. Strain and counterstrain. The Indianapolis, IN: American Academy of Osteopathy; 1981:11–14. 18. Travell JG, Simons DG. Myofascial pain and dysfunction, Vol 2. Baltimore: Williams and Wilkins; 1992. 19. Chaitow L. An introduction to muscle energy techniques. In: Chaitow L, ed. Muscle energy techniques, 2nd edn. Edinburgh: Churchill Livingstone; 2001:1–17. 20. Lewitt K. Manipulative therapy in rehabilitation of the motor system. London: Butterworths; 1985. 21. Leahy PM, Active Release soft tissue management system. Course Manual 1999. 22. Schiottz-Christensen BMV, Azad S, Selstad D, et al. The role of active release manual therapy for upper extremity overuse syndromes – a preliminary report. J Occup Rehabil 1999; 9:210.
1256
23. Flynn TW, Fritz JM, Wainner RS, et al. The audible pop is not necessary for successful spinal high-velocity thrust manipulation in individuals with low back pain. Arch Phys Med Rehabil 2003; 84(7):1057–1060.
45. Keating JG, Avillar MD, Price M. Sacroiliac joint arthrodesis in selected patients with low back pain. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability and low back pain. New York: Churchill Livingstone; 1999: 573–586. 46. Lippitt AB. Percutaneous fixation of the sacroiliac joint. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability and low back pain. New York: Churchill Livingstone; 1999:587–594. 47. Dorman TA. Pelvic mechanics and prolotherapy. In: Vleeming A, Mooney V, Dorman T, et al., eds. Movement, stability and low back pain. New York: Churchill Livingstone; 1999:501–522. 48. Dorman TA. Prolotherapy: A survey. J Orthop Med 1993; 15:2. 49. Ongley MJ, Klein RG, Dorman TA, et al. A new approach to the treatment of chronic low back pain. Lancet 1987; 2:143–146. 50. Herring SA. Rehabilitation of muscle injuries. Med Sci Sports Exerc 1990; 22:455.
Section 1: Sacroiliac Joint Syndrome 51. Godges JJ, Varnum DR, Sand KM. Impairment-based examination of disability management of an elderly woman with sacroiliac region pain. Phys Ther 2002; 82(8):812–821. 52. Fast A, Ducommun EJ, Friedmann LW, et al. Low-back pain in pregnancy. Spine 1987; 11:368–371. 53. MacArthur C, Knox EG, Crawford JS. Epidural anaesthesia and long term backache after childbirth. Br Med J 1990; 301:9–12. 54. Ostgaard HC, Karlsson K. Prevalence of back pain in pregnancy. Spine 1991; 16:549–551. 55. Heckman JD. Musculoskeletal considerations in pregnancy. J Bone Joint Surg 1994; 76A:1720–1730.
65. Mantle MJ, Currey HLF. Backache in pregnancy II: Prophylactic influences of back care classes. Rheumatol Rehabil 1981; 20:227–232. 66. Skaggs CD, Ducar D, Prather H. Musculoskeletal intervention for low back and pelvic pain in pregnancy. 2003. 67. Suputtitada A, Chaisayan P. Effect of the ‘sitting pelvic tilt exercise’ during the third trimester in primigravides on back pain. J Med Assoc Thai 2002; 85:S170–S178. 68. Duffy S. Chronic pelvic pain: defining the scope of the problem. Int J Gynaecol Obstet 2001; 74(Suppl 1):S3–S7. 69. Mens JMA, Stam HJ. Diagonal trunk muscle exercises in peripartum pelvic pain: A randomized clinical trial. Phys Ther 2000; 80:1164–1173.
56. Endresen EH. Pelvic pain and low back pain in pregnant women – an epidemiological study. Scand J Rheumatol 1995; 24:135–141.
70. Stuge BM. The efficacy of a specific stabilization exercise program in the treatment of patients with peripartum pelvic pain after pregnancy. A randomized controlled trial. Montreal: 2001.
57. Kristiansson P, Von Schoultz B. Back pain during pregnancy: A prospective study. Spine 1996; 21:702–709.
71. Rath J, Mielscarski E, Waldman R. Low back pain during pregnancy: Helping patients take control. J Musculoskel Med 2000; 223–232.
58. Bullock JE, Bullock MI. The relationship of low back pain to postural changes during pregnancy. Austr J Physiother 1987; 33:10–17.
72. Kihlstrand M, Nilsson S, Axelsson O. Water-gymnastics reduced the intensity of back/low back pain in pregnancy women. Acta Obstet Gynecol Scand 1999; 78:180–185.
59. Stapleton DB, Kristiansson P. The prevalence of recalled low back pain during and after pregnancy: A South Australian population survey. Aust NZ J Obstet Gynaecol 2002; 42: 482–485. 60. Berg G, Moller-Nielsen J, Linden U, et al. Low back pain during pregnancy. Obstet Gynecol 1988; 71:71–75.
73. Requejo SM, Kulig K, Landel R, et al. The use of a modified classification system in the treatment of low back pain during pregnancy: A case report. J Orthop Sports Phys Ther 2002; 32:318–326.
61. Orvieto R, Ben-Rafael Z, Gelernter I, et al. Low-back pain of pregnancy. Acta Obstet Gynecol Scand 1994; 73:209–214.
74. Vleeming A, de Vries HJ, Mens JM, et al. Possible role of the long dorsal sacroiliac ligament in women with peripartum pelvic pain. Acta Obstet Gynecol Scand 2002; 81(5):430–436.
62. Ostgaard HC, Roos-Hansson E. Back pain in relation to pregnancy. Spine 1997; 22:2945–2950.
75. McIntyre IN, Broadhurst NA. Effective treatment of low back pain in pregnancy 1996; 9(Suppl 2):S65–S67.
63. Nilsson-Wikmar L, Harms-Ringdahl K, Pilo C, et al. Back pain in women postpartum is not a unitary concept. Physiother Res Int 1999; 4(3):201–213.
76. Daly JM, Rapoza PA. Sacroiliac subluxation: a common, treatable cause of low back pain in pregnancy. Family Pract Res J 1991; 22:149–159.
64. Noren L, Johansson G, Ostgaard HC. Lumbar back and posterior pelvic pain during pregnancy: A 3-year follow-up. Eur Spine J 2002; 11:267–271.
77. Fung BKP, Ho ESC. Low back pain of women during pregnancy in the mountainous district of central Taiwan. Chin Med J 1993; 51:103–106.
1257
PART 4
EXTRA-SPINAL DISORDERS
Section 1
Sacroiliac Joint Syndrome
CHAPTER
Therapeutic Injections and Radiofrequency Denervation
116
Way Yin
INTRODUCTION For more than 70 years, the sacroiliac joint complex has been implicated as a significant and discreet structural source of low back pain. However, of the three major groups of spinal structures identified as contributing to chronic low back pain, the sacroiliac joint complex (SIJC) stands apart from the zygapophyseal joints and intervertebral discs as the least understood from a neuroanatomic, diagnostic, and therapeutic standpoint. The prevalence of low back pain arising from the SIJC has been estimated at 15–30%,1,2 and is likely higher in the older population. The SIJC possesses a unique and complex three-dimensional anatomy with multisegmental sensory innervation. Unlike the zygapophyseal joints and intervertebral discs, the sensory innervation of the SIJC has been described in a detailed fashion only recently, and the definitive gold standard for successful treatment of SIJC pain has not yet been rigorously defined. Numerous studies have demonstrated a lack of pathognomonic historical, symptom, physical examination, or imaging findings specific for the individual diagnosis of zygapophyseal joint, disc, or SIJC pain.1,3–7 The identification of specific structural sources of low back pain must currently be made through validated interventional diagnostic means. A structure-specific diagnosis is ultimately essential for the eventual consideration of appropriate evidence-supported treatment options. A specific structural diagnosis also leads to a definable prognosis, as the long-term outcomes following treatment for zygapophyseal joint pain differ from disc pain, and from SIJC pain as well.8–14 A rational, evidence-based diagnostic algorithm for the identification of the structural source of low back pain is thus invaluable (Fig. 116.1). The area of the SIJC is frequently involved with referred pain patterns associated with other lumbar structures,2,3,15–17 and pain of SIJC origin frequently involves somatic referred pain to various areas of the low back, pelvis, abdomen, and lower extremities,18 with nearly one in seven patients experiencing pain radiating to the foot in a pseudoradicular pattern. Successful implementation of such a diagnostic algorithm is therefore ultimately dependent not only on the physician’s understanding of the technical aspects of diagnostic interventions, but also the overlapping distributions of referred somatic pain arising from different lumbar structures, and the defined sensitivities and specificities of each test considered. The current gold standard for the diagnosis of SIJC pain involves controlled intra-articular anesthetic injections (IAI).1,2,6,7,19 Pain may also arise from the deep interosseous ligament (DIOL), which is exquisitely innervated. The nociceptive potential of the DIOL is supported by anatomic and histologic findings. Although a technique for injection of the DIOL has been described, the clinical overlap in diagnostic sensitivity and specificity between controlled SIJC IAI and DIOL anesthetic injections has yet to be determined,10,20–22 and represents an ongoing area of clinical and anatomical research. Once the
diagnosis of SIJC pain has been established and the presence of other sources of lumbar spine pain excluded, definitive SIJC therapeutic intervention may be considered. A definitive, highly successful, and durable intervention for the treatment of SIJC pain may be just around the corner. Limited reports of the efficacy of surgical fusion23,24 and radiofrequency denervation10,25,26 are available; however, long-term prospective, controlled or comparative studies are currently lacking or are under investigation. This chapter will focus on current evidence supporting therapeutic injection and radiofrequency SIJC denervation.
RELEVANT ANATOMY The sacroiliac joint (SIJ) is the largest syndesmotic joint in the human body. Although possessing a cartilaginous articular surface and synovial component, the sacroiliac joint primarily functions as a stress-relieving joint, insulating the lumbar spine from transmitted shock associated with ambulation. The SIJ is not bounded by capsular tissue like other synovial joints. The joint capsule is composed of ligamentous fibers, and posteriorly, contiguous with the deep interosseous ligament. The joint as a whole is intimately associated with a multitude of surrounding ligaments, which provide structural integrity to the joint complex. The synovial component of the SIJC is composed of two divergent joint planes, a larger lateral (or anterior) pole and the smaller medial (or posterior) pole. Percutaneous access to the medial pole traverses a minimum of ligamentous tissue, whereas access to the lateral pole must traverse the DIOL (Fig. 116.2). The total volume of the synovial component of the SIJC (1.5 mL) is small compared to its surface area.15,27 The ‘capsule’ of the sacroiliac joint is frequently incompetent, even in asymptomatic patients. In one series, 61% of intra-articular injections demonstrated extracapsular extravasation,22 and 25% of asymptomatic volunteers undergoing intra-articular injection demonstrated ventral capsular insufficiencies,27 with contrast extravasating in the region of the traversing lumbosacral plexus. Detailed dissection of the ventral joint capsule in cadavers suggests that these ventral capsular ‘defects’ often appear as small foramina rather than traumatic capsular rents.28
Neuroanatomy of the sacroiliac joint complex Early studies of the sacroiliac joint suggested a combination of ventral and dorsal innervation,29,30 but recent investigation has demonstrated a predominant dorsal innervation in humans21,22 arising from the lateral branches of the L5 dorsal ramus and S1–4 dorsal rami, and composed of a wide range of sensory fiber types.21,30 The lateral branch nerves arise from a lateral dorsal sacral plexus, and divide into multiple smaller branches, some of which enter the DIOL whereas 1259
Part 4: Extra-Spinal Disorders
Low back pain? Yes
Pain above L5 level?
Yes
Exit algorithm, SIJ pain unlikely, pursue lumbar sources of pain
No Evaluate zygapophysial joints via intra-articular LA injection
Pain completely relieved?
Yes
Exit algorithm, Pt. blinded comparative LA block z-joints
No Evaluate lumbar intervertebral discs with provocative discography
IASP validated discography positive?
Yes
Exit algorithm, consider treatment options for disc pain
No Evaluate SIJ with IAI, IOL LA injection
Yes
Pain completely relieved?
No
Exit algorithm, reassess for other sources of LBP
Pt. blinded comparative local anesthetic block Concordant complete relief?
No Yes
1260
SIJ RF denervation
Fig. 116.1 Sample SIJ diagnostic algorithm flowchart depicts an evidence-supported interventional diagnostic algorithm for the identification and treatment of SIJC pain.
Section 1: Sacroiliac Joint Syndrome
Fig. 116.2 Medial and lateral poles, SIJ. An ipsilateral oblique image of SIJ arthrography, with needle penetrating the posterior joint capsule of the medial pole. The heavy dark line separates the medial from the lateral pole of the joint. Note capsular redundancy of the distal (caudal) medial pole (white arrow), and the small amount of dorsal capsular contrast extravasation (black arrow).
others do not. The segmental location and number of lateral branch nerves innervating the SIJC is extremely variable. On the posterior aspect of the sacrum, these branches are often closely related (Fig. 116.3).20 Unlike the lumbar medial branch nerves of the dorsal rami supplying innervation to the zygapophyseal joints, the complex three-dimensional anatomy of the lateral branch nerves innervating
Left
Right
L5 L5/S1
S1 PSIS S2
LDSIL S3
ST
Fig. 116.3 Dorsal sacral plexus and lateral branch nerves. A representative illustration of the lateral branch nerves supplying sensation to the dorsal sacral joint complex (arrows) from L5 through S3. Note the variability in lateral branch topography between right and left. LDSIL, long dorsal sacroiliac ligament; PSIS, posterior superior iliac spine; ST, sacral tubercle; L5–S1, L5–S1 zygapophyseal joint (superior articular process). (Courtesy of Frank Willard, PhD.)
Fig. 116.4 Incomplete lateral branch staining. Dissection in nonembalmed cadaver of lateral branch nerves, left dorsal sacral plexus following injection of 0.5 mL of colored dye lateral to S1 and S2 dorsal sacral foramina. Note incomplete staining of lateral branch nerves at S2 (black arrows). Unlike similar diagnostic injection techniques to identify painful zygapophyseal joints, it is not possible to selectively anesthetize the lateral branch nerves supplying the sacroiliac joint. (Courtesy of Paul Dreyfuss, M.D. and Frank Willard, PhD, used with permission.)
the SIJC combined with their close proximity to the dorsal sacral foramina renders consideration of selective anesthetic blockade futile (Fig. 116.4).27 The DIOL is richly innervated with nociceptive mechanoreceptors. Sensory fibers must traverse the DIOL to reach the posterior SIJ capsule, and understanding the topographic neuroanatomy of the SIJC becomes invaluable in consideration of the design and performance of diagnostic injection techniques and therapeutic interventions.
DIAGNOSTIC INJECTION TECHNIQUES With the exception of imaging findings on magnetic resonance imaging (MRI) characteristic of sacroiliitis (and in the absence of tumor, fracture, or infection), there are no pathognomonic imaging findings specific for the diagnosis of SIJC pain. As previously discussed, there are also no physical examination findings that accurately identify patients with SIJC pain, although a combination of pain below L5 and localized just medial to the posterior superior iliac spine (PSIS) is suggestive. The diagnosis of SIJC pain therefore rests on a combination of interventional tests to exclude other lumbar sources of pain, and objectively verify the presence of SIJC pain. Once other structures of low back pain have been excluded, consideration of SIJC-specific diagnostic interventions may be entertained. The current gold standard involves blinded, controlled intra-articular local anesthetic injections of the SIJC, or saline placebo-controlled blocks. Because the synovial component of the SIJC is rarely accessed successfully without image guidance, injection of the joint must be performed under fluoroscopy, or possibly computed tomography (CT) guidance.31,32 However, it must be remembered that the sacroiliac joint capsule is frequently incompetent, and extravasation of local anesthetic into surrounding structures, especially from the ventral joint capsule in the region of the traversing lumbosacral plexus, will render such an injection non-specific, and therefore nondiagnostic. Additionally, since the false-positive rate of single anesthetic injections may approach 40%,33–36 no therapeutic decisions regarding ablation or surgery should be made based on a single response to an isolated analgesic test. Patient responses to controlled, comparative or placebo-controlled anesthetic testing must be rigorously assessed and documented. As with any diagnostic procedure, analgesic tests generate negative, indeterminate, and positive results, and have associated false-negative and false-positive rates. Understanding what 1261
Part 4: Extra-Spinal Disorders
constitutes a negative, indeterminate, and positive result is essential. The methodology of comparative and placebo-controlled analgesic testing has been extensively validated elsewhere, and should be considered mandatory reading for all interventional spine diagnosticians.34,35,37–39 It is further recommended that any analgesic test be performed without sedation. Patient responses in the immediate postprocedural period should be rigorously documented, preferably with a q15 minute or q30 minute pain log. Sedation is an inadequate excuse for poor injection technique. Access techniques for the medial40–44 and lateral poles10,45 of the synovial component of the SIJC have been described, as has a technique for isolated injection of the DIOL.10,45 Any image-guided injection of the SIJC must include the use of radiopaque contrast to obviate vascular uptake, and verify contained distribution of injected local anesthetic. Fluoroscopy offers several intrinsic advantages over CT, including the capability for real-time imaging (and detection of vascular uptake of contrast), although the superior contrast and spatial resolution of CT may offer potential advantages in documenting extracapsular or extraligamentous extravasation patterns. In patients with spinal or pelvic hardware, advanced fluoroscopic imaging technologies, such as digital subtraction algorithm (DSA) imaging permits imaging free of the metallic imaging artifacts common to CT.
THERAPEUTIC INTERVENTIONS Injections of the SIJC have not been demonstrated to have therapeutic value except in the isolated instance of sacroiliitis associated with seronegative spondyloarthropathies.46–50 No structure-specific diagnostic information can be gleaned from steroid injection; if a patient experiences relief beyond the duration of action of local anesthetic, all that can be ascertained is that a steroid response may be present. A prolonged steroid response implies that a component of inflammation may be present, but is not structure-specific; local anesthetic injection in and of itself may also provide prolonged analgesia, well beyond the expected duration of conduction block.37 Once the diagnosis of SIJC pain has been established, therapeutic intervention may be considered. Therapeutic options for SIJC pain may be categorized into surgical interventions, other interventions, and denervation procedures. Surgical intervention for SIJC pain is covered elsewhere in this text. Some religiously advocate other therapeutic options, such as manipulation and proliferative therapies. Regrettably, the efficacy of manual medicine techniques and proliferative treatments remain anecdotal. Several denervation procedures for SIJC pain have described targeting the lateral branch nerves of the dorsal rami at various points between the dorsal sacral foramina and the posterior SIJ capsule. Among the first techniques is that described by Kline, involving the generation of a series of bipolar radiofrequency (RF) lesions along the posterior joint line (Fig. 116.5).51 Recognizing the multisegmental innervation of the SIJC, Kline reasoned that the lateral branch nerves must converge along the posterior joint capsule, and serial lesions along the posterior joint line should effectively denervate the joint. However, a study by Ferrante et al., utilizing uncontrolled single anesthetic diagnostic blocks, found that only 36% of patients experienced more than 6 months of >60% relief, and no patients experienced complete relief.26 A more rigorous evaluation with controlled anesthetic blocks and rigorous postblock assessment may have yielded better results, as initial false-positive block responders would have been eliminated from consideration. Another approach toward denervation of lateral branch nerves at L5 and S1 has been described under CT guidance by Gevargez 1262
Fig. 116.5 Bipolar SIJ RF lesioning technique. Cone down anteroposterior radiograph of bipolar electrode placement over caudal dorsal sacroiliac joint capsule. (Courtesy of Matthew T. Kline, M.D.)
et al.25 Like the Ferrante study, a single anesthetic block was used for patient selection. Thirty-five of 38 patients were followed for 3 months, with 34.2% reporting complete relief, and an additional 32% reporting ‘substantial relief.’ Based on a detailed neuroanatomic study of the dorsal sacral plexus and lateral branch topography, Yin et al. published results of a pilot study utilizing a sensory stimulation-guided approach to select pain-conducting from non pain-conducting lateral branch nerves for subsequent RF denervation.10 Dual analgesic injections of the SIJC DIOL were utilized to identify patients with probable SIJC pain after no relief was reported following anesthetic blocks of the lumbar zygapophyseal joints. In this study, provocative discography was not performed to rule out disc pain. Sensory stimulation-guided localization of the lateral branch nerves was performed to identify painful versus nonpainful nerves. The frequency of painful L5 and S1 lateral branch nerves identified in this group of patients was 100%, with 78% of patients demonstrating a painful branch arising from S2 and 42% with painful S3 branches. Although follow-up was limited to 6 months, preliminary results were encouraging, with 64% of patients experiencing longer than 6 months of >60% relief, and among responders, more than half (36% of total) experiencing 100% relief. No complications were noted. A prospective, long-term follow-up study is currently in progress. Ultimately, prospective, controlled studies will be required to identify a gold standard for the treatment of SIJC pain.
DESCRIPTION OF SENSORY STIMULATION-GUIDED LATERAL BRANCH RADIOFREQUENCY NEUROTOMY TECHNIQUE Background Detailed neuroanatomic examination of the dorsal sacral plexus and associated lateral branch nerves innervating the SIJC demonstrates that these nerves follow a complex and variable course to the DIOL and posterior joint capsule. Penetrating numerous ligaments along their course, the segmental lateral branch nerves are inconsistent with regard to number and location in three dimensions soon after exiting the dorsal sacral foramina (Fig. 116.6).10,28 Because consistent lateral branch contributions to the SIJC have been demonstrated to arise from the S2 and S3 dorsal rami, procedures that only target the lateral branch nerves at L5 and S1 may miss pain-bearing conducting from these lower dorsal rami. A description of the sensory stimulation-guided radiofrequency neurotomy targeting the L5 through S3 lateral branch nerves follows.
Section 1: Sacroiliac Joint Syndrome
Fig. 116.6 Wire study of LB topography. Thin gauge wires have been placed directly overlying lateral branch nerves seen entering the dorsal sacroiliac deep interosseous ligament arising from the dorsal sacral foramina of S1 in this cadaver. Heavier gauge wire has been placed at the dorsal margin of the dorsal sacral foramina. Note the variability or number and location of lateral branch nerves entering the dorsal SIJC.
Patient preparation Prior to surgery, the patient must understand that consistent reporting during sensory stimulation significantly contributes to the success or failure of the procedure. Further, the patient should understand that in order to map the lateral branch nerves, it is not feasible to anesthetize the target area prior to electrical stimulation. Movement and repositioning of the radiofrequency electrode is uncomfortable, but once positioned, the pain associated with electrode movement rapidly extinguishes, permitting detailed recording of patient’s sensory responses. Because consistent and clear communication with the patient is an essential component of any stereotactic surgery, no intraoperative sedation is recommended. A mild preoperative analgesic may be administered (e.g. meperidine 25–50 mg i.m.) if indicated. As the likelihood of infection from a percutaneous dorsal sacral RF procedure is low, no preoperative antibiotics are typically required. Contraindications to the procedure include (but are not limited to): a bleeding diathesis, ongoing infectious process, lack of (or refusal to provide) informed consent, organic or nonorganic pathology that would preclude accurate patient–physician communication during the procedure, or the presence of comorbidities that represent a greater threat to well-being than chronic back pain.
Procedural details The patient is brought to the operating theater and placed in the prone position on a radiolucent operating room table. If unilateral, the side of the procedure is verified with the patient. Anesthetic monitors are applied, and supplemental oxygen is provided, if needed. Although the requirement for intraoperative analgesia or anesthesia is exceedingly rare, the presence of a qualified anesthesia provider is invaluable in the event of a significant vasovagal episode or other unexpected intraoperative occurrence. The patient’s back and buttocks are sterilized with an antiseptic skin preparation (e.g. Betadine) and draped in a sterile fashion. Meticulous aseptic technique is observed. Fluoroscopic imaging is utilized to visualize the sacrum in real time, and the fluoroscope is angled parallel to the ring apophysis of S1. A skin entry site is marked and anesthetized with 1% lidocaine just medial to the posterior superior iliac spine on the operative side. To facilitate subsequent introduction of a blunt radiofrequency electrode, a 1.25", 16-gauge
intravenous catheter is introduced percutaneously, through which a 100 mm, 5 or 10 mm active tip, blunt, curved radiofrequency electrode may be advanced. Through this single entry site, the lateral branch nerves from L5 through S3 may be accessed. Initially, the RF electrode is advanced under fluoroscopic imaging to overlie the superior-medial aspect of the sacral ala, in the region of the medial dorsal ramus of L5. It is often helpful to provide the patient with an initial stimulation sensation that is expected to be nonpainful (and if L5–S1 zygapophyseal joint pain has been adequately excluded, stimulation over the medial dorsal ramus should not result in a painful response). Localization of the medial dorsal ramus of L5 is then achieved with application of stimulation (50 Hz, 1 msec pulse duration) at an initial ‘seeking’ voltage of 0.2–0.4 volts. The L5 medial dorsal ramus has an occasional motor component to the multifidus, but gross tetanic contraction of the multifidus at this level is often not seen, especially in older patients with multifidus atrophy. A strong sensory response to patient-blinded stimulation indicates successful localization of the L5 medial dorsal ramus. Nonpainful responses to stimulation include the sensation of ‘buzzing,’ ‘tingling,’ ‘vibration,’ or ‘pulsing.’ Occasionally patients will describe the sensation as ‘thumping.’ These nonpainful sensations are nearly always clearly differentiated from pain. Painful stimulation is most commonly described as sharp,’ ‘burning,’ ‘aching,’ or ‘stabbing.’ Stimulation threshold is then decreased to a minimum voltage necessary to elicit a sensation, as excessive stimulation of a nonpain-bearing nerve may be incorrectly perceived as painful. Because the proximity of the electrode to the target nerve is inversely (and nonlinearly) proportional to the voltage (or, more accurately, current) required for a sensory response, finely manipulating the electrode to achieve the lowest stimulation threshold will maximize the juxtaposition of electrode to target nerve. Ultimately, this close apposition of electrode to nerve is important for RF lesioning, as the size of an RF lesion is relatively small. To minimize the possibility of a false-positive or false-negative response to stimulation, patient-blinded stimulation, including faux stimulation is performed at the minimum threshold stimulation voltage (ideally 27). It is believed that the pelvic volume in obese subjects restricts the natural movements of pelvic rotation. Other factors can restrict pelvic rotation, including loss of mobility of the lumbosacral junction as a result of degenerative disc changes, sequelae of discectomy and arthrodesis, or, more simply, a high seat. Hyperlaxity of the ligaments and a low seat can also increase rotation. Such factors can affect the occurrence of coccygeal pain. The absence of movement when sitting can be due to ossification of coccygeal joints or the presence of immobile discs. The coccyx is usually less mobile in men than women.
HISTORICAL ASSESSMENT Interviewing the patient with coccydynia should include the following four steps: ● ● ● ●
Confirm the diagnosis. Obtain a detailed history of the symptoms. Identify a cause Assess the potential repercussions.
Confirm the diagnosis: where do you feel the pain? Common coccydynia is primarily characterized by its localization to the coccygeal region, the absence of significant symptom referral, and the fact that the pain may be increased or only present in the sitting position. 1289
Part 4: Extra-Spinal Disorders
It is therefore essential to ask the patient to turn his or her back toward the examiner and point to the painful area. The identified region must correspond to the coccyx. Diffuse pain or pain present in both the standing and sitting positions does not indicate common coccydynia. Frequent differential diagnoses include pain associated with depression, low back pain radiating to the coccyx, pudendal neuralgia, anal pathology, or certain sacroiliac pains.
Obtain a detailed history of the symptoms: is this acute or chronic coccydynia? It is important to differentiate acute from chronic coccydynia. Initially, coccydynia is acute and by definition becomes chronic after 2 months. Management will depend on how long the patient has been suffering; acute coccydynia usually resolves spontaneously within a few weeks.
Identify a cause Trauma is a classical cause of coccydynia. Sometimes, patients blame a traumatic event sustained several years earlier, although the role of this past event is questionable. Based on the fact that luxation (see below) is the most commonly observed condition after a trauma, it was demonstrated that the interval between the trauma and the onset of coccydynia is a determining factor.7 A very short or nonexistent interval (such as in postpartum coccydynia) is almost certainly indicative of trauma-related pain. Traumatic coccydynia is very likely if the pain occurs within a month of an injury. After 3 months, it is unlikely that trauma is the cause. It is important to know whether the traumatic event is an occupational injury or not, as the treatment results may be less effective when the trauma is work related. In some cases, coccydynia may develop after moderate trauma, as a result of a long car journey, or riding a bicycle or a horse. In obese patients, excess weight in conjunction with the particular way of changing from standing to sitting (see below), and even sitting itself can be considered as repeated microtraumas. Generally, posttraumatic coccydynia is more frequent in straight coccyges that move into extension when the subject sits down than in curved coccyges that move into flexion.7,9 Curved coccyges are actually relatively well protected during the impact of sitting. Thus, contrary to a common opinion, hooked coccyges are less at risk than straight ones regarding post-traumatic coccygodynia. Apart from a possible trauma, it has been shown that other factors such as BMI and the presence of pain when standing up from sitting could have diagnostic value.6 Determining body mass index is essential, as this factor greatly affects coccygeal biomechanics and, therefore, the culprit lesion. Luxation is more frequently observed in the obese population. The obese subject has a low angle of sagittal pelvic rotation when sitting down. As a result, the coccyx is more or less perpendicular to the seat surface, which increases the risk of luxation. In a normal-weight or lean person, the angle of sagittal pelvic rotation is greater, and the coccyx is parallel to the seat and prone to flexion and hypermobility. In lean patients, a spicule may cause significant irritation due to the absence of perineal fat (see below). PAIN ON STANDING UP FROM SITTING The presence of sharp pain on passing from the sitting to the standing position is a sign that suggests a lesion that can be identified with radiologic imaging. These radiographic abnormalities are usually luxation or osseous spicules.7 As with any information gleaned during history taking, this element is of greater value if the patient mentions it spontaneously. LOW BACK PAIN It is essential to know if the back pain was present before or after the onset of coccydynia. If such pain has developed after the onset of coccydynia, it can be due to bad postures adopted 1290
by the patient to avoid or decrease coccygeal pain. If the low back pain occurred before, it may be a key factor in causing coccydynia (see below).
Assessing potential repercussions Pain tolerance is highly variable. Discomfort is best assessed after a car journey, as virtually all patients experience pain in this case. In some cases, any driving may prove to be impossible. Physical requirements of job-related activities also play a role, as patients who can work standing up are less disadvantaged.
Red flags As with any vertebral pain, identifying red flags is essential, as coccygeal pain may rarely reveal a severe pelvic or lumbar condition. It should be noted that information obtained from the patient is generally sufficient and an MRI is requested only if a red flag is observed.
PHYSICAL EXAMINATION The physical examination takes less time than obtaining the history. In addition to the routine comprehensive interventional spine examination some additional elements are added. The patient is asked to assume the prone position, at which time inspection for the presence of a skin pit or a pilonidal sinus in the natal cleft is conducted. Such findings could indicate the presence of a boney spicule. The patient is asked again to point out the painful area. Palpation of the entire coccyx is conducted to determine the most painful area (where pressure results in the most pain), and if the site corresponds to a disc (sacroor intercoccygeal) or to the tip of the coccyx. It is at this time that an osseous spicule may be palpated, jutting out under the skin. Based on the author’s experience, the rectal examination should be optional. Rectal examination is not recommended in patients under the age of 20–25, as it is often poorly accepted. In men, it can be difficult and painful to reach the coccyx by rectal route. In other cases, the rectal examination makes it possible to mobilize the flexible part of the coccyx to see which movement (flexion or extension) best reproduces coccydynia. The rest of the consultation should be focused upon the radiologic procedure and the therapeutic management. An etiologic diagnosis is sometimes possible at this stage. Failing this, it may be possible to identify elements suggesting the presence of a radiologic lesion (Table 120.1).
INITIAL MANAGEMENT Acute coccydynia (less than 2 months) is best treated with nonnarcotic analgesics. Radiographs are not indicated, except in case of severe pain (or pain related to violent trauma). Most acute coccydynia cases heal spontaneously. Conversely, in cases of chronic coccydynia, dynamic radiographs are essential.
Standard radiographs The standard lateral standing film of the coccyx may be sufficient in acute hyperalgic coccydynia. Such films can detect fractures and crystal arthritis. In all other cases, dynamic radiographs are essential.
Fractures Coccygeal fractures are very rare (two in a thousand according to the author’s findings, where the fracture only involved the first coccygeal vertebra). This is easily understood as the weak point of the coccyx is the sacrococcygeal or intercoccygeal joint and not the
Section 2: Sacral Disorders
Table 120.1: Clinical Elements Suggesting the Presence of a Radiologic Lesion on Dynamic Films Versus no Lesion Items Suggesting a Radiologic Lesion
Items Suggesting Normal Radiographs
Local coccygeal pain
Pain radiating to the buttocks and thighs
Pain only in the sitting position
Significant pain also present in the standing position
Pain on standing up from sitting (especially if mentioned spontaneously)
Absence of pain on standing up from sitting
Pain occurring immediately after sitting down
Pain occurring after 30–60 minutes of sitting
Painful sitting position from the beginning of the day
Painful sitting position especially at the end of the day
Pain relieved for at least a month by a steroid injection
Pain unresponsive to a steroid injection
coccyx itself. Luxation is the most common trauma-related injury. However, fractures of the distal portion of the sacrum are slightly more common (1% in the author’s cases). The real figure may be higher, as most of the author’s patients are referred with chronic coccydynia. Fractures are only responsible for acute coccydynia, since they resolve spontaneously, typically within 3 weeks. Pseudoarthrosis seems to be exceedingly rare as this entity has never been observed in the author’s patients.
Calcifications The presence of a small, rounded calcification into a disc is sometimes observed. Calcification appears to have no diagnostic value, although this aspect has not been studied specifically. However, the author had the opportunity to observe five cases of crystal arthritis (probably hydroxyapatite), i.e. a frequency of 0.5%. The clinical pattern is characterized by very intense, permanent pain, appearing suddenly and spontaneously, and which makes any sitting position unbearable. This type of pain usually responds to oral steroid antiinflammatory agents within a few days.
Fig. 120.1 Standard technique for the ‘sitting’ film.
Dynamic radiographs Since coccydynia is more pronounced in the sitting position, it is essential to compare lateral sitting and lateral standing radiographs when evaluating chronic coccydynia. Radiographs should be taken immediately when there is a history of violent trauma or acute pain. The author has termed this examination ‘dynamic exploration.’10 The author has had the opportunity to evaluate in excess of a thousand cases in this manner. The lateral standing X-ray is taken first. In order for the coccyx to be in a neutral position, it is important that the patient avoids sitting for the 5–10 minutes preceding the X-ray examination. Otherwise, in some cases of hypermobility or luxation, there is not enough time for the coccyx to regain a neutral position. Next, the patient sits on a hard stool with the feet on a footrest (if necessary) so that the thighs are horizontal (as in the usual sitting position) until pain is experienced (Fig. 120.1). If necessary, the subject can lean slightly backward to feel the pain. If the pain cannot be triggered after a few minutes, interpretation of the sitting film will be difficult, since it has been taken in a position of no pain. The radiograph must then be taken in the sitting position, the position that regularly provokes the most intense pain for that patient. The two radiographs are read separately to compare the general appearance, number of vertebrae, curves, sacrococcygeal and intercoccygeal joints, and the presence of a possible fracture, or coccygeal spicule. The two films are then superimposed over a bright source of light, with both sacrums superimposed upon each other to compare and measure sagittal movement of the coccyx (Fig. 120.2).
Fig. 120.2 The range of motion of the coccyx is measured in degrees, after superposition of the two radiographs matching the sacrum. This superposition is obtained by pivoting the sitting film through an angle representing sagittal pelvic rotation. The arrow indicates the most mobile disc. 1291
Part 4: Extra-Spinal Disorders
Angle of mobility It is possible to determine the angle of coccygeal mobility, the apex of which is in the center of the first mobile disc. In two-thirds of cases, coccygeal movement is forward (flexion). Normal values in a control group range from 0° to 25°. An angle of mobility exceeding 30° in women (25° in men) is abnormal.6 In one-third of cases, the coccyx moves backward (extension), resulting in an angle of usually less than 15°. This angle can be increased to 20° only in exceptional cases. As the angle of mobility is the one of greatest importance, it should be measured systematically, except in cases of luxation, which precludes its measurement and is therefore irrelevant. Other angles differ from the angle of mobility, as their significance is purely biomechanical.
Incidence The incidence is the angle at which the coccyx strikes the seat surface. Unfortunately, neither the lateral standing nor the sitting radiograph truly shows the coccyx in this transient position. The solution is to superimpose the two radiographs with both sacra on top of each other. The coccyx of the standing film is then drawn on the sitting film. The angle of this ‘virtual’ coccyx with the horizontal plane is the angle of incidence. The incidence determines the direction in which the coccyx moves.
Sagittal pelvic rotation To superimpose the two sacra, by placing the sitting film on the standing film, the sitting film must be pivoted through an angle representing sagittal pelvic rotation, when the patient passes from the standing to the sitting position (not taking into account the sacroiliac mobility). In a lean subject, the angle of rotation is usually greater than 40°, while in the obese it is usually less than 30°. Sagittal pelvic rotation and incidence are closely associated together (patients with a high pelvic rotation have a low incidence and vice versa). Both are affected by the BMI.
Lesions observed on dynamic radiographs Posterior coccygeal luxation Luxation is the most striking coccygeal lesion (Fig. 120.3). It represents about 20% of the chronic coccydynia cases. Except in very rare
cases of permanent luxation, it occurs only in the sitting position, and spontaneously reduces when the patient stands up. This explains why such a lesion had not been identified prior to the author’s findings. Luxation occurs on straight coccyges, with limited pelvic rotation and a greater angle of incidence. Sacrococcygeal and intercoccygeal discs are equally affected. The coccyx always moves backward. A control-group analysis showed that its displacement had to exceed 20% (based on a measurement method used for spondylolisthesis) to be significant.11 Generally, the backward movement ranges from 50% to 100%, and its implication in pain is almost never an issue. Luxation is by far the most common post-traumatic lesion. Poor pelvic rotation and an increased angle of incidence denotes that the coccyx moves backward if the subject falls, thus increasing the risk of injury if one admits that a fall on the buttocks involves the same pelvic movement pattern as does sitting down. Luxation is also the lesion most often seen in overweight subjects. This is not because obese patients risk more serious injury when falling, but is due to the specific way they sit. Obese individuals have a limited sagittal pelvic rotation (average 15 mm, and spinal stenosis was present if the diameter was
