Physical Medicine and Rehabilitation: Expert Consult- Online and Print 4th Edition

Associate Editors

RANDALL L. BRADDOM MD, MS

LEIGHTON CHAN, MD MPH, MS

Clinical Professor University of Medicine and Dentistry New Jersey Medical School Clinical Professor Robert Wood Johnson Medical Schools New Brunswick, New Jersey

Chief Department of Rehabilitation Medicine Clinical Center National Institutes of Health Bethesda, Maryland

MARK A. HARRAST, MD Director Sports Medicine Fellowship Clinical Associate Professor Department of Rehabilitation Medicine University of Washington Seattle, Washington

KAREN J. KOWALSKE, MD Associate Professor and Chair Department of Physical Medicine and Rehabilitation University of Texas Southwestern Medical Center Dallas, Texas

DENNIS J. MATTHEWS, MD Associate Clinical Professor Department of Rehabilitation Medicine University of Colorado School of Medicine Chair and Medical Director The Children’s Hospital Rehabilitation Center Denver, Colorado

KRISTJAN T. RAGNARSSON, MD Lucy G. Moses Professor and Chair Department of Rehabilitation Medicine Mount Sinai School of Medicine New York, New York

KATHRYN A. STOLP, MD Associate Professor and Chair Department of Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota

Physical Medicine and Rehabilitation FOURTH EDITION

1600 John F. Kennedy Boulevard Suite 1800 Philadelphia, PA 19103-2899 Physical Medicine and Rehabilitation Copyright © 2011 by Saunders, an imprint of Elsevier Inc.

978-1-4377-0884-4

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Notice Knowledge and best practice in this field are constantly changing. As new research and ­experience broaden our understanding, changes in research methods, professional practices, or medical ­treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in ­evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods, they should be mindful of their own safety and the safety of others, ­including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or ­editors, assume any liability for any injury and/or damage to persons or property as a matter of ­product ­liability, negligence, or otherwise, or from any use or operation of any methods, products, ­instructions, or ideas contained in the material herein. Previous editions copyrighted 2007, 2000, 1996 Library of Congress Cataloging-in-Publication Data Physical medicine & rehabilitation / [edited by] Randall L. Braddom ; associate editors, Leighton Chan, Mark A. Harrast. -- 4th ed.     p. ; cm.   Other title: Physical medicine and rehabilitation   Includes bibliographical references and index.   ISBN 978-1-4377-0884-4 (alk. paper)   1. Physical therapy. 2. Medical rehabilitation. I. Braddom, Randall L. II. Chan, Leighton. III. Harrast, Mark A. IV. Title: Physical medicine and rehabilitation.   [DNLM: 1. Physical Therapy Modalities. 2. Rehabilitation--methods. WB 460 P5774 2011]   RM700.P465 2011   615.8’2--dc22 2010002590

Acquisitions Editor: Daniel Pepper Developmental Editor: Ann Ruzycka Anderson Publishing Services Manager: Anne Altepeter Team Manager: Radhika Pallamparthy Senior Project Manager: Beth Hayes Design Direction: Ellen Zanolle

Printed in China. Last digit is the print number:  9  8  7  6  5  4  3  2  1

To my wife, Diana Verdun Braddom How do I love thee? Let me count the ways . . . Elizabeth Barrett Browning, 1850 Diana The giggling princess of delight She dances through my dreams. Her hazel eyes brightly twinkling Light my life with golden beams. Randall L. Braddom, 2002

CONTRIBUTORS Chulhyun Ahn, MD, MS Resident Physician Department of Physical Medicine and Rehabilitation Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Prevention and Management of Chronic Wounds Michael Andary, MD, MS Professor Michigan State University College of Osteopathic Medicine East Lansing, Michigan Electrodiagnostic Medicine I: Fundamental Principles Karen L. Andrews, MD Assistant Professor Department of Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota Quality and Outcome Measures for Medical Rehabilitation Susan D. Apkon, MD Associate Professor Department of Rehabilitation Medicine University of Washington; Director Department of Rehabilitation Medicine Seattle Children’s Hospital Seattle, Washington Examination of the Pediatric Patient Patricia M. Arenth, PhD Assistant Professor Department of Physical Medicine and Rehabilitation University of Pittsburgh Pittsburgh, Pennsylvania Traumatic Brain Injury Jan Avent, BS, MA, PhD Professor Emerita Department of Communicative Sciences and Disorders California State University – East Bay Hayward, California Adult Neurogenic Communication Disorders Karen P. Barr, MD Associate Professor Department of Rehabilitation Medicine University of Washington Seattle, Washington Low Back Pain

Brent A. Bauer, MD, FACP Director Complementary and Integrative Medicine Program Professor of Medicine Department of Internal Medicine Mayo Medical School Rochester, Minnesota Integrative Medicine in Rehabilitation Fin Biering-Sorensen, MD, DMSc Professor and Chair Clinic for Spinal Cord Injuries The Neuroscience Center Rigshospitalet Copenhagen University Hospital Faculty of Health Sciences University of Copenhagen Copenhagen, Denmark Spinal Cord Injury Rina M. Bloch, MD Associate Professor Department of Physical Medicine and Rehabilitation Tufts University School of Medicine Boston, Massachusetts Geriatric Rehabilitation Cathy Bodine, PhD, CCC-SLP Associate Professor Departments of Physical Medicine and Rehabilitation   and Pediatrics Executive Director Assistive Technology Partners Anshutz Medical Campus University of Colorado – Denver Denver, Colorado Computer Assistive Devices and Environmental Controls Andrea J. Boon, MBChB Assistant Professor Department of Physical Medicine and Rehabilitation Assistant Professor Department of Neurology College of Medicine Consultant Department of Physical Medicine and Rehabilitation Mayo Clinic and Foundation Rochester, Minnesota Electrodiagnostic Medicine III: Case Studies Jeffrey S. Brault, DO Consultant Department of Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota Manipulation, Traction, and Massage vii

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Contributors

Andrew D. Bronstein, MD Medical Director Radiology Consultants of Washington Center for Diagnostic Imaging Bellevue, Washington Neurologic and Musculoskeletal Imaging Studies Theodore R. Brown, MD, MPH Director of Neurorehabilitation Multiple Sclerosis Center Evergreen Hospital Medical Center Kirkland, Washington Multiple Sclerosis Thomas N. Bryce, MD Associate Professor Department of Rehabilitation Medicine The Mount Sinai Medical Center New York, New York Spinal Cord Injury Bruce Caplan, PhD Independent Practice Wynnewood, Pennsylvania Psychological Assessment and Intervention in Rehabilitation Diana D. Cardenas, MD, MHA Professor and Chair Chief of Service Jackson Memorial Rehabilitation Hospital Department of Rehabilitation Medicine University of Miami Miller School of Medicine Miami, Florida Management of Bladder Dysfunction Gregory T. Carter, MD, MS Professor Department of Rehabilitation Medicine University of Washington School of Medicine Seattle, Washington Motor Neuron Diseases, Myopathic Disorders Pablo Celnik, MD Medical Director Outpatient Neurorehabilitation Program Director Human Brain Physiology and Stimulation Laboratory Associate Professor Department of Physical Medicine and Rehabilitation Johns Hopkins University Baltimore, Maryland Stroke Syndromes Leighton Chan, MD, MPH Chief Department of Rehabilitation Medicine Clinical Center National Institutes of Health Bethesda, Maryland Pulmonary Rehabilitation Andrea L. Cheville, MD, MSCE Associate Professor Department of Physical Medicine and Rehabilitation Mayo Clinic College of Medicine Rochester, Minnesota Cancer

Anthony Chiodo, MD, MBA Department of Physical Medicine and Rehabilitation University of Michigan Health System Ann Arbor, Michigan Management of Bladder Dysfunction Dexanne B. Clohan, MSA, MD Chief Medical Officer HealthSouth Birmingham, Alabama Quality and Outcome Measures for Medical Rehabilitation Andrew J. Cole, MD Clinical Professor Department of Physical Medicine and Rehabilitation University of Washington President Northwest Spine & Sports Physicians Bellevue, Washington Neurologic and Musculoskeletal Imaging Studies Rory Cooper, PhD Senior Career Scientist Human Engineering Research Laboratories Department of Veterans Affairs FISA/PVA Chair and Distinguished Professor Department of Rehabilitation Science and Technology University of Pittsburgh Pittsburgh, Pennsylvania Wheelchairs and Seating Systems Anita Craig, DO Assistant Professor University of Michigan Ann Arbor, Michigan Rehabilitation of Patients With Neuropathies Loren Davidson, MD Assistant Professor Department of Physical Medicine and Rehabilitation University of California – Davis Sacramento, California Cerebral Palsy R. Drew Davis, MD, FAAPMR, FAAP Assistant Professor Department of Pediatrics Department of Physical Medicine and Rehabilitation University of Alabama – Birmingham Children’s Hospital of Alabama Birmingham, Alabama Myelomeningocele and Other Spinal Dysraphisms Michael J. DePalma, BS, MD Medical Director Virginia Commonwealth University Spine Center Director Interventional Spine Care Fellowship Associate Professor Department of Physical Medicine and Rehabilitation Virginia Commonwealth University Medical College of Virginia Hospitals Richmond, Virginia Common Neck Problems

Contributors

Timothy R. Dillingham, MD, MS Professor and Chair Medical College of Wisconsin Milwaukee, Wisconsin Electrodiagnostic Medicine II: Clinical Evaluation and Findings Carole V. Dodge, BS, CHT Supervisor and Clinical Specialist Occupational Therapy University of Michigan Ann Arbor, Michigan Upper Limb Orthotic Devices Jeanne Doherty, MD Assistant Medical Director Magee Rehabilitation Hospital Director Utilization Management Magee Rehabilitation Hospital Philadelphia, Pennsylvania Degenerative Movement Disorders of the Central Nervous System Bart E. Drinkard, MSPT Senior Physical Therapist Medicine Department National Institutes of Health Bethesda, Maryland Pulmonary Rehabilitation Daniel Dumitru, MD, PhD Professor Department of Rehabilitation Medicine Deputy Chair University of Texas Health Science Center San Antonio, Texas Electrodiagnostic Medicine I: Fundamental Principles Gisli Einarsson, MD, PhD Associate Professor Department of Rehabilitation Medicine Landspitali University Hospital Faculty of Medicine University of Iceland Reykjavik, Iceland Cardiac Rehabilitation Alberto Esquenazi, MD Chair and Professor Department of Physical Medicine and Rehabilitation MossRehab Albert Einstein Health Network Director Gait and Motion Analysis Laboratory Regional Amputee Center MossRehab Elkins Park, Pennsylvania Gait Analysis: Technology and Clinical Applications

Karen Ethans, BSc, MD Associate Professor Department of Medicine Section of Physical Medicine and Rehabilitation University of Manitoba Service Chief Spinal Cord Injury Health Sciences Centre Winnipeg, Manitoba, Canada Spasticity Management Elizabeth Feldbruegge, MPT Physical Therapist Arthritis Center Rehabilitation Institute of Chicago Chicago, Illinois Rheumatic Diseases Jonathan T. Finnoff, DO Assistant Professor Mayo Clinic Rochester, Minnesota Musculoskeletal Disorders of the Upper Limb Colleen M. Fitzgerald, MD, BS Medical Director Women’s Health Rehabilitation Department of Physical Medicine and Rehabilitation Assistant Professor Northwestern University Chicago, Illinois Sexual Dysfunction and Disability Brian S. Foley, MD, MBA Medical Director Community Spine Center Indianapolis, Indiana Occupational Rehabilitation Robert G. Frank, PhD Provost, Senior Vice President for Academic Affairs,   and Professor College of Public Health Kent State University Kent, Ohio Psychological Assessment and Intervention in Rehabilitation Guy Fried, MD Chief Medical Officer and Associate Professor Department of Rehabilitation Medicine Jefferson University Hospital Philadelphia, Pennsylvania Degenerative Movement Disorders of the Central Nervous System Vincent Gabriel, MD, MSc, FRCPC Assistant Professor Division of Physical Medicine and Rehabilitation Foothills Medical Center University of Calgary Calgary, Alberta, Canada Burn Rehabilitation

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Contributors

Ralph E. Gay, MD, DC Assistant Professor Department of Physical Medicine and Rehabilitation Mayo Clinic College of Medicine Rochester, Minnesota Integrative Medicine in Rehabilitation Robert J. Goldman, MD, FAAPM&R, CWS Medical Director Fort HealthCare Wound and Edema Center Fort Medical Group Fort Memorial Hospital Fort Atkinson, Wisconsin Prevention and Management of Chronic Wounds Brian E. Grogg, BS, MD Rochester, Minnesota Manipulation, Traction, and Massage Ellen Guess, OTR, BS Occupational Therapy Clinical Training Coordinator   for Rehabilitation Department of Occupational Therapy The Children’s Hospital Aurora, Colorado Achieving Functional Independence Nelson Hager, MD, MS Associate Clinical Professor Department of Physical Medicine and Rehabilitation Department of Orthopedics and Sports Medicine University of Washington Woodinville, Washington Spinal Injection Techniques Jay J. Han, MD Associate Professor Department of Physical Medicine and Rehabilitation Davis School of Medicine University of California Sacramento, California Myopathic Disorders Pamela A. Hansen, MD Assistant Professor Physical Medicine and Rehabilitation University of Utah Salt Lake City, Utah Musculoskeletal Disorders of the Lower Limb R. Norman Harden, MD Director Center for Pain Studies Rehabilitation Institute of Chicago Physical Medicine and Rehabilitation Northwestern University Chicago, Illinois Chronic Pain

Mark A. Harrast, MD Director Sports Medicine Fellowship Clinical Associate Professor Department of Rehabilitation Medicine Department of Orthopaedics and Sports Medicine University of Washington Seattle, Washington Low Back Pain, Sports Medicine Richard L. Harvey, MD Medical Director Stroke Rehabilitation Wesley and Suzanne Dixon Stroke Chair Rehabilitation Institute of Chicago Feinberg School of Medicine Northwestern University Chicago, Illinois Stroke Syndromes William J. Hennessey, MD President Pennsylvania Physical Medicine Greensburg, Pennsylvania Lower Limb Orthotic Devices Radha Holavanahalli, PhD Assistant Professor Department of Physical Medicine and Rehabilitation University of Texas Southwestern Medical Center Dallas, Texas Burn Rehabilitation Chang-Zern Hong, MD Research Professor Hung-Kuang University Sha-Lu, Taiwan Clinical Professor University of California – Irvine Irvine, California Muscle Pain Syndromes Kurtis M. Hoppe, MD Consultant Mayo Clinic Instructor Department of Physical Medicine and Rehabilitation Mayo Clinic College of Medicine Rochester, Minnesota Physical Agent Modalities Mark E. Huang, MD Associate Professor Department of Physical Medicine and Rehabilitation Chief Medical Information Officer Feinberg School of Medicine Rehabilitation Institute of Chicago Chicago, Illinois Rehabilitation and Prosthetic Restoration in Lower Limb Amputation

Contributors

Joseph Ihm, MD Assistant Professor Department of Physical Medicine and Rehabilitation Feinberg School of Medicine Northwestern University Rehabilitation Institute of Chicago Chicago, Illinois Peripheral Joint and Soft Tissue Injection Techniques Marta Imamura, MD, PhD Chief Technical Service Division of Physical Medicine Collaborative Professor Department of Orthopaedics and Traumatology School of Medicine University of São Paulo São Paulo, Brazil International Physical Medicine and Rehabilitation Jeffrey G. Jenkins, MD Associate Professor and Residency Program Director Department of Physical Medicine and Rehabilitation University of Virginia Charlottesville, Virginia Therapeutic Exercise Jose Jimenez, MD, FRCPC Professor Emeritus University of Toronto Toronto, Ontario, Canada International Physical Medicine and Rehabilitation Shana Johnson, MD Physician Department of Physical Medicine and Rehabilitation Providence Physical Medicine Clinic – Olympia Olympia, Washington Multiple Sclerosis Nanette Joyce, BA, DO Neuromuscular Disease Clinical Fellow Department of Physical Medicine and Rehabilitation Davis Health System University of California – Davis Sacramento, California Motor Neuron Diseases Robert E. Kappler, DO Professor Midwestern University Downers Grove, Illinois Manipulation, Traction, and Massage Amol M. Karmarkar, PhD Post Doctoral Fellow Department of Rehabilitation Sciences University of Texas Medical Branch Galveston, Texas Wheelchairs and Seating Systems

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Marla Kaufman, MD Clinical Assistant Professor Departments of Rehabilitation Medicine   and ­Orthopaedics and Sports Medicine University of Washington Medicine Sports and Spine Physicians University of Washington Medical Center Seattle, Washington Spinal Injection Techniques Brian M. Kelly, DO Associate Professor Department of Physical Medicine and Rehabilitation University of Michigan Ann Arbor, Michigan Upper Limb Orthotic Devices David J. Kennedy, MD Assistant Professor Department of Orthopaedics and Rehabilitation University of Florida Gainesville, Florida Peripheral Joint and Soft Tissue Injection Techniques Michelle Kennedy, MS Exercise Physiologist Rehabilitation Medicine Clinical Research Center The National Institutes of Health Bethesda, Maryland Pulmonary Rehabilitation Mary F. Kessler Administrative Projects Coordinator Department of Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota Quality and Outcome Measures for Medical Rehabilitation Randall E. Keyser, PhD Associate Professor Center for the Study of Chronic Illness and Disability College of Health and Human Services George Mason University Fairfax, Virginia Clinical Investigator Rehabilitation Medicine Mark O. Hatfield Clinical Research Center National Institutes of Health Bethesda, Maryland Pulmonary Rehabilitation John C. King, MD Professor Department of Rehabilitation Medicine University of Texas Health Sciences Center – San Antonio Director Reeves Rehabilitation Center University Health System – San Antonio San Antonio, Texas Neurogenic Bowel: Dysfunction and Rehabilitation

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Contributors

Heidi Klingbeil, MD, BS Columbia University Medical Center New York, New York Employment of Persons With Disabilities Susan Knapton, MD Assistant Professor Department of Physical Medicine and Rehabilitation University of Texas Southwestern Medical Center Dallas, Texas Lower Limb Peripheral Vascular Disease Alicia M. Koontz, PhD Research Biomedical Engineer Human Engineering Research Laboratories Department of Veterans Affairs Associate Professor Rehabilitation Science and Technology University of Pittsburgh Pittsburgh, Pennsylvania Wheelchairs and Seating Systems Karen J. Kowalske, MD Associate Professor and Chair Department of Physical Medicine and Rehabilitation University of Texas Southwestern Medical Center Dallas, Texas George H. Kraft, MD, MS Alvord Professor of Multiple Sclerosis Research Professor Department of Rehabilitation Medicine Adjunct Professor Department of Neurology Director Western Multiple Sclerosis Center Co-Director Muscular Dystrophy Clinic Director Department of Electrodiagnostic Medicine University of Washington Seattle, Washington Multiple Sclerosis Todd A. Kuiken, MD, PhD Professor and Director Center for Bionic Medicine Department of Physical Medicine and Rehabilitation   and Biomechanical Engineering Rehabilitation Institute of Chicago Northwestern University Chicago, Illinois Rehabilitation and Prosthetic Restoration in Lower Limb Amputation Christina Kwasnica, MD Medical Director Neurorehabilitation Barrow Neurological Institute Phoenix, Arizona Traumatic Brain Injury

Scott Laker, MD Clinical Assistant Professor Department of Rehabilitation Medicine University of Washington Seattle, Washington Sports Medicine Alison E. Lane, Phd, OTR/L Assistant Professor School of Allied Medical Professions College of Medicine The Ohio State University Columbus, Ohio Charles Law, MD Associate Professor Department of Pediatrics University of Alabama Birmingham, Alabama Myelomeningocele and Other Spinal Dysraphisms Paul Lento, MD Associate Professor Temple University School of Medicine Department of Physical Medicine and Rehabilitation Temple University Hospital Philadelphia, Pennsylvania Peripheral Joint and Soft Tissue Injection Techniques C. David Lin, MD Assistant Professor Department of Rehabilitation Medicine Weill Cornell Medical College New York, New York The Physiatric History and Physical Examination Robert Lipschutz, BS Department of Mechanical Engineering Drexel University Philadelphia, Pennsylvania Certificate Prosthetics and Orthotics Post Graduate Medical School New York University New York, New York Certified Prosthetist and Director Department of Prosthetics and Orthotics Education Rehabilitation Institute of Chicago Instructor Clinical Physical Medicine and Rehabilitation Northwestern University Neural Engineering Center for Artificial Limbs Rehabilitation Institute of Chicago Department of Physical Medicine and Rehabilitation Northwestern University Chicago, Illinois Rehabilitation and Prosthetic Restoration in Lower Limb Amputation Erin Maslowski, MD Sports and Spine Fellow Rehabilitation Medicine University of Washington Seattle, Washington Sports Medicine

Contributors

Koichiro Matsuo, DDS, PhD Department of Special Care Dentistry Matsumoto Dental University Shiojiri, Nagano, Japan Rehabilitation of Patients With Swallowing Disorders Dennis J. Matthews, MD Associate Clinical Professor Department of Rehabilitation Medicine University of Colorado School of Medicine Chair and Medical Director The Children’s Hospital Rehabilitation Center Denver, Colorado R. Samuel Mayer, MD Vice Chair for Education Deputy Director Quality Improvement Department of Physical Medicine and Rehabilitation Johns Hopkins Hospital Baltimore, Maryland Transplantation of Organs: Rehabilitaion to Maximize Outcomes Craig M. McDonald, MD Chair Department of Physical Medicine and Rehabilitation Professor Pediatric Physical Medicine and Rehabilitation Director NIDRR, RRTC in Neuromuscular Diseases Director MDA Neuromuscular Disease Clinics University of California School of Medicine Davis, California Myopathic Disorders John Melvin, BSc, MD, MMSc Chair and Michie Professor Rehabilitation Medicine Jefferson Medical College Philadelphia, Pennsylvania International Physical Medicine and Rehabilitation Laura Ann Miller, PhD, CP Assistant Professor Physical Medicine and Rehabilitation Neural Engineering Center for Artificial Limbs Rehabilitation Institute of Chicago Chicago, Illinois Rehabilitation and Prosthetic Restoration in Lower Limb Amputation Daniel P. Moore, MD Chair Physical Medicine and Rehabilitation East Carolina University Department of Physical Medicine and Rehabilitation Greenville, North Carolina Spinal Orthoses

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Patricia W. Nance, MD, FRCPC, FAAPMR Professor University of California – Irvine Chief Rehabilitation Service Veterans Administration Long Beach Healthcare System Long Beach, California Spasticity Management Michael W. O’Dell, MD Chief of Clinical Services Department of Rehabilitation Medicine NewYork–Presbyterian Hospital Weill Cornell Medical Center Professor Clinical Rehabilitation Medicine Division of Rehabilitation Medicine Weill Cornell Medical College New York, New York The Physiatric History and Physical Examination Bryan J. O’Young, MD Clinical Associate Professor Rehabilitation Medicine New York University School of Medicine Rusk Institute of Rehabilitation Medicine Langone Medical Center New York University New York, New York Transplantation of Organs: Rehabilitaion to Maximize Outcomes Heather S. Ohl, RN, BSN, CRRN Coordinator Prospective Payment System Physical Medicine and Rehabilitation Mayo Clinic Rochester, Minnesota Quality and Outcome Measures for Medical Rehabilitation Joyce Oleszek, MD Assistant Professor Department of Rehabilitation University of Colorado – Denver Aurora, Colorado Cerebral Palsy Jeffrey B. Palmer, MD Lawrence Cardinal Shehan Professor of Physical Medicine and Rehabilitation Chair Department of Physical Medicine and Rehabilitation Professor of Otolaryngology and Head and Neck Surgery Functional Anatomy and Evolution School of Medicine Johns Hopkins University Physiatrist-in-Chief Johns Hopkins Hospital Chair Department of Physical Medicine and Rehabilitation The Good Samaritan Hospital of Maryland Baltimore, Maryland Rehabilitation of Patients With Swallowing Disorders

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Contributors

André Panagos, MD, MSC Spine & Sports Medicine of New York New York, New York The Physiatric History and Physical Examination Geetha Pandian, MD Clinical Professor Physical Medicine and Rehabilitation University of Texas Southwestern Medical Center Dallas, Texas Lower Limb Peripheral Vascular Disease Atul T. Patel, MD, MHSA Medical Director Rehabilitation Unit Research Medical Center Kansas City Bone and Joint Clinic Kansas City, Missouri Upper Limb Orthotic Devices Debra Paul, BS, OTR Program Manager Department of Occupational Therapy The Children’s Hospital Aurora, Colorado Achieving Functional Independence Cathy A. Pelletier, PhD, MS, CCC-SLP Assistant Professor Physical Medicine and Rehabilitation Johns Hopkins Hospital Baltimore, Maryland Rehabilitation of Patients With Swallowing Disorders Kristjan T. Ragnarsson, MD Lucy G. Moses Professor and Chair Department of Rehabilitation Medicine Mount Sinai School of Medicine New York, New York Spinal Cord Injury Stephanie A. Reid-Arndt, PhD, ABPP Associate Chair and Assistant Professor Department of Health Psychology University of Missouri Columbia, Missouri Psychological Assessment and Intervention in Rehabilitation James K. Richardson, MD Associate Professor Department of Physical Medicine and Rehabilitation University of Michigan Health Systems Ann Arbor, Michigan Rehabilitation of Patients With Neuropathies James P. Robinson, MD, PhD Clinical Associate Professor Department of Rehabilitation Medicine University of Washington Seattle, Washington Impairment Rating and Disability Determination

Gianna Rodriguez, BS, MD Assistant Professor Physical Medicine and Rehabilitation University of Michigan Ann Arbor, Michigan Neurogenic Bowel: Dysfunction and Rehabilitation Emily H. Rogers, MPH Department of Physical Medicine and Rehabilitation University of Pittsburgh Pittsburgh, Pennsylvania Traumatic Brain Injury Elliot J. Roth, MD Paul B. Magnuson Professor and Chair Department of Physical Medicine and Rehabilitation Feinberg School of Medicine Northwestern University Chicago, Illinois Stroke Syndromes Michele J. Rustin, PhD,  ABPP Independent Practice Atlanta, Georgia Psychological Assessment and Intervention in Rehabilitation Richard Salcido, MD Chair Physical Medicine and Rehabilitation Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Prevention and Management of Chronic Wounds Gregory Samson, MD Voluntary Assistant Professor Staff Physician Department of Rehabilitation Medicine Spinal Cord Injury Service Miami Veterans Administration Healthcare System Miller School of Medicine University of Miami Miami, Florida Management of Bladder Dysfunction Lalith Satkunam, MBBS, FRCPC Professor Divisions of Physical Medicine and Rehabilitation   and Anatomy and Cell Biology University of Alberta Medical Lead Regional Spasticity Program for Adults Glenrose Rehabilitation Hospital Edmonton, Alberta Spasticity Management Michael Saulino, MD, PhD Assistant Professor Thomas Jefferson University Philadelphia, Pennsylvania Physiatrist MossRehab Elkins Park, Pennsylvania Degenerative Movement Disorders of the Central Nervous System

Contributors

Mark R. Schmeler, PhD, OTR/L, ATP Assistant Professor Department of Rehabilitation Science and Technology School of Health and Rehabilitation Sciences University of Pittsburgh Pittsburgh, Pennsylvania Wheelchairs and Seating Systems Kelly M. Scott, MD Assistant Professor Physical Medicine and Rehabilitation University of Texas Southwestern Medical Center Dallas, Texas Sexual Dysfunction and Disability Richard E. Seroussi, MD, MSc Clinical Assistant Professor Department of Rehabilitation Medicine University of Washington Medical Center Seattle Spine & Sports Medicine Seattle, Washington Impairment Rating and Disability Determination Craig K. Seto, MD, FAAFP, CAQ (Sports Medicine) Associate Professor Family Medicine Director Primary Care Sports Medicine Fellowship Assistant Residency Director Department of Family Medicine University of Virginia Health System Charlottesville, Virginia Therapeutic Exercise Terrence P. Sheehan, MD Chief Medical Officer Adventist Rehabilitation Hospital of Maryland Rockville, Maryland Rehabilitation and Prosthetic Restoration in Upper Limb Amputation

Beth S. Slomine, PhD, ABPP Clinical Neuropsychologist Associate Professor Department of Neuropsychology Kennedy Krieger Institute School of Medicine Johns Hopkins University Baltimore, Maryland Psychological Assessment and Intervention in Rehabilitation Donald M. Spaeth, PhD Rehabilitation Science Adjunct Assistant Professor School of Health and Rehabilitation Sciences Department of Rehabilitation Science   and Technology University of Pittsburgh Health Research Scientist Human Engineering Research Laboratories Department of Veterans Affairs Veterans Administration Pittsburgh Healthcare System Pittsburgh, Pennsylvania Wheelchairs and Seating Systems Kevin Sperber, MD Assistant Professor Clinical Rehabilitation Medicine Assistant Professor Clinical Rehabilitation Medicine   in Anesthesiology Columbia University College Physicians   and Surgeons Adjunct Assistant Professor Clinical Rehabilitation Medicine Weill Cornell Medical College New York, New York Employment of Persons With Disabilities

Mehrsheed Sinaki, MD, MS Professor Department of Physical Medicine and Rehabilitation Mayo Clinic College of Medicine Consultant Department of Physical Medicine and Rehabilitation Rochester, Minnesota Osteoporosis

Steven P. Stanos, DO Medical Director Center for Pain Management Rehabilitation Institute of Chicago Assistant Professor Department of Physical Medicine and Rehabilitation Feinberg School of Medicine Northwestern University Chicago, Illinois Chronic Pain

Mark A. Skirgaudas, MD Musculoskeletal Radiologist Radiology Consultants of Washington and Center   for Diagnostic Imaging Kirkland, Washington Neurologic and Musculoskeletal Imaging Studies

Siobhan Statuta, MD Sports Medicine Fellow Department of Family Medicine University of Virginia Charlottesville, Virginia Therapeutic Exercise

Curtis W. Slipman, MD Retired Miami Beach, Florida Common Neck Problems

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Contributors

Adam B. Stein, MD Chair Department of Physical Medicine and Rehabilitation North Shore – Long Island Jewish Health System Chair and Associate Professor Department of Physical Medicine and Rehabilitation School of Medicine Hofstra University Great Neck, New York Spinal Cord Injury Steven A. Stiens, MD, MS Director Spinal Cord Medicine, Fellowship Program Associate Professor Department of Rehabilitation Medicine University of Washington Attending Physician University Hospital Harborview Medical Center Veterans Administration Puget Sound Health Care System Seattle, Washington Neurogenic Bowel: Dysfunction and Rehabilitation, Transplantation of Organs: Rehabilitaion to Maximize Outcomes Alison Stout, DO Director Spine and Musculoskeletal Medicine Rehabilitation Medicine Veterans Affairs Puget Sound Health Care Services Department of Rehabilitation Medicine University of Washington Seattle, Washington Spinal Injection Techniques Jeffrey A. Strommen, MD Assistant Professor Physical Medicine and Rehabilitation and Neurology Mayo Clinic Rochester, Minnesota Electrodiagnostic Medicine III: Case Studies Paul Sugg, BS, CPO, CPed, FAAOP EastPoint Prosthetics and Orthotics Kinston, North Carolina Spinal Orthoses Mukul Talaty, PhD Biomechanics Researcher Gait and Motion Analysis Laboratory MossRehab Albert Einstein Healthcare Network Elkins Park, Pennsylvania Gait Analysis: Technology and Clinical Applications Edward Tilley, CO Manager, Orthotics Services University Health Systems of Eastern North Carolina Pitt County Memorial Hospital Greenville, North Carolina Spinal Orthoses

Santiago Toledo, MD Medical Director Orthopaedics Rehabilitation Physical Medicine and Rehabilitation Rehabilitation Institute of Chicago Assistant Professor Physical Medicine and Rehabilitation Feinberg School of Medicine Northwestern University Chicago, Illinois Rheumatic Diseases Kathleen Trapani, BA, MPT Physical Therapist Little Company of Mary Hospital Evergreen Park, Illinois Rheumatic Diseases Mark D.Tyburski, MD Assistant Chief Physical Medicine and Rehabilitation Spine Clinic The Permanente Medical Group Sacramento and Roseville, California Chronic Pain Jay M. Uomoto, PhD Liaison and Senior Consultant Traumatic Brain Injury Veterans Administration and Department of Defense Office of Rehabilitation Services U.S. Department of Veterans Affairs Washington, DC Psychological Assessment and Intervention in Rehabilitation Christopher J.Visco, MD Assistant Professor Department of Rehabilitation and Regenerative Medicine College of Physicians and Surgeons Columbia University New York Presbyterian Hospital New York, New York Peripheral Joint and Soft Tissue Injection Techniques Amy K. Wagner, MD Associate Professor and Vice Chair Research Department of Physical Medicine and Rehabilitation Associate Director Rehabilitation Research Safar Center for Resuscitation Research Graduate Training Faculty Center for Neuroscience University of Pittsburgh Pittsburgh, Pennsylvania Traumatic Brain Injury

Contributors

Delaina Walker-Batson, PhD Director The Stroke Center Professor Department of Communication Sciences and Disorders Texas Women’s University Dallas, Texas Adult Neurogenic Communication Disorders David C. Weber, MD Mayo Clinic Rochester, Minnesota Physical Agent Modalities Jonathan H. Whiteson, MD Assistant Professor Rehabilitation Medicine Department of Physical Medicine and Rehabilitation School of Medicine New York University New York, New York Cardiac Rehabilitation Robert P. Wilder, MD Associate Professor Department of Physical Medicine and Rehabilitation Medical Director The Runner’s Clinic Team Physician University of Virginia Athletics University of Virginia Charlottesville, Virginia Therapeutic Exercise Stuart E. Willick, MD, FACSM Associate Professor Orthopaedic Center University of Utah Salt Lake City, Utah Musculoskeletal Disorders of the Lower Limb Pamela E. Wilson, MD Department of Physical Medicine and Rehabilitation Medicine University of Colorado The Children’s Hospital Aurora, Colorado Examination of the Pediatric Patient Joshua G. Woolstenhulme, DPT Research Fellow Physical Therapist Department of Rehabilitation Medicine Clinical Research Center National Institutes of Health Bethesda, Maryland Pulmonary Rehabilitation

Sam S.H. Wu, MD, MA, MPH, MBA Associate Professor and Vice Chair Clinical Operations Department of Physical Medicine and Rehabilitation University of Pennsylvania Health System Chief Medical Officer Good Shepherd Penn Partners Medical Director Penn Institute for Rehabilitation Medicine Medical Director Stroke Program Penn Institute for Rehabilitation Medicine Medical Director Delaware Valley Stroke Council President, Board of Directors Delaware Valley Stroke Council Department of Physical Medicine and Rehabilitation University of Pennsylvania Health System Philadelphia, Pennsylvania Prevention and Management of Chronic Wounds Robert K.Yang, MD, MHA Clinical Assistant Professor Department of Orthopedics and Rehabilitation University of Iowa Iowa City, Iowa Integrative Medicine in Rehabilitation Mark A.Young MD, MBA, FACP Chair Department of Physical Medicine and Rehabilitation The Workforce and Technology Center Maryland Vocational Rehabilitation Center Division of Rehabilitation Services Department of Education Faculty Physical Medicine and Rehabilitation Johns Hopkins School of Medicine Baltimore, Maryland Faculty Department of Rehabilitation New York University Faculty Department of Neurology University of Maryland White Marsh, Maryland Transplantation of Organs: Rehabilitation to Maximize Outcomes David T. Y   u, MD Physical Medicine and Rehabilitation Virginia Mason Medical Center Seattle, Washington Electrical Stimulation, Stroke Syndromes

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PREFACE The goal of the fourth edition (and all editions of the textbook) has been to create a practical, clinically useful, and user-friendly textbook encompassing the breadth of the field of physical medicine and rehabilitation. This continues to be a moving target because the field is dynamic. New treatments constantly come on the scene, and pioneering physiatrists are consistently expanding the field by reaching out to new areas of patient care. Feedback from readers indicates that one of the reasons the first three editions enjoyed worldwide popularity was their readability. In this edition I have made every effort to make the book even more readable and to maximize “reader efficiency.” A sincere effort has been made to write and edit the book in such a way that the reader can learn the “most per minute.” Thanks to our friends at Elsevier, the fourth edition has additional upgrades in production values. The majority of the illustrations are in color. The website has additional information to enhance that included in the book, including multiple-choice self-assessment questions for each chapter. These questions will help readers determine how well they have mastered the material. The website for this edition will provide important updates as they become available. The website is now available at no additional cost to all who purchase the textbook.

The book is again divided into four major sections. Section 1 discusses the evaluation of patients typically seen in the practice of physical medicine and rehabilitation (Chapters 1 to 11). Section 2 examines treatment techniques and special equipment used in this field (Chapters 12 to 25). Section 3 discusses the therapeutic issues and problems commonly seen in the practice of physical medicine and rehabilitation (Chapters 26 to 35). Section 4 covers specific diagnoses faced by the physiatrist both in physical medicine and in rehabilitation (Chapters 36 to 61). It is true that one could write an entire book about the topic of each of the chapters in this text. One of the tasks of the authors and editors was to take the huge body of information that now comprises the field of physical medicine and rehabilitation and condense it into a textbook of reasonable size. The fourth edition has been carefully edited to still fit into one volume, and we have been able to use the massive publishing resources and efficiencies of Elsevier to overcome inflationary pressures and actually slightly lower the price. As with the first three editions, we welcome comments, suggestions, and constructive criticism from members of the physical medicine and rehabilitation community and from all readers.

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ACKNOWLEDGMENTS My sincerest thanks to: The 155 contributors and many others, without whom this edition of the book could not have been completed. My wife, Diana Verdun Braddom, whose constant encouragement and support made this undertaking a labor of love. The excellent staff of Elsevier, especially Dolores Meloni, Ann Ruzycka Anderson, and Beth Hayes. The Associate Editorial Board, Leighton Chan, MD, MPH; Mark A. Harrast, MD; Karen J. Kowalske, MD;  Dennis J. Matthews, MD; Kristjan Ragnarsson, MD; and Kathryn A. Stolp, MD

The readers of the first three editions who have sent their suggestions, many of which have been incorporated into the fourth edition. The hundreds of contributors for the first three  editions, who laid a solid foundation for the content of this edition. The translators of one or more of the previous  editions into Italian and Turkish. Randall L. Braddom, MD, MS

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CHAPTER 1 THE PHYSIATRIC HISTORY AND PHYSICAL EXAMINATION Michael W. O’Dell, C. David Lin, and André Panagos

The physiatric history and physical examination (H&P) serves several purposes. It is the data platform from which a treatment plan is developed. It also serves as a written record that communicates to other rehabilitation and nonrehabilitation health care professionals. Finally, the H&P provides the basis for physician billing16 and serves as a medicolegal document. Physician documentation has become the critical component in inpatient rehabilitation reimbursement under prospective payment, as well as proof for continued coverage by private insurers. The scope of the physiatric H&P varies enormously depending on the setting, from the focused assessment of an isolated knee injury in an outpatient setting, to the comprehensive evaluation of a patient with traumatic brain or spinal cord injury admitted for inpatient rehabilitation. An initial evaluation is almost always more detailed and comprehensive than subsequent or follow-up evaluations. An exception would be when a patient is seen for a follow-up visit with substantial new signs or symptoms. Physicians in training tend to overassess, but with time the experienced physiatrist develops an intuition for how much detail is needed for each patient given a particular presentation and setting. The physiatric H&P resembles the traditional format taught in medical school but with an additional emphasis on history, signs, and symptoms that affect function (performance). The physiatric H&P also identifies those systems not affected that might be used for compensation.22 Familiarity with the 1980 and 1997 World Health Organization classifications is invaluable in understanding the philosophic framework for viewing the evaluation of persons with physical and cognitive disabilities (Table 1-1).76,77 Identifying and treating the primary impairments to maximize performance becomes the primary thrust of physiatric evaluation and treatment. Because patients cared for in rehabilitation medicine can be extremely complicated, the H&P is many times a work in progress. Confirmation of historical and functional items by other team members, health care professionals, and family members can take several days. Many of the functional items discussed in this chapter will actually be assessed and explored more fully by other interdisciplinary team members during the course of inpatient or outpatient treatment. It is imperative that the physiatrist stays abreast of additional information and findings as they become available, and that lines of verbal or written communication be directed through the medical leadership of the team. The exact structure of the physiatric assessment is determined in part by personal preference, training background,

and institutional requirements (physician billing compliance expectations, forms committees, and regulatory oversight). The use of templates can be invaluable in maximizing the thoroughness of data collection and minimizing documentation time. Pertinent radiologic and laboratory findings should be clearly documented. The essential elements of the physiatric H&P are summarized in Table 1-2. Assessment of some or all of these elements is required for a complete understanding of the patient’s state of health and the illness for which he or she is being seen. These elements also form the basis for a treatment plan. An emergence in the use of electronic medical records (EMR) has significantly altered the landscape for documentation of the physiatric H&P in both the inpatient and outpatients settings.23 Among the advantages of the EMR are increased legibility, time efficiency afforded by the use of templates and “smart phrases” that can be tailored to individual practitioners, and automated warnings regarding medication interactions or errors, as well as faster and more accurate billing. Disadvantages include overuse of the “copy and paste” function, leading to the appearance of redundancy among consecutive notes and the perpetuation of potentially inaccurate information, automated importation of data not necessarily reviewed by the practitioner at the time of service, and “alarm fatigue.” As regulation of hospital and physician practice and billing increases, the EMR will become more important in ensuring the proper, and sometimes convoluted, documentation required for safety initiatives40 and physician payment.15

The Physiatric History History-taking skills are part of the art of medicine and are required to fully assess a patient’s presentation. One of the unique aspects of physiatry is the recognition of functional deficits caused by illness or injury. Identification of these deficits allows for the design of a treatment program to restore performance. In a person with stroke, for example, the most important questions for the physiatrist are not just the etiology or location of the lesion but also “What functional deficits are present as a result of the stroke?” The answer could include deficits in swallowing, communication, mobility, cognition, activities of daily living (ADL), or a combination of these. The time spent in taking a history also allows the patient to become familiar with the physician, establishing rapport and trust. This initial rapport is critical for a constructive and productive doctor–patient–family relationship and 3

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Table 1-1  World Health Organization Definitions Term

Definition

1980 Impairment

Any loss or abnormality of psychologic, physiologic, or anatomic structure or function

Disability

Any restriction or lack resulting from an impairment of the ability to perform an activity in the manner or within the range considered normal for a human being

Handicap

A disadvantage for a given individual, resulting from an impairment or a disability, that limits or prevents the fulfilment of a role that is normal for that individual

words. A patient can present with several related or unrelated complaints, in which case it is helpful to have the patient rank problems from “most bothersome” to “least bothersome.” The specific circumstance of a patient offering a chief complaint can also allude to a degree of disability or handicap. For example, knowing that an obese mail carrier presents with the chief complaint of difficulty in walking because of knee pain could suggest not only the impairment but also an impact on his vocation and role as a provider for his family (participation, handicap).

History of the Present Illness

1997 Impairment

Any loss or abnormality of body structure or of a physiologic or psychologic function (essentially unchanged from the 1980 definition)

Activity

The nature and extent of functioning at the level of the person

Participation

The nature and extent of a person’s involvement in life situations in relationship to impairments, activities, health conditions, and contextual factors

From World Health Organization 198076 and 1997,77 with permission of the World Health Organization.

can also help the physician learn about such sensitive areas as the sexual history and substance abuse. It can also have an impact on outcome, as a trusting patient tends to be a more compliant patient.62 Assessing the tone of the patient and/or family (such as anger, frustration, resolve, and determination), understanding of the illness, insight into disability, and coping skills are also gleaned during history taking. In most cases, the patient leads the physician to a diagnosis and conclusion. In other cases, such as when the patient is rambling and disorganized, frequent redirection and refocus are required. Patients are generally the primary source of information. However, patients with cognitive or mood deficits (denial or decreased insight) or with communication problems, as well as small children, might not be able to fully express themselves. In these cases, the history taker might rely on other sources such as family members; friends; other physicians, nurses, and medical professionals; or previous medical records. This can also have an impact on physician billing. Caution must be exercised in using previous medical records because inaccuracies are sometimes repeated from provider to provider, sometimes referred to as “chart lore.”

Chief Complaint The chief complaint is the symptom or concern that caused the patient to seek medical treatment. The most common chief complaints seen in an outpatient physiatric practice are pain, weakness, or gait disturbance of various musculoskeletal or neurologic origins. On a physiatric consultation on an inpatient rehabilitation service, the predominant chief complaints are related to mobility, ADL, communication, or cognitive deficits and candidacy for inpatient rehabilitation. Unlike the relatively objective physical examination, the chief complaint is purely subjective and, when possible, the physician should use the patient’s own

The history of the present illness (HPI) details the chief complaint(s) for which the patient is seeking medical attention, as well as any related or unrelated functional deficits. It should also explore other information relating to the chief complaint such as recent and past medical or surgical procedures, complications of treatment, and potential restrictions or precautions. The HPI should include some or all of eight components related to the chief complaint: location, time of onset, quality, context, severity, duration, modifying factors, and associated signs and symptoms (see Table 1-2). In this case example, the patient is a 70-year-old man referred by his neurologist for physical therapy because the patient cannot walk properly (chief complaint). Over the past few months (duration), he has noted slowly progressive weakness of his left leg (location). Subsequent workup by his neurologist suggested amyotrophic lateral sclerosis (context). The patient was active in his life and working up until a few months previously, ambulating without an assistive device (context). Now he uses a straight cane for fear of falling (modifying factor). Besides difficulty with walking, the patient also has some trouble swallowing foods (associated signs and symptoms).

Functional Status Detailing the patient’s current and prior functional status is an essential aspect of the physiatric HPI. This generally entails better understanding the issues surrounding mobility, ADL, instrumental activities of daily living (I-ADL), communication, cognition, work, and recreation, among others. The data should be as accurate and detailed as possible to guide the physical examination and develop a treatment plan with reasonable short- and long-term goals. Assessing the potential for functional gain or deterioration requires an understanding of the natural history, cause, and time of onset of the functional problems. For example, most spontaneous motor recovery after stroke occurs within 3 months of the event.68 For a recent stroke patient with considerable motor impairments, there is a greater expectation for significant functional gain than in a patient with minor deficits related to a stroke that occurred 2 years ago. It is sometimes helpful to assess functional status using a standardized scale. No single scale is appropriate for all patients, but the Functional Independence Measure (FIM) is the most commonly used in the inpatient rehabilitation setting (Table 1-3; see Chapter 8).3 Measuring only activity

CHAPTER 1  The Physiatric History and Physical Examination

limitation (disability) or performance, each of 18 different activities is scored on a scale of 1 to 7, with a score of 7 indicating complete independence. Intermediate scores indicate varying levels of assistance from very little (from an assistive device, to supervision, to hands-on assistance) to a score of 1 indicating complete dependence on caregiver assistance. FIM scores also serve as a kind of rehabilitation shorthand among team members to quickly and accurately describe functional deficits.

Table 1-2  Essential Elements of the Physiatric History and Physical Examination Component Chief complaint History of present illness

Exploring location, onset, quality, context, severity, duration, modifying factors, and associated signs and symptoms

Functional history

Mobility: Bed mobility, transfers, wheelchair mobility, ambulation, driving, and devices required Activities of daily living: Bathing, toileting, dressing, eating, hygiene and grooming, etc. Instrumental activities of daily living: Meal preparation, laundry, telephone use, home maintenance, pet care, etc. Cognition Communication

Past medical and surgical history

Specific conditions: Cardiopulmonary, musculoskeletal, neurologic, and rheumatologic Medications

Social history

Home environment and living ­circumstances, family and friends support system, ­substance abuse, sexual history, vocational activities, finances, recreational activities, psychosocial history (mood disorders), spirituality, and litigation

Mobility Mobility is the ability to move about in one’s environment and is taken for granted by most healthy people. Because it plays such a vital role in society, any impairment related to mobility can have major consequences for a patient’s quality of life. A clear understanding of the patient’s functional mobility is needed to determine independence and safety, including the use of, or need for, mobility assistive devices. There is a range of mobility assistive devices that patients can use, such as crutches, canes, walkers, orthoses, and manual and electric wheelchairs (Table 1-4; see Chapters 15 and 17). Bed mobility includes turning from side to side, going from the prone to supine positions, sitting up, and lying down. A lack of bed mobility places the patient at greater risk for skin ulcers, deep vein thrombosis, and pneumonia. In severe cases, bed mobility can be so poor as to require a caregiver. In other cases, bed rails might be appropriate to facilitate movement. Transfer mobility includes getting in and out of bed, standing from the sitting position (whether from a chair or toilet), and moving between a wheelchair and another seat (car seat or shower seat). Once again, the history taker should assess the level of independence, safety, and any changes in functional ability. Wheelchair mobility can be assessed by asking if patients can propel the wheelchair independently, how far or how long they can go without resting, and whether they need assistance with managing the wheelchair parts. It is also important to assess the extent to which they can move about at home, in the community, and up and down ramps. Whether the home is potentially wheelchair-­accessible is particu­­larly important in cases of new onset of severe disability. Ambulation can be assessed by how far or for how long patients can walk, whether they require assistive devices, and their need for rest breaks. It is also important to know whether any symptoms are associated with ambulation, such as chest pain, shortness of breath, pain, or dizziness. Patients should be asked about any history of falling or instability while walking, and their ability to navigate uneven surfaces. Stair mobility, along with the number of stairs the patient must routinely climb and descend at home or in the community, and the presence or absence of handrails should also be determined. Driving is a crucial activity for many people, not only as a means of transportation but also as an indicator and facilitator of independence. For example, elders who stop driving have an increase in depressive symptoms.50 It is important to identify factors that might prevent driving, such as decreased cognitive function and safety awareness, and decreased vision or reaction time. Other factors affecting driving can include lower limb weakness, contracture, tone, or dyscoordination. Some of these conditions might

Examples

Family history Review of systems General Medical Physical Examination Cardiac Pulmonary Abdominal Other Neurologic Physical Examination Level of consciousness Attention Orientation Memory General fund of knowledge Abstract thinking Insight and judgment Mood and affect Communication Cranial nerve ­examination Sensation Motor control

Strength Coordination Apraxia Involuntary movements Tone

Reflexes

Superficial Deep Primitive

Musculoskeletal Physical Examination Inspection

Behavior Physical symmetry, joint deformity, etc.

Palpation

Joint stability Range of motion (active and passive) Strength testing (see above) Painful joints and muscles

Joint-specific provocative maneuvers

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Table 1-3  Levels of Function on the Functional Independence Measure Level of Function

Score

Definition

Independent

7 6

Another person is not required for the activity (no helper). Complete independence: all the tasks described as making up the activity are performed safely, without modification, assistive devices, or aids, and within a reasonable amount of time. Modified independence—one or more of the following can be true: • The activity requires an assistive device. • The activity takes more than a reasonable time. • There are safety considerations.

Dependent

5

4

3 2 1

The patient requires another person for either supervision or ­physical ­assistance for the activity to be ­performed (requires helper). Supervision or set-up: the patient requires no more help than stand-up or cueing without physical contact, or the helper sets up needed items. Minimal contact assistance: the patient requires no more help than touching and expends 75% or more of the effort. Moderate assistance: the patient requires more help than touching and expends 50%-75% of the effort. Maximal assistance: the patient expends 25%-50% of the effort. Total assistance: the patient expends less than 25% of the effort.

From Anonymous3 1997, with permission of the State University of New York at Buffalo.

Table 1-4  Commonly Used Mobility Assistive Devices Category

Example

Crutches

Axillary crutches Forearm crutches Platform crutches

Canes

Straight cane Wide- or narrow-based quad cane Hemiwalker or pyramid cane

Walkers

Standard or pick-up walker Rolling walker Platform walker

Wheelchairs Types Common modifications or ­specifications

Manual Powered Lightweight Folding or solid frame Elevated or removable leg rests Removable armrests Reclining

Off-the-Shelf Ankle-Foot Orthoses Common custom orthoses

Plastic ankle-foot orthosis Metal ankle-foot orthosis Knee orthosis Knee-ankle-foot orthosis

BOX 1-1

Activities of Daily Living (ADL) and Instrumental Activities of Daily Living (I-ADL) ADL • Bathing and showering • Bowel and bladder management • Dressing • Eating • Feeding • Functional mobility • Personal device care • Personal hygiene and grooming • Sexual activity • Sleep and rest • Toilet hygiene I-ADL • Care of others (including selecting and supervising caregivers) • Care of pets • Child rearing • Communication device use • Community mobility • Financial management • Health management and maintenance • Home establishment and management • Meal preparation and cleanup • Safety procedures and emergency responses • Shopping

  Modified from [Anonymous]: Occupational Therapy Practice Framework: domain and process. Am J Occup Ther 56:609-639, 2002 (Erratum in: Am J Occup Ther 2003; 57:115) with permission.

require use of adaptive hand controls for driving. Cognitive impairment sufficient to affect the ability to drive can be due to medications or organic disease (dementia, brain injury, stroke, or severe mood disturbance). Ultimately, the risks of driving are weighed against the consequences of not being able to drive. If the patient is no longer able to drive, alternatives to driving should be explored, such as the use of public or assisted transportation. Laws differ widely from state to state on the return to driving after a neurologic impairment develops. Activities of Daily Living and Instrumental Activities of Daily Living ADL encompass activities required for personal care including feeding, dressing, grooming, bathing, and toileting. I-ADL encompass more complex tasks required for independent living in the immediate environment such as care of others in the household, telephone use, meal preparation, house cleaning, laundry, and in some cases use of public transportation. In the Occupational Therapy Practice Framework, there are 11 activities for both ADL and I-ADL (Box 1-1).4 The clinician should identify and document ADL the patient can and cannot perform, and determine the causes of limitation. For example, a woman with a stroke might state that she cannot put on her pants. This could be due to a combination of factors such as a visual field cut, balance problems, weakness, pain, contracture, hypertonia, or deficits in motor planning. Some of these factors can be confirmed later in the physical examination. A more detailed follow-up to a positive response to the question is frequently

CHAPTER 1  The Physiatric History and Physical Examination

needed. For example, a patient might say “yes” to the question “Can you eat by yourself?” On further questioning,  it might be learned that she cannot prepare the food by herself or cut the food independently. The most accurate assessment of ADL and mobility deficits often comes from the hands-on assessment by therapists and nurses on the rehabilitation team. Cognition Cognition is the mental process of knowing (see Chapters 3 and 4). Although objective assessment of cognition comes under physical examination (memory, orientation, and the ability to assimilate and manipulate information), impairments in cognition can also become apparent during the course of the history taking. Because persons with cognitive deficits often cannot recognize their own impairments (anagnosia), it is important to gather information from family members and others familiar with the patient. Cognitive deficits and limited awareness of these deficits are likely to interfere with the patient’s rehabilitation program unless specifically addressed. These deficits can pose a safety risk as well. For example, a man with a previous stroke who falls, sustaining a hip fracture requiring replacement, might not be able to follow hip precautions, resulting in possible refracture or hip dislocation. Executive functioning is another aspect of cognition, which includes the mental functions required for planning, problem solving, and self-awareness. Executive functioning correlates with functional outcome because it is required in many real-world situations.45 Communication Communication skills are used to convey information including thoughts, needs, and emotions. Verbal expression deficits can be very subtle and might not be noticed in a first encounter. If there is a reason to think that speech or communication has been affected by a recent event, it is advisable to ask family members if they have noticed recent changes. Patients who cannot communicate through speech might or might not be able to communicate through other means, known as augmentative communication, depending on the type of communication dysfunction and other physical and cognitive limitations. This can include writing and physicality (such as sign language, gestures, and body language). They can also use a variety of augmentative communication aids ranging from simple picture, letter, and word boards to electronic devices.

Past Medical and Surgical History The physiatrist should understand the patient’s past medical and surgical history. This knowledge allows the physiatrist to understand how preexisting illnesses affect current status, and how to tailor the rehabilitation program for precautions and limitations. The patient’s past medical history can also have a major impact on rehabilitation outcome. Cardiopulmonary Mobility, ADL, I-ADL, work, and leisure can be severely compromised by cardiopulmonary deficits. The patient should be asked about any history of congestive heart failure, recent and distant myocardial infarction, arrhythmias,

7

and coronary artery disease. Past surgical procedures such as bypass surgery, heart transplantation, stent placement, and recent diagnostic testing (stress test or echocardiogram) should be ascertained. This information is important to ensure that exercise prescriptions do not exceed cardiovascular activity limitations. Patients should also be asked about their activity tolerance, surgery such as lung volume reduction or lung transplant, and whether they require home oxygen. Dyspnea from chronic obstructive pulmonary disease can be a significant contributor to functional limitations. Often medication adjustment to maximize cardiac and pulmonary function accompanies mobilization. It is also important to identify modifiable risk factors for cardiac disease such as smoking, hypertension, and obesity. Musculoskeletal There can be a wide range of musculoskeletal disorders from acute traumatic injuries to gradual functional decline with chronic osteoarthritis. The patient should be asked about a history of trauma, arthritis, amputation, joint contractures, musculoskeletal pain, congenital or acquired muscular problems, weakness, or instability. It is important to understand the functional impact of such impairments or disabilities. Patients with chronic physical disability often develop overuse musculoskeletal syndromes, such as the development of shoulder pain secondary to chronically propelling a wheelchair.33 Neurologic Disorders Preexisting congenital or acquired neurologic disorders can have a profound impact on the patient’s function and recovery from both neurologic and nonneurologic illness. It is helpful to know whether a neurologic disorder is congenital versus acquired, progressive versus nonprogressive, central versus peripheral, demyelinating versus axonal, or sensory versus motor. This information can be helpful in understanding the pathophysiology, location, severity, prognosis, and implications for management. The interviewer must assess the premorbid need for assistive devices, orthoses, and the degree of speech, swallowing, and cognitive impairments. Rheumatologic The history should assess the type of rheumatologic disorder, time of onset, number of joints affected, pain level, current disease activity, and past orthopedic procedures. Discussions with the patient’s rheumatologist might address whether medication changes could improve activity tolerance in a rehabilitation program (see Chapter 36). Medications All medications should be documented including prescription and over-the-counter drugs, as well as nutraceuticals, supplements, herbs, and vitamins. Medications should be documented from both the last institutional venues (acute care, nursing home) and from home before institutionalization. Decreasing medication errors via medication reconciliation is a major thrust of the National Patient Safety Goals initiative.40 Patients typically do not mention medications that they do not think are relevant to their current problem, unless asked about them in detail. Drug

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and food allergies should be noted. It is especially important to gather the complete list of medications being used in patients who are seeing multiple physicians. Particular attention should be paid to nonsteroidal antiinflammatory agents because these are commonly prescribed by physiatrists for musculoskeletal disorders, and care must be taken not to double-dose the patient.27,32 The indications, precautions, and side effects of all drugs prescribed should be explained to the patient.

Social History Home Environment and Living Situation Understanding the patient’s home environment and living situation includes asking if the patient lives in a house or an apartment, if there is elevator access, whether it is wheelchair accessible, if there are stairs, whether the bathroom is accessible from the bedroom, and whether the bathroom has grab bars or handrails (and on which side). A home visit might be required to gain the best assessment. If there is no caregiver at home, the patient could require a home health aide. These factors help determine many aspects of the discharge plan. Family and Friends Support Patients who have lost function might require supervision, emotional support, or actual physical assistance. Family, friends, and neighbors who can provide such assistance should be identified. The clinician should discuss the level of assistance they are willing and able to provide. The assistance provided by caregivers can be limited if they are elderly, have some type of impairment, work, or are not willing to assist with bowel or bladder hygiene. Substance Abuse Patients should be asked about their history of smoking, alcohol use or abuse, and drug abuse. Because patients often deny substance abuse, this topic should be discussed in a nonjudgmental manner. Patients frequently feel embarrassment or guilt in admitting substance abuse, and also fear the legal consequences of such an admission. Substance abuse can be a direct and an indirect cause of disability, and is often a contributing factor in traumatic brain injury.19 It can also have an impact on community reintegration, because patients with pain and/or depression are at risk for further abuse. Patients who are at risk should be referred to social work to explore options for further assistance, either during the acute rehabilitation or later in the community.

elderly. Sexual orientation and safer sex practices should be addressed when appropriate. Vocational Activities Vocation is not only a source of financial security; it also significantly relates to self-confidence and even identity. The history should include the patient’s educational level, recent work history, and the ability to fulfill job requirements subsequent to the injury or illness. If an individual cannot fully regain the previous function level, the vocational options available should be explored. It is possible that the work environment can be modified to compensate for a functional loss or minimize musculo­ skeletal pain complaints. An example of this would be the installation of a wheelchair ramp for an accountant with paraplegia. Finances and Income Maintenance Patients can have financial concerns that are due to or exacerbated by their illness or injury. These concerns can also be addressed by the rehabilitation team social worker. Whether a patient has the financial resources or insurance to pay for adaptive devices such as a ramp or mobility equipment can significantly affect discharge planning. If patients cannot safely be discharged home, skilled nursing facility placement might need to be explored, at least on a temporary basis. Recreation The ability to engage in hobbies and recreational activities is important to most people, and any loss or limitation of the ability to perform these activities can be stressful. Recreation is a primary outcome in sports medicine. The recreational activity affected can involve physical exercise, such as a sporting activity, or can be more sedentary, such as playing cards. The team recreational therapist can be helpful in helping to restore the patient’s favorite recreations and offer new ones. Psychosocial History The history taker must recognize the psychosocial impact of impairment. Beyond the loss of function, the patient can also feel a loss of overall health, body image, mobility, or independence. The loss of function, and possibly of income as well, can place great stress on the family unit and caregivers. The treatment plan should recognize the patient’s psychosocial context and provide assistance in developing coping strategies, especially for depression and anxiety. This can help accelerate the patient’s process of adjusting to a new disability.

Sexual History

Spirituality and Belief

Patients and health care practitioners alike are often uncomfortable discussing the topic of sexuality, so developing a good rapport during history taking can be helpful. Discussion of this topic is made easier if the health care practitioner has a basic knowledge of how sexual function can be changed by illness or injury (see Chapter 31). Sexuality is particularly important to patients in their reproductive years (such as with many spinal cord– and brain-injured persons), but the physician should enquire about sexuality in adolescents and adults, as well as in the

Spirituality is an important part of the lives of many patients, and some preliminary studies indicate that it can have positive effects on rehabilitation, life satisfaction, and quality of life.13 Health care providers should be sensitive to the patient’s spiritual needs, and appropriate referral or counseling should be provided.17 Pending Litigation Patients should be asked in a nonjudgmental fashion whether they are involved in litigation related to their

CHAPTER 1  The Physiatric History and Physical Examination

illness, injuries, or functional impairment. The answer should not change the treatment plan, but litigation can be a source of anxiety, depression, or guilt. In some cases the patient’s legal representative can play an important role in obtaining needed services and equipment.

Family History Patients should be asked about the health, or cause and age of death, of parents and siblings. It is always important to know whether any family members have a similar condition. They should also be asked about any family history of heart disease, diabetes, cancer, stroke, arthritis, hypertension, or neurologic illness. This will help to identify genetic disorders within the family. Knowledge of the general health of family members can also provide insight into their ability to provide functional assistance to the patient.

Review of Systems A detailed review of organ systems should be done discover any problems or diseases not previously identified during the course of the history taking. Table 1-5 lists some questions that can be asked about each system.24 Note that this list is not comprehensive, and more detailed questioning might be necessary.

Table 1-5  Sample Questions for the Review of Systems System

Questions

Systemic

Any general symptoms such as fever, weight loss, fatigue, nausea, and poor appetite?

Skin

Any skin problems? Sores? Rashes? Growths? Itching? Changes in the hair or nails? Dryness?

Eyes

Any changes in vision? Pain? Redness? Double vision? Watery eyes? Dizziness?

Ears

How are the ears and hearing? Running ears? Poor hearing? Ringing ears? Discharge?

Nose

How are your nose and sinuses? Stuffy nose? ­Discharge? Bleeding? Unusual odors?

Mouth

Any problems with your mouth? Sores? Bad taste? Sore tongue? Gum trouble?

Throat and neck

Any problems with your throat and neck? Sore throat? Hoarseness? Swelling? Swallowing?

Breasts

Any problems with your breasts? Lumps? Nipple discharge? Bleeding? Swelling? Tenderness?

Pulmonary

Any problems with your lungs or breathing? Cough? Sputum? Bloody sputum? Pain in the chest on taking a deep breath? Shortness of breath?

Cardiovascular

Do you have any problems with your heart? Chest pain? Shortness of breath? Palpitations? Cough? Swelling of your ankles? Trouble lying flat in bed at night? Fatigue?

Gastrointestinal

How is your digestion? Any changes in your appetite? Nausea? Vomiting? Diarrhea? Constipation? Changes in your bowel habits? Bleeding from the rectum? Hemorrhoids?

Genitourinary

Male: Any problems with your kidneys or urination? Painful urination? Frequency? Urgency? Nocturia? Bloody or cloudy urine? Trouble starting or ­stopping? Female: Number of pregnancies? Abortions? Miscarriages? Any menstrual problems? Last menstrual period? Vaginal bleeding? Vaginal discharge? Cessation of periods? Hot flashes? Vaginal itching? Sexual dysfunction?

Endocrine

Any problems with your endocrine glands? Feeling hot or cold? Fatigue? Changes in the skin or hair? Frequent urination? Fatigue?

Musculoskeletal

Do you have any problems with your bones or joints? Joint or muscle pain? Stiffness? Limitation of motion?

Nervous system

Numbness? Weakness? Pins and needles sensation?

The Physiatric Physical Examination Neurologic Examination Neurologic problems are common in the setting of inpatient and outpatient rehabilitation, including functional deficits in persons with such conditions as stroke, multiple sclerosis, peripheral neuropathy, spinal cord injury, brain injury, and neurologic cancers. The neurologic examination should be conducted in an organized fashion to confirm or reconfirm the neurologic disorder, and subsequently to identify which components of the nervous system are the most and the least affected. The precise location of the lesion should be identified, if possible, and the impact of the neurologic deficits on the overall function and mobility of the patient should be noted. If a cause of the patient’s condition has not been identified at presentation to the rehabilitation service, a differential diagnosis list should be developed, the neurologic examination tailored appropriately, and consultations garnered, if indicated. An accurate and efficient neurologic examination requires that the examiner have a thorough knowledge of both central and peripheral neuroanatomy before the examination. Weakness is a primary sign in neurologic disorders and is seen in both upper (UMN) and lower motor neuron (LMN) disorders. UMN lesions involving the central nervous system (CNS) are typically characterized by hypertonia, weakness, and hyperreflexia without significant muscle atrophy, fasciculation, or fibrillation (on electromyography). They tend to occur in a hemiparetic, paraparetic, and tetraparetic pattern. UMN etiologies include stroke, multiple sclerosis, traumatic and nontraumatic brain and spinal cord injuries, and neurologic cancers, among others. LMN defects are characterized by hypotonia, weakness,

9

From Enelow AJ, Forde DL, Brummel-Smith K: Interviewing and patient care, ed 4, New York, 1996, Oxford University Press,24 with permission of Oxford University Press.

hyporeflexia, significant muscle atrophy, fasciculations, and electromyographic changes. They occur in the distribution of the affected nerve root, peripheral nerve, or muscle. UMN and LMN lesions often coexist; however, the LMN system is the final common pathway of the nervous system. An example of this is an upper trunk brachial plexus injury on the same side as spastic hemiparesis in a person with traumatic brain injury.51 Similar to physical examination in other organ systems, testing of one neurologic system is often predicated by the normal functioning of other systems. For example, severe visual impairment can be confused with cerebellar dysfunction, as many cerebellar tests have a visual component. The integrated functions of all organ systems should be considered to provide an accurate clinical assessment,

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SECTION 1  Evaluation

and potential limitations of the examination should be considered. Mental Status Examination The mental status examination (MSE) should be performed in a comfortable setting where the patient is not likely to be disturbed by external stimuli such as televisions, telephones, pagers, conversation, or medical alarms. The bedside MSE is often limited secondary to distractions from within the room. Having a familiar person such as a spouse or relative in the room can often help reassure the patient. The bedside MSE might need to be supplemented by far more detailed and standardized evaluations performed by neuropsychologists, especially in cases of vocational and educational reintegration (see Chapters 4 and 35). Language is the gateway to assessing cognition and is therefore limited in persons with significant aphasia. Level of Consciousness. Consciousness is the state of awareness of one’s surroundings. A functioning pontine reticular activating system is necessary for normal conscious functioning. The conscious patient is awake and responds directly and appropriately to varying stimuli. Decreased consciousness can significantly limit the MSE and the general physical examination. The examiner should understand the various levels of consciousness. Lethargy is the general slowing of motor processes (such as speech and movement) in which the patient can easily fall asleep if not stimulated, but is easily aroused. Obtundation is a dulled or blunted sensitivity in which the patient is difficult to arouse, and once aroused is still confused. Stupor is a state of semiconsciousness characterized by arousal only by intense stimuli such as sharp pressure over a bony prominence (e.g., sternal rub), and the patient has few or even no voluntary motor responses.56 The Aspen Neurobehavioral Conference proposed, and several leading medical organizations have endorsed, three terms to describe severe alterations in consciousness.29 In coma, the eyes are closed with absence of sleep-wake cycles and no evidence of a contingent relationship between the patient’s behavior and the environment.29 Vegetative state is characterized by the presence of sleep-wake cycles but still no contingent relationship. Minimally conscious state indicates a patient who remains severely disabled but demonstrates sleep-wake cycles and even inconsistent, nonreflexive, contingent behaviors in response to a specific environmental stimulation. In the acute settings, the Glasgow Coma Scale is the most often used objective measure to document level of consciousness, assessing eye opening, motor response, and verbal response (Table 1-6).39 Attention. Attention is the ability to address a specific stimulus for a short period without being distracted by internal or external stimuli.65 Vigilance is the ability to hold attention over longer periods. For example, with inadequate vigilance a patient can begin a complex task but be unable to sustain performance to completion. Attention is tested by digit recall, where the examiner reads a list of random numbers and the patient is asked to repeat those numbers. The patient should repeat digits both forward and backward. A normal performance is repeating seven numbers

Table 1-6  Glasgow Coma Scale Function Eye opening Spontaneous To speech To pain Nil

Rating E 4 3 2 1

Best motor response

M

Obeys Localizes Withdraws Abnormal flexion Extensor response Nil

6 5 4 3 2 1

Verbal response Oriented Confused conversation Inappropriate words Incomprehensible sounds Nil Coma score (E + M + V)

V 5 4 3 2 1 3-15

From Jennett B, Teasdale G: Assessment of impaired consciousness, Contemp Neurosurg 20:78, 1981 with permission.

in the forward direction, with fewer than five indicating significant attention deficits.52,65 Orientation. Orientation is necessary for basic cognition. Orientation is composed of four parts: person, place, time, and situation. After asking the patient’s name, place can be determined by asking the location the patient is currently in or her or his home address. Time is assessed by asking the patient the time of day, the date, the day of the week, or the year. Situation refers to why the patient is in the hospital or clinic. Time sense is usually the first component lost, and person is typically the last to be lost. Temporary stress can account for a minor loss of orientation; however, major disorientation usually suggests an organic brain syndrome.69 Memory. The components of memory include learning, retention, and recall. During the bedside examination, the patient is typically asked to remember three or four objects or words. The patient is then asked to repeat the items immediately to assess immediate acquisition (encoding) of the information. Retention is assessed by recall after a delayed interval, usually 5 to 10 minutes. If the patient is unable to recall the words or objects, the examiner can provide a prompt (e.g., “It is a type of flower” for the word “tulip”). If the patient still cannot recall the words or objects, the examiner can provide a list from which the patient can choose (e.g., “Was it a rose, a tulip, or a daisy?”). Although abnormal scores must be interpreted within the context of the remaining neurologic examination, normal individuals younger than 60 years should recall three of four items.65 Recent memory can also be tested by asking questions about the past 24 hours, such as “How did you travel here?” or “What did you eat for breakfast this morning?” Assuming the information can be confirmed, remote memory is tested by asking where the patient was born or the school

CHAPTER 1  The Physiatric History and Physical Examination

or college attended.46 Visual memory can be tested by having the patient identify (after a few minutes) four or five objects hidden in clear view. General Fundamentals of Knowledge. Intelligence is a global function derived from the general tone and content of the examination and encompasses both basic intellect and remote memory. The examiner should note the patient’s educational level and highest grade completed during the history. Examples of questions that can be asked include names of important elected officials, such as the current president of the United States or recent past presidents. It can be very difficult to identify when a patient with a very high intelligence premorbidly drops to a more average level after injury or illness. The history of memory or intellectual decline from a family member or close friend should prompt further evaluation of the patient. Abstract Thinking. Abstraction is a higher cortical function and can be tested by the interpretation of common proverbs such as “a stitch in time saves nine” or “when the cat’s away the mice will play,” or by asking similarities, such as “How are an apple and an orange alike?” A concrete explanation for the first proverb would be “You should sew a rip before it becomes bigger,” whereas an abstract explanation would be “Quick attention to a given problem would prevent bigger troubles later.” An abstract response to the similarity would be “They are both kinds of fruit,” and a concrete response would be “They are both round” or “You can eat them both.” Most normal individuals should be able to provide abstract responses. A patient also demonstrates abstraction when he or she understands a humorous phrase or situation. Concrete responses are given by persons with dementia, mental retardation, or limited education. Abstract thinking should always be considered in the context of intelligence and cultural differences.69 Insight and Judgment. Insight has been conceptualized into three components: awareness of impairment, need for treatment, and attribution of symptoms. Insight can be ascertained by asking what brought the patient into the hospital or clinic.10 Recognizing that one has an impairment is the initial step for recovery. A lack of insight can severely hamper a patient’s progress in rehabilitation and is a major consideration in developing a safe discharge plan. Insight can be difficult to distinguish from psychological denial. Judgment is an estimate of a person’s ability to solve real-life problems. The best indicator is usually simply observing the patient’s behavior. Judgment can also be assessed by noting the patient’s responses to hypothetical situations in relation to family, employment, or personal life. Hypothetical examples of judgment that reflect societal norms include “What should you do if you find a stamped, addressed envelope?” or “How are you going to get around the house if you have trouble walking?” Judgment is a complex function that is part of the maturational process and is consequently unreliable in children and variable in the adolescent years.69 Assessment of judgment is important to assess the patient’s capacity for independent functioning.

11

Mood and Affect. Mood can be assessed by asking the “Yale question”: “Do you often feel sad or depressed?”72 Establishing accurate information pertaining to the length of a particular mood is important. The examiner should document if the mood has been reactive (e.g., sadness in response to a recent disabling event or loss of independence), and whether the mood has been stable or unstable. Mood can be described in terms of being, including happy, sad, euphoric, blue, depressed, angry, or anxious. Affect describes how a patient feels at a given moment, which can be described by terms such as blunted, flat, inappropriate, labile, optimistic, or pessimistic. It can be difficult to accurately assess mood in the setting of moderate to severe acquired brain injury. A patient’s affect is determined by the observations made by the examiner during the interview.11 General Mental Status Assessment. The Folstein MiniMental Status Examination is a brief and convenient tool to test general cognitive function. It is useful for screening patients for dementia and brain injuries. Of a maximum 30 points, a score 24 or above is considered within the normal range.25 Also available is the easily administered Montreal Cognitive Assessment.54 The clock-drawing test is another quick test sensitive to cognitive impairment. The patient is instructed to “Without looking at your watch, draw the face of a clock, and mark the hands to show 10 minutes to 11 o’clock.” This task uses memory, visual spatial skills, and executive functioning. The drawing is scored on the basis of whether the clock numbers are generally intact or not intact out of a maximum score of 10.66 The use of the threeword recall test in addition to the clock-drawing test, which is known collectively as the Mini-Cog Test, has recently gained popularity in screening for dementia. The MiniCog can usually be completed within 2 to 3 minutes.60 The reader is referred to other excellent descriptions of the MSE for further reading.65 Communication Aphasia. Aphasia involves the loss of production or comprehension of language. The cortical center for language resides in the dominant hemisphere. Naming, repetition, comprehension, and fluency are the key components of the physician’s bedside language assessment. The examiner should listen to the content and fluency of speech. Testing of comprehension of spoken language should begin with single words, progress to sentences that require only yes– no responses, and then progress to complex commands. The examiner should also assess visual naming, repetition of single words and sentences, word-finding abilities, and reading and writing from dictation and then spontaneously. Circumlocutions are phrases or sentences substituted for a word the person cannot express, such as responding “What you tell time with on your wrist” when asked to name a watch. Alexia without agraphia is seen in dominant occipital lobe injury. Here the patient is able to write letters and words from a spoken command but is unable to read the information after dictation.12 Some commonly used standardized aphasia measures include the Boston Diagnostic Aphasia Examination and the Western Aphasia Battery (see Chapter 3).67

12

SECTION 1  Evaluation

Dysarthria. Dysarthria refers to defective articulation, but with the content of speech unaffected. The examiner should listen to spontaneous speech and then ask the patient to read aloud. Key sounds that can be tested include “ta ta ta,” which is made by the tongue (lingual consonants); “mm mm mm,” which is made by the lips (labial consonants); and “ga ga ga,” which is made by the larynx, pharynx, and palate.46 There are several subtypes of dysarthria including spastic, ataxic, hypokinetic, hyperkinetic, and flaccid.52 Dysphonia. Dysphonia is a deficit in sound production and can be secondary to respiratory disease, fatigue, or vocal cord paralysis. The best method to examine the vocal cords is by indirect laryngoscopy. Asking the patient to say “ah” while viewing the vocal cords is used to assess vocal cord abduction. When the patient says “e,” the vocal cords will adduct. Patients with weakness of both vocal cords will speak in whispers with the presence of inspiratory stridors.46 Verbal Apraxia. Apraxia of speech involves a deficit in motor planning (i.e., awkward and imprecise articulation in the absence of impaired strength or coordination of the motor system). It is characterized by inconsistent errors when speaking. A difficult word might be spoken correctly, but trouble is experienced when repeating it. People with verbal apraxia of speech often appear to be “groping” for the right sound or word, and might try to speak a word several times before saying it correctly. Apraxia is tested by asking the patient to repeat words with an increasing number of syllables. Oromotor apraxia is seen in patients with difficulty organizing nonspeech, oral motor activity. This can adversely impact swallowing. Tests for oromotor apraxia include asking patients to stick out their tongue, show their teeth, blow out their cheeks, or pretend to blow out a match.1 Cognitive Linguistic Deficits. Cognitive linguistic deficits involve the pragmatics and context of communication. Examples can include confabulation after a ruptured aneurysm of the anterior communicating artery, or disinhibited or sexually inappropriate comments from a patient with frontal lobe damage after a traumatic brain injury. Cognitive linguistic deficits are distinguished from fluent aphasias (Wernickeʼs) by the presence of relatively normal syntax and grammar. Cranial Nerve Examination Cranial Nerve I: Olfactory Nerve. The examiner should test both perception and identification of smell using aromatic nonirritating materials that avoid stimulation of the trigeminal nerve fibers in the nasal mucosa. Irritant substances such as ammonia should be avoided. The patient is asked to close the eyes while the opposite nostril is compressed separately. The patient should identify the smell in a test tube containing a common substance with a characteristic odor, such as coffee, peppermint, or soap. The olfactory nerve is the most commonly injured cranial nerve (CN) in head trauma, resulting from shearing injuries that can be associated with fractures of the cribiform plate.5

Cranial Nerve II: Optic Nerve. The optic nerve is assessed by testing for visual acuity and visual fields and by performing an ophthalmologic examination. Visual acuity refers to central vision, while visual field testing assesses the integrity of the optic pathway as it travels from the retina to the primary visual cortex. Testing visual fields by confrontation is most commonly performed. The patient faces the examiner while covering one eye so the other eye fixates on the opposite eye of the examiner directly in front. The examiner wiggles a finger at the outer boundaries of the four quadrants of vision while the patient points to the quadrant where he or she senses movement. More accurately, a red 5-mm pin can be used to map out the visual field.5 For patients with visual field and extraocular movement deficits (see following discussion), further assessment by a neurooptometrist or visually trained occupational therapists can be helpful. Cranial Nerves III, IV, and VI: Oculomotor, Trochlear, and Abducens Nerves. These three cranial nerves are best tested together because they are all involved in ocular motility. The oculomotor nerve (III) provides innervation to all the extraocular muscles except the superior oblique and lateral rectus, which are innervated by the trochlear (IV) and abducens nerves (VI), respectively. The oculomotor nerve also innervates the levator palpebrae muscle, which elevates the eyelid, the pupilloconstrictor muscle that constricts the pupil, and the ciliary muscle that controls the thickness of the lens in visual accommodation. The primary action of the medial rectus is adduction (looking in) and that of the lateral rectus is abduction (looking out). The superior rectus and inferior oblique primarily elevate the eye, whereas the inferior rectus and superior oblique depress the eye. The superior oblique muscle controls gaze looking down, especially in adduction.46 Examination of the extraocular muscles involves assessing the alignment of the patient’s eyes while at rest and when following an object or finger held at an arm’s length. The examiner should observe the full range of horizontal and vertical eye movements in the six cardinal directions.5 The optic (afferent) and oculomotor (efferent) nerves are involved with the pupillary light reflex. A normal pupillary light reflex (CNs II and III) should result in constriction of both pupils when a light stimulus is present to either eye separately. A characteristic head tilt when looking down is sometimes seen in CN IV lesions.75 Cranial Nerve V: Trigeminal Nerve. The trigeminal nerve provides sensation to the face and mucous ­membranes of the nose, mouth, and tongue. There are three sensory ­divisions of the trigeminal nerve: the ophthalmic, maxillary, and mandibular branches. These branches can be tested by pinprick sensation, light touch, or temperature along the forehead, cheeks, and jaw on each side of the face. The motor branch of the trigeminal nerve also innervates the muscles of mastication, which include the masseters, the pterygoids, and the temporalis. The patient is asked to clamp the jaws together, and then the examiner will try to open the patient’s jaw by pulling down on the lower mandible. Observe and palpate for contraction of

CHAPTER 1  The Physiatric History and Physical Examination

13

both the temporalis and the masseter muscles. The pterygoids are tested by asking the patient to open the mouth. If one side is weak, the intact pterygoid muscles will push the weak muscles, resulting in a deviation toward the weak side. The corneal reflex tests the ophthalmic division of the trigeminal nerve (afferent) and the facial nerve (efferent). Cranial Nerve VII: Facial Nerve. The facial nerve provides motor innervation to all muscles of facial expression; provides sensation to the anterior two thirds of the tongue and the external acoustic meatus; innervates the stapedius muscle, which helps dampen loud sounds by decreasing excessive movements of the ossicles in the inner ear; and provides secretomotor fibers to the lacrimal and salivary glands. The facial nerve is first examined by watching the patient as she or he talks and smiles, watching specifically for eye closure, flattening of the nasolabial fold, and asymmetric elevation of one corner of the mouth. The patient is then asked to wrinkle the forehead (frontalis), close the eyes while the examiner attempts to open them (orbicularis oculi), puff out both cheeks while the examiner presses on the cheeks (buccinator), and show the teeth (orbicularis oris). A peripheral injury to the facial nerve, such as Bell’s palsy, affects both the upper and the lower face, whereas a central lesion typically affects mainly the lower face. Cranial Nerve VIII: Vestibulocochlear Nerve. The vestibulocochlear nerve, also known as the auditory nerve, comprises two divisions. The cochlear nerve is the part of the auditory nerve responsible for hearing, while the vestibular nerve is related to balance. The cochlear division can be tested by checking gross hearing. A rapid screen can be done if the examiner rubs the thumb and index fingers near each ear of the patient. Patients with normal hearing usually have no difficulty hearing this. The vestibular division is seldom included in the routine neurologic examination. Patients with dizziness or vertigo associated with changes in head position or suspected of having benign paroxysmal positional vertigo should be assessed with the Dix-Hallpike maneuver (Fig­ ure 1-1). The absence of nystagmus indicates normal vestibular nerve function. With peripheral vestibular nerve dysfunction, however, the patient complains of vertigo, and rotary nystagmus appears after an approximately 2- to 5-second latency, toward the direction in which the eyes are deviated. With repetition of maneuvers, the nystagmus and sensation of vertigo fatigue and ultimately disappear. In central vestibular disease, such as from a stroke, the nystagmus has latency and is nonfatigable.26 Rehabilitation therapists with training in vestibular rehabilitation can also provide invaluable data for developing a differential diagnosis of balance deficits. Cranial Nerves IX and X: Glossopharyngeal Nerve and Vagus Nerve. The glossopharyngeal nerve supplies taste to the posterior one third of the tongue, along with sensation to the pharynx and the middle ear. The glossopharyngeal nerve and vagus nerve are usually examined together. The patient’s voice quality should be noted,

45 degrees

FIGURE 1-1 The Dix-Hallpike maneuver is performed with the patient initially seated upright. The patient is asked to fall backward so that the head is below the plane of his or her trunk.The examiner then turns the patient’s head to one side and asks the patient to look in the direction to which the head is turned.

as hoarseness is usually associated with a lesion of the recurrent laryngeal nerve, a branch of the vagus nerve. The patient is asked to open the mouth and say “ah.” The examiner should inspect the soft palate, which should elevate symmetrically with the uvula in midline. In an LMN vagus nerve lesion, the uvula will deviate to the side that is contralateral to the lesion. A UMN lesion presents with the uvula deviating toward the side of the  lesion.31 The gag reflex can be tested by depressing the patient’s tongue with a tongue depressor and touching the pharyngeal wall with a cotton tip applicator until the patient gags. The examiner should compare the sensitivity of each side (afferent: glossopharyngeal nerve) and observe the symmetry of the palatal contraction (efferent: vagus nerve). The absence of a gag reflex indicates loss of sensation and/or loss of motor contraction. The presence of a gag reflex does not imply the ability to swallow without risk of aspiration (see Chapter 27).57 Cranial Nerve XI: Accessory Nerve. The accessory nerve innervates the trapezius and sternocleidomastoid muscles. While standing behind the patient, the examiner should look for atrophy or spasm in the trapezius and compare the symmetry of both sides. To test the strength of the trapezius, the patient is asked to shrug the shoulders and hold them in this position against resistance. To test the strength of the sternocleidomastoid muscle, ask the patient to rotate the head against resistance. The ipsilateral sternocleidomastoid muscle turns the head to the contralateral side. The ipsilateral muscle brings the ear to the shoulder.

14

SECTION 1  Evaluation

Cranial Nerve XII: Hypoglossal Nerve. The hypoglossal nerve is a pure motor nerve innervating the muscles of the tongue. It is tested by asking the patient to protrude the tongue, noting evidence of atrophy, fasciculation, or deviation. Fibrillations in the tongue are common in patients with amyotrophic lateral sclerosis.30 The tongue typically points to the side of the lesion in peripheral hypoglossal nerve lesions, but toward the opposite side of the lesion in UMN lesions such as stroke. Sensory Examination The examiner should be familiar with the normal dermatomal and peripheral nerve sensory distribution (Figure 1-2). Evaluation of the sensory system requires testing of both superficial sensation (light touch, pain, and temperature) and deep sensation (involves the perception of position and vibration from deep structures such as muscle, ligaments, and bone). Light touch can be assessed with a fine wisp of cotton or a cotton tip applicator. The examiner should touch the skin lightly, avoiding excessive pressure. The patient is asked to respond when a touch is felt, and to say whether there is a difference between the two sides. Pain and temperature both travel via the spinothalamic tracts and are assessed using a safety pin or other sharp sanitary object, while occasionally interspersing the examination with a blunt object. Patients with peripheral neuropathy might have a delayed pain appreciation and often change their minds a few seconds after the initial stimuli. Some examiners use the single or double pinprick of brief duration to test for pain, while others use a continuous sustained pinprick to better test for delayed pain.50 Temperature testing is not often used and rarely provides additional information, but it is sometimes easier for patients to delineate insensate areas. Thermal sensation can be checked by using two different test tubes, one filled with hot water (not hot enough to burn) and one filled with cold water and ice chips. Joint position sense or proprioception travel via the dorsal columns along with vibration sense. Proprioception is tested by vertical passive movement of the toes or ­fingers. The examiner holds the sides of the patient’s fingers or toes and asks the patient if the digits are in the upward or downward direction. It is important to grasp the sides of the digits rather than the nailbed, because the patient might be able to perceive pressure in these areas, reducing the accuracy of the examination. Most normal persons make no errors on these maneuvers. Vibration is tested in the limbs with a 128-Hz tuning fork. The tuning fork is placed on a bony prominence such as the dorsal aspect of the terminal phalange of the great toe or finger, the malleoli, or the olecranon. The patient is asked to indicate when the vibration ceases. The vibration stimulus can be controlled by changing the force used to set the tuning fork in motion, or by noting the amount of time that a vibration is felt as the stimulus dissipates. Assuming the examiner is normal, both patient and examiner should feel the vibration cease at approximately the same time. Two-point discrimination is most commonly tested using calipers with blunt ends. The patient is asked to close the eyes and indicate if one or two stimulation points are felt. The normal distance of separation that can be felt as

two distinct points depends on the area of body being tested. For example, the lips are sensitive to a point separation of 2 to 3 mm, normally identified as two points. Commonly tested normal two-point discrimination areas include the fingertips (3 to 5 mm), the dorsum of the hand (20 to 30 mm), and the palms (8 to 15 mm).46 Graphesthesia is the ability to recognize numbers, letters, or symbols traced onto the palm. It is performed by writing recognizable numbers on the patient’s palm with his or her eyes closed. Stereognosis is the ability to recognize common objects placed in the hand, such as keys or coins. This requires normal peripheral sensation as well as cortical interpretation. Motor Control Strength. Manual muscle testing provides an important method of quantifying strength and is outlined in the musculoskeletal examination section below. Coordination. The cerebellum controls movement by comparing the intended activity with actual activity that is achieved. The cerebellum smoothes motor movements and is intimately involved with coordination. Ataxia or motor coordination can be secondary to deficits of sensory, motor, or cerebellar connections. Ataxic patients who have intact function of the sensory and motor pathways usually have cerebellar compromise. The cerebellum is divided into three areas: the midline, the anterior lobe, and the lateral hemisphere. Lesions affecting the midline usually produce truncal ataxia in which the patient cannot sit or stand unsupported. This can be tested by asking the patient to sit at the edge of the bed with the arms folded so they cannot be used for support. Lesions that affect the anterior lobe usually result in gait ataxia. In this case, the patient is able to sit or stand unsupported but has noticeable balance deficits on walking. Lateral hemisphere lesions produce loss of ability to coordinate movement, which can be described as limb ataxia. The affected limb usually has diminished ability to correct and change direction rapidly. Tests that are typically used to test for limb coordination include the finger-to-nose test and the heel-to-shin test.51 Rapid alternating movements can be tested by observing the amplitude, rhythm, and precision of movement. The patient is asked to place the hands on the thighs and then rapidly turn the hands over and lift them off the thighs for 10 seconds. Normal individuals can do this without difficulty. Dysdiadochokinesis is the clinical term for an inability to perform rapidly alternating movements. The Romberg test can be used to differentiate a cerebellar deficit from a proprioceptive one. The patient is asked to stand with the heels together. The examiner notes any excessive postural swaying or loss of balance. If loss of balance is present when the eyes are open and closed, the examination is consistent with cerebellar ataxia. If the loss of balance occurs only when the eyes are closed, this is classically known as a positive Romberg sign indicating a proprioceptive (sensory) deficit.46 Apraxia. Apraxia is the loss of the ability to carry out programmed or planned movements despite adequate understanding of the tasks. This deficit is present even though

CHAPTER 1  The Physiatric History and Physical Examination

15

Great auricular nerve Anterior cut. nerve of neck Supraclavicular nerves Axillary nerve (circumflex) Lower lateral cut. nerve of arm (from radial nerve) Lateral cut. nerve of forearm (from musculocut. nerve) Ilioinguinal nerve

T2 3 4 5 6 7 8 9 10 11 12

Medical cut. nerve of arm and intercostobrachial nerve Medial cut. nerve of forearm Illiohypogastric nerve Radial nerve Median nerve Ulnar nerve

Fermoral branch of genitofemoral nerve (lumboinguinal nerve)

Genital branch of genitofemoral nerve

Lat. cut. nerve of thigh

Dorsal nerve of penis

Intermed. c med.cut nerves of thigh (from femoral nerve)

Scrotal branch of perineal nerve Obturator nerve

Saphenous nerve (from femoral nerve)

A

Lateral cut. nerve of calf (from common peroneal nerve)

Deep peroneal nerve (from common peroneal nerve)

Superficial peroneal nerve (from common peroneal nerve)

Medial & lateral plantar nerves (from post. tibial nerve)

Sural nerve (from tibial nerve)

Greater occipital nerve Lesser

Axillary nerve (circumflex)

Great auricular nerve

Posterior cut. nerve of arm (from radial nerve) Lower lateral cut. nerve of arm (radial nerve) Posterior cut. nerve of forearm (from radial nerve) Iliohypogastric nerve Inferior medial clunical nerve Lateral cut. nerve of thigh Posterior cut. nerve of thigh Lateral cut. nerve of calf (from common peroneal nerve) Saphenous nerve (from femoral nerve) Superfical peroneal nerve (from common peroneal nerve)

Anterior cut. nerve of neck T2 Post. 3 cut. 4 rami 5 6 of 7 thor. 89 nerves 10 11 12 Post. rami of lumbar, sacral and coccygeal nerves

Supraclavicular nerves Medial cut. nerve of arm and intercostobrachial nerve Medial cut. nerve of forearm Lateral cut. nerve of forearm (from musculocut. nerve) Radial nerve Inferior lateral clunical nerves Median nerve Ulnar nerve Obturator Medial cut. nerve of thigh (from femoral nerve) Medial plantar nerve Lateral plantar nerve

Sural nerve (from tibial nerve) Calcanean branches of sural and tibial nerves

B

Calcanean branches of sural and tibial nerves

Saphenous nerve

FIGURE 1-2  Distribution of peripheral nerves and dermatomes. (Redrawn from Haymaker W, Woodhall B: Peripheral nerve injuries, Philadelphia, 1953, Saunders, with permission.) Continued

16

SECTION 1  Evaluation

C2

C3

C2 C3 C4 C5

T2

C5

C7

S3 C8

C6

T1

L1

C7

T2

C6 T1

L2 Coc S5 S4

S3

C8

S4

C5

5 6 7 8 9 10 11 12

T2

T1 C6

10 11 12 L1

C4

T2 3 4

C5

T2

7 8 9

C6 T1

C4

C4

T2 3 4 5 6

C8

L2

L2

L2

C7

C7 S2 L3

L5

S2

L3

L4 L4

C8

L3

L5

L5

L4 L4

L5

L5 L5 S1

S1

C

L5

S1

S1

D

L4

S1

L4 L5

S1

FIGURE 1-2—cont’d

the patient has no weakness or sensory loss. To accomplish a complex act, there first must be an idea or a formulation of a plan. The formulation of the plan then must be transferred into the motor system where it is executed. The examiner should watch the patient for motor-planning problems during the physical examination. For example, a patient might be unable to perform transfers and other mobility tasks but has adequate strength on formal manual muscle testing. Ideomotor apraxia associated with a lesion of the dominant parietal lobe occurs when a patient cannot carry out motor commands but can perform the required movements under different circumstances. These patients usually can perform many complex acts automatically but cannot carry out the same acts on command. Ideational apraxia refers to the inability to carry out sequences of acts, although each component can be performed separately. Other forms of apraxia are constructional, dressing, oculomotor, oromotor, verbal, and gait apraxia. Dressing and constructional apraxia are often related to impairments of the nondominant parietal lobe, which typically are the result of neglect rather than actual deficit in motor planning.46 Involuntary Movements. Documenting involuntary move­ ments is important in the overall neurologic examination. A careful survey of the patient usually shows the presence or absence of voluntary motor control. Tremor is the most common type of involuntary movement and is a rhythmic movement of a body part. Lesions in the basal

ganglia produce characteristic movement disorders. Chorea describes movements that consist of brief, random, nonrepetitive movements in a fidgety patient unable to sit still. Athetosis consists of twisting and writhing movements and is commonly seen in cerebral palsy. Dystonia is a sustained posturing that can affect small or large muscle groups. An example is torticollis, in which dystonic neck muscles pull the head to one side. Hemiballismus occurs when there are repetitive violent flailing movements that are usually caused by deficits in the subthalamic nucleus.52 Tone. Tone is the resistance of muscle to stretch or passive elongation (see Chapter 30). Spasticity is a velocitydependent increase in the stretch reflex, whereas rigidity is the resistance of the limb to passive movement in the relaxed state (non–velocity dependent). Variability in tone is common, as patients with spasticity can vary in their presentation throughout the day and with positional changes or mood. Some patients will demonstrate little tone at rest (static tone) but experience a surge of tone when they attempt to move the muscle during a functional activity (dynamic tone). Accurate assessment of tone might require repeated examinations.56 Initial observation of the patient usually shows abnormal posturing of the limbs or trunk. Palpation of the muscle also provides clues, because hypotonic muscles feel soft and flaccid on palpation, whereas hypertonic muscles feel firm and tight. Passive range of motion (ROM) provides information about the muscle in response to stretch. The examiner provides firm and constant contact while moving

CHAPTER 1  The Physiatric History and Physical Examination

17

Table 1-7  Important Normal Superficial Reflexes Reflex

Elicited by

Response

Segmental Level

Corneal

Touching cornea with hair

Contraction of orbicularis oculi

Pons

Pharyngeal

Touching posterior wall of pharynx

Contraction of pharynx

Medulla

Palatal

Touching soft palate

Elevation of palate

Medulla

Scapular

Stroking skin between scapulae

Contraction of scapular muscles

C5–T1

Epigastric

Stroking downward from nipples

Dimpling of epigastrium ipsilaterally

T7–9

Abdominal

Stroking beneath costal margins and above inguinal ligament

Contraction of abdominal muscles in quadrant stimulated

T8–12

Cremasteric

Stroking medial surface of upper thigh

Ipsilateral elevation of testicle

L1, L2

Gluteal

Stroking skin of buttock

Contraction of glutei

L4, L5

Bulbocavernous (male)

Pinching dorsum of glans

Insert gloved finger to palpate anal contraction

S3, S4

Clitorocavernous (female)

Pinching clitoris

Insert gloved finger to palpate anal contraction

S3, S4

Superficial anal

Pricking perineum

Contraction of rectal sphincters

S5, coccygeal

Modified from Mancall EL: Examination of the nervous system. In Alpers and Mancall’s essentials of the neurologic examination, ed 2, Philadelphia, 1993, FA Davis, with permission of FA Davis.

Table 1-8  Muscle Stretch Reflexes Muscle

Peripheral nerve

Root level

Biceps

Musculocutaneous nerve

C5, C6

Brachioradialis

Radial nerve

C5, C6

Triceps

Radial nerve

C7, C8

Pronator teres

Median nerve

C6, C7

V1 is taken as slow as possible, slower than the natural drop of the limb segment under gravity. V2 is taken at the speed of the limb falling under gravity. V3 is taken with the limb moving as fast as possible, faster than the natural drop of the limb under gravity. Responses are recorded at each velocity and the degrees of angle at which the muscle reaction occurs.34

Patella (quadriceps)

Femoral nerve

L2–L4

Reflexes

Medial hamstrings

Sciatic (tibial portion) nerve

L5–S1

Achilles

Tibial nerve

S1, S2

Superficial Reflexes. The plantar reflex is the most common superficial reflex examined. A stimulus (usually by the handle end of a reflex hammer) is applied on the sole of the foot from the lateral border up and across the ball of the foot. A normal reaction consists of flexion of the great toe or no response. An abnormal response consists of dorsiflexion of the great toe with an associated fanning of the other toes. This response is the Babinski sign and indicates dysfunction of the corticospinal tract but no further localization. Stroking from the lateral ankle to the lateral dorsal foot can also produce dorsiflexion of the great toe (Chaddock sign). Flipping the little toe outward can produce the upgoing great toe also, and is called the Stransky sign. Other superficial reflexes include the abdominal, cremasteric, bulbocavernous, and superficial anal reflexes (Table 1-7).52

the limbs in all directions. The limb should move easily and without resistance when altering the direction and speed of movement. Hypertonic limbs feel stiff and resist movement, while flaccid limbs are unresponsive. The patient should be told to relax because these responses should be examined without any voluntary control. Clonus is a cyclic alternation of muscular contraction in response to a sustained stretch, and is assessed using a quick stretch stimulus that is then maintained. Myoclonus refers to sudden, involuntary jerking of a muscle or group of muscles. Myoclonic jerks can be normal because they occasionally happen in normal individuals and are typically part of the normal sleep cycle. Myoclonus can result from hypoxia, drug toxicity, and metabolic disturbances. Other causes include degenerative disorders affecting the basal ganglia and certain dementias.61 Tone can be quantified by the Modified Ashworth Scale, a six-point ordinal scale. A pendulum test can also be used to quantify spasticity. While in the supine position, the patient is asked to fully extend the knee and then allow the leg to drop and swing like a pendulum. A normal limb swings freely for several cycles, whereas a hypertonic limb quickly returns to the initial dependent starting position.67 The Tardieu Scale has been suggested to be a more appropriate clinical measure of spasticity than the Modified Ashworth Scale. It involves assessment of resistance to passive movement at both slow and fast speeds. Measurements are usually taken at 3 velocities (V1, V2, and V3).

Muscle Stretch Reflexes. Muscle stretch reflexes (which in the past were called deep tendon reflexes) are assessed by tapping over the muscle tendon with a reflex hammer (Table 1-8). In order to elicit a response, the patient is positioned into the midrange of the arc of joint motion and instructed to relax. Tapping of the tendon results in visible movement of the joint. The response is assessed as 0, no response; 1+, diminished but present and might require facilitation; 2+, usual response; 3+, more brisk than usual; and 4+, hyperactive with clonus. If muscle stretch reflexes are difficult to elicit, the response can be enhanced by reinforcement maneuvers such as hooking together the fingers of both hands while attempting to pull them apart (Jendrassik maneuver). While pressure is still maintained, the lower limb reflexes can be tested. Squeezing the knees together and clenching the teeth can reinforce responses to the upper limbs.46

18

SECTION 1  Evaluation

Primitive Reflexes. Primitive reflexes are abnormal adult reflexes that represent a regression to a more infantile level of reflex activity. Redevelopment of an infantile reflex in an adult suggests significant neurologic abnormalities. Examples of primitive reflexes include the sucking reflex, in which the patient sucks the area around which the mouth is stimulated. The rooting reflex is elicited by stroking the cheek, resulting in the patient turning toward that side and making sucking motions with the mouth. The grasp reflex occurs when the examiner places a finger on the patient’s open palm. Attempting to remove the finger causes the grip to tighten. The snout reflex occurs when a lip-pursing movement occurs when there is a tap just above or below the mouth. The palmomental response is elicited by quickly scratching the palm of the hand. A positive reflex is indicated by sudden contraction of the mentalis (chin) muscle. It arises from unilateral damage of the prefrontal area of the brain.53 Gait Gait evaluation is an important and often neglected part of the neurologic evaluation. Gait is described as a series of rhythmic, alternating movements of the limbs and trunks that result in the forward progression of the center of gravity.9 Gait is dependent on input from several systems including the visual, vestibular, cerebellar, motor, and sensory systems. The cause of dysfunction can be determined by understanding the aspects of gait involved. One example is difficulty getting up, which is consistent with ­Parkinson’s disease, or a lack of balance and wide-based gait, which is suggestive of cerebellar dysfunction. The examination starts by asking the patient to walk across the room in a straight line. This can also be assessed by observing the patient walking from the waiting area into the examination room. The patient is then asked to stand from a chair, walk across the room, and come back toward the examiner. The examiner should pay particular attention to the following: 1. Ease of arising from a seated position. Can the patient easily arise from a sitting position? Difficulty with a sitto-stand task may indicate proximal muscle weakness, movement disorders with difficulty initiating movements, or a balance problem. 2. Balance. Does the patient lean or veer off to one side, which is an indication of cerebellar dysfunction? Patients with medullary lesions and cerebellar lesions tend to push to the side of the lesion. Diffuse disease affecting both cerebellar hemispheres can cause a generalized loss of balance. Patients with cerebellar disorders usually have balance issues with or without their eyes open. Patients with proprioceptive dysfunction can use their visual input to compensate for their sensory deficit. 3. Walking speed. Does the patient start off slow and then accelerate uncontrollably? Patients with Parkinson’s disease will have problems initiating movements, but then lose their balance once they are in motion. Patients with pain such as knee or hip arthritis often have limitations of ROM affecting gait speed. It has been shown that a self-selected gait speed of less than 0.8 m/s is a risk factor for falls in the stroke population.59 The speed of walking remains stable until about age 70 when there is a 15% decline per decade. Gait speed is lower because elderly people take shorter steps. 7

4. Stride and step length. Does the patient take a small step or shuffle while walking? Patients with normal pressure hydrocephalus and Parkinson’s disease usually take small steps or shuffle (decreasing their step and stride length). Stride length is the linear distance between successive corresponding points of heel contact of the same foot, whereas step length is the distance between corresponding successive contact points of opposite feet.9 An average step length is approximately 2 feet for women and 2.5 feet for men.73 5. Attitude of arms and legs. How does the patient hold his or her arms and legs? Loss of movement as in a spastic or contracted patient should be assessed. Patients with knee extension weakness might swing their knees into terminal extension, thereby locking their knee (genu recurvatum). The patient is then asked to also walk heel to toe in a straight line. Ask the patient to walk in a straight line by putting one heel of one foot directly in front of the toe of the other. This is also called tandem gait and is a test of higher balance. Tandem gait can be difficult for older patients, and in some other medical conditions (even without neurologic disease). Other tests to assess gait function include observing patients walk on their toes and heels. Balance can also be assessed by asking patients to hop in place and to do a shallow knee bend. Gait disorders have stereotypical patterns that reflect injury to various aspects of the neurologic system (Table 1-9).

Musculoskeletal Examination Caveats The musculoskeletal examination (MSK examination) confirms the diagnostic impression and lays the foundation for the physiatric treatment plan. It incorporates inspection, palpation, passive and active ROM, assessment of joint stability, manual muscle testing and joint-specific provocative maneuvers, or special tests (Table 1-10).28,35,48 The functional unit of the musculoskeletal system is the joint. The comprehensive examination of a joint includes related structures such as muscles, ligaments, and the synovial membrane and capsule.63 The physiatric MSK examination also indirectly tests coordination, sensation, and endurance.28,44 There is overlap between the examination (and clinical presentation) of the neurologic and musculoskeletal systems. The primary impairment in many cases in neurologic disease is the secondary musculoskeletal complications of immobility and suboptimal movement (in which the concept of the kinetic chain is important for evaluation). The MSK examination should be performed in a routine sequence for efficiency and consistency, and must be approached with a solid knowledge of the anatomy. The reader is referred to several excellent references that provide in-depth reviews of the MSK examination.* Inspection and Palpation Inspection of the musculoskeletal system begins during the history. Attention to subtle cues and behaviors can guide the approach to the examination. Inspection includes observing mood, signs of pain or discomfort, functional *References 21, 35, 36, 41, 47, 52.

CHAPTER 1  The Physiatric History and Physical Examination

19

Table 1-9  Common Gait Disturbances Gait Type

Disease or Anatomic Location

Gait Characteristics

Hemiplegic

Unilateral upper motor neuron lesions with spastic hemiplegia

The affected lower limb is difficult to move, and knee is held in extension. With ­ambulation, the leg swings away from the center of the body, and the hip hikes upward to prevent the toes and foot from striking the floor. This is known as “circumduction.” If the upper limb is involved, there may be decreased arm swing with ambulation.30 The upper limb has a flexor synergy pattern resulting in shoulder adduction, elbow and wrist flexion, and a clinched fist.

Scissoring

Bilateral corticospinal tract lesions often seen in patients with cerebral palsy, incomplete spinal cord injury, and multiple sclerosis

Hypertonia in the legs and hips results in flexion and the appearance of a crouched stance. The hip adductors are overactive causing the knees and thighs to touch or cross in a “scissor-like” movement. In cerebral palsy, there can be associated ankle plantar flexion forcing the patient to tiptoe walk. The step length is shortened by the severe adduction or scissoring of the hip muscles.30

Ataxic

Cerebellar dysfunction or severe sensory loss (such as tabes dorsalis)

Ataxic gait is characterized by a broad-based stance and irregular step and stride length. In ataxic gait from proprioceptive dysfunction (tabes dorsalis), gait will markedly worsen with the eyes closed. There is a tendency to sway, while watching the floor usually helps guide the uncertain steps. Ataxic gait from cerebellar dysfunction will not worsen with eyes closed. Movement of the advancing limb starts slowly, and then there is an erratic movement forward or laterally. The patient will try to correct the error but usually overcompensates. Tandem gait exacerbates cerebellar ataxia.74

Myopathic

Myopathies cause weakness of the ­proximal leg muscles.

Myopathies result in a broad-based gait and a “waddling-type” appearance as the patient tries to compensate for pelvic instability. Patients will have problems with climbing stairs or rising from a chair without using their arms. When going floor to standing, the patient will use their arms and hands to climb up their legs—known as Gower’s sign.13

Trendelenberg

Caused by weakness of the abductor muscles (gluteus medius and gluteal minimus) as in superior gluteal nerve injury, poliomyelitis, or myopathy

During the stance phase, the abductor muscle allows the pelvis to tilt down on the opposite side. In order to compensate, the trunk lurches to the weakened side to maintain the pelvis level during the gait cycle. This results in a waddling-type gait with an exaggerated compensatory sway of the trunk toward the weight-bearing side. It is important to understand that the pelvis sags on the opposite side of the weakened abductor muscle.13

Parkinsonian

Seen in Parkinson’s disease and other disorders of the basal ganglia

Patients have a stooped posture, narrow base of support, and a shuffling gait with small steps. As the patient starts to walk, the movements of the legs are usually slow with the appearance of the feet sticking to the floor. They might lean forward while walking so the steps become hurried, resulting in shuffling of the feet (festination). Starting, stopping, or changing directions quickly is difficult, and there is a tendency for retropulsion (falling backwards when standing). The whole body moves rigidly requiring many short steps and there is loss of normal arm swing. There can be a “pill-rolling” tremor while the patient walks.74

Steppage

Diseases of the peripheral nervous ­system including L5 radiculopathy, lumbar plexopathies, and peroneal nerve palsy

The patient with foot drop has difficulty dorsiflexing the ankle. The patient compensates for the foot drop by lifting the affected extremity higher than normal to avoid dragging the foot. Weak dorsiflexion leads to poor heel strike with the foot slapping on the floor.30 An ankle-foot orthosis can be helpful.

Apraxic

Gait impairment when there is no evidence of sensory loss, weakness, vestibular dysfunction, or cerebellar deficit; seen in frontal lobe injuries such as a stroke and traumatic brain injury

Despite difficulty with ambulation, patients can perform complex coordinated activities with the lower limbs.70

impairments, or evidence of malingering. The spine should be specifically inspected for scoliosis, kyphosis, and lordosis. Limbs should be examined for symmetry, circumference, and contour. In persons with amputation, the level, length, and shape of the residual limb should be noted. Depending on the clinical situation, it can be important to assess for muscle atrophy, masses, edema, scars, and fasciculations.63 Joints should be inspected for abnormal positions, swelling, fullness, and redness. These isolated findings can coalesce to influence global movement patterns that affect the kinetic chain. The term kinetic chain refers to the fact that the joints of the human body are not isolated but instead are linked in a series. Joint motion is always accompanied by motion at adjacent as well as distant joints, resulting in asymmetric patterns causing pathology of seemingly unrelated sites. This is especially true with a fixed distal limb. For example, very tight hamstring muscles decrease the lumbar lordosis, resulting in an increased risk of lower back pain. It is

important to include this concept in any musculoskeletal assessment. Palpation is used to confirm initial impressions from inspection, helping to determine the structural origins of soft tissue or bony pain and localize trigger points, muscle guarding, or spasm and referred pain.63 Joints and muscles should be assessed for swelling, warmth, masses, tight muscle bands, tone, and crepitus.36 Tone is typically determined while assessing the ROM. It is important to palpate the limbs and cranium for evidence of fracture in patients with a change in mental status after a fall or trauma.52 Assessment of Joint Stability. The assessment of joint stability judges the capacity of structural elements to resist forces in nonanatomic directions.52,63 Stability is determined by several factors including bony congruity, capsular and cartilaginous integrity, and the strength of ligaments and muscles.52 Assessing the “normal” side establishes a patient’s unique biomechanics. The examiner first identifies Text continued on page 25.

20

SECTION 1  Evaluation

Table 1-10  Musculoskeletal Provocative Maneuvers Test

Description

Reliability (%)

Spurling’s/neck compression test

A positive test is reproduction of radicular symptoms distant from the neck with passive lateral flexion and compression of the head.

Sensitivity: 40-60 Specificity: 92-100

Shoulder abduction (relief) sign

A positive test is relief or reduction of ipsilateral cervical radicular symptoms with active abduction of the ipsilateral arm with the hand on the head.

Sensitivity: 43-50 Specificity: 80-100

Neck distraction test

A positive test is relief or reduction of cervical radicular symptoms with an axial traction force applied by the examiner under the occiput and the chin while the patient is supine.

Sensitivity: 40-43 Specificity: 100%

Lhermitte’s sign

A positive test is the presence of electric-like sensations down the extremities with passive cervical forward flexion.

Sensitivity: 20,000 Hz). Medical uses of ultrasound can be diagnostic or therapeutic. Diagnostic ultrasound is used for a variety of obstetric, urologic, cardiovascular, and other imaging studies, and is outside the scope of this chapter. Therapeutic ultrasound involves the use of high-frequency acoustic energy to produce thermal

i

r

Incident wave

Reflected wave

Tissue 1 Tissue 2

Transmitted wave t

FIGURE 20-5  Example of reflection and refraction at a tissue interface. ϕi, Angle of incident wave; ϕr , angle of reflected wave; ϕt, angle of transmitted wave.

and nonthermal effects in tissue. Ultrasonic signals are typically generated using the reverse piezoelectric effect. Certain quartz crystals and synthetic ceramics have piezoelectric characteristics, such that when they vibrate they produce an electric current.188 The reverse happens when an electric current is passed across such crystals, causing vibration at a specific frequency. As ultrasonic waves travel through tissue, they lose a proportion of their energy, a process called attenuation.208 Attenuation in tissue is produced by several mechanisms: absorption, beam divergence, and deflection.208 Absorption is the major cause of ultrasound attenuation.208 Ultrasonic energy is absorbed by the tissue and is ultimately converted into heat.208 For most tissues, attenuation increases as frequency increases, so a 1.0-MHz signal would penetrate deeper than a 3.0-MHz signal because of its lower attenuation by the tissue.208 Beam divergence is the amount that the beam spreads out from the transducer. Beam divergence decreases as frequency increases, so a higher frequency signal has a more focused beam. Deflection includes the processes of reflection, refraction, and scattering.208 The angle of the reflected wave is equal to the angle of the incident wave (Figure 20-5). The magnitude of the reflected wave depends on the difference in acoustic impedance between the tissues on each side of the reflecting surface.208 Acoustic impedance is a measure of the resistance to the transmission of a sound wave, and is the product of the velocity of sound and the density of the medium.188,208 The magnitude of the reflected wave is proportional to the following formula208: A2   −  A1 / A2   +  A1

where A2 is the acoustic impedance of tissue 2 and A1 is the acoustic impedance of tissue 1. The greater the mismatch of acoustic impedance of the two tissues, the greater the magnitude of the reflected wave. Because the impedance mismatch between skin and air is extremely high, essentially all the acoustic signal is reflected if a coupling agent is not used (see below).208 Refraction is a deviation of beam direction as it is transmitted between two media (see ­Figure 20-5). The angle of the transmitted (refracted) wave is determined by the velocity of sound in the two media, and is given by Snell’s law208: sine 1 / sine 2  =  velocity 1 / velocity 2 where sine 1 is the sine of the incident wave, sine 2 is the sine of the transmitted wave, velocity 1 is the velocity of sound in the first tissue, and velocity 2 is the velocity of sound in the second tissue. Scattering is the last

CHAPTER 20  Physical Agent Modalities

Table 20-2  Ultrasound Parameters Parameter

Details

Frequency

Millions of cycles per second (MHz)

Power

Total energy per unit time (W)

Effective radiating area

The area of the transducer that actually ­radiates ultrasonic waves (cm2)

Intensity Spatial average intensity Spatial peak intensity Temporal average intensity Temporal peak intensity

May be expressed in terms of peak or average and spatial or temporal (W/cm2) Total power output divided by effective ­radiating area Maximal intensity anywhere within the beam Average intensity of “on” and “off” periods of a pulsed signal Maximal intensity of “on” period of a pulsed signal

Duration

Generally 5-10 minutes per site

Additional parameters for pulsed ultrasound Pulse duration Pulse repetition period Pulse repetition frequency Duty factor

Time of actual ultrasound pulse (“time on”) Time interval from one pulse to the next (“time on” and “time off”) Number of pulses per second Fraction of total time during which ultrasound is emitted (calculated by dividing pulse duration by pulse repetition period)

mechanism of beam deflection. It occurs when surface irregularities scatter the signal. Scattering is minimized when surface irregularities are small with respect to the wavelength. Parameters for therapeutic ultrasound are noted in Table 20-2. Frequency is generally in the range of millions of cycles per second (or megahertz). The most commonly used frequencies in the United States are in the range of 0.8 to 1.1 MHz, although frequencies around 3.0 MHz are also fairly common. Power is total energy per unit time, whereas intensity is power per unit area. Intensity can be expressed in terms of peak or average intensity, and spatial or temporal intensity, and is indicated in units of watts per square centimeter. These different measures of intensity are defined in Table 20-2. The World Health Organization and the International Electrical Commission both recommend limiting spatial average intensity to 3 W/cm2.88 Most clinically used intensities of therapeutic ultrasound are in the range of 0.5 to 2.0 W/cm2. Temperatures of up to 46° C (114.8° F) in deep tissues (e.g., bone-muscle interface) are easily achieved with ultrasound.115-117 If very deep heating (e.g., of the hip joint) is the goal, ultrasound appears to be superior to microwave or SWD.121 Ultrasound delivery can be continuous or pulsed. Pulsed delivery involves the emission of brief bursts or pulses of ultrasound, interspersed with periods of silence (Figure 20-6). For pulsed ultrasound delivery, additional parameters should be indicated.188 These include pulse duration, pulse repetition period, pulse repetition frequency, and duty factor, and are defined in Table 20-2. In most machines available for use in the United States, selecting a duty factor automatically determines the other parameters. Duty factor commonly ranges from 10% to 50%. For example, a 2-ms pulse duration might be interspersed with 8 ms of silence. The pulse repetition period would be 10 ms, the pulse repetition frequency would be 100 Hz, and the

455

Pulse repetition period

Pulse duration FIGURE 20-6  Example of a pulsed ultrasound signal.

duty factor would be 20%. Pulsed delivery, especially at low duty factors, results in less heating than ­continuous wave ultrasound, and thereby presumably emphasizes nonthermal effects. The physiologic effects of ultrasound can be divided into thermal and nonthermal effects. Thermal effects are produced when acoustic energy is absorbed, producing molecular vibration, which results in heat production.36 Nonthermal effects include cavitation, media motion (acoustic streaming, microstreaming), and standing waves. Cavitation is the production of gas bubbles in a sound field.36 These bubbles can expand and contract with alternating compressions and rarefactions of a sound wave.36 Stable cavitation refers to bubbles that oscillate in size within the sound field.57 Unstable cavitation refers to bubbles that continue to grow in size and then collapse. The high temperatures and pressures generated by this can produce platelet aggregation, localized tissue damage, and cell death.57 Both forms of cavitation are capable of mechanical distortion, movement of material, and alteration of cellular function, but their clinical significance is not yet clearly defined.36,138 Media motion includes acoustic streaming and micro­ streaming. Acoustic streaming is defined as unidirectional movement in an ultrasonic pressure field, and results from an ultrasonic wave traveling through a compressible medium.57 Acoustic microstreaming is produced by stable cavitation. As the stable cavitation bubbles oscillate in size, the surrounding fluid is set in motion, with nearby particles being attracted to the oscillating bubble.57 In addition to movement of material, acoustic streaming and microstreaming can result in cell membrane damage and accelerate metabolic processes.57 Standing waves are produced by the superimposition of incident and reflected sound waves, and can result in focal heating at tissue interfaces of different densities.57 Stasis of red blood cells at one-half wavelength intervals in a sound field has also been demonstrated in the laboratory.58 Although numerous subcellular, cellular, and tissue nonthermal ultrasound effects have been reported, their clinical significance remains to be elucidated.36,43,57,58,138 Certain measures can minimize the nonthermal effects of ultrasound. Higher frequency, lower intensity, and pulsed delivery mode minimizes acoustic cavitation.43 Stroking technique of application minimizes standing wave formation.57 As noted previously, the amount of ultrasound reflected at an interface between two media depends on the difference in acoustic impedance, so the ideal coupling medium is one with acoustic impedance similar to that of tissue. Three factors have an impact on the effectiveness of a coupling medium:

456

SECTION 2  Treatment Techniques and Special Equipment

1. Absorption by the medium, which attenuates the ultrasound power 2. Impedance match between the coupling media and the transmitter sound head, which determines the amount of power reflected into the ultrasound source 3. Impedance match between the coupling medium and the body tissue, which determines the amount of power reflected into the medium8 Degassed water is a commonly used coupling medium and is used to prevent bubble formation on the skin surface. Allowing tap water to stand overnight typically allows for adequate gas evaporation. In tests of acoustic transmissivity, mineral oil and several commercially available coupling gels had similar transmissivities to the reference standard of distilled degassed water.195 However, the hydrocortisone phonophoresis coupling agents tested had a significantly lower transmissivity, presumably related to microscopic air bubbles introduced into the media. Variation in transducer pressure produced dramatic differences in transmissivity, which outweighed the differences between the various coupling media. The investigators concluded that coupling media can be chosen primarily on the basis of cost and convenience, without compromising function.195 Encased silicon gel shows promise for use as a coupling agent over irregular body surfaces, sensitive skin areas, and open wounds, if the issue of impedance mismatch with the sound head can be rectified.8 In addition to accommodating for impedance mismatches, coupling media also lubricate to permit smooth movement of the transducer over the skin. The most common technique of ultrasound application is the stroking technique. It allows a more even energy distribution over the site being treated. The applicator is moved slowly over an area of approximately 25 cm2 (4 square inches) in a circular or longitudinal manner.112 The applicator size (usually 5 to 10 cm2) limits the size of the area that can be treated, so multiple fields of treatment might be needed for larger areas (i.e., shoulder and hip may require anterior, lateral, and posterior ports). The stationary technique generally should be avoided because of the potential for standing waves and the production of hot spots.148 Intensity is indicated by specifying the particular watts per square centimeter or by titrating to just below pain threshold. In surveys of performance of ultrasonic therapy equipment, variations in frequency and power output were common.88,182 Although the frequency of commercially available ultrasound applicators was typically within 5% of manufacturer’s specifications, the overwhelming majority (85%) of applicators tested had power output variations of over 20%.182 Consequently it is important to have ultrasound applicators recalibrated regularly. More than 35 clinical uses of ultrasound have been described, but many of these are not well supported by experimental evidence.186 More recent systematic reviews have not conclusively shown the benefits of ultrasound in the care of a number of musculoskeletal and related conditions, for similar lack of evidential support.* The purported clinical uses of ultrasound continue to expand, however, as witnessed by the current clinical interest in fracture healing, especially of bony nonunions,63,64,102 104 and in chronic wound healing.† *References 21, 28, 84, 130, 192, 193. †References 24, 61, 78, 86, 105, 111, 120, 145.

BOX 20-6

Ultrasound Precautions

 

• General heat precautions • Near brain, eyes, reproductive organs • Gravid or menstruating uterus • Near pacemaker • Near spine, laminectomy sites • Malignancy • Skeletal immaturity • ? Arthroplasties • ? Methyl methacrylate or high-density polyethylene

Ultrasound precautions are summarized in Box 20-6.133,148,186 Concern about the use of heat near malignancies was discussed previously. Deep heating over an open epiphysis could result in either increased growth (from hyperemia) or decreased growth (from thermal injury). Avoiding ultrasound near pacemakers is reasonable because of potential thermal or mechanical injury to the pacemaker. Ultrasound over laminectomy sites could theoretically result in spinal cord heating. Ultrasound at therapeutic dosage over the peroneal nerve has been shown to produce a reversible conduction block in some patients with polyneuropathy.94 There are also case reports of increased radicular pain with ultrasound.72 There are even case reports of patient abuse of ultrasound.125 The concern with ultrasound use over arthroplasties and other metallic implants is the potential for focal heating. Gersten71 reported that temperature rises near metal were actually lower than temperature rises near bone, so metal per se should not be a contraindication to ultrasound. ­Lehmann112 cautioned against the use of ultrasound near methyl methacrylate or high-density polyethylene because of their high coefficient of absorption. The effect of ultrasound on bony ingrowth arthroplasties is not yet well defined. Because the effects of ultrasound on arthroplasties are not yet completely delineated, the most prudent course would be to avoid ultrasound over these areas whenever possible. Shortwave Diathermy SWD is a modality that produces deep heating via conversion of electromagnetic energy to thermal energy. Oscillation of high-frequency electrical and magnetic fields produces movement of ions, rotation of polar molecules, and distortion of nonpolar molecules, with resultant heat generation.73,99 The Federal Communications Commission limits industrial, scientific, and medical use to 13.56 MHz (wavelength, 22 m), 27.12 MHz (wavelength, 11 m), and 40.68 MHz (wavelength, 7.5 m).101 The 27.12-MHz ­frequency is most commonly used. The heating pattern produced depends on the type of shortwave unit and on the water content and electrical properties of the tissue. ­Tissues can be grossly divided into those with high water content (muscle, skin, blood, etc.) and those with low water content (bone, fat, etc.).99 SWD units can be inductive or capacitive. Inductive applicators use induction coils that apply a magnetic field to induce circular electrical fields in the tissue.80 They achieve higher temperatures in water-rich tissues with higher conductivity.101 These applicators typically have a cable or drum

CHAPTER 20  Physical Agent Modalities

457

BOX 20-7

Shortwave Precautions

 

FIGURE 20-7  Example of shortwave diathermy application with capacitive applicator (condenser plates). (From Kotke FJ, Lehmann JF, editors: Krusen’s handbook of physical medicine and rehabilitation, ed 4, Philadelphia, 1990, Saunders, with permission.)

configuration.101 Cables are semiflexible induction coils that can be formed to the contour of the area to be treated. Drum applicators consist of induction coils enclosed in a rigid housing or drum. For a capacitive applicator, the patient is placed between two metal condenser plates (Figure 20-7). The plates and the patient’s intervening tissue act as a capacitor (an object that stores electrical charge), and heat is generated by rapid oscillations in the electric field from one plate to the other.73 Capacitive applicators might achieve higher temperatures in water-poor tissues such as subcutaneous adipose tissue.80,101 Currently available shortwave applicators do not allow precise dosimetry, so initial pain perception is used to monitor intensity. Terrycloth towels are used for spacing and to absorb sweat, which is highly conductive and could result in potentially severe focal heating.112 Typical treatment time is 20 to 30 minutes. Specific applicator configuration can greatly affect the distribution of heating.101,120 In a review of several different induction applicators, the ratio of muscle heating versus fat heating ranged from 0.39 to 2.67 for the various applicators tested.120 Lehmann et al.114 evaluated the effect of subcutaneous fat thickness and technique of SWD application. In comparing distance from the applicator, 2 cm of air space between patient and applicator produced a more desirable heating pattern than did 3 mm of terrycloth between patient and applicator. Depth of subcutaneous fat also had a significant effect on temperature distribution. Muscle temperature rise in subjects with less than 1 cm of subcutaneous fat was 9.5° C, compared with 5.6° C in subjects with more than 2 cm of subcutaneous fat.114 After application of pulsed SWD, Draper et al.54 noted mean temperature increases of 1.36° C at 5 minutes, 2.87° C at 10 minutes, 3.78° C at 15 minutes, and 3.49° C at 20 minutes, at a depth of 3 cm in the gastrocnemius muscle. SWD may also decrease musculotendinous stiffness and facilitate soft tissue extensibility.139,168 SWD has been purported to be useful in a variety of musculoskeletal conditions, although, as with most of the physical agent modalities, there are conflicting data regarding efficacy.* SWD precautions are listed in Box 20-7. Metal can result in focal heating and should be strictly avoided. All jewelry should be removed, and the *References 29, 53, 59, 66, 73, 97, 131, 141, 165.

• General heat precautions • Metal (jewelry, pacemakers, intrauterine devices, surgical implants, deep brain stimulators, etc.) • Contact lenses • Gravid or menstruating uterus • Skeletal immaturity

treatment table ideally should not contain metal. Likewise, electromagnetic energy can seriously interfere with pacemaker function, so a pacemaker is an absolute contraindication. Severe central nervous system damage has been reported after use of SWD near a deep brain stimulator.147 Contact lenses are a concern because of the potential for focal heating.174 The other precautions listed are self-explanatory. Regular maintenance and calibration of equipment should be performed to ensure safe operation of SWD.5 Special attention should also be given to ensure operator safety during SWD use.177,179 Microwave Diathermy Microwave diathermy is another form of electromagnetic energy that uses conversion as its primary form of heat production. Thermal energy is produced by increased kinetic energy of molecules within the microwave field.153 Federal Communications Commission–approved frequencies for therapeutic microwave are 915 MHz (wavelength, 33 cm) and 2456 MHz (wavelength, 12 cm).112 The lower frequency has the advantage of increased depth of penetration but also the disadvantages of greater beam dispersion and the requirement of larger applicators.153 Temperature distribution in a particular tissue is affected largely by its water content. The fraction of power absorbed in a particular tissue depends on several factors, including the frequency of the electromagnetic wave, the dielectric constant, and the electrical conductivity of the tissue.153 In general, tissues with high water content absorb greater amounts of energy and are selectively heated.112 If muscle heating is a primary objective, 915-MHz applicators are preferable to 2456-MHz applicators.118 Nonthermal effects of microwave diathermy have been documented, but Lehmann112 points out that there is no evidence that these are of any therapeutic significance. Average temperatures of approximately 41°C (105.8°F) at a depth of 1 to 3 cm have been demonstrated.46 Microwave, although once quite popular, has been largely replaced by other modalities.177 General heat precautions should be observed with microwave. Metal implants, pacemakers, sites of skeletal immaturity, reproductive organs and brain, and fluid-filled cavities (eye, bullae, effusions, etc.) should be avoided.100,112

Cryotherapy All forms of cryotherapy (therapeutic use of cold) are considered superficial cooling agents, usually transferring thermal energy by conduction. Exceptions include convective cooling in the whirlpool and evaporative cooling with vapocoolant sprays (Table 20-3). This section reviews the physiologic

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Table 20-3  Classification of Various Types of Cooling Type of Cooling

Depth

Main Form of Energy Transfer

Cold packs

Superficial

Conduction

Ice massage

Superficial

Conduction

Cold water immersion

Superficial

Conduction

Cryotherapy-compression units

Superficial

Conduction

Vapocoolant spray

Superficial

Evaporation

Whirlpool baths

Superficial

Convection

BOX 20-9

 

General Uses of Cryotherapy in Physical Medicine • Musculoskeletal conditions (sprains, strains, tendonitis, tenosynovitis, bursitis, capsulitis, etc.) • Myofascial pain • After certain orthopedic surgeries • Component of spasticity management • Emergency treatment of minor burns

BOX 20-10

General Precautions for the Use of Cold

BOX 20-8

Physiologic Effects of Cold

 

Hemodynamic • Immediate cutaneous vasoconstriction • Delayed reactive vasodilatation • Decreased acute inflammation Neuromuscular • Slowing of conduction velocity • Conduction block and axonal degeneration with prolonged exposure • Decreased group 1a fiber firing rates (muscle spindle) • Decreased group 2 fiber firing rates (muscle spindle) • Decreased group 1b fiber firing rates (Golgi tendon organ) • Decreased muscle stretch reflex amplitudes • Increased maximal isometric strength • Decreased muscle fatigue • Temporarily reduced spasticity Joint and Connective Tissue • Increased joint stiffness • Decreased tendon extensibility • Decreased collagenase activity Miscellaneous • Decreased pain • General relaxation

effects (Box 20-8), general uses (Box 20-9), and general precautions (Box 20-10) for cryotherapy, followed by a discussion of the agents currently used in physical medicine.

Physiologic Effects of Cold Hemodynamic Application of cold to the skin results in immediate cutaneous vasoconstriction through sympathetically mediated reflex mechanisms and by directly stimulating smooth muscle contraction.81,156 Lewis127 observed phasic oscillations of temperature in the fingers after initial vasoconstriction during cold water immersion. The initial vasoconstriction is thought to be due to a cold-induced increase in the affinity of the postjunctional α-adrenergic receptors for existing norepinephrine in vascular smooth muscle.178 Reactive vasodilatation occurs as further cooling interrupts noradrenaline release. Vasodilatation warms the tissues, again releasing norepinephrine to sensitized receptors, and the cycle repeats. This “hunting” of temperature is believed to be a mechanism by which peripheral exposed

 

• Cold intolerance • Cryotherapy-induced neurapraxia or axonotmesis • Arterial insufficiency • Impaired sensation • Cognitive or communication deficits that preclude ­reporting of pain • Cryopathies • Cryoglobulinemia • Paroxysmal cold hemoglobinuria • Cold hypersensitivity • Raynaud disease or phenomenon

parts of the body are protected from cold injury. Others have demonstrated vasodilatation after cooling of the hand and forearm, without the phasic oscillations observed by Lewis.35,67 The effects of localized cooling on heart rate and blood pressure are variable and have been summarized elsewhere.134 Cryotherapy has also been shown to moderate inflammation, more effectively in the acute phase than in the chronic phase.173 Neuromuscular The initial response of peripheral nerves to cold application is a marked slowing of conduction velocity.1,49 With more prolonged exposure, there is conduction block, cessation of axoplasmic transport, and eventual axonal degeneration.146 Decreased muscle spindle (both group 1a and 2 fibers) and Golgi tendon organ (group 1b fibers) firing rates have been demonstrated after local cooling in animals.62 The clinical neuromuscular effects of cooling include a decrease in gastrocnemius muscle stretch reflex amplitude,17,109 an increase in maximal isometric strength,34,132 and slowing in the rate of muscle fatigue.34 Cold has also been shown to temporarily reduce spasticity in patients with hemiplegia and multiple sclerosis, improving exercise tolerance and enhancing function.87,137 Other investigators, however, have noted increased spasticity after cold application in some subjects.31,164 Joint and Connective Tissue Topical cold application (approximately 4° C) to the knee in dogs induced significant and sustained depression of intraarticular temperature without significant effect on core temperature.18 Synovial collagenase activity also decreases with temperature. In vitro experiments demonstrate negligible synovial collagenase activity after cooling to 30° C (86° F), suggesting that therapy that decreases intraarticular temperature in inflammatory arthropathies could slow

CHAPTER 20  Physical Agent Modalities

the rate of collagenolysis.82 It should be noted, however, that in one study of the use of cryotherapy after cruciate ligament surgery, skin temperature had to be lowered to 20° C to produce significant intraarticular temperature declines.41 Potentially negative effects such as decreased tendon extensibility and increased joint stiffness have also been demonstrated after cooling.119,205

459

urticaria and angioedema on exposure to cold. Raynaud disease is an idiopathic condition characterized by arteriolar spasm precipitated by cold exposure or stress. Raynaud phenomenon is secondary to other rheumatologic conditions (rheumatoid arthritis, scleroderma, systemic lupus erythematosus, etc.) and is classically manifested by digital pallor, followed by cyanosis and eventual reactive hyperemia.

Miscellaneous Effects of Cold The analgesic effect of cold can be related to reflex muscle relaxation, cutaneous counterirritation, or its effects on nerve conduction.134 As with heat, some patients note cold to produce a general relaxation, although the mechanisms are not well defined.

General Uses of Cryotherapy in Physical Medicine The general uses for therapeutic cold are summarized in Box 20-9. Cryotherapy is most commonly used acutely after musculoskeletal injury to minimize formation of edema, and for symptomatic relief in painful soft tissue and articular inflammatory states.75,92,134,135,189 Two recent reviews nicely summarize the use of modalities in arthritis.83,151 Studies of the use of cryotherapy after orthopedic procedures have produced mixed results: some investigators report favorable effects on factors such as range of motion, pain, analgesic use, swelling, postoperative blood loss, and hospital length of stay, while others demonstrate no significant effect from cryotherapy.* There have also been mixed results with the use of cryotherapy in spasticity management.31,87,137,164,196 Cryotherapy in the form of immediate ice water immersion is advocated as emergent primary treatment for minor burns.181

General Precautions for the Use of Cold The general precautions for the use of cold are outlined in Box 20-10. The most common relative contraindication to the use of cold is simple cold intolerance. A patient who does not tolerate cold application will tend to increase muscle guarding and cocontraction, which is directly counterproductive to the therapeutic goals. Simple cold intolerance should be distinguished from true cold hypersensitivity, which is discussed below. Caution should also be used when applying cold over the course of superficial nerves, because peroneal and ulnar palsies have been reported after cryotherapy.55 Application of cold over areas of compromised arterial vascularity can theoretically produce further ischemia from local vasoconstriction and should be avoided. Likewise, because of the potential for cold injury, cryotherapy should be used with caution in areas of impaired sensation or in patients who have cognitive or communication deficits that preclude reporting of pain. The cryopathies are also contraindications to the use of cold.167 Cryoglobulinemia is a condition that results in the precipitation of immune complexes at low temperatures. Paroxysmal cold hemoglobinuria is a rare disorder resulting from an antibody directed against a red blood cell surface antigen, with hemolysis precipitated by cold exposure. Cold hypersensitivity is a mast cell–mediated process producing *References 10, 37, 42, 60, 85, 96, 124, 126, 170, 198, 203.

Cryotherapy Agents Cold packs Cold packs include hydrocollator packs, endothermic chemical gel packs, and ice packs. Hydrocollator packs are cooled in a freezer to –12° C (10° F) and applied over a moist towel.109 Endothermic chemical gel packs have separate compartments with compounds such as ammonium nitrate and water that when mixed, undergo a heatabsorbing reaction. They are portable, pliable, and easily used in the field. Although many endothermic chemical gel packs are designed for one-time use, some have the advantage that they can be refrozen and reused as a simple cryogel pack. Ice packs are easily used at home and might be best applied by elastic bandage or tape, as external compression appears to increase their cooling effectiveness.12 The duration of application is typically 20 to 30 minutes. With application of a cooled hydrocollator pack, the skin is cooled immediately, subcutaneous tissues are cooled within minutes, and muscle at a depth of 2 cm is cooled by approximately 5° C after 20 minutes.109 Precautions for cold packs are as listed in Box 20-10. Ice Massage Ice massage is the direct application of ice to the skin using gentle stroking motions. It combines the therapeutic effects of cooling with the mechanical effects of massage. Water is frozen in a paper cup, with the ice being exposed by tearing the top rim of paper off as the ice melts (Figure 20-8). Alternatively, a wooden tongue depressor can be placed in the water, to be used as a handle after the water is frozen. Ice massage is generally used for localized symptoms and applied for 5 to 10 minutes per site, depending on the amount of subcutaneous adipose tissue.129 There is typically a phasic response to ice massage, beginning with an initial perception of coolness, followed by a burning or aching, then hypoesthesia and analgesia.75 Intramuscular temperatures at a depth of 2 cm after 5 minutes of ice massage have been reported to be reduced by 4.1° C in the posterior thigh197 to as much as 15.9° C in the biceps brachii muscle.129 In his initial description of ice massage, Grant75 reported a “satisfactory treatment result” in over 80% of a series of more than 7000 patients with a variety of painful musculoskeletal conditions treated with ice massage and mobilization exercises, although no statistical analysis was reported. Precautions for ice massage are as listed under general cold precautions. Cold Water Immersion Immersion in cold water is best suited for circumferential cooling of the limbs, usually at temperatures of 5° to 13° C (41° to 55.4° F).181 It is often uncomfortable and poorly tolerated, although reportedly effective with localized burns, as skin temperature rapidly approaches

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SECTION 2  Treatment Techniques and Special Equipment

primary uses are in arthritis and a variety of musculoskeletal conditions, and in the cleansing and debridement of burns and other dermal injuries.

Whirlpool Baths and Hubbard Tanks

FIGURE 20-8  Example of ice massage.

water temperature.181 Gastrocnemius muscle temperature decreases to approximately 6° C below baseline after 30 minutes of cold water immersion.137,158 Precautions for cold water immersion are listed in Box 20-10. Cryotherapy-Compression Units Cryotherapy-compression units consist of a cuff or boot through which cold water is circulated, and can be pneumatically compressed statically or in a serial, distal-toproximal pumping action. They are designed to combine the beneficial effects of cryotherapy with the advantages of pneumatic compression. They are used primarily after acute musculoskeletal injury with soft tissue swelling, and after some surgical procedures.171 Typical temperatures of 7.2° C (45° F) and pressures up to 60 mm Hg are used. Vapocoolant Spray Vapocoolant spray and stretch methods are used by some practitioners to treat myofascial and musculoskeletal pain syndromes. The technique consists of a series of unidirectional applications of Fluori-Methane spray, which has replaced the highly flammable ethyl chloride spray in clinical usage.189 Treatment begins in the “trigger area” (area of deep myofascial hypersensitivity) and extends over the “reference zone” (area of referred pain) while passively stretching the muscle.189 The spray and stretch are performed parallel to the muscle fibers, at an approximate rate of 4 inches/s. Waiting briefly between applications helps prevent skin freezing. The therapeutic effect of spray and stretch is postulated to result from a counterirritant phenomenon.189 Precautions include general cold precautions and avoidance of cutaneous freezing.

Hydrotherapy Hydrotherapy is defined as the external application of hot or cold water, in any form, for the treatment of disease.69 The main forms of hydrotherapy are whirlpool baths, the Hubbard tank, the shower cart, and contrast baths. Their

Whirlpool baths and Hubbard tanks control water temperature and agitate it by aeration, dispersing thermal energy by convection (although as noted previously, the actual transfer of heat to or from the body is by conduction). Whirlpool baths come in a variety of sizes and are typically used for treatment of a limb or localized lesion. Because only a portion of the body is immersed, greater extremes of temperature can be tolerated without significant core body temperature change.69,158 As more body surface area is immersed and the extremes of temperature increase, there is increasing potential for alteration of core body temperature. Hubbard tanks are larger tanks generally used for whole-body immersion, so neutral temperatures (34° to 36° C, 93° to 97° F) should be used to prevent core temperature fluctuations. An immersed body experiences a vertical antigravity force equal to that of the volume of the displaced water, decreasing stress on bones and joints.69 This property, along with the therapeutic effects of the water temperature, makes hydrotherapy appropriate for adjunctive treatment of degenerative arthritis, acute musculoskeletal injuries, burns, and skin ulceration23 and infection.69 Antiseptic conditions can be used for hydrotherapy of burns or infected areas, but truly sterile conditions are not easily achieved, necessitating provider vigilance in patient selection, given reports of Pseudomonas infections.190 Sodium hypochlorite is the most commonly used antibacterial solution used in burn programs.187 For Hubbard tank treatment of large wounds, salt can also be added to minimize fluid shifts. Isotonic saline is 0.9% sodium chloride (0.9 g of NaCl, 100 mL of H2O), so 900 g (approximately 2 lb) of salt should be added per 100 L (approximately 25 gallons) of water.

Shower Cart Hydrotherapy has several features that are desirable for treatment of burns or other wounds. It loosens adherent dressings to facilitate removal, allows for removal of antimicrobial cream before reapplication, and softens eschar to facilitate debridement.194 There is a risk for autocontamination and cross-contamination, however, with conventional whirlpool baths or Hubbard tanks.194 The shower cart was developed in response to this risk.194 It allows for gentle spray or shower hydrotherapy during mechanical debridement of large surface area burns and other wounds under relatively sterile conditions.194 Typical units have overhead retractable shower heads (Figure 20-9), with independently adjustable water temperature and pressure. A shower cart also uses significantly less water and less space, and requires less maintenance than a Hubbard tank (see Chapter 58).

Contrast Baths Contrast baths consist of alternating immersion of the distal limbs in hot (42° to 45° C, 108° to 113° F) then cold (8.5° to 12.5° C, 47° to 55° F) water.204 The effect

CHAPTER 20  Physical Agent Modalities

461

delivery of medicines. For systemic drug delivery, it avoids the problems associated with oral or intravenous routes such as gastric irritation, first-pass hepatic metabolism, and variable serum concentrations.32,33 Iontophoresis in physical medicine is used to deliver medicines directly to soft tissues, limiting systemic absorption.30,38,128 Ionic medications (local anesthetics, corticosteroids, analgesics, and antibiotics) or plain tap water has been used with this technique. The ionic solution to be iontophoresed is placed on the electrode of the same polarity, and then the negative, positive, and ground electrodes are applied to the skin. A direct current, typically between 10 and 30 mA, is applied to drive the solution away from the electrode and into the surrounding tissues.180 The quantity of solution transported appears to be dependent on the local current density, the duration of treatment, and the solution concentration.150 Although the mechanism of action and the clinical efficacy of iontophoresis continue to be debated, it is a modality commonly used by practitioners to treat a variety of conditions.* Iontophoresis is generally well tolerated, although miliariasis has been reported when treating hyperhydrosis.180 FIGURE 20-9  Shower cart.

is thought to be related to the cyclic vasoconstriction and vasodilatation produced by the temperature extremes. Thirty-minute treatment sessions are typical, beginning with a 10-minute immersion in hot water, followed by alternating immersions of 1 minute in cold and 4 minutes in hot water, and ending the session with a cold water immersion to theoretically limit swelling. The technique might be beneficial in the treatment of rheumatologic disease, neuropathic pain, or other chronic pain syndromes such as complex regional pain syndrome.

Other Modalities Ultraviolet Ultraviolet radiation is that part of the electromagnetic spectrum adjacent to the short-wavelength, high-frequency (violet) end of the visible light spectrum. Ultraviolet radiation has historically been used in physical medicine for the treatment of skin ulcers, but now its therapeutic use is almost exclusively dermatologic.143 Most current treatments with ultraviolet radiation use either ultraviolet A (wavelength 320 to 400 nm) or ultraviolet B (wavelength 290 to 320 nm) radiation.143 The minimal erythema dose can be used to titrate intensity, and is determined by exposing small areas of skin to different durations of ultraviolet radiation. The minimal erythema dose is that duration of exposure that produces erythema. Although originally used mainly in the treatment of psoriasis, there are now more than 30 dermatologic disorders for which ultraviolet radiation could be efficacious.143 Potential adverse effects include premature aging of the skin, nonmelanoma skin cancer, and cataracts.143

Iontophoresis Iontophoresis is the migration of charged particles across biologic membranes under an imposed electrical field.123 Its primary use has been in transcutaneous systemic or local

Phonophoresis Phonophoresis involves the use of ultrasound to facilitate transdermal migration of topically administered medications. Corticosteroids are the most frequently used phonophoresis agents. The antiinflammatory effects of ultrasound and corticosteroids are thought to be synergistic.144 The actual mechanism of transdermal migration has not been well defined but could involve increased cell permeability from the thermal effects of ultrasound.144 Ultrasonic coupling gel is mixed with various chemical substances to produce the phonophoresis coupling agent.144 Studies have documented significant differences in acoustic transmission among different phonophoresis agents, and these differences should be considered in choosing an agent.27 Typical phonophoresis treatment parameters are similar to those of standard ultrasound: pulsed mode, 1-MHz transducer frequency, stroking technique, at 1.0 to 1.5 W/cm2, for approximately 5 minutes per site.144 There is also lowfrequency phonophoresis that typically uses frequencies less than 100 kHz.140 Proposed indications for phonophoresis include osteoarthritis, bursitis, capsulitis, tendonitis, strains, fasciitis, epicondylitis, tenosynovitis, contracture, scar tissue, neuromas, and adhesions.77,144 Phonophoresis is a modality with some measure of clinical effectiveness, but there continue to be differences of opinion about its mechanism of action, clinical efficacy, and the extent of transdermal migration of agents.† The precautions for and contraindications to phonophoresis are listed in Box 20-6.

Low-Energy Laser Laser is the acronym for light amplification by stimulated emission of radiation. It consists of a coherent (in phase), collimated (restricted in area) beam of photons of identical frequency. Low-energy lasers typically deliver less *References 9, 30, 38, 40, 48, 79, 90, 128, 142, 152, 157, 166, 180, 183, 184, 206. †References 11, 25, 26, 44, 90, 93, 106, 154, 169.

SECTION 2  Treatment Techniques and Special Equipment

Interferential Current Therapy Interferential current therapy (IFC) is a modality that uses two alternating current signals of slightly different frequency. To understand the mechanism of IFC, one must have an understanding of how waves interact. Figure 20-10 illustrates that interaction. At the intersection of two sinusoidal waveforms, the “interference” of the two waves produces a summated wave. When the two waves are in phase, there is constructive interference; the summated wave has an amplitude equal to the sum of the individual wave amplitudes.74 When the two waves are out of phase, there is destructive interference; the summated wave has a lower amplitude because the opposite polarities of the waves partially cancel each other.74 When two waves of equal amplitude and frequency are exactly in phase, the amplitude of the summated wave is exactly twice that of the individual waves. When two waves of equal amplitude and frequency are out of phase by exactly one-half wavelength (i.e., the peak of one wave intersects with the trough of the other wave), the amplitude of the summated wave is zero. As noted, IFC uses two alternating current signals of slightly different frequencies. As these two waveforms intersect, they are periodically in phase (constructive interference) and periodically out of phase (destructive interference). This periodic interference results in a new wave with cyclic modulation of amplitude, because of the cyclic constructive and destructive interference. The amplitude of the summated wave modulates at a beat frequency, equal to the difference in frequency between the two signals.74 For example, if one applicator channel frequency is 5100 Hz and the other is 5000 Hz, the beat frequency would be 100 Hz (5100 – 5000 = 100). IFC machines typically use medium-frequency currents of approximately 4000 to 5000 Hz. Alternating currents of medium frequency (1000 to 10,000 Hz) have lower skin resistance than low-frequency currents (1 month) are unknown. These treatments do not appear to be effective in aborting headaches. There is little evidence to suggest that manipulation or mobilization can correct or reduce idiopathic scoliosis.107,113 There is, however, a suggestion that spinal manipulation therapy is helpful in controlling chronic mechanical back pain associated with scoliosis.133 Although manual medicine practitioners have reported alleviation of symptoms caused by carpal tunnel syndrome and normalization of nerve conduction studies,136 there is little evidence to suggest a therapeutic effect.45 Shekelle123 has noted that “there appears to be little evidence to support the value of spinal manipulation for nonmusculoskeletal conditions.” Randomized controlled trials of chiropractic treatment for asthma have demonstrated no change in measured lung functions in either children15 or adults.105 Although otitis media is sometimes treated by chiropractors, there have been no randomized trials. A review of the literature concluded that the effect of spinal manipulation on enuresis is similar to the natural remission rate.78 Primary dysmenorrhea has been reported to respond to spinal manipulative therapy.32,85 A single randomized trial demonstrated reduction in pain and menstrual distress. The control (sham manipulation) and treatment groups had similar elevations in circulating prostaglandins, indicating that the effect may have been the result of nonspecific factors.75 There is no evidence that manual therapies are beneficial for central nervous system– based disorders such as epilepsy.

Movement Therapies Feldenkrais Method The Feldenkrais Method is a system of body movement education that is believed to enhance awareness of movement and improve functional movement. The underlying theory is that poor habitual movement patterns result in injury and pain. The expected results of Feldenkrais therapy (awareness through movement classes or functional integration sessions) are that a person will be able to move more efficiently and comfortably, and with less pain. Feldenkrais practitioners undergo an extensive apprentice-like training program. Although the popular press promotes this therapy for many conditions, there are few randomized studies of the Feldenkrais Method. A nonrandomized study in patients with nonspecific musculoskeletal pain syndromes found no difference between conventional physical therapy, body awareness therapy, and the Feldenkrais Method as reflected by medical outcomes study 36-Item Short-Form Health Survey subscale scores.92 A small randomized study of the effect of Feldenkrais on pain found the affective dimension (attitude toward the pain) to be reduced, but no change was measured in other dimensions.129 A small randomized trial found patients with neck and shoulder complaints to benefit more from Feldenkrais than physical therapy.91 There is theoretic potential for benefit in numerous conditions because of possible effects on motor control, but this therapeutic paradigm has been inadequately studied.69

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SECTION 2  Treatment Techniques and Special Equipment

Alexander Technique The Alexander technique is a psychophysical reeducation method that proposes to relieve muscular tension and improve the efficiency of movement. The technique involves examination of posture, breathing, balance, and coordination, and has three underlying principles: (1) an organism functions as a whole; (2) a person’s ability to function optimally is dependent on the relationship of the head, neck, and spine; and (3) body function is affected by habitual patterns of use. The Alexander technique is often advocated in the treatment of asthma, headaches, arthritis, and pain, and is often used by performing artists.51 The evidence supporting the use of the Alexander technique is very limited and at this point inconclusive,52 although at least one randomized trial has demonstrated benefit for persons with chronic low back pain.89 T'ai Chi Tái chi is an ancient exercise form that originated in China. Various forms of it are practiced today, and it has become a popular physical activity in North America and Europe. It has been advocated as a therapeutic exercise, particularly in the elderly. Tái chi has been reported to improve balance, flexibility, and cardiovascular fitness in geriatric patients.139,145,146 A Cochrane systematic review found only four trials that had appropriate control groups. No statistically significant or clinically meaningful effect was found for most outcomes measured, although significant increases in range of motion were noted.65 In spite of this, tái chi appears to be a safe form of exercise for most individuals, even the elderly. Pilates Pilates exercises were originally designed for and used by performance artists, but have enjoyed wider popularity in recent years. It is estimated that 5 million people now use them, largely because of mass marketing. There are at least two randomized studies examining the effects of Pilates exercises on back pain. A randomized controlled trial (n = 39) with 12-month follow-up comparing specific Pilates exercises (using specialized exercise equipment) with usual medical care found the Pilates group to have lower disability scores and pain ratings after the intervention, with the improved disability scores maintained at 12 months.119 In another study 53 subjects were randomized to receive either pilates treatment or referral to a back school and exercise program for chronic low back pain, with blinded observers and 6-month follow-up. Both groups improved similarly in regard to disability and pain, although the Pilates group had better compliance and perceived benefit.47 Yoga Yoga is part mind-body therapy and part stretching and breathing exercise. It is most appropriately addressed with movement therapies. It is commonly advocated as treatment for musculoskeletal conditions including arthritis58 and carpal tunnel syndrome.58 There are few controlled studies in the literature. Yoga appears to have some beneficial effect on asthma, but the mechanism of effect is unclear.95 It might be beneficial for hypertension as well.111 A randomized trial of yoga, exercise, or a self-care book for

A

B

C

D

E

FIGURE 22-1  Acupuncture needles. A, A 30-mm stainless steel needle with green plastic handle (diameter, 0.14 mm). B, A 30-mm stainless steel needle with pipestem handle (diameter, 0.20 mm). C, A 30-mm stainless steel needle with wire-wrapped handle (diameter, 0.20 mm). D, A 40-mm stainless steel needle with copper wire–wrapped handle (diameter, 0.25 mm). E, A 125-mm stainless steel needle (diameter, 0.30 mm).

low back pain found the yoga group to have improved function compared with the book and exercise groups at 12 weeks, but there were no significant differences in the “bothersomeness” of symptoms. At 26 weeks, back-related function in the yoga group continued to be superior to the book group.126

Energy Therapies Acupuncture Originating in ancient China, acupuncture is one of the best recognized CAM treatments. Acupuncture consists of the insertion of thin, flexible needles into the body at specific points to improve health (Figure 22-1). The needles are inserted to varying depths and angles, and typically are inserted superficially (Figure 22-2). The needles can be further stimulated in a number of ways, including twirling the needles, electrical stimulation, or burning an herb placed on the end of the needle outside the patient. In the United States acupuncture is most widely used for analgesia or relief of pain, but it is also used to treat a wide range of other conditions including asthma, fatigue, gastrointestinal disturbance, and infertility. A wide range of practitioners perform acupuncture. State laws vary, but acupuncture practitioners include physicians (MDs), osteopaths (DOs), chiropractors (DCs), and licensed acupuncturists (LAcs). In some states, acupuncture can be performed as part of a religious ceremony. With such a diverse group of practitioners, there is considerable

CHAPTER 22  Integrative Medicine in Rehabilitation

A

491

C

B

FIGURE 22-2  A, The acupuncture needle sits in a guide tube on the patient’s skin. The length of the needle is slightly longer than the guide tube. The guide tube acts to guide the needle, keep the skin taut, and when tapped, provide a sensation that distracts from the needle insertion. B, The needle has been tapped into the skin and the guide tube removed. The tip of the needle is subcutaneous but has not reached the muscle. The needle is almost parallel to the skin, as it has not been inserted deeply enough to support its weight. C, The needle tip has been advanced into the first dorsal interosseous muscle. It is now able to stand perpendicular to the skin surface.

variability in the approach to acupuncture. Given its historical origin, acupuncture is most commonly associated with TCM (see earlier discussion). Acupuncture in this setting is often provided with recommendations regarding diet, herbal remedies, exercises, massage, and lifestyle modification. Qi flows through the body in specific patterns, and these pathways are known as meridians. Meridian-based acupuncture is invoked to alter the flow of qi or energy through the body. The specific technique to produce the desired result requires knowledge of the nature of the qi circulation, a diagnosis (often based on TCM), and an understanding of how insertion of the needles affects such flows. Another common style of acupuncture is termed neuroanatomic acupuncture. This style incorporates a modern understanding of the nervous and musculoskeletal systems with empiric knowledge of acupuncture point selection. For example, the point stomach 31 can relieve lateral thigh pain and lies over the lateral femoral cutaneous nerve. Although the classic interpretation of acupuncture’s mechanism of effect has been a change in the qi of the body, scientific studies have uncovered many different mechanisms of action. These range from local effects such as vasodilation, torsion of the connective tissue, and changes in local autonomic activity, to more remote endocrine effects. The endocrine effects include release of endorphins and influence of the hypothalamic-pituitary axis. Remote neurologic effects can also occur, such as changes on functional magnetic resonance imaging (MRI) of the brain. Acupuncture is a modality that is generally safe, with a growing but not definitive evidence base regarding its effectiveness for many conditions frequently seen in a physical medicine and rehabilitation practice. Conditions commonly treated with acupuncture in the rehabilitation medicine setting are listed in Box 22-3. It is most often used after therapies with more evidence of efficacy have been tried and failed. There is considerable anecdotal evidence and a large number of clinical trials that support its use. In the 1990s, high-quality evidence for the efficacy of acupuncture was scant.1 Individual studies

BOX 22-3

Conditions Commonly Treated by Acupuncturists in North America

 

• Back pain (upper and lower) • Neck pain • Headaches • Perioperative pain • Osteoarthritic pain • Tennis elbow (lateral epicondylitis) • Fibromyalgia • Myofascial pain

often demonstrated benefit for multiple conditions, but they were usually small, less rigorous, and difficult to reproduce. In addition, there was a question of publication bias; Asian studies tended to report more favorable results than those studies performed in the United States. Larger, more rigorous trials have now demonstrated less favorable results for many conditions. Several difficulties continue to produce controversy in acupuncture research. The difficulty of establishing adequate sham procedures and the variability in study design continue to be of concern. Also, the precision of the diagnosis is lacking, because patients are classified by symptoms rather than by objective criteria or specific medical diagnoses. Acknowledging this complex background, recent trials show a generally positive effect on knee osteoarthritis symptoms,22,70,93,117 chronic low back pain,56 and headaches.86,87 There is also evidence that acupuncture added to standard treatment is beneficial for fibromyalgia.132 The literature regarding acupuncture safety indicates only a low rate of complications, even among acupuncture students.1 Risks for acupuncture include bleeding, infection, and organ puncture (including pneumothorax).81 Needle shock is an uncommon side effect that typically occurs during the first acupuncture treatment. The description of this event is similar to a vasovagal episode: sweating, flushing,

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and the sensation that the world is being seen from down a long tunnel. Treatment of needle shock is the immediate removal of the needles. A technique that is particularly prone to complications is the permanent placement of needles. These needles are inserted, and the handles are broken off.39 Unfortunately, they can migrate and cause damage to internal organs.

Acupressure Acupressure is similar to acupuncture in terms of its analysis of the human body, but it uses pressure rather than needles to achieve its effects. Acupressure is used for many of the same complaints and conditions as acupuncture, and is thought to produce similar effects. Acupressure practitioners might incorporate massage as part of their practice. Japanese shiatsu massage and Chinese tui na both use acupressure principles. Direct manipulation of the tissues is believed to open up channels to the flow of qi. Topical herbal treatments and salves can be used as well. Compared with acupuncture, acupressure can be applied differently, which may be advantageous in some patients. Most obviously, the lack of needles eliminates the potential complications of bleeding and infection, and expands the range of patients who might benefit from this treatment to include individuals receiving anticoagulants, those with needle phobia, and those who are severely immunosuppressed. Acupressure can also be taught to the patient, who can subsequently apply self-treatment on a more frequent basis. This can be very helpful in the early stages of treatment when the duration of the relief from acupressure might be short-lived. Acupuncture needles are currently classified as class II devices by the Food and Drug Administration, limiting their sale to acupuncture practitioners. They cannot be given to a patient so they can administer the treatment at home. Acupressure forces a practitioner to treat each individual area sequentially, whereas acupuncture allows more points to be simultaneously stimulated. This potentially allows a practitioner to determine which points are more effective in achieving the desired effect. Studies on acupressure and evidence of benefit are limited at present.

Reiki and Healing Touch Reiki and healing touch are both energy-based methods of healing. They both posit the ability of one human being to positively influence the energy field of another individual and thus improve that individual’s health. This energy influence or transfer is also an “intelligent” one, as the specifics of energy manipulation are automatic for the most part. Healing touch requires specific hand positions only for certain conditions. Both disciplines propose the possibility of healing at a distance, as close physical contact is not always required. A number of trials using reiki and healing touch are currently being conducted by the National Institutes of Health. Completed studies suggest that both of these modalities might be effective in reducing psychologic sequelae of disease, such as pain. A Cochrane review concluded that use of reiki (versus other touch modalities) by experienced practitioners might result in a greater degree of pain relief.131

Reflexology Reflexology is a healing art based on the theory that there are reflexes in the feet and hands that correspond to every part of the body. Reflexology relies on the concept of a microsystem, with the entire body mapped out on a small part of the brain. This concept is seen in conventional medicine, such as the topographic mapping of the somatosensory cortex in the brain. Pressure can be applied to specific parts of the hands and feet to influence the parts of the body being treated. Research on reflexology has produced mixed results. As with many of the other energy treatments listed above, methodological flaws are prevalent in a large number of studies. Large well-designed studies are not available. Small studies suggest that it might be helpful for some conditions. For instance, it can possibly help spasticity, paresthesias, and urinary symptoms associated with multiple sclerosis.127 Yet it was found not to be helpful for irritable bowel syndrome.134 It is uncertain whether this variability is secondary to reflexology’s efficacy, the variation in how reflexology is practiced, or poor study design.

Electromagnetic Fields and Magnets Unlike the energy medicine techniques discussed above that defy scientific attempts to characterize their energies, electromagnetic fields are well-defined physical phenomena that are widely used in technology. Electromagnetic fields are very familiar to physical medicine and rehabilitation physicians and are used in testing, such as MRI scans, electromyography, and electrocardiograms. The human body is composed of multiple structures and molecules that are highly charged and therefore particularly sensitive to strong magnetic fields. Magnets of varying field strengths and polarity can be applied to the body. Although the theoretic framework is in place, clinical effects of magnetic therapy have not been demonstrated. The data from trials on this modality are mixed, with the majority reporting no significant improvement in the condition being studied. Most studies have investigated magnetic therapy as a treatment for a specific condition, such as rotator cuff disorder,23,83 rather than for a general class of conditions. In summary, biofield CAM treatments are safe, but systematic studies regarding their efficacy are lacking, with a few notable exceptions. This suggests that these modalities might be appropriate as second-line therapies, to be used when proven or better studied treatments have not been shown to be effective.

How to Discuss Integrative Medicine With Your Patient Many physicians feel challenged by CAM topics, particularly those whose training occurred before the boom in interest in CAM. They can feel inadequately trained or educated to make sound recommendations regarding the use or avoidance of supplements, interventions, or both. At the same time, many patients feel that they have been dismissed when raising questions regarding CAM or integrative medicine. As a result, they become “gun shy” about asking such questions of their

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physician. Additionally, surveys have shown that patients frequently consider therapies such as herbs “natural” and therefore not of interest to their physician. As a result, patients may withhold information because they do not recognize the importance of their physician knowing about their use of CAM therapies. Either way, both physicians and patients need to make a concerted effort to discuss integrative medicine approaches as part of the physician-patient encounter. Perhaps one of the most important first steps in discussing integrative medicine with a patient is to simply incorporate questions regarding integrative medicine into the routine patient interview. In the medical setting, physicians routinely inquire about a patient’s medication use. This simple nonjudgmental question can be easily expanded by inquiring about the use of herbs, dietary supplements, medicinal teas, megadoses of vitamins, and other supplements. By asking the question simultaneously with inquiries about medication use, patients are taught that these other substances are important and are of interest to their medical provider. If asked in a nonjudgmental tone, it typically allows patients to be forthcoming and to openly and freely share their interests in or use of such therapies.

Some physicians find that this a natural point to also ask about other modalities or therapies that the patient might be using. This can also be done in a nonjudgmental fashion by simply asking, in the context of herbs and other dietary supplements, whether the patient is using other techniques or therapies to improve health or deal with any ongoing issues. The physician can then list a few common examples that the patient might identify with, such as meditation, chiropractic, or massage therapy. By specifying a few concrete examples, the patient can see that this is an important topic that the physician is willing to discuss. The obvious challenge in this setting is for the physician who has not had significant training in integrative medicine or CAM to know how to respond when the patient does reply in the affirmative to these inquiries. Many institutions have physicians or pharmacists who have received extra training in dietary supplements, including their risks and potential benefits. These individuals can be excellent resources. For dietary supplements, there is a wealth of reliable websites that can be queried. Online sources are of particular help in finding information regarding other specific therapies as well (Table 22-1).

Table 22-1  CAM and Integrative Medicine Information on the Web (Selected References) Databases

URL

Cost/yr

Comments

Natural Medicines Comprehensive Database

www.naturaldatabase.com

$92

▪ Very comprehensive (herbs and DS only) ▪ Up-to-date, well-referenced, good pt handouts

Herbmed

http://www.herbmed.org

Free

▪ Moderately comprehensive (herbs and DS only) ▪ Well-referenced, not as intuitive to navigate as above ­database

MD Anderson Complementary/ Integrative Medicine

www.mdanderson.org/departments/ CIMER

Free

▪ Mod. comprehensive (herbs, DS and therapies) ▪ Cancer-specific, well-referenced

Memorial Sloan Cancer Center IM Service Herb/Botanical Info

http://www.mskcc.org/mskcc/html/ 11570.cfm

Free

▪ Small database (herbs and DS only) ▪ Cancer-specific, brief monographs

MayoClinic.com

www.mayoclinic.com

Free

▪ Small database (herbs, DS and therapies) ▪ Patient-friendly language, not referenced

Dr. Duke’s Phytochemical and Ethnobotanical Databases

http://www.ars-grin.gov/duke/

Free

▪ Detailed summary of chemical constituents and biological activity ▪ Research-focused

http://mayoclinic.com/health/meditation/ MM00623

Free

▪ Nice, brief video introduction to meditation

NIH

www.healthfinder.gov/

Free

▪ Guide to reliable consumer health information

National Center for CAM (NCCAM)

http://nccam.nih.gov

Free

▪ Growing number of articles and references ▪ Many links to other quality sites

NIH-NLM

http://www.nlm.nih.gov/medlineplus/ druginfo/herb_All.html

Free

▪ Content from Natural Standard

The Office of Cancer CAM (OCCAM) – NCI

http://www.cancer.gov/cancertopics/ treatment/cam

Free

▪ Mod. comprehensive (herbs, DS and therapies)

ACS

http://www.cancer.org/docroot/ETO/ ETO_5.asp?sitearea=ETO

Free

▪ Mod. comprehensive (herbs, DS and therapies)

CAM on PubMed

http://www.ncbi.nlm.nih.gov/entrez/query. fcgi?db=PubMed&orig_db=PubMed&cmd_ current=Limits&pmfilter_Subsets=Com plementary+Medicine

Free

▪ Limits searches to articles that are identified as having Complementary Medicine theme

IOM Report on CAM

http://www.iom.edu/CMS/3793/4829/ 24487.aspx

Free/$

▪ Institute of Medicine report on CAM ▪ Can be read online or downloaded for ~$50

On-line Tools MayoClinic.com “Take a Break to Meditate” General Information

Continued

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SECTION 2  Treatment Techniques and Special Equipment

Table 22-1  CAM and Integrative Medicine Information on the Web (Selected References)—cont’d Databases

URL

Cost/yr

Comments

The Consortium of Academic Health Centers for Int. Med.

http://www.imconsortium.org/

Free

▪ Membership currently includes 33 academic medical centers ▪ Integrative Medicine curriculum guide

Quackwatch

http://www.quackwatch.org

Free

▪ Nonprofit corporation whose purpose is to “combat health-related frauds, myths, fads, and fallacies”

Mayo Clinic CIM Program

http://mayoresearch.mayo.edu/mayo/ research/cimp/

Free

▪ Summary of Complementary and Integrative Medicine research activities at Mayo Clinic

Mayo Clinic Book of Alternative Medicine

http://bookstore.mayoclinic.com/products/ bookDetails.cfm?mpid=35

$30

▪ Written by Mayo Clinic clinicians and researchers ▪ A good, basic introduction to CAM and Integrative ­Medicine

Log On: Two Steps to Mindful Awareness

http://www.amazon.com

$26

▪ Author is Director of Research for Mayo CIM Program ▪ Scientific review of the benefits of meditation

http://bookstore.mayoclinic.com/products/ bookDetails.cfm?mpid=45

$20

▪ Integrating yoga, meditation and nutrition into care plans ▪ Heart health, insomnia, arthritis, back pain, weight loss, etc.

http://itunes.apple.com/us/app/mayo-clinicmediatation/id348265081?mt=8

$5

▪ Basic introduction to meditation ▪ More useful if user has already undergone training in meditation

www.consumerlab.com

$24

▪ Provides independent test results on many dietary supplements ▪ Products that pass testing can display the CL Seal of Approval

Books

DVDs Mayo Clinic Wellness Solutions Downloads Mayo Clinic Meditation

Herb Quality Info. ConsumerLab.com

Consumer Reports

www.consumerreports.org

$24

▪ Occasional articles on herbs, DS

United States Pharmacopeia

www.usp.org

Free

▪ Discusses the Dietary Supplement Verification Program and the meaning of the USP label

AMA

www.ama-assn.org/ama/pub/category/19 05.html

Free

▪ Guidelines for Medical and Health Information Sites on the Internet

Health on the Net Foundation

www.hon.ch

Free

▪ Promotes guidelines that create a “code of conduct” for websites delivering medical information

FDA

http://www.cfsan.fda.gov/~dms/ supplmnt.html

Free

▪ Nice background on DSHEA, current regulatory environment in US ▪ Recent adverse events associate with DS reported here

FTC

www.ftc.gov

Free

▪ Reviews regulations re: advertising DS ▪ Link to file complaints

http://www.experienceispa.com/

Free

▪ Excellent resource for information regarding spas as part of a wellness lifestyle

Massage therapist

http://www.amtasmassage.org/ findamassage/locator.htm

Free

▪ Maintained by AMTA

Licenced acupuncturist

http://www.aaoma.org/45000.asp

Free

▪ Maintained by AAOM

Yoga class

http://www.yogafinder.com/index.html

Free

▪ Commercial site

Internet Info. Quality

Regulatory Info.

Spa International Spa Association Practitioners

The goal of discussing integrative medicine with a patient is to provide patient education. This is a critically important goal. Much of the information that patients are otherwise exposed to is commercial in intent and fraught with misinformation. The physician can fulfill the classic role of healers throughout the centuries, that of a teacher, by providing

a safe environment for the patient to obtain information about these CAM therapies. By providing the patient with reliable, evidence-based information about the risks and benefits of a therapy, and by collaborating with the patient, the clinician can be an ally to the patient who is trying to navigate the complex realm of integrative medicine.

CHAPTER 22  Integrative Medicine in Rehabilitation

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53. Foerster KK, Schmid K, Rovati LC: Efficacy of glucosamine sulfate in osteoarthritis of the lumbar spine: a placebo controlled, randomized, double-blind study, 64th Annual Scientific Meeting of the American College of Rheumatology, Denver, Co, October 29–November 2. 54. Fors E, Sexton H, Gotestam K: The effect of guided imagery and amitriptyline on daily fibromyalgia pain: a prospective, randomized, controlled trial, J Psychiatr Res 36:179-187, 2002. 55. Frumkin LR, Baloh RW: Wallenberg’s syndrome following neck manipulation, Neurology 40:611-615, 1990. 56. Furlan AD, van Tulder M, Cherkin D, et al: Acupuncture and dryneedling for low back pain: an updated systematic review within the framework of the Cochrane collaboration, Spine 30:944-963, 2005. 57. Garfinkel M, Schumacher H, Husain A, et al: Evaluation of a yoga based regimen for treatment of osteoarthritis of the hands, J Rheumatol 21:2341-2343, 1994. 58. Garfinkel MS, Singhal A, Katz WA, et al: Yoga-based intervention for carpal tunnel syndrome: a randomized trial, JAMA 280:1601-1603, 1998. 59. Glorioso S, Todesco S, Mazzi A, et al: Double-blind multicentre study of the activity of S-adenosylmethionine in hip and knee osteoarthritis, Int J Clin Pharmacol Res 5:39-49, 1985. 60. Gross AR, Hoving JL, Haines TA, et al: A Cochrane review of manipulation and mobilization for mechanical neck disorders, Spine 29:1541-1548, 2004. 61. Hack GD, Koritzer RT, Robinson WL, et al: Anatomic relation between the rectus capitis posterior minor muscle and the dura mater, Spine 20:2484-2486, 1995. 62. Haldeman S, Kohlbeck FJ, McGregor M: Risk factors and precipitating neck movements causing vertebrobasilar artery dissection after cervical trauma and spinal manipulation, Spine 24:785-794, 1999. 63. Haldeman S, Rubinstein SM: Cauda equina syndrome in patients undergoing manipulation of the lumbar spine, Spine 17:1469-1473, 1992. 64. Haldeman S, Rubinstein SM: Compression fractures in patients undergoing spinal manipulative therapy, J Manipulative Physiol Ther 15:450-454, 1992. 65. Han A, Robinson V, Judd M, et al: Tai chi for treating rheumatoid arthritis, Cochrane Database Syst Rev CD004849, 2004. 66. Hanna J: The power of dance: health and healing, J Altern Complement Med 1:323-331, 1995. 67. Hart RG: Vertebral artery dissection, Neurology 38:987-989, 1988. 68. Hurwitz EL, Aker PD, Adams AH, et al: Manipulation and mobilization of the cervical spine, a systematic review of the literature, Spine 21:1746-1759, 1996. 69. Ives JC, Shelley GA: The Feldenkrais Method in rehabilitation: a review, Work 11:75-90, 1998. 70. Jubb RW, Tukmachi ES, Jones PW, et al: A blinded randomised trial of acupuncture (manual and electroacupuncture) compared with a non-penetrating sham for the symptoms of osteoarthritis of the knee, Acupunct Med 26:69-78, 2008. 71. Keefer L, Blanchard E: A one year follow-up of relaxation response meditation as a treatment for irritable bowel syndrome, Behav Res Ther 40:541-546, 2002. 72. Kelly G: The role of glucosamine sulfate and chondroitin sulfates in the treatment of degenerative joint disease, Altern Med Rev 3:27-39, 1998. 73. Klein G, Kullich W: Short-term treatment of painful osteoarthritis of the knee with oral enzymes, Clin Drug Investig 19:15-23, 2000. 74. Klougart N, Leboeuf-Yde C, Rasmussen LR: Safety in chiropractic practice. Part I: the occurrence of cerebrovascular accidents after manipulation to the neck in Denmark from 1978-1988, J Manipulative Physiol Ther 19:371-377, 1996. 75. Kokjohn K, Schmid DM, Triano JJ, et al: The effect of spinal manipulation on pain and prostaglandin levels in women with primary dysmenorrhea, J Manipulative Physiol Ther 15:279-285, 1992. 76. Komori T, Fujiwara R, Tanida M, et al: Effects of citrus fragrance on immune function and depressive states, Neuroimmunomodulation 2:174-180, 1995. 77. Konig B: A long-term (two years) clinical trial with S-adenosylmethionine for the treatment of osteoarthritis, Am J Med 83:89-94, 1987. 78. Kreitz BG, Aker PD: Nocturnal enuresis; treatment implications for the chiropractor, J Manipulative Physiol Ther 17:465-473, 1994. 79. Krueger B, Okazaki H: Vertebal-basilar distribution infarction following chiropractic cervical manipulation, Mayo Clin Proc 55:322-332, 1980. 80. Lane D: Music therapy: gaining an edge in oncology management, J Oncol Manag, 44-46, 1993.

81. Lao L, Hamilton GR, Fu J, et al: Is acupuncture safe? A systematic review of case reports, Altern Ther Health Med 9:72-83, 2003. 82. Lawrence DJ, Meeker W, Branson R, et al: Chiropractic management of low back pain and low back-related leg complaints: a literature synthesis, J Manipulative Physiol Ther 31:659-674, 2008. 83. Leclaire R, Bourgouin J: Electromagnetic treatment of shoulder periarthritis: a randomized controlled trial of the efficiency and tolerance of magnetotherapy, Arch Phys Med Rehabil 72:284-287, 1991. 84. Leeb B, Schweitzer H, Montag K, et al: A metaanalysis of chondroitin sulfate in the treatment of osteoarthritis, J Rheumatol 27:205-211, 2000. 85. Liebl NA, Butler LM: A chiropractic approach to the treatment of dysmenorrhea, J Manipulative Physiol Ther 13:101-106, 1990. 86. Linde K, Allais G, Brinkhaus B, et al: Acupuncture for migraine prophylaxis, Cochrane Database Syst Rev: CD001218, 2009. 87. Linde K, Allais G, Brinkhaus B, et al: Acupuncture for tension-type headache, Cochrane Database Syst Rev: CD007587, 2009 (1). 88. Linton SJ, Nordin E: A 5-year follow-up evaluation of the health and economic consequences of an early cognitive behavioral intervention for back pain: a randomized, controlled trial, Spine 31:853-858, 2006. 89. Little P, Lewith G, Webley F, et al: Randomised controlled trial of Alexander technique lessons, exercise, and massage (ATEAM) for chronic and recurrent back pain, BMJ 337:a884, 2008. 90. Lopes Vaz A: Double-blind clinical evaluation of the relative efficacy of ibuprofen and glucosamine sulphate in the management of osteoarthrosis of the knee in out-patients, Curr Med Res Opin 8:145-149, 1982. 91. Lundblad I, Elert J, Gerdle B: Randomized controlled trial of physiotherapy and Feldenkrais interventions in female workers with neckshoulder complaints, J Occup Rehabil 9:179-194, 1999. 92. Malmgren-Olsson E, Branholm I: A comparison between three physiotherapy approaches with regard to health-related factors in patients with non-specific musculoskeletal disorders, Disabil Rehabil 24:308-317, 2002. 93. Manheimer E, Linde K, Lao L, et al: Meta-analysis: acupuncture for osteoarthritis of the knee, Ann Intern Med 146:868-877, 2007. 94. Mannix L, Chandurkar R, Rybicki L, et al: Effect of guided imagery on quality of life for patients with chronic tension-type headache, Headache 39:326-334, 1999. 95. Manocha R, Marks GB, Kenchington P, et al: Sahaja yoga in the management of moderate to severe asthma: a randomised controlled trial, Thorax 57:110-115, 2002. 96. McAlindon TE, LaValley MP, Felson DT: Efficacy of glucosamine and chondroitin for treatment of osteoarthritis, JAMA 284:1241, 2000. 97. Mierau D, Cassidy JD, McGregor M, et al: A comparison of the effectiveness of spinal manipulative therapy for low back pain patients with and without spondylolisthesis, J Manipulative Physiol Ther 10:49-55, 1987. 98. Morone NE, Greco CM, Weiner DK: Mindfulness meditation for the treatment of chronic low back pain in older adults: a randomized controlled pilot study, Pain 134:310-319, 2008. 99. Morreale P, Manopulo R, Galati M, et al: Comparison of the antiinflammatory efficacy of chondroitin sulfate and diclofenac sodium in patients with knee osteoarthritis, J Rheumatol 23:1385-1391, 1996. 100. Mur E, Hartig F, Eibl G, et al: Randomized double blind trial of an extract from the pentacyclic alkaloid-chemotype of uncaria tomentosa for the treatment of rheumatoid arthritis [comment], J Rheumatol 29:678-681, 2002. 101. Nachemson A: The load on lumbar discs in different positions of the body, Clin Orthop Relat Res 45:107-122, 1966. 102. Najm WI, Reinsch S, Hoehler F, et al: S-adenosyl methionine (SAMe) versus celecoxib for the treatment of osteoarthritis ­symptoms: a ­double-blind cross-over trial, BMC Musculoskelet Disord 5:6, 2004. 103. NCCAM: What is complementary and alternative medicine (CAM)? Bethesda, 2002, National Institutes of Health/National Center for Complementary and Alternative Medicine. 104. Nelson CF, Bronfort G, Evans R, et al: The efficacy of spinal manipulation, amitriptyline and the combination of both therapies for the prophylaxis of migraine headache, J Manipulative Physiol Ther 21:511-519, 1998. 105. Nielsen NH, Bronfort G, Bendix T, et al: Chronic asthma and chiropractic spinal manipulation: a randomized clinical trial, Clin Exp Allergy 25:80-88, 1995.

CHAPTER 22  Integrative Medicine in Rehabilitation 106. Nilsson N, Christensen HW, Hartvigsen J: The effect of spinal manipulation in the treatment of cervicogenic headache, J Manipulative Physiol Ther 20:326-330, 1997. 107. Nykoliation JW, Cassidy JD, Arthur BE, et al: An algorithm for the management of scoliosis, J Manipulative Physiol Ther 9:1-14, 1986. 108. Orme-Johnson D: Medical care utilization and the transcendental meditation program, Psychosom Med 49:493-507, 1987. 109. Paris A, Gonnet N, Chaussard C, et al: Effect of homeopathy on analgesic intake following knee ligament reconstruction: a phase III monocentre randomized placebo controlled study, Br J Clin Pharmacol 65:180-187, 2008. 110. Parker GB, Tupling H, Pryor DS: A controlled trial of cervical manipulation of migraine, Aust N Z J Med 8:589-593, 1978. 111. Patel C, North W: Randomised controlled trial of yoga and bio-­ feedback in management of hypertension, Lancet 2:93-95, 1975. 112. Piscoya J, Rodriguez Z, Bustamante S, et al: Efficacy and safety of freeze-dried cat’s claw in osteoarthritis of the knee: mechanisms of action of the species Uncaria guianensis, Inflamm Res 50:442-448, 2001. 113. Plaugher G, Cremata EE, Phillips RB: A retrospective consecutive case analysis of pretreatment and comparative static radiological parameters following chiropractic adjustments, J Manipulative Physiol Ther 13:498-506, 1990. 114. Powell FC, Hanigan WC, Olivero WC: A risk/benefit analysis of spinal manipulation therapy for relief of lumbar or cervical pain, Neurosurgery 33:73-78, 1993. 115. Reginster J, Deroisy R, Rovati L, et al: Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, ­placebo-controlled clinical trial, Lancet 357:251-256, 2001. 116. Reibel D, Greeson J, Brainard G, et al: Mindfulness-based stress reduction and health-related quality of life in a heterogeneous patient population, Gen Hosp Psychiatry 23:183-192, 2001. 117. Reinhold T, Witt CM, Jena S, et al: Quality of life and cost-effectiveness of acupuncture treatment in patients with osteoarthritis pain, Eur J Health Econ 9:209-219, 2008. 118. Rosenstein E: Topical agents in the treatment of rheumatic disorders, Rheum Dis Clin North Am 25:899-918, 1999:viii. 119. Rydeard R, Leger A, Smith D: Pilates-based therapeutic exercise: effect on subjects with nonspecific chronic low back pain and functional disability: a randomized controlled trial, J Orthop Sports Phys Ther 36:472-484, 2006. 120. Sajedi F, Alizad V, Alaeddini F, et al: The effect of adding homeopathic treatment to rehabilitation on muscle tone of children with spastic cerebral palsy, Complement Ther Clin Pract 14:33-37, 2008. 121. Schneider C, Klein P, Stolt P, et al: A homeopathic ointment preparation compared with 1% diclofenac gel for acute symptomatic treatment of tendinopathy, Explore (NY) 1:446-452, 2005. 122. Senstad O, Leboeuf-Yde C, Borchgrevink CF: Side-effects of chiropractic spinal manipulation: types frequency, discomfort and course, Scand J Prim Health Care 14:50-53, 1996. 123. Shekelle PG: What role for chiropractic in health care? N Engl J Med 339:1074-1075, 1998. 124. Shekelle PG, Adams AH, Chassin MR, et al: Spinal manipulation for low-back pain, Ann Intern Med 117:590-598, 1992. 125. Shekelle PG, Coulter I: Cervical spine manipulation: summary report of a systematic review of the literature and a multidisciplinary expert panel, J Spinal Disord 10:223-228, 1997. 126. Sherman KJ, Cherkin DC, Erro J, et al: Comparing yoga, exercise, and a self-care book for chronic low back pain: a randomized, controlled trial, Ann Intern Med 143:849-856, 2005.

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127. Siev-Ner I, Gamus D, Lerner-Geva L, et al: Reflexology treatment relieves symptoms of multiple sclerosis: a randomized controlled study, Mult Scler 9:356-361, 2003. 128. Sloman R: Relaxation and imagery for anxiety and depression control in community patients with advanced cancer, Cancer Nurs 25:432-435, 2002. 129. Smith AL, Kolt GS, McConville JC: The effect of the Feldenkrais Method on pain and anxiety in people experiencing chronic low back pain, N Z J Physiother 29:6-14, 2001. 130. Smith M, Neubauer D: Cognitive behavior therapy for chronic insomnia, Clin Cornerstone 5:28-40, 2003. 131. So PS, Jiang Y, Qin Y: Touch therapies for pain relief in adults, Cochrane Database Syst Rev: CD006535, 2008. 132. Targino RA, Imamura M, Kaziyama HHS, et al: A randomized controlled trial of acupuncture added to usual treatment for fibromyalgia, J Rehabil Med 40:582-588, 2008. 133. Tarola GA: Manipulation for the control of back pain and curve progression in patients with skeletally mature idiopathic scoliosis: two cases, J Manipulative Physiol Ther 17:253-257, 1994. 134. Tovey P: A single-blind trial of reflexology for irritable bowel syndrome, Br J Gen Pract 52:19-23, 2002. 135. Trice J, Pinals R: Dimethyl sulfoxide: a review of its use in the rheumatic disorders, Semin Arthritis Rheum 15:45-60, 1985. 136. Valente R, Gibson H: Chiropractic manipulation in carpal tunnel syndrome, J Manipulative Physiol Ther 17:246-249, 1994. 137. Vernon HT, Humphreys BK, Hagino CA: A systematic review of conservative treatments for acute neck pain not due to whiplash, J Manipulative Physiol Ther 28:443-448, 2005. 138. Walker AF, Bundy R, Hicks SM, et al: Bromelain reduces mild acute knee pain and improves well-being in a dose-dependent fashion in an open study of otherwise healthy adults, Phytomedicine 9:681-686, 2002. 139. Wang C, Collet JP, Lau J: The effect of tai chi on health outcomes in patients with chronic conditions: a systematic review, Arch Intern Med 164:493-501, 2004. 140. Warnock M, McBean D, Suter A, et al: Effectiveness and safety of Devil’s Claw tablets in patients with general rheumatic disorders, Phytother Res 21:1228-1233, 2007. 141. Watkins G: Music therapy: proposed physiological mechanisms and clinical implications, Clin Nurse Spec 11:43-50, 1997. 142. Wegener T, Lupke N-P: Treatment of patients with arthrosis of hip or knee with an aqueous extract of devil’s claw (Harpagophytum procumbens), Phytother Res 17:1165-1172, 2003. 143. Williams D: Psychological and behavioural therapies in fibromyalgia and related syndromes, Best Pract Res Clin Rheumatol 17:649-665, 2003. 144. Williams H, Furst D, Dahl S, et al: Double-blind, multicenter controlled trial comparing topical dimethyl sulfoxide and normal saline for treatment of hand ulcers in patients with systemic sclerosis, Arthritis Rheum 28:308-314, 1985. 145. Wu G: Evaluation of the effectiveness of Tai Chi for improving balance and preventing falls in the older population: a review, J Am Geriatr Soc 50:746-754, 2002. 146. Zwick D, Rochelle A, Choksi A, et al: Evaluation and treatment of balance in the elderly: a review of the efficacy of the Berg Balance Test and Tai Chi Quan, Neuro-Rehabilitation 15:49-56, 2000.

CHAPTER 23 COMPUTER ASSISTIVE DEVICES AND ENVIRONMENTAL CONTROLS Cathy Bodine This chapter provides an overview of assistive technology (AT) devices and services, including definitions, history, and legislation. It also discusses the use of AT by people with communication disorders, impaired mobility, hearing and visual impairments, and cognitive and learning disabilities. It describes the selection of appropriate technology and training in its use, suggests ways to avoid the abandonment of AT by clients and caregivers, and discusses the principles of clinical assessment and physician responsibility. Finally, it briefly discusses the future in terms of research and development, and application of emerging technologies to the needs of people with disabilities.

Defining Assistive Technology The term assistive technology is fairly new, although history records the use of tools to enable people with disabilities to walk, eat, and see as far back as the sixth or seventh century bc.14,17 Public Law 100-40725 defines AT as “any item, piece of equipment or product system whether acquired commercially off the shelf, modified, or customized that is used to increase or improve functional capabilities of individuals with disabilities.” This definition also includes a second component defining AT services as “any service that directly assists an individual with a disability in the selection, acquisition or use of an AT device.” Public Law 100-407 specifies the following: • Evaluate individuals with disabilities in terms of their goals, needs, and functional abilities in their customary environments. • Purchase, lease, or otherwise provide for the acquisition of AT by persons with disabilities. • Select, design, fit, customize, adapt, apply, retain, repair, or replace AT devices. • Coordinate and use other therapies, interventions, or services with AT devices, such as those associated with existing education and rehabilitation plans and programs. • Provide training or technical assistance for persons with disabilities or, if appropriate, their families. • Provide training or technical assistance for professionals (including individuals providing education or rehabilitation services), employers, or other individuals who provide services to, employ, or are otherwise substantially involved in the major life functions of children with disabilities.25

Since 1988, this definition has also been used in other federal legislation authorizing services or supports for persons with disabilities. The Individuals with Disabilities Education Act3 (IDEA) and Reauthorization of the Rehabilitation Act24 are both examples of legislation that further codifies Public Law 100-407.

History, Legislation, and Utilization of Assistive Technology Education: The Individuals with Disabilities Education Act IDEA originated in 1997 and was reauthorized most recently as Public Law 108-446 by the 108th Congress. IDEA strengthens academic expectations and accountability for the nation’s 5.8 million children with disabilities. One important impact of IDEA legislation is that it specifies that AT devices and services be provided to children from birth to 21 years of age to facilitate education in a regular classroom if such devices and services are required as part of the student’s special education, related services, or supplementary aids and services (Code of Federal Regulations, Title 34, Sections 300.308) (Box 23-1). For students with disabilities, AT supports their acquisition of a free and appropriate public education. All individualized education plans developed for children needing special education services must indicate that AT has been considered as a way “to provide meaningful access to the general curriculum.”27 AT devices and services included as a component of an individualized education plan must also be provided at no cost to the student or parents. The school, however, can use other public and private funding sources that are available to fund the AT (34 CFR). Part C of IDEA also includes children before they start school. It covers the needs of children as soon as their developmental differences are noted. It intends that infants and toddlers receive services in the home or in other places, such as preschool settings, where possible. The services provided for these children are described in individualized family service plans. Individualized family service plans include parents, extended family, and early childhood interventionists and other related services personnel in planning and identifying goals and necessary services. IDEA also recognizes that coordination is needed to help families and children with the transition from infant and toddler programs to preschool programs. As a result, students with disabilities are being educated in preschool 499

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BOX 23-1

Summary of the Individuals with Disabilities Education Act Assistive Technology Requirements

 

• Assistive technology (AT) must be provided by the school district at no cost to the family. • AT must be determined on a case-by-case basis; if needed to ensure access to free and appropriate public education, AT is required. • If the individual education plan team determines that AT is needed for home use to ensure free and appropriate public education, it must be provided. • The student’s individual education plan must reflect the nature of the AT and the amount of supportive AT services required. • A parent is accorded an extensive set of procedural safeguards, including the provision of AT to the child.

settings along with typically developing children in an effort to help all children reach the same developmental milestones.

The Americans with Disabilities Act and the Reauthorization of the Rehabilitation Act The American Rehabilitation Act with Disabilities Act (ADA) was originally passed in 1990, and clarified the civil rights of persons with disabilities and specified equal access to public places, employment, transportation, and telecommunications. The ADA built on the foundation of the Rehabilitation Act of 1973 (updated in 2003 as the Reauthorization of the Rehabilitation Act) in recognizing the role of employment in enabling individuals with disabilities to become economically self-sufficient and integrated into communities. The ADA was amended in 2008, and these amendments became effective January 1, 2009. The amended ADA retains the original Act’s basic definition of “disability” as an impairment that substantially limits one or more major life activities, a record of such an impairment, or being regarded as having such an impairment.38,39 However, it changes the way that these statutory terms should be interpreted in several ways. Most significantly, the amended Act does the following: • Directs the Equal Employment Opportunity Commission (EEOC) to revise that portion of its regulations defining the term “substantially limits” • Expands the definition of “major life activities” by including two nonexhaustive lists: • The first list includes many activities that the EEOC has recognized (e.g., walking) as well as activities that the EEOC has not specifically recognized (e.g., reading, bending, and communicating). • The second list includes major bodily functions (e.g., “functions of the immune system, normal cell growth, digestive, bowel, bladder, neurologic, brain, respiratory, circulatory, endocrine, and reproductive functions”). • States that mitigating measures other than “ordinary eyeglasses or contact lenses” shall not be considered in assessing whether an individual has a disability • Clarifies that an impairment that is episodic or in remission is a disability if it would substantially limit a major life activity when active

• Changes the definition of “regarded as” so that it no longer requires showing that the employer perceived the individual to be substantially limited in a major life activity, and instead says that an applicant or employee is “regarded as” disabled if he or she is subject to an action prohibited by the ADA (e.g., failure to hire or termination) based on an impairment that is not transitory and minor • Provides that individuals covered only under the “regarded as” prong are not entitled to reasonable accommodation (For more information regarding the ADA, please see the following website: http://www.eeoc .gov/types/ada.html) Vocational rehabilitation services are often the key to enabling employment for adults with disabilities. The Rehabilitation Act mandates that AT devices and services should be considered and provided as a means to acquire vocational training, as well as to enter into and maintain employment. It also requires that AT be considered during the development and implementation of the Individualized Written Rehabilitation Plan, the document that guides a person’s vocational rehabilitation process. For example, if an individual has limited sight and needs to fill out paperwork to determine eligibility for vocational rehabilitation services, assistive devices to facilitate reading must be provided at that time. In recent years the Offices of Vocational Rehabilitation have become an important source of funding for AT devices and services to support employment for adults with disabilities.37

Assistive Technology and the International Classification of Functioning The term disability is not always precise and quantifiable. The concept of disability is not even agreed on by persons who self-identify as having a disability, by professionals who study disability, or by the general public.23 This lack of agreement creates an obstacle to the study of disability and to the fair and effective administration of programs and policies intended for people with disabilities.4-8,18 With this issue in mind, the World Health Organization (WHO) developed a global common health language, one that includes physical, mental, and social well-being. The International Classification of Impairment, Disabilities, and Handicaps was first published by the WHO in 1980 as a tool for classification of the “consequences of disease.” The newest version, International Classification of Functioning, Disability and Health (ICF), moves away from a “consequence of disease” classification (1980 version) to a more positive “components of health” classification. This latest version provides a common framework and language for the description of health and health-related domains and uses the following language: • Body functions are the physiologic functions of body systems (including psychologic functions). • Body structures are anatomic parts of the body such as organs, limbs, and their components. • Impairments are problems in body function or structure such as a significant deviation or loss. • Activity is the execution of a task or action by an individual. • Participation is involvement in a life situation.

CHAPTER 23  Computer Assistive Devices and Environmental Controls

• Activity limitations are difficulties an individual might have in executing activities. • Participation restrictions are problems an individual might experience in involvement in life situations. • Environmental factors make up the physical, social, and attitudinal environments in which people live and conduct their lives.41 The ICF and its language help professionals define the need for health care and related services, such as the provision of AT. It recognizes that physical, mental, social, economic, or environmental interventions can improve lives and levels of functioning for persons with diseases. These might include medical, rehabilitation, psychosocial, or other person-based interventions.41 It also characterizes physical, mental, social, economic or environmental interventions that will improve lives and levels of functioning. Because AT has the potential to improve daily activities and participation in social and physical environments and thus improve the quality of life of individuals with disabilities, it clearly fits within the ICF. The WHO common health language is used throughout this chapter to discuss the potential impact of appropriate AT.

501

FIGURE 23-1  A head switch.

Direct Selection

AT devices are designed to facilitate functional abilities and to meet the needs of humans throughout their varied life stages and roles. It is important to remember that AT device usage and requirements will change over time as individuals mature and take on different life roles. Consequently there is no “one size fits all” technology available.

Once optimal positioning is established, assessment of an individual’s reliable, low-effort, high-accuracy hand movements, vision, communication, and hearing will help an evaluator decide whether the individual is able to use a typical “interface” or needs one that is adapted. Using a typical interface (e.g., a computer keyboard, steering wheel, or television remote control) is typically called direct selection, because all possible options are presented at once and can be directly selected by the individual. For those without the ability to accurately choose an intended item within the available selection set, a different selection method must be considered.

The Human-Technology Interface

Indirect Selection

AT devices have the potential to compensate for immobility; low endurance; difficulty reaching, grasping, or accurately touching keys or switches; and problems with seeing or hearing, verbal communication, and the complex skills necessary for reading, writing, and learning. This section focuses on specific categories of AT devices as they are related to these areas of human function. Considering one’s own interaction with technology gives insight into the issues involved in the concept of the human-technology interface. Devices await activation or input from the people who use them. This commonly occurs through dials, switches, keyboards, handlebars, joysticks, or handgrips. This interface typically requires fine motor control, adequate hearing, vision, or both. People know they have successfully interacted with devices by the physical, visual, or auditory feedback these devices provide (e.g., the sight of brewing coffee, images on a computer monitor, or the sound of a phone ringing). Individuals with impairments that affect their interaction with items in their environment need special consideration in the design, function, or placement of the devices they want or need to use. It is essential for many individuals to first be seated or positioned by using orthotic or ergonomic seating and positioning interventions, so they can optimally use their residual abilities17 (see Chapter 17).

Scanning is the most common indirect selection method used by persons with significant motor impairments. A selection set is presented on a display (e.g., a series of pictures or letters) and is sequentially scanned by a light or cursor on the device. The user chooses the desired item by pressing a switch when the indicator reaches the desired location or choice on the display. Switches come in many styles and are selected based on the body part that will be activating them (e.g., elbow or chin) and the task or setting for using them (e.g., watching television in bed or using a communication device while eating). A switch can be as simple as a “wobble” switch that is activated by a gross motor movement such as hitting the switch with the head (Figure 23-1), hand, arm, leg, or knee. Other switches are activated by tongue touch, by sipping and puffing on a straw, or through very fine movements such as an eye blink or a single muscle twitch. Regardless, switch use and timing accuracy can be very difficult for new users and must be taught. One common method to teach switch activation and use is to interface a switch with battery-operated toys and games, or home or work appliances to increase motivation and teach the concepts used in indirect selection. Fairly recent developments include eye-gaze switches, which calibrate intentional eye movement patterns and select targets such as individual keys on an onscreen

Overview of Assistive Technology Devices

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keyboard. Other new developments include brain wave technology (Eye and Muscle Operated Switch [EMOS]) that responds to excitation of alpha waves to trigger a selection.

Displays The human-technology interface also applies to completing the feedback loop from devices back to the user. Examples include software that enlarges images on a computer display for persons with low vision, installing flashing alarms for persons without hearing, and using devices that convert printed text into synthesized speech or Braille for persons with blindness or learning disabilities. These human-technology interface concepts apply to all forms of AT, whether it is being used for seating, mobility, communication, computer operation, or control of the environment. Good assessment skills and a focus on clients and their goals and needs are essential for humantechnology interface success and prevention of assistive devices abandonment.33

Assistive Technology for Communication Disorders Vocal communication allows humans to interact, form relationships, and direct the events of their lives to enable choice and participation. Human communication is based on having both receptive and expressive language abilities and the physical capacity to reliably produce intelligible speech sounds. Communication impairment can result from congenital conditions such as mental retardation, cerebral palsy, developmental verbal apraxia, and developmental language disorders. Other impairments can be acquired through traumatic brain injury, stroke, multiple sclerosis, amyotrophic lateral sclerosis, tetraplegia, ventilator dependence, and laryngectomy resulting from cancer.3 AT devices that meet the needs of persons with many types of speech and language impairment are commonly called augmentative and alternative communication (AAC) devices, because they can either support or substitute for expressive language impairments. More recently the term speech-generating device has entered into the medical vocabulary to differentiate AAC devices from basic computer devices, especially when seeking third-party funding such as that from Medicaid and Medicare.8 Some individuals are completely unable to speak or have such severe expressive difficulties that only those very familiar with them are able to communicate effectively with them. Many devices are available for these individuals, ranging from simple, low-tech picture books to high-end, sophisticated electronic devices with digitally recorded or synthetic text-to-speech output capable of producing complex language interactions (Figure 23-2). Although AAC devices are extremely useful to nonspeaking individuals, they do not replace natural communication. AAC device use should be encouraged along with all other available communication modalities such as gestures, vocalizations, sign language, and eye gaze.28 There are no firm cognitive, physical, or developmental prerequisites for using an AAC device. Instead,

comprehensive evaluation techniques are used to match the individual’s abilities and communication needs with the appropriate AAC technologies. A qualified team of clinicians performs this evaluation, with input from the individual, family members, teachers, employers, and others. Because speaking is considered to be a critical human function, many parents and family members wait to seek out AAC devices in the hope that natural speech will develop. Research shows, however, that using an AAC device can actually support verbal language development, and can, in fact, increase the potential for natural speech to develop.3 Children and adults with severe communication impairments can benefit socially, emotionally, academically, and vocationally from using a device that allows them to communicate their thoughts, learn and share ideas, and participate in life activities.2

Nonelectronic Systems Low-tech, nonelectronic AAC systems are often used in addition to an electronic voice output system (or as a backup system in case an electronic device fails or cannot be used during certain activities, such as during a swimming lesson). Low-tech systems can be made by using digital photographs, pictures from books or catalogs, or by simply using a marker to draw letters, words, phrases, or pictures. Picture library software is also available commercially. These software programs (e.g., BoardMaker and PCS Symbols) incorporate thousands of line drawings and pictures that can be used to quickly and easily fabricate a low-tech, nonelectronic communication system. Adults with progressive diseases such as amyotrophic lateral sclerosis or multiple sclerosis can also choose to use low-tech picture or alphabet boards as a supplement to verbal communication when they are fatigued, or as their ability to verbally communicate decreases. Many of these adults choose to use both low- and high-tech communication systems depending on their environment and their comfort level with technology.9

FIGURE 23-2  Use of the Liberator, an augmentative and alternative communication device.

CHAPTER 23  Computer Assistive Devices and Environmental Controls

Electronic Voice Output Systems: Digital Speech A variation in low-tech communication systems has developed as a result of the manufacture of low-cost microprocessors capable of storing digitized speech. These low-tech, digital voice output devices work like a tape recorder, allowing recording and storing of simple phrases into memory within the device. When users want to speak, they simply press a button and the device speaks the prerecorded message. Devices such as One Step, Step by Step, and Big Mac (Figure 23-3) are simple and relatively inexpensive, and are designed to communicate quick, simple messages such as “hi,” “let’s play,” or “leave me alone.” These technologies are often used by very young children who are beginning communicators, or by those who have significant cognitive impairments. They are not appropriate for individuals needing or wanting to communicate complex thoughts and feelings.12 Complex digitized devices store several minutes of recorded voice that is usually associated with representative pictures or icons on a keyboard. These devices are often used by people who are not yet literate, have developmental disabilities, or simply wish to have a simple device to use when going to the store or out to eat. Examples are the SuperTalker, the ChatBox (Figure 23-4), and the Springboard. Synthesized speech is created by software that uses rules of phonics and pronunciation to translate alphanumeric text into spoken output through speech synthesizer hardware. Voice output systems such as Tango, VMax, and ECO2 are examples of high-tech text-to-speech devices with builtin speech synthesis that speak words and phrases that have been typed or previously stored in the device, or both. The advantage of these systems is that they allow users to speak on any topic and use any words they wish to use. These systems, which can encode several thousand words, phrases, and sentences, are expensive ($6000 to $9000). They form, however, an essential link to the world for people with severe expressive communication disabilities. All of these voice output systems, whether digital or textto-speech, can be activated by direct selection (e.g., using a finger or a pointing device such as a mouth stick or head

FIGURE 23-3  The Big Mac electronic voice output system.

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pointer). They can also be activated using indirect selection (e.g., using a scanning strategy or an infrared or wireless switch). In AAC device use, individuals will most commonly use a scanning strategy called row-column scanning, in which they activate a switch to begin the scan. When the row containing the desired key or icon is highlighted, the user hits the switch again to scan by column. The process is repeated until the desired word or phrase is assembled. Although the process can be slow and tedious, indirect selection often provides the only means many people have to communicate with others. Among the latest developments for persons who are completely locked in are speech-generating devices that can be activated by a simple eye blink, or by visually gazing or “dwelling” on the desired area of the screen. The DynaVox EyeMax System is one example of this new, advanced access method for communicators who use the DynaVox Vmax. It comprises two parts: a DynaVox VMax and a DynaVox EyeMax Accessory. AAC devices differ in the mapping and encoding strategies used to represent language, and in the storing and retrieving methods used for vocabulary. However, all systems use either orthographic or pictographic symbols, which vary in ease of learning. When selecting a set of symbols for an individual as part of the user interface, it is important to consider these factors and compare them with the individual’s cognitive and perceptual abilities.

Portable Amplification Systems For people who speak quietly because of low breath support or other difficulties with phonation, portable amplification systems that function like a sound system in a large

FIGURE 23-4 The ChatBox electronic voice output system.

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lecture hall are available. The Speech Enhancer processes speech sounds for people with dysarthria and enables improved recognition by others. Users wear a headset with a microphone attached to a portable device, and their clarified voice is projected via speakers attached to the unit.

Assistive Technology for Mobility Impairments Motor impairments greatly affect the ability of individuals to interact with their environment. Infants are compelled to roll, then crawl and toddle, to explore their surroundings. Any motor impairment can greatly affect overall development. This is often the situation with cerebral palsy, spina bifida, arthogryposis, and other diagnoses that affect motor skills. Early intervention, and having supportive families able to create modifications and incorporate AT devices into activities, can help children achieve developmental milestones. The loss of acquired motor abilities through trauma or disease is experienced as a severe loss for children and adults and occurs with spinal cord injury, stroke, multiple sclerosis, and amputation. There are many forms of AT that help compensate for impaired motor skills, and they should be introduced as early as possible in rehabilitation to ensure the best outcome possible.

Upper Body Mobility Devices Given the importance of computer use in education, training, and employment, many AT devices have been developed to provide access to computers for individuals with upper body mobility impairment, such as poor hand control or paralysis. For individuals who are unable to use a standard mouse and keyboard, multiple AT options are available. Alternate computer keyboards come in many shapes and sizes. Expanded keyboards such as the Intellikeys (Figure 23-5) provide a larger target or key surrounded by inactive space than is found in a standard keyboard. Options such as delayed activation response help individuals who have difficulty with pointing accuracy or removing a finger after activating a key. Individuals unfamiliar with a standard QWERTY keyboard layout have the option for alphabetical layout. This is often helpful for young children who are developing literacy skills, as well as for adults with cognitive or visual impairments. There are also smaller keyboards (e.g., Tash Mini Keyboard) designed for persons with limited range of motion and endurance. They are also helpful for individuals who type with one hand, or use a head pointer or mouth stick to type. These keyboards use a “frequency of occurrence” layout. The home or middle row in the center of the keyboard holds the space bar and the letters in English words that occur most frequently (e.g., “a” and “e”). All other characters, numbers, and functions (including mouse control) fan out from the center of the keyboard based on how frequently they are used in common computer tasks. Voice recognition (VR) is a mass-market technology that has become essential for computer access for many persons with motor impairment. Instead of writing via the

keyboard, VR users write by speaking words into a microphone. The computer processor uses information from the user’s individual voice file, compares it with digital models of words and phrases, and produces computer text. If the words are accurate, the user proceeds; if not, the user corrects the words to match what was said. As the process continues, the computer updates its voice file and VR accuracy improves. This software is cognitively demanding yet can offer “hands-free” or greatly reduced keyboarding to many individuals with motor impairment. Another group of computer input methods includes devices that rely on an onscreen keyboard visible on the computer monitor, such as the Head Mouse Extreme and TrackerPro. The user wears a head-mounted signaling device or a reflective dot on the forehead to select keys on the onscreen keyboard, choose commands from pulldown menus, or direct mouse movement. Onscreen keyboards are typically paired with rate enhancement options like word prediction or abbreviation expansion to increase a user’s word-per-minute rate. Because so many tasks can be accomplished through computers, individuals with disabilities—even those with the most severe motor impairments—can fully participate in life. They can perform education- and work-related tasks, and monitor and control an unlimited array of devices and appliances at home, work, and school.

Lower Body Mobility Devices Individuals with spinal cord injury, spina bifida or cerebral palsy often have lower body mobility impairments. AT solutions can include crutches, a rolling walker, a powered scooter, or a manual or powered wheelchair (see Chapter 17). Simple environmental modifications or adaptations, such as installing a ramp instead of stairs, raising the height of a desk, or widening doorways, can be critical facilitators for these individuals and might be all that is needed. For other activities or to increase participation, adding automobile hand controls, adapting saddles for horseback riding, or using sit-down forms of downhill skiing is possible (Figure 23-6).

FIGURE 23-5 The Intellikeys expanded keyboard.

CHAPTER 23  Computer Assistive Devices and Environmental Controls

Literally thousands of low-tech assistive devices are available for persons with motor impairments. Commonly referred to as aids or adaptive devices for completing activities of daily living, these devices include weighted spoons and scoop plates to facilitate eating, aids for personal hygiene such as bath chairs and longhandled hairbrushes, items for dressing such as sock aides and one-handed buttoners, adapted toys for play, builtup pencil grips for writing and drawing, and many others. Many low-tech mobility aids can be handmade for just a few dollars, whereas others, such as an adult rolling bath chair, can cost several hundred dollars. All share the common goal of reducing barriers and increasing participation in daily life.

Assistive Technology for Ergonomics and Prevention of Secondary Injuries A rapidly growing area of concern for AT practitioners is the development of repetitive strain injuries (RSIs) among both able-bodied and disabled individuals. Although specialized keyboards and mouse control have provided computer access for many individuals, the pervasiveness of computer technology has also increased the possibility of RSIs. During the past few years, an entire industry of AT has developed to deal with repetitive motion disorders. Computer desks, tables, and chairs used in computer laboratories, classrooms, and offices do not always match the physical needs of users. When people with and without disabilities spend hours repetitively performing the same motor movement, they can and do develop RSIs. Potential solutions include properly supporting seated posture, raising or lowering a chair or desk for optimal fit, implementing routine breaks, and using ergonomically designed keyboards and other assistive technologies. Many of the AT devices described in this chapter (i.e., alternate and specially designed ergonomic keyboards, VR

FIGURE 23-6 The hand bike, an example of a low-tech recreation aid.

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software, and other technologies designed to minimize keystrokes) can also provide useful solutions for individuals with RSIs. There are also Internet-based resources that target ergonomic issues, such as those found in Table 23-1.

Electronic Aids to Daily Living Electronic aids to daily living (EADLs) provide alternative control of electrical devices within the environment and increase independence in tasks of daily living. This technology is also referred to as environmental control units (ECUs). Within the home, EADLs can control audiovisual equipment (e.g., television, video players and recorders, cable, digital satellite systems, stereo), communication equipment (e.g., telephone, intercom, and call bells), doors, electric beds, security equipment, lights, and appliances (e.g., fan, wave machine). EADLs are controlled directly by pressing a button with a finger or pointer or by voice command, or indirectly by scanning and switch activation. Some AAC devices or computer systems also provide EADL control of devices within the environment. Almost anyone with limited control over his or her environment can benefit from this technology. Children and adults with developmental delays often benefit from lowtech EADLs that increase independence in play through intermittent switch control of battery-operated toys or electrical devices, such as a disco light. For those unable to operate a television remote control, switches or voice commands to an EADL device allow access to devices they would otherwise be unable to control. Many EADLs also accommodate cognitive and visual deficits. For example, an AAC device can display an icon instead of text for a client without literacy or who cannot read English. The same device can also use auditory scanning so that choices can be heard if the client has impaired vision. EADLs are primarily used in the home, but can also be used in a work or school setting. An individual can use EADL technology to turn on the lights at a workstation and use the telephone. A child who uses a switch can participate more fully in the classroom by advancing slides for a presentation or by activating a tape player with a story on cassette for the class. The term EADL was chosen over ECU for two primary reasons. First, the term more accurately defines this area of AT by emphasizing the task (e.g., communication is a daily living activity) rather than the item being controlled (e.g., the telephone). Second, the term was chosen to improve reimbursement by third-party providers because the category of ECUs has been poorly funded in the past. In contrast, aids to daily living (ADL) equipment is traditionally funded very well. ADL equipment, which is designed to make the client more independent in a specific daily living task, includes bath seats, toileting aids, built-up spoon handles, and zipper pulls. This equipment is defined by the “daily living” task it “aids.” ECU devices had the same general goal, but the name failed to reflect the goal, particularly to funding agencies. EADLs expand ADL equipment to include equipment that happens to use batteries or plug into the wall, but still shares the same goal—increasing independence in tasks of daily living.

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Table 23-1  Internet-Based Resources for Ergonomics Organization

Website Address

Government Sites NASA Ergo Resources

http://ohp.ksc.nasa.gov/topics/ergo/

NIOSH Web

http://www.cdc.gov/niosh/topics/ergonomics/

OSHA Web

http://www.osha.gov/SLTC/ergonomics/index.html

Military Sites Department of Defense Design Criteria MIL-1472F

http://safetycenter.navy.mil/instructions/osh/MILSTD1472F.pdf

Educational Institution Sites Cornell University Ergonomics

http://ergo.human.cornell.edu/

Ergonomic Design Standard—University of Melbourne

http://www.unimelb.edu.au/ehsm/Ergonomic_design.pdf

Ergonomic Guidelines for Video Display Terminal

http://www.fiu.edu/~ehs/general_safety/general_ergonomics_video.htm

Ergonomic Standard and Guidelines—University of Maryland

http://www.otal.umd.edu/guse/standards.html

Ergonomic Workstation Guidelines—NC State University

http://www.ncsu.edu/ehs/www99/right/handsMan/office/ergonomic.html

Loughborough University Ergonomics

http://www.lboro.ac.uk/research/esri/

Louisville University Ergonomics

http://louisville.edu/speed/ergonomics/

Office Ergo Guidelines—University of Sydney

http://www.usyd.edu.au/ohs/ohs_manual/ergonomics/ergoguide.shtml

Office Ergonomic Standard—University of Toronto

http://www.ehs.utoronto.ca/services/Ergonomics.htm

Ohio State University Ergonomics

http://ergonomics.osu.edu/#

University of California, Berkeley, San Francisco Ergonomics

http://ergo.berkeley.edu/

University of California Los Angeles Ergonomics

http://ergonomics.ucla.edu/

University of Michigan Ergonomics

http://www.engin.umich.edu/dept/ioe/C4E/

University of Nebraska Ergonomics

http://eeshop.unl.edu/rsi.html

Additional Ergonomic Resources ANSI BHMA Search

http://www.buildershardware.com/20.html

Ergonomics for Notebooks

http://www.ergoindemand.com/laptop-workstation-ergonomics.htm

Human Factors Standards

http://www.12207.com/human_factors.htm

Ergonomic Edge

http://www.ergonomicedge.com/

Ergonomic Product Guidelines

http://www.cccd.edu/facultystaff/riskservices/erg_resource_center.aspx

Ergonomic Resources

http://www.ergoweb.com/

Ergonomics for Teacher and Student

http://www.ergonomics4schools.com/

Next Gen Ergo

http://www.nexgenergo.com/

Stress Ergonomics

http://www.spineuniverse.com/displayarticle.php/article1484.html

Industry Sites 3MErgo

http://solutions.3m.com/wps/portal/3M/en_US/ergonomics/home/advice/ workspacecomfortguide/

American Ergonomics Corporation

http://americanergonomics.com/

Basic Ergo Standard

http://www.ergoweb.com/resources/reference/guidelines/

Ergonomic for Writers and Editors

http://www.sfwa.org/ergonomics/

Hewlett Packard Ergo Guidelines-Working in Comfort

http://www.hp.com/ergo/and http://www.hp.com/ergo/pdfs/ 297660-002.pdf

IBM Ergo Guide-Healthy Computing

http://www.pc.ibm.com/ww/healthycomputing/

Office Ergonomics Training

http://www.office-ergo.com/

Office Ergonomics

http://www.healthycomputing.com/office/

Repetitive Strain Injury FAQs by CTD Resource Network, Inc

http://www.tifaq.org/information.html

Work-Related Musculoskeletal Disorders

http://www.nsc.org/osh/Training/ergonomics.aspx

ANSI, Almerican National Standards Institute; BHMA, Builders Hardware Manufacturers Association; FAQs, frequently asked questions; NASA, National Aeronautics and Space Administration; NIOSH, National Institute for Occupational Safety and Health; OSHA, Occupational Safety and Health Administration.

CHAPTER 23  Computer Assistive Devices and Environmental Controls

Assistive Technology for Hearing Impairments Hearing impairment and deafness affect the feedback loop in the human environment interaction. Because most individuals can hear, it is commonly recognized as a significant barrier in communication and can compromise safety in situations where sound is used to warn of danger.

Hearing Aids Individuals who are deaf or hard of hearing deal with two major issues: lack of auditory input and compromised ability to monitor speech output and environmental sound. AT devices such as hearing aids and frequency modulation (or radio wave) systems can be used to facilitate both auditory input and speech output. Other types of AT devices provide a visual representation of the auditory signal. These include flashing lights as an alternative emergency alarm (e.g., for fire or tornado) or the ring of a phone or doorbell.

Cochlear Implants When the hearing system is impaired at the level of the middle ear or the cochlea, a highly specialized form of AT is used to create an alternate means of stimulating the auditory nerve. This technology is implanted surgically with an electrode array placed within or around the cochlear structure. The external portion, a microphone, relays speech and environmental sound to the implanted portion, which is programmed to process, synchronize, and stimulate electrodes appropriately. This system requires a battery pack worn on the body or behind the ear.8 It also requires an experienced audiologist to teach the individual to use the acoustic cues produced by the cochlear implant as a substitute for natural hearing.

loop,” which acts as an antenna and is capable of broadcasting directly to a hearing aid. A microphone placed near the speaker transmits directly to the neck loop, eliminating background sound. This is also an excellent solution for office and school environments. The Whisper Voice is similar, except it uses a smaller microphone and is more portable. It can be passed from speaker to speaker with sound transmitted to the neck loop and then to the hearing aid for amplification. Environmental adaptations can frequently support individuals who are deaf or hard of hearing. For example, a person speaking to someone who has difficulty hearing can take care not to stand in front of a light source (windows, lamps, etc.) and not to overexaggerate or hide lip movements. Gestures can also be helpful.

Assistive Technology for Visual Impairments The term visual impairment technically encompasses all types of permanent vision loss, including total blindness. Low vision refers to a vision loss that is severe enough to impede performing everyday tasks, but still provides some useable visual information. Low vision cannot be corrected to normal by eyeglasses or contact lenses.

Low-Tech Visual Aids A variety of AT devices and strategies can help individuals with visual impairments become more mobile; perform daily activities, such as reading, writing, and personal care; and participate in recreational activities. Among low-tech solutions are simple handheld magnifiers, the use of large print, and mobility devices for safe and efficient travel (e.g., a white cane; Figure 23-7). High-contrast tape or markers can also be used to indicate hazards, what an item is, or where it is located.

Other Hearing Technologies Another recent adaptation for persons with significant hearing impairments is computer-assisted real-time translation. This AT solution involves a specially trained typist or stenographer who captures what is being spoken on a computer. The text is then projected onto a display, resulting in close to “real-time” translation. The advantage of this technology is that it can be used by hearing-impaired individuals who are not fluent in sign language, as well as others who might need listening help, such as those who use English as a second language. In addition to use in group environments like conferences or meetings, a variation of this technology can be used to assist a single student or employee in a small setting.

Environmental Adaptations For individuals who wear hearing aids, additional technologies are available that can facilitate hearing in large rooms or in noisy, crowded environments such as a restaurant. The Conference Mate and Whisper Voice are especially designed for these environments. In the case of the Conference Mate, the person with the hearing loss wears a “neck

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FIGURE 23-7  Use of a cane by a person with visual impairment.

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Other low-tech solutions include using wind chimes to help with direction finding, using easily legible type fonts such as Verdana (16 point or larger), and using beige paper rather than white to improve the visibility of text. In recreational activities, solutions include beeper balls, three-dimensional puzzles, and outdoor trails with signage (called “Braille trails”) designed to improve access to wilderness and other outdoor activities. Braille text is still the first choice of many individuals for reading, although it is less used than in the past because of the advances in computer and other technologies. Many restaurants now provide large-print, Braille, and picturebased menus for customers with a variety of abilities. Books on tape are another resource for individuals with severe visual impairments. In addition to commercially available tapes for sale and at public libraries, special

libraries provide print materials in alternate formats for persons with visual, physical, and learning impairments. Borrowers can arrange to have textbooks and other materials translated into alternate formats. For more information, contact the American Federation for the Blind or the National Library Service for the Blind and Physically Handicapped (http://www.loc.gov/nls/) (Box 23-2).

High-Tech Visual Aids Numerous high-tech solutions exist for persons with visual impairments. Computers outfitted with a speech synthesizer and specialized software, such as Jaws or WindowEyes, allow navigation of the desktop, operating system, applications, and documents, as well as the entire Internet. Any digital text can be heard aloud by the person using this

BOX 23-2

Resources for Persons With Low Vision or Blindness • American Academy of Ophthalmology PO Box 7424 San Francisco, CA 94120 Tel 415 561-8500 http://www.eyenet.org • American Council of the Blind 2200 Wilson Boulevard, Suite 650 Arlington, VA 22201 Tel 202 467-5081 http://www.acb.org • American Council of the Blind in Colorado 1536 Wynkoop Street, Suite 201 Denver, CO 80202 Tel 888 775-2221 http://www.acbco.org • American Foundation for the Blind 11 Penn Plaza, Suite 300 New York, NY 10001 Tel 800 232-5463 http://www.afb.org • American Printing House for the Blind 1839 Frankfort Avenue Louisville, KY 40206 Tel 502 895-2405 http://www.aph.org • National Association for Visually Handicapped 22 West 21st Street, 6th Floor New York, NY 10010 Tel 212 889-3141 http://www.navh.org • National Braille Association, Inc 95 Allen Creek Road, Building 1, Suite 202 Rochester, NY 14618 Tel 585 427-8260 http://www.nationalbraille.org • National Braille Press, Inc. 88 St. Stephen Street Boston, MA 02115 Tel 617 266-6160 http://www.nbp.org • Recordings for the Blind and Dyslexic 20 Roszel Road Princeton, NJ 08540 Tel 866 732-3585 http://www.rfbd.org

• Rehabilitation Engineering and Assistive Technology Society of North America State Technology Projects 1700 N Moore Street, Suite 1540 Arlington, VA 22209-1903 Tel 703 524-6866 http://www.resna.org • Aspen Braille Nature Trail White River National Forest Aspen, CO 81611 Tel 970 945-2521 http://www.fs.fed.us/r2/whiteriver • Assistive Technology Partners 601 East 18th Avenue, Suite 130 Denver, CO 80203 Tel 303-315-1280 http://www.uchsc.edu/atp • Guide Dogs for the Blind, Inc. PO Box 151200 San Rafael, CA 94915-1200 Tel 415 499-4000 http://www.guidedogs.com • Guide Dogs for the Blind, Inc. 32901 Southeast Kelso Road Boring, OR 97009 Tel 503 668-2100 http://www.guidedogs.com • Helen Keller National Center for Deaf-Blind Youth and Adults 141 Middle Neck Road Sand Point, NY 11050 Tel 516 944-8900 http://www.helenkeller.org • National Federation of the Blind 1800 Johnson Street Baltimore, MD 21230 Tel 410 659-9314 http://www.nfb.org • National Library Services for the Blind–Physically Handicapped Library of Congress 1291 Taylor Street, Northwest Washington, DC 20011 Tel 888 657-7323 www.loc.gov/nls  

CHAPTER 23  Computer Assistive Devices and Environmental Controls

software. For text that is printed, such as menus, memos, and letters, using a technology called optical character recognition allows a page scanner and software to convert print into digital form. It can then be listened to through the computer’s speech synthesizer or converted to Braille or large print. Another category of high-tech aids is portable note takers with either Braille or speech synthesizer feedback for the user. These devices are specialized personal digital assistants with calendars, contacts, and memo and document capabilities, and can be purchased with either a QWERTY or Braille keyboard. For individuals with some degree of visual ability, screen magnification software such as Zoomtext (Figure 23-8) or MAGic enables the user to choose the amount (2 to 20 times) and type of magnification preferred for optimal computer access. Many magnification applications combine enlargement with speech synthesis or text to speech. A recent addition to the list of screen magnification software is called Bigshot. This software is less expensive ($99) and provides fewer features than some other programs. However, it appears to be a highly affordable alternative for users who do not need access to the more sophisticated computer functions.

Environmental Adaptations Persons with visual impairments usually keep the setup of their home and work environments constant because this helps in locating items. However, they usually need specialized training for mobility in the community. They learn to use environmental cues such as traffic sounds, echoes, or texture of the sidewalk in combination with mobility aids such as a white cane or a guide dog. To supplement these less technical aids, some individuals use electron ic travel aids that have the capability of detecting obstacles missed by a cane, such as overhanging branches or objects that have fallen. This technology (Talking Signs) uses ultrasound or information embedded in the environment expressly for users who have limited vision. The demands for independence in community mobility

FIGURE 23-8  Zoomtext screen magnification software for the visually impaired.

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by persons with significant visual impairments are huge because of the high cognitive demand for remembering routes and because environments constantly change. Many individuals use these types of technologies to increase their independent mobility in both familiar areas and the larger community.

Assistive Technology for Cognitive and Learning Disabilities Cognitive disabilities include disorders such as traumatic brain injury, mental retardation, developmental disabilities, autism, Alzheimer disease, learning disability, fragile X syndrome, and other disorders, both developmental and acquired. Most individuals in this group have not had the benefit of using AT devices because relatively few products have been specifically developed for intellectual impairments. In addition, families, teachers, and others providing support services for individuals with cognitive impairments have generally not been aware of the potential usefulness of AT.40 Most have looked to simple solutions for persons with learning impairments, cognitive impairments, or both, using strategies such as colored highlighter tape, pencil grips, enlarged text, reminder lists, and calendars. Others try low-tech adaptations such as using a copyholder to hold print materials for easy viewing, and making cardboard windows to help the eyes follow text when reading. In 2004 the U.S. Department of Education, National Institute on Disability Research and Rehabilitation, recognizing the need to increase AT development for persons with cognitive disabilities by funding, funded the nation’s first Rehabilitation Engineering Research Center for the Advancement of Cognitive Technologies (RERC-ACT; www.rerc-act.org). The RERC-ACT is developing a wide range of new ATs designed to facilitate vocational and literacy skills, service provision, and enhanced caregiving supports for persons with significant cognitive impairments. One of the newer developments from the RERC-ACT is the use of intelligent agents to interactively help people with everyday tasks in education, health care, and workforce training. The systems are designed to assess, instruct, or assist new readers and learners, as well as people who have speech, language, reading, or cognitive difficulties. The intelligent or “animated” agent is available on desktop or mobile computing devices. It is being used to assist persons with cognitive disabilities to learn new job tasks or to prompt them through various steps within a task, or both (Figure 23-9). Other RERC-ACT work includes the development of “batteryless” micropower sensors. Access to low levels of power and the elimination of batteries in sensor technologies for persons with cognitive and physical disabilities enable additional prompts or inputs based on time, weight, location awareness, and other context-aware sensoring capabilities. This technology enables developers to use context-aware sensors in a multitude of environments and other ATs to facilitate the safety, capacity, and wellbeing of persons with cognitive disabilities. This new field of “cognitive technologies” promises numerous advances during the next decade.

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FIGURE 23-9  An example of a handheld intelligent animated agent. These devices are used to help persons with cognitive disabilities to learn new job tasks or to prompt them through various steps within a task, or both. (Courtesy Sarel Van Vuuren, PhD, University of Colorado.)

Literacy Technologies A number of both low- and high-technology solutions are available to assist literacy development. Individuals who are unable to read print materials often use books on tape or some of the text-to-speech software solutions mentioned earlier, such as Jaws. Co:Writer is an example of a specially designed application that predicts the word or phrase an individual is trying to spell as he or she begins to type a word. Other applications (e.g., Write Outloud and Kurzweil 3000) provide multisensory feedback by both visually highlighting and speaking the text an individual is generating on the computer. In addition to helping persons with mobility impairment, VR software can sometimes be helpful for persons with learning disabilities so significant they are unable to develop writing skills. VR software enables such individuals to speak words, phrases, or sentences into a standard computer word-processing program such as Microsoft Word. A review or playback feature in the application allows writers to hear the text they have written. Although VR software is a rapidly developing technology, the user must currently have a fifth grade reading ability to read the text used to generate a voice file, which hinders its usability by those with significant learning disabilities. Dragon Naturally Speaking has developed a VR version for children 9 years and older, but its success rate for children with learning and other cognitive disabilities has not yet been published. Other limitations of VR include reduced accuracy in the presence of ambient noise, such as that found in a typical classroom, and fluctuating vocal abilities related to fatigue or some types of disabilities. In general, it takes more than 20 hours to train the software to an acceptable level of accuracy (greater than 90%). Caution is currently in order when prescribing this type of software, but the rapid pace of development bodes well for future use of this type of software for persons with disabilities. Other applications for persons with cognitive impairment focus on a range of topics, including academics, money management, personal skills development, behavior training, development of cognitive skills, memory improvement, problem solving, time concepts, safety awareness, speech and language therapy, telephone usage, and recreation and games.

FIGURE 23-10  Prompting technology: the Pocket Coach.

Prompting Technologies Recent mainstream technology developments include handheld personal digital assistants. AbleLink Technologies, Inc. have used this technology and developed software applications (PocketCoach; Figure 23-10) that provide auditory prompts for individuals with cognitive disabilities. This software can be set up to prompt an individual through each step of a task as simple as mopping a floor, or a task as complex as solving a math problem. The latest version of this software combines both voice prompts with visual prompts (Visual Assistant). The individual setting up the system for a user can simply take digital pictures with the accompanying camera and combine them with digitally recorded voice prompts to further facilitate memory and cognition.

Selecting Appropriate Assistive Technologies  Abandonment Practitioners are sometimes surprised to learn that not everyone with a disability enjoys using technology, however useful it might appear. Depending on the type of technology, nonuse or abandonment can be as low as 8% or as high as 75%. On average, one third of more optional assistive technologies are abandoned, most within the first 3 months.23 Research has not yet been done to determine the number of individuals who are unhappy with their devices, but who must continue to use them because they cannot abandon them without severe consequences.22,29-31 For example, an individual who has just received a new wheelchair that does not meet expectations simply cannot stop using the chair, but must wait until third-party funding becomes available again (typically several years). Alternatively, the individual must engage in potentially difficult and unproductive discussions with the vendor, who has more than likely provided the chair as it was prescribed by the assessment team.

CHAPTER 23  Computer Assistive Devices and Environmental Controls

Research does tell us that the main reason individuals with disabilities choose not to use assistive devices is because practitioners failed to consider their opinions and preferences during the process of selecting the device. In other words, the person with a disability was not included as an active member of the team during the evaluation process.10,11,22,27

Principles of Clinical Assessment The goal of an AT evaluation is to determine whether AT devices and services have the potential to help an individual meet his or her activity or participation goals at home, school, work, or play. Other goals include (1) providing a safe and supportive environment for the person with a disability and his or her family to learn about and review available assistive devices; (2) identifying the need for AT services, such as training support staff or integrating an AT device into daily activities; (3) determining the modification or customization needed to make the equipment effective; and (4) developing a potential list of recommended devices for trial usage before a final selection of technology is made. In addition, the individual and family, as well as the AT team, should specify exactly what they hope to achieve as a result of the evaluation (e.g., equipment ideas, potential success with vocational or educational objectives). When selecting team members to conduct an AT evaluation, professional disciplines should be chosen based on the identified needs of the person with the disability. For example, if the individual has both severe motor and communication impairments, team members should include an occupational or physical therapist with expertise in human-technology interface, as well as a speech-language pathologist with a background in working with persons with severe communication impairments and alternative forms of communication. If a cognitive impairment has been identified, someone versed in learning processes, such as a psychologist, neurolinguist, teacher, or special educator, would be an appropriate member of the team. If there is an ergonomic issue (e.g., repetitive stress injury), an evaluator with training in ergonomic assessment or a background in physical or occupational therapy is a necessary component for a successful experience. It is not appropriate for an AT vendor to be called in to perform an AT evaluation. Although vendors can and should be members of the evaluation team, it must be recognized that they have a conflict of interest because they earn a living by selling products. When working with a manufacturer or vendor, it is important to work with a credentialed provider. When requested by the team, vendors demonstrate their products, discuss pertinent features, and assist in setting up the equipment for evaluation and trial usage. However, other team members, including the end user and family, should perform the evaluation and make the final recommendations.

Phase 1 of the Assessment Process Knowledge within the field of AT continues to expand and change, sometimes on a daily basis. This directly affects whether the AT device recommended by the assessment team will be used or abandoned by the consumer.15,19 As a

511

result of rapidly changing information, the evaluation process continues to be refined. Many researchers are working to develop standardized AT measurement tools,* but the fact remains that few resources are available to guide practitioners who have not received formalized training in AT assessment. As mentioned earlier in this chapter, the most common reason AT is abandoned is because the needs and preferences of the consumer are not taken into account during the evaluation process. Other reasons cited for abandonment of devices include the following22: • Changes in consumer functional abilities or activities • Lack of consumer motivation to use the device or do the task • Lack of meaningful training on how to use the device • Ineffective device performance or frequent breakdown of the device • Environmental obstacles to use, such as narrow doorways • Lack of access to and information about repair and maintenance • Lack of sufficient need for the device functions • Device aesthetics: Device’s weight, size, and appearance Given the relationship that must develop between individuals and AT devices, it is common sense that these factors be considered during the evaluation process. The AT assessment process has evolved from a random process of trying out any number of devices with the individual, to a team process that begins with the technology out of sight. Phase 1 of the assessment process begins when a referral is received. Standard demographic and impairment-related information is collected, usually over the phone. In most cases, cognitive, motor, vision, and other standard clinical assessments have already been performed, and a release of information is requested from the individual or caregiver so information can be forwarded to the team. If appropriate assessments have not been conducted, they are scheduled as a component of phase 2 of the assessment process. Based on the preliminary information, an appropriate team of professionals is assembled, and a date is chosen for the evaluation. The team leader takes responsibility for ensuring that the individual with the disability, the family, and any other significant individuals are invited to the evaluation. At the initial meeting, team members spend some time getting to know the individual. Using methods described by Cook and Hussey8 and Galvin and Scherer,10 the team identifies the life roles of the consumer (e.g., student, brother, or musician) and the specific activities engaged in by the individual to fulfill that life role. For example, if a young man is a “brother,” that means he might play hide and seek with a sibling, squabble over toys, or otherwise engage in brotherly activities. If he is a musician, then he might want or need to have access to musical instruments, sheet music, or simply a radio. Next, the team identifies any problems that might occur during the individual’s daily activities. For example, the musician might not have enough hand control to manage recording equipment, or could experience visual or cognitive difficulties with sheet music. The team asks specific *References 7, 10, 15, 20, 21, 30, 31, 34-36.

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questions about where and when these difficulties occur (activity limitations). Perhaps problems occur when the individual is tired or not properly positioned, or when trying to communicate with others. The individual is also asked to describe instances of success with these activities and to discuss what made them successful (prior history with and without technology). By now the team is usually able to recognize patterns of success and failure from the individual’s perspective as common limitations across environments emerge. Finally, the team prioritizes the order in which to address barriers to participation, and a specific plan of action is developed. This specific plan of action contains “must statements” such as “the device must have a visible display in sunlight,” or “the technology chosen must weigh less than 2 lb.” It is at this point that the team might be reconfigured. For example, if the individual is not properly seated and positioned, he or she is referred to the occupational or physical therapist for a seating and positioning evaluation before proceeding further. Some members of the team may leave after determining that further assessment from their perspective is not needed. In other situations as additional needs becomes apparent, new members are invited to join the team (e.g., a vision specialist). At all times the assessment team includes the individual and caregivers as the primary members.

Phase 2 of the Assistive Technology Assessment Once the team has agreed on the specific plan of action and those things that “must” occur, phase 2 of the assessment process begins. The person with the disability, the caregivers, or both, are asked to preview any number of AT devices that might serve to reduce activity limitations and increase participation in chosen environments. These AT devices are tried along with various adaptations, modifications, and placements to ensure an appropriate match of the technology to the individual. It is at this point that the clinician’s AT skills become critical. If trial devices are not properly configured or if the wrong information is given to the consumer, he or she will be unable to make an appropriate selection. Because many devices require extensive training and follow-up, it is essential that realistic information about training and learning time is provided and appropriate resources within the local community identified. With very few exceptions the wise course of action involves borrowing or renting the AT device before making a final purchase decision. For many individuals the actual use of technologies on a dayto-day basis raises new issues that must be resolved. For instance, there might not be the local supports necessary for the technology that appears to be best for an individual. In these cases it is best to first identify local resources or local AT professionals willing to seek additional training before sending the device home with the user. Consumers and their families should always be informed so they can make the final decision regarding when and where the equipment will be delivered. Unexpected benefits of trial use occur as a result of improved functioning, including changes in role and

status. In some cases these unexpected benefits create an entirely new set of problems. For most individuals these problems can be resolved with time, energy, and patience. Others decide that they either prefer the old way of doing things or that they are interested in adding or changing the technology once they have had a chance to experiment with it in different settings. AT professionals, in consultation with the physician, should also anticipate future needs (e.g., physical and cognitive maturation), and final decisions should consider both the expected performance and durability of the device.31

Writing the Report The evaluation report documents the AT assessment process and must include several components. It is important to use layman’s terms to help case managers, educators, and others unfamiliar with ATs understand the process. In cases where medical insurance is being used to purchase technology, it is essential to document the medical need for the device(s) within the report. This information will be included in the “letter of medical necessity” required by medical insurers before funding approval. For example, the evaluation report might state, “Mr. Jones will use this wheelchair to enable safe and independent mobility in the home and community and to meet the functional or activities of daily living goals as listed.” In instances where educational or vocational funding is being requested to purchase the technology, the report should focus on the educational or vocational benefit of the assistive devices and how relevant goals will be met with the recommended equipment. It is also extremely important that all components of the AT device be included in the list of recommended equipment (e.g., cables, ancillary peripherals, and consumable supplies). In many instances devices are recommended for purchase as a “system.” As a result, acquisition can be delayed for months because an item was not included in the initial list. An estimate of the amount of time, cost, and source of training should also be included at this point. Purchasing AT devices without paying for the AT services needed to learn how to use and integrate the devices into identified life activities will result in low use or abandonment.29-31 Finally, it is also important to include contact information for the vendors who sell the equipment. Many purchasers are unfamiliar with rehabilitation technology supply companies, and acquisition can be delayed if this information is not included in the report.

Physician Responsibilities Prescribing the Technologies The American Medical Association36 recommends the following items be considered when prescribing AT and certifying medical necessity: The physician must provide evidence of individual medical necessity for the specific AT being prescribed and be prepared to talk with insurance company representatives about the medical necessity of complex assistive technologies (e.g., power wheelchairs

CHAPTER 23  Computer Assistive Devices and Environmental Controls

and AAC devices). Reviewing a comprehensive assessment report from the AT assessment team should supply all the needed information. Health insurance requires an “appropriate” prescription that includes mention of the comprehensive assessment process, the individual’s motivation, the availability of training, and the potential functional outcomes for the patient, as compared with the cost of the products. Success with reimbursement also includes using the appropriate medical necessity forms and prior authorization procedures.

Documentation in the Medical Record In addition to prescribing and certifying medical necessity on various forms, physicians must maintain complete patient records that include the following: • Patient diagnosis or diagnoses • Duration of the patient’s condition • Expected clinical course • Prognosis • Nature and extent of functional limitations • Therapeutic interventions and results • Past experience with related items • Consultations and reports from other physicians, an interdisciplinary team, home health agencies, etc. • A complete listing of all assistive devices the patient is using, including copies of prescriptions and certification forms or letters • A system to track device performance, including followup assessment schedules and lists of professionals and vendors to contact if problems occur This comprehensive medical record supplies the background information needed to substantiate the need for the AT devices and services regardless of the funding source.

Letters of Medical Necessity Physicians are frequently asked to write “letters of medical necessity.” Well-written letters of medical necessity help ensure that the AT needs of patients are met. These letters should include the diagnoses (International Classification of Diseases codes) and the functional limitations of the individual (e.g., balance disorder or developmental delay). There should also be a statement about the patient’s inability to perform specific tasks, such as activities of daily living, work activities, and the ability to walk functionally. For example, individuals with severe communication disorders typically cannot communicate verbally and/or in writing, and are often unable to communicate independently over the phone. This would also mean they are unable to adequately communicate their health care needs to medical personnel and are therefore unsafe or at risk. These details should be included in a letter of medical necessity. The letter should also include a paragraph stating why the equipment is necessary. For example, the use of the equipment will allow the patient to do the following: • Function independently or improve the ability to function • Perform independent wheelchair mobility in the home and community • Return home or move to a less expensive level of care

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Sometimes the equipment may simply be required as a lifetime need, such as a wheelchair or specialized medical bed. Next, the letter needs a rationale for choosing the specific equipment. This requires describing the specific equipment features and listing all required components. This might include the following: • Features that provide safety or safe positioning for an activity • Cost-effectiveness of preventing secondary complications (e.g., pressure ulcers) • Mobility restrictions preventing independent activity • Access to areas in home, such as bathroom and kitchen • Durability of the product over its alternatives • Past experience, interventions, and results (failure of less expensive solutions)

Funding Assistive Technology The funding sources for AT devices and services fall into several categories. The AT assessment process often helps to identify which source will be used. One source is private or government medical or health insurance. Health insurance defines AT as “medical equipment necessary for treatment of a specific illness or injury,” and a physician’s prescription is usually required. When writing a prescription for an AT device, it is important that physicians are aware of the costs and benefits of the devices and be prepared to justify their prescriptions to third-party payers. Funding includes not only the initial cost of the device, but the expense involved in equipment maintenance and patient education or training, as well as the potential economic benefits it provides to the patient (e.g., a return to work). AT is usually covered under policy provisions for durable medical equipment, orthoses and prostheses, or ADL and mobility aids. With private health insurance and with government insurance programs, such as Medicaid and Medicare, coverage is based on existing law and regulations. In 2002, AAC devices were included for reimbursement by Medicare. AT professionals and other health care providers should continually advocate for adequate coverage of AT in all health care plans Funding for AT is also available from other federal and state government entities, such as the Veterans Administration, State Vocational Rehabilitation Agencies, State Independent Living Rehabilitation Centers, and State Department of Education Services. Local school districts might also fund education-related AT for children.13 Each agency or program sets criteria for the funding of AT devices based on its mission and the purpose of the technology. For example, vocational rehabilitation agencies pay for AT devices and services that facilitate or help maintain paid employment, and education systems fund AT that enables students to perform or participate in school. Funding is generally available for AT, but persistence and advocacy by the AT provider are required for success.32,35 The AT provider must also keep abreast of the requirements of various funding sources, to direct the client to appropriate organizations. Private funding is often available through subsidized loan programs, churches, charitable organizations, and disability‑related nonprofit groups. Often funding from several sources is needed to

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reduce personal out‑of‑pocket costs. It is important that the presumed availability of funding not drive the evaluation process and limit the options that are considered for an individual. When the need and justification for a particular AT solution are clear, it becomes much easier to locate a source of funding and make the case for purchase of the AT device or service. Beukelman and Mirenda3 identify five steps in developing a funding strategy: 1. Survey the funding resources available to the individual. 2. Identify various funding sources for the various steps in the AT intervention (i.e., assessment, funding, and training). 3. Prepare a funding plan with the client and family members or advocates. 4. Assign responsibility to specific individuals for the funding of each step of the AT intervention. 5. Prepare the necessary written documentation for the funding source so there is a record in the event an appeal is needed.3

Summary and Future Directions The world of AT is moving at a very rapid pace, fed in large part by the growth in mainstream technologies and the culture of inclusion that is changing traditional concepts about disability and impairment. Space travel, satellitesupported telecommunications, wireless networks, robotics, new materials with advanced performance properties, miniaturization of integrated circuits, and innovation in batteries and power sources are all crossing over into the field of AT. Federal funding supports Rehabilitation and Engineering Research Centers for the development and testing of new AT concepts. Funds also support the transfer of technologies from the federal laboratory system to AT manufacturers. The convergence of these factors is leading to AT products more likely to meet the needs of persons with disabilities. REFERENCES 1. [Anonymous]. The Rehabilitation Act of 1973, as amended. 1973. 2. Ball L, Beukelman D, Patee G: Augmentative and alternative communication clinical decision making for persons with ALS, Augment Altern commun. 2002:7–12. 3. Beukelman DR, Mirenda P: Augmentative and alternative communication: management of severe communication disorders in children and adults, ed 2, Baltimore, 1998, Paul H Brookes. 4. Blake DJ, Bodine C: An overview of assistive technology for persons with multiple sclerosis, J Rehabil Res Dev 39:299-312, 2002. 5. Bodine C, Beukelman DR: Prediction of future speech performance among potential users of AAC systems: a survey, Augment Altern Commun 7:100-111, 1991. 6. Bromley BE: Assistive technology assessment: a comparative analysis of five models. Proc CSUN 2001. 7. Chatman A, Hyams S, Neel J, et al: The Patient-Specific Functional Scale: measurement properties in patients with knee dysfunction, Phys Ther 77:820-829, 1997. 8. Cook AM, Hussey SM: Assistive technologies: principles and practice, ed 2, St Louis, 2002, Mosby. 9. De Ruyter F, Kennedy MR, Doyle M: Augmentative communication and stroke rehabilitation: who is doing what and do the data tell the whole story? Third Annual National Stroke Rehabilitation Conference, Boston, May 10-11,1990.

10. Galvin JC, Scherer M: Evaluating, selecting, and using appropriate assistive technology, Gaithersburg, 1996, Aspen. 11. Gray DB, Quatrano LA, Lieberman M: Designing and using assistive technology: the human perspective, Baltimore, 1998, Paul H Brookes. 12. Grove N: Augmentative and alternative communication: management of severe communication disorders in children and adults, J Intellect Disabil Res 38:219-220, 1994. 13. Hager RM: Funding of assistive technology: state vocational rehabilitation agencies and their obligation to maximize employment, Buffalo, 1999, Neighborhood Legal Services. 14. James P, Thorpre N: Ancient inventions, New York, 1994, Ballentine Books. 15. Jutai J: Quality of life impact of assistive technology, Rehabil Eng 14:27, 1999. 16. King TW: Assistive technology: essential human factors, Needham Heights, 1999, Allyn & Bacon. 17. Klund J: A crash course on alternative access, Technol Spec Interest Sect Q :1-3, 2001. 18. La Plante MP: The demographics of disability, Milbank Q 69:55-77, 1991. 19. Nagi S: Some conceptual issues in disability and rehabilitation. In Sussman M, editor: Sociology and rehabilitation, Washington DC, 1965, American Sociological Association. 20. Patterson DJ, Liao L, Fox D, et al: Inferring high-level behavior from low-level sensors. In McCarthy AD, Kautz H: UBICOMP 2003: the Fifth International Conference on Ubiquitous Computing, New York, 2003, Springer-Verlag. 21. Pentland A: Machine understanding of human action. In 7th International Forum on Frontier of Telecom Technology November, 1995. Available at: http:\\www.white.media.mit.edu/vismod/demos/ive/. Accessed August 8, 2010. 22. Phillips B, Zhao H: Predictors of assistive technology abandonment, Assist Technol 5:36-45, 1993. 23. Pope AM, Tarlove AR: Disability in America: toward a national agenda for prevention, Washington, DC, 1991, National Academy Press. 24. Public Law 93-113. Section 508 of the Rehabilitation Act of 1973, as amended 29 USC 794 (d). 1998. 25. Public Law 100-407: Technology Related Assistance for Individuals with Disabilities Act of 1988, Federal Register 19:41272, August 1991. 26. Public Law 108-446. The Individuals with Disabilities Education Act Amendments of 1997. 27. Riermer-Reiss ML, Wacker Robbyn R: Factors associated with assistive technology discontinuance among individuals with disabilities, J Rehabil 66:44-49, 2000. 28. Romski MA, Sevcik RA: Language learning through augmented means: the process and its products, Baltimore, 1993, Paul H Brookes. 29. Scherer M: Assistive technology use, avoidance and abandonment: what we know so far. Proceedings of the 6th Annual Technology and Person with Disability Conference, Los Angeles, 1991. 30. Scherer M: Assistive technology: matching device and consumer for successful rehabilitation, Washington, 2002, American Psychological Association. 31. Scherer M, Coombs FK: Ethical issues in the evaluation and selection of assistive technology. Available at: http://www.gatfl.org/publications/ ethical.pdf. Accessed August 8, 2010. 32. Scherer MJ: Living in a state of stuck: how technology impacts the lives of people with disabilities, Cambridge, MA, 1993, Brookline Books. 33. Scherer MJ: Living in the state of stuck: how technology impacts the lives of people with disabilities, ed 3, Cambridge, 2000, Brookline Books. 34. Scherer MJ, Cushman LA: Measuring subjective quality of life ­following spinal cord injury: a validation study of the assistive technology device predisposition assessment, Disabil Rehabil 23:387-393, 2001. 35. Scherer MJ, McKee BG: Assessing predispositions to technology use in special education: music education majors score with the ‘Survey on Technology Use.’ RESNA ‘94 Annual Conference, Arlington, 1994, Rehabilitation Engineering and Assistive Technology Society of North America. 36. Schwartzberg JG, Kakavas VK, Malkind S: Guidelines for the use of assistive technology evaluation, referral, prescription, ed 2, Chicago, 1996, American Medical Association. 37. The Rehabilitation Act Amendments of 1992 and Assistive Technology. Rehabilitation Engineering and Assistive Technology Society of North America: Assistive Technology Quarterly; 1993. 38. US Congress: Americans with Disabilities Act of 1990.

CHAPTER 23  Computer Assistive Devices and Environmental Controls 39. US Congress: Americans with Disabilities (ADA) accessibility guidelines for buildings and facilities, Washington, DC, 1991, US Architectural and Transportation Barriers Compliance Board, 91. 40. Wehmeyer ML, Kelchner K, Richards S: Individual and environmental factors related to the self-determination of adults with mental retardation, J Vocat Rehabil 5:291-305, 1995.

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41. World Health Organization: International classification of functioning, disability and health: literature review on environmental factors, Geneva, 2000, WHO. 42. World Health Organization Committee for the International Classification of Functioning: International classification of functioning: ICF checklist, Geneva, 2002, WHO.

CHAPTER 24 PERIPHERAL JOINT AND SOFT TISSUE INJECTION TECHNIQUES Paul Lento, Joseph Ihm, David J, Kennedy, and Christopher J. V   isco

Physical medicine and rehabilitation specialists often inject soft tissues and peripheral joints when treating various musculoskeletal conditions. This chapter reviews the more common techniques used to perform these injections, as well as the properties of the medications used, their adverse effects, and efficacy rates. Because the injections have a known “miss rate” when done without image guidance, techniques using both fluoroscopy and ultrasound (US) guidance are described. Where applicable, the literature regarding the efficacy of these various injections is reviewed.

Overview and History The first published description of intraarticular corticosteroid injection was by Hollander et al.79 in 1951, who demonstrated clinical improvement with the injection of hydrocortisone in a case series of patients with inflammatory joint conditions. Hollander78 subsequently reported on 250,000 injections in 8000 patients and was the first to describe complications associated with intraarticular corticosteroid injections. These included postinjection flare, aseptic necrosis in weight-bearing joints, and infection (infections occurred at a frequency of 1 in 15,000 injections). Practitioners have since expanded the use of corticosteroids to include injections near tendon insertions for enthesitis and other periarticular structures such as bursae.183 These injections have other known complications including localized fat atrophy and tendon rupture.25 Despite these known complications, physicians continue to use corticosteroids as evidenced by a survey showing that 89% of physiatrists171 and 93% of rheumatologists use intraarticular and soft tissue corticosteroid injections for the treatment of pain.75 Fortunately, other medications such as local anesthetics and hyaluronan derivatives are available that can also be used to help with musculoskeletal pain conditions when corticosteroids are not indicated or are not beneficial.

Purpose: Diagnostic or Therapeutic Intraarticular space or soft tissue injections can be used either for diagnostic or therapeutic purposes. Obtaining fluid from a joint, bursa, or cystic structure can help determine the cause of a fluid collection. Although a

complete discussion is beyond the scope of this chapter, certain laboratory studies and bedside analyses can help categorize the nature of the fluid (Table 24-1). Cell count classifies the type of fluid as being noninflammatory, inflammatory, infectious, or septic. Culture and sensitivity help in the identification of a specific organism and its susceptibility to antibiotics. Birefringence classifies the type of crystals present. Although laboratory analysis is the most specific and sensitive way to analyze aspirated fluid, the string test allows for a nonspecific bedside screen for inflammation. Because of its highly viscous nature, healthy synovial fluid should be able to stretch at least 2.5 cm before breaking when dripped from a syringe. Inflammation decreases the overall viscosity and makes the fluid drip instead of stretch. If the aspirated fluid is noninflammatory, it should be clear enough to read 0.25-inch font through a test tube.134 The fluid should be sent for formal analysis when an infection or a crystal arthropathy is suspected, or when the cause of the fluid collection is uncertain.92 Although aspiration can help classify the etiology of the fluid, injecting an anesthetic into a structure might aid in identifying or confirming whether the structure is a pain generator.94 For example, a diagnostic injection into the hip joint using fluoroscopic guidance can help distinguish whether pain is emanating from a pathologic disorder of the hip joint or is referred from the lumbar spine. Because single anesthetic diagnostic injections have a known falsepositive rate, a second confirmatory injection might be necessary.45 Not only can injections be used for diagnostic purposes, they can also be effective in the treatment of painful conditions. Although isolated aspiration of accumulated fluid can be helpful in some cases, any benefits obtained from solely removing fluid are often short-lived.201 Consequently various injected medications and preparations have been used alone or in combination to provide a longer therapeutic benefit for various musculoskeletal conditions. Performing these injections should help lessen the need for oral medication, improve function, and reduce disability. Optimally injections should not be performed in isolation, but in combination with physical therapy and exercise.26 Injected medications such as anesthetics, corticosteroids, and various preparations of viscosupplementation have different adverse effects, durations of action, and costs. These factors should be thoroughly understood before use of injections in the clinical setting. 517

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Table 24-1  Synovial Fluid Analysis Synovial Fluid

Common Diseases

Normal

Clarity

Color

Viscosity

WBC Count (cc)

Clear

Yellow

High

0-200

90

Absent

Hemorrhagic

Trauma, hemophilia, hemangioma, anticoagulant therapy, tumors

Turbid

Red-brown

Reduced

50-10,000

200 mg/24 hours) begins about 4 weeks after injury, reaches a maximum at 16 weeks, and can persist for 12 to 18 months. Renal stone incidence in the first 9 months is approximately 1.0% to 1.5% and is due mainly to hypercalciuria. Over the next 10 years upper tract stones are found in 8%, with many of these secondary to infection. The incidence of bladder stones in the first 9 months in patients on intermittent catheterization is 2.3%. In the presence of an indwelling catheter, and despite greater urine output, the prevalence is much higher (8.8%).13

Bladder stones are effectively treated with cystoscopy and holmium:yttrium–aluminum–garnet laser lithotripsy. Small stones and particles can be dissolved by daily bladder irrigations with 30 mL of 10% hemiacidrin (Renacidin) solution, which is left in the bladder for 30 minutes. Some patients with recurrent stones use this once or twice a week for prophylaxis. In patients who have ureteral reflux, it should be used with caution because of potential nephrotoxicity and absorption of magnesium. Calyceal calculi that are small (3 cm diameter), a percutaneous approach is preferred because clearance of fragments is poor if patients are inactive. Ureteral stones are potentially dangerous in patients with no renal sensation. These can be managed expectantly if they pass down within 2 to 3 weeks. Patients with reduced sensation might not perceive continuous pain, which would normally suggest severe continuing obstruction. This results in an increased risk of renal damage. When obstruction and infection occur together, they require a drainage procedure as an emergency with a percutaneous nephrostomy or a retrograde stent. This is typically followed by an endoscopic lithotripsy, stone removal, or ESWL. Lower Urinary Tract Changes Trabeculation occurs in the majority of patients after spinal cord injury. In many cases trabeculation happens despite appropriate management strategies. Sacculation and diverticula can occur when obstruction and high pressure are severe. If a diverticulum occurs at the ureteral hiatus, ureteral reflux is almost inevitable. Chronic infection of dilated prostatic ducts can be an important source for relapsing UTIs in men. Ureteral Reflux and Upper Tract Dilation Ureteral reflux or high bladder pressure in the absence of reflux can cause upper tract dilation (Figure 28-9). Dilation without reflux is said to be caused by decreased compliance, but data from long-term monitoring suggest that baseline pressure elevations are minimal with natural rates of filling, and that increased phasic activity might be more important.40 With reflux, or ureteral dilation without reflux, the bladder pressure should be lowered with intermittent catheterization and anticholinergics. If bladder pressure responds but reflux fails to improve, a surgical procedure to repair the reflux can be considered. If bladder

pressures do not improve, the options are to augment the bladder or, in men, to perform a sphincterotomy and rely on free drainage.

Summary The ultimate goal of bladder management is to create a bladder management system for the patient that optimizes quality of life while preventing renal deterioration and reducing morbidity such as UTIs. A history and physical examination followed by appropriate testing will allow classification of the patient’s bladder dysfunction. This will allow, with careful consideration of other medical problems and social issues, choice of the best method of bladder management to meet these stated goals. REFERENCES 1. Abrams P, Amarenco G, Bakke A, et al: Tamsulosin: efficacy and safety in patients with neurogenic lower urinary tract dysfunction due to suprasacral spinal cord injury, J Urol 170(4):1242-1251, 2003. 2. Abrams P, Blaivas JG, Stanton SL, et al: Standardization of terminology of lower urinary tract function. In Krane RJ, Siroky MB, editors: Clinical neurology, ed 2, Boston, 1991, Little, Brown. 3. Berger Y, Blaivas JG, DeLaRocha ER, et al: Urodynamic findings in Parkinson’s disease, J Urol 138(4):836-838, 1987. 4. Blaivas JG: Videourodynamics. In Krane RJ, Siroky MB, editors: Clinical neurology, ed 2, Boston, 1991, Little, Brown. 5. Bors E, Comarr AE: Neurological urology, Baltimore, MD 1971, University Park Press. 6. Bradley WE: Physiology of the urinary bladder. In Walsh PC, Gittes RF, Perlmutter AD, et al, editors: Campbell’s neurology, Philadelphia, 1986, WB Saunders. 7. Brindley GS, Rushton DN: Long-term follow-up of patients with sacral anterior root stimulator implants, Paraplegia 28(8):469-475, 1990. 8. Cardenas DD, Hooton TM: Urinary tract infection in persons with spinal cord injury, Arch Phys Med Rehabil 75(3):272-280, 1995. 9. Cardenas DD, Kelly E, Krieger JN, et al: Residual urine volumes in patients with spinal cord injury: measurement with a portable ultrasound instrument, Arch Phys Med Rehabil 69(7):514-516, 1988.

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10. Cardenas DD, Kelly E, Mayo ME: Manual stimulation of reflex voiding after spinal cord injury, Arch Phys Med Rehabil 66(7):459-462, 1985. 11. Cardenas DD, Mayo ME: Bacteriuria with fever after spinal cord injury, Arch Phys Med Rehabil 68:291-293, 1987. 12. Consortium for Spinal Cord Medicine: Linsenmeyer TA, Baker ER, et al: Clinical practice guidelines for health-care professionals: acute management of autonomic dysreflexias: individuals with spinal cord injury presenting to health-care facilities, J Spinal Cord Med 25(S1):S67-S88, 2002. 13. DeVivo MJ, Fine PR, Cutter GR, et al: The risk of renal calculi in spinal cord injury patients, J Urol 131(5):857-860, 1984. 14. Dewire DM, Owens RS, Anderson GA, et al: A comparison of the urological complications associated with long-term management of quadriplegics with and without chronic indwelling urinary catheters, J Urol 147(4):1069-1071, 1992. 15. Dmochowski RR, Miklos JR, Norton PA, et al: Duloxetine versus placebo for the treatment of North American women with stress urinary incontinence, J Urol 170(4):1259-1263, 2003. 16. Dykstra DD, Sidi AA: Treatment of detrusor-sphincter dyssynergia with botulinum A toxin: a double-blind study, Arch Phys Med Rehabil 71(1):24-26, 1990. 17 Feifer A, Corcos J: Contemporary role of suprapubic cystostomy in treatment of neuropathic bladder dysfunction in spinal cord injured patients, Neurourol Urodyn 27(6):475-479, 2008. 18. Finkbeiner AE: Is bethanechol chloride clinically effective in promoting bladder emptying? A literature review, J Urol 134(3):443-449, 1985. 19. Gasparini ME, Schmidt RA, Tanagho EA: Selective sacral rhizotomy in the management of the reflex neuropathic bladder: a report on 17 patients with long-term followup, J Urol 148(4):1207-1210, 1992. 20. Giannantoni A, Di Stasi SM, Stephen RL, et al: Intravesical resiniferatoxin versus botulinum-A toxin injections for neurogenic detrusor overactivity: a prospective randomized study, J Urol 172(1):240-243, 2004. 21. Glowacki LS, Beecroft ML, Cook RJ, et al: The natural history of asymptomatic urolithiasis, J Urol 147(2):319-321, 1992. 22. Iwatsubo E, Komine S, Yamashita H, et al: Over-distension therapy of the bladder in paraplegic patients using self-catheterization: a preliminary study, Paraplegia 22(4):210-215, 1984. 23. Kim JH, Rivas DA, Shenot PJ, et al: Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebo-controlled trial, J Spinal Cord Med 26(4):358-363, 2003. 24. Kiviat MD, Zimmermann TA, Donovan WH: Sphincter stretch: a new technique resulting in continence and complete voiding in paraplegics, J Urol 114(6):895-897, 1975.

25. Lapides J, Diokno AC, Silber SJ, et al: Clean, intermittent self-catheterization in the treatment of urinary tract disease, J Urol 107(3):458461, 1972. 26. MacDonald R, Monga M, Fink H, et al: Neurotoxin treatments for urinary incontinence in subjects with spinal cord injury or multiple sclerosis: a systematic review of effectiveness and adverse effects, J Spinal Cord Med 31:157-165, 2008. 27. Madersbacher H, Jilg G: Control of detrusor hyperreflexia by the intravesical instillation of oxybutynin hydrochloride, Paraplegia 29(2):8490, 1991. 28. Mayo ME: The value of sphincter electromyography in urodynamics, J Urol 122(3):357-360, 1979. 29. Mayo ME, Chetner MP: Lower urinary tract dysfunction in multiple sclerosis, Urology 39(1):67-70, 1992. 30. McInerney PD, Vanner TF, Harris SA, et al: Permanent urethral stents for detrusor sphincter dyssynergia, Br J Urol 67(3):291-294, 1991. 31. McLellan FC: The neurogenic bladder, Springfield, IL, 1939, Charles C Thomas. 32. Montgomerie JZ, Chan E, Gilmore DS, et al: Low mortality among patients with spinal cord injury and bacteremia, Rev Infect Dis 13(5):867-871, 1991. 33. National Institute on Disability and Rehabilitation Research Consensus Statement: The prevention and management of urinary tract infection among people with spinal cord injuries, J Am Paraplegia Soc 15:194-204, 1992. 34. Sidi AA, Becher EF, Reddy PK, et al: Augmentation enterocystoplasty for the management of voiding dysfunction in spinal cord injury patients, J Urol 143(1):83-85, 1990. 35. Steers WD: Physiology and pharmacology of the bladder and urethra. In Walsh PC, Retch AB, et al, editors: Campbell’s urology, ed 7, Philadelphia, 1998, WB Saunders. 36. Steers WD, Meythaler JM, Haworth C, et al: Effects of acute bolus and chronic continuous intrathecal baclofen on genitourinary dysfunction due to spinal cord pathology, J Urol 148(6):1849-1855, 1992. 37. Subramonian K, Cartwright RA, Harnden P, et al: Bladder cancer in patients with spinal cord injuries, BJU Int 93(6):739-743, 2004. 38. Swierzewski SJI, Gormley EA, Belville WD, et al: The effect of terazosin on bladder function in the spinal cord injured patient, J Urol 151(4):951954, 1994. 39. Tanagho EA, Schmidt RA, Orvis BR: Neural stimulation for control of voiding dysfunction: a preliminary report in 22 patients with serious neuropathic voiding disorders, J Urol 142(2):340-345, 1989. 40. Webb RJ, Styles RA, Griffiths CJ, et al: Ambulatory monitoring of bladder pressure in low compliance neurogenic bladder dysfunction, J Urol 48:1477-1488, 1992.

CHAPTER 29 NEUROGENIC BOWEL: DYSFUNCTION AND REHABILITATION Gianna Rodriguez, John C. King, and Steven A. Stiens

Gastrointestinal dysfunction is most often characterized by a conglomeration of symptoms that most often indicate lower gastrointestinal impairment, including constipation, diarrhea, and fecal incontinence (FI). It can also present as upper gastrointestinal impairment heralded by bloating, nausea, early satiety, burning, and gaseousness. Neurogenic bowel dysfunction can be a clinically elusive impairment. It is often eclipsed by other, more noticeable associated motor deficits. Neurogenic bowel dysfunction itself can be particularly life-limiting if it is not thoroughly assessed and treated using rehabilitation principles. Interdisciplinary rehabilitative interventions focus on establishing a total management plan for bowel function, termed a bowel program, and for assisted defecation, known as bowel care.107 Sensation and mobility might be limited, affecting a person’s ability to anticipate the need for and to physically perform independent bowel care and hygiene. In spite of many abilities regained during the rehabilitation process, bowel care capabilities at the time of discharge are not always comparable to other skills that would be expected for a given level of function. Bowel incontinence is one of the greatest predictors of return to home for stroke survivors.29 In fact, bowel management has been found to be one of the areas of least competence among rehabilitated persons with spinal cord injury (SCI).14,50 More than one third of surveyed persons with SCI rated bowel and bladder dysfunction as having the most significant effect on their lives after SCI.51 In a recent Swedish review of medical problems after SCI, 41% of subjects rated bowel dysfunction as a moderately to severely life-limiting problem.74

Epidemiology Gastrointestinal dysfunction is frequently seen in persons with neurologic diseases who require rehabilitation. Besides the direct effects of neurologic disease on gut function, other factors can also play a huge role in the development of enteric problems, including debility, insufficient fluid intake, and the use of anticholinergics and other medications. Digestive tract problems in stroke, brain injury, multiple sclerosis, Parkinson’s disease, neuromuscular diseases, dysautonomias, peripheral nerve injuries, SCIs, and other neurologic disorders have been shown to be difficult and challenging to manage. Neurogenic bowel difficulties can be a primary disabling and handicapping feature for

patients with SCI, stroke, amyotrophic lateral sclerosis, multiple sclerosis, diabetes mellitus, myelomeningocele, and muscular dystrophy.* Neurogenic bowel dysfunction results from autonomic and somatic denervation, and produces FI, constipation, and difficulty with evacuation (DWE). These symptoms are common. The prevalence of FI and fecal impaction ranges from 0.3% to 5.0% in the general population. The prevalence of DWE ranges from 10% to 50% among the hospitalized or institutionalized elderly.100,115 Although many gastrointestinal disorders can contribute to FI or DWE, disorders that impair the extrinsic (sympathetic, parasympathetic, or somatic) nervous control of the bowel and anorectal mechanisms are more common among the patient populations seen by physiatrists.

Impact Living with nausea, vomiting, bloating, abdominal pain, constipation, diarrhea, or FI profoundly affects the quality of life. It significantly affects nutrition, overall health, and sense of well-being. Loss of voluntary control over bowel function alters every facet of a person’s life at home, at work, and in the community. The ability to spontaneously regulate and direct bowel function is essential for participation in everyday activities at home, work, or school. It plays a major role in one’s ability to create and maintain relationships. It has a significant effect on such activities as recreation or travel. Problems with constipation and FI can create considerable psychologic, social, and emotional trauma. FI decreases the return-to-home rates for stroke patients.49 Almost one third of persons with SCI report or exhibit worsening of bowel function 5 years beyond their injury, with 33% developing megacolon, suggesting inadequate long-term management.52,110 Recent evidence has shown some improvement in outcomes for SCI bowel management.67 When restoring normal defecation is not possible, social continence becomes the goal. Social continence is defined as predictable, scheduled, adequate defecations without incontinence at other times. It is often achievable by persons with neurogenic bowel dysfunction. Embarrassment and humiliation from FI frequently result *References 2, 20, 29, 61, 107, 119.

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SECTION 3  Common Clinical Problems

in extreme vocational and social disability. Vocational disability and excessive institutionalization add substantial costs to the care related to neurogenic bowel dysfunction. Nursing home costs are higher for patients with FI.115 A 1983 report estimated that $8 billion per year is spent in the United States for the care of fecally incontinent institutionalized patients.100

Brain

Spinal cord

Neuroanatomy and Physiology of the Gastrointestinal Tract In the last two decades, there has been significant advancement in the science of neurogastroenterology. This includes new discoveries in the basic physiology of the gastrointestinal tract and interactions with the brain and spinal cord, autonomic and enteric nervous systems, and somatomotor system (pharyngeal muscles and swallowing, pelvic floor muscles and defecation, continence and pelvic pain). Normal functioning of the stomach and intestines entails coordination of muscle contraction, digestion and absorption of nutrients, and regulation of blood flow. The neural schema of the gastrointestinal tract is much more complex than previously thought. Neural control of the gastrointestinal tract is an extremely organized and integrated hierarchy of mechanisms that involve the central nervous system (CNS; brain and spinal cord), autonomic nervous system (sympathetic and parasympathetic), and enteric nervous system (ENS) (Figures 29-1 and 29-2).123,126

Intrinsic Autonomic

Gut

Somatic

IS ES

Enteric Nervous System The ENS is a distinct system that has its own set of neurons that coordinate sensory and motor functions. In the ENS the ganglia are interconnected, which allows for integration and processing of data (as opposed to autonomic ganglia, which only serve as relay centers for stimuli transmitted from the CNS). There are three different types of neurons in the ENS based on function: sensory neurons, interneurons, and motor neurons.123,126 Sensory neurons perceive thermal, chemical, or mechanical stimuli and transform these sensations into action potentials that are conducted to the nervous system. Interneurons serve as conduits between the sensory and motor neurons. The numerous synapses between interneurons create a highly organized circuitry that processes sensory input from the gut and other parts of the nervous system, and integrates and generates reflex responses to these stimuli. Motor neurons are the final common pathway. They receive and translate signals to the gut (mucosa, muscle, vasculature) that affect digestive, interdigestive, and emetic functions based on the transmitters released.123,126 Automatic feedback control is present in the ENS, with the neurons being in close proximity to the stomach and intestines. This can be manifested as reflex circuits that systematize reflex responses to sensory signals, as integrative circuits that coordinate motor patterns (migrating motor complex, digestive activity, giant migratory contractions),123,126 or as a pattern-generating activity occurring when a “command neuron” is actuated with a resulting rhythmic, repetitive behavior.11,126

FIGURE 29-1 The bowel has three nervous systems: somatic, autonomic, and enteric. ES, External sphincter; IS, internal sphincter.

The ENS is the key to proper functioning of the entire gastrointestinal tract. This collection of highly organized neurons is situated in two primary layers: the submucosal (Meissner’s) plexus and the intramuscular myenteric (Auerbach’s) plexus. These plexi have an estimated 10 to 100 million neurons, plus two to three glial cells per neuron. The ENS glial cells resemble CNS astrocytes and are much less abundant than the 20 to 50 glial cells per neuron in the CNS.46 The coordination of segment-to-segment function is largely regulated by the ENS.121 The ENS also has its own blood-nerve barrier, similar to the blood-brain barrier of the CNS.24

Gastrointestinal Neurosensory System Enteric Nervous System Sensory Neurons The ENS relays chemical, mechanical, and thermal sensory information to the CNS through vagal afferents and spinal afferents. Vagal and spinal sensory neuron endings supply the muscle, mucosa, and ganglia of the ENS. Spinal sensory neurons also supply the serosa and mesentery and their blood vessels.11,47 Vagal afferent nerve endings act as chemical, thermal, and mechanical receptors. These directly monitor various changes in the gastrointestinal tract such as chemical milieu, temperature, muscle tension, and mucosal brushing.11,47

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

621

Vagus nerve

Sympathetic chain

T10 T11 T12 L1 L2

S1 S2 S3 S4 S5

Inferior mesenteric ganglion

Hypogastric nerve

Pelvic ganglion

Nervi erigentes Direct sacral root branches Pudendal nerve

Levator ani Puborectalis Internal Exernal

Anal sphincters

FIGURE 29-2  Neurologic levels and pathways for the sympathetic, parasympathetic, and somatic nervous system innervation of the colon and anorectum. Not shown is the enteric nervous system, which travels along the bowel wall from esophagus to internal anal sphincter and forms the final common pathway to control the bowel wall smooth muscle.

Chemical receptors are located in the mucosal epithelium of the stomach and intestinal lumen in close proximity with the lamina propria, constantly determining acidity, osmolarity, and the concentration of glucose, fatty acids, and amino acids.11,47 The existence of nociceptors (C or Aδ fibers) in the gastrointestinal tract has not been established.21,22,126 Temperature change in the lumen is detected by thermoreceptors that play a role in the brain’s perception and regulation of core temperature.126 Mechanical receptors are classified as intramuscular arrays or intraganglionic laminar endings. Intramuscular arrays are adjacent to the intramuscular interstitial cells of Cajal and run contiguously with the long muscle layers.43,47 Intraganglionic laminar endings that follow circular and longitudinal muscle fibers provide data on distention or contraction, and connect with myenteric ganglia.47,129 They are also found in rectal muscles and contribute to pelvic innervation.47,78 Spinal afferent nerve endings are distributed extensively throughout the bowel, relaying chemical, thermal, and mechanical information. In the mucosa they detect chemical changes related to injury, ischemia, infection, or

inflammation that contribute to pain and discomfort.47,66 Spinal nerve endings express receptors for bradykinin, adenosine triphosphate (ATP), adenosine, prostaglandins, leukotrienes, histamine, mast cell proteases, and serotonin 5-hydroxytryptamine3 (5-HT3). In the serosa and mesentery, they recognize visceral distention and contraction.70,82,83 Those that innervate the blood vessels and ENS ganglia release neurotransmitters that affect gastrointestinal blood flow, motility, and secretory reflexes.47,83 Mechanoreceptors (whether derived from vagal or spinal afferents) are either low or high in threshold.101 Lowthreshold receptors detect normal nonconscious and conscious sensations such as satiety, hunger, gaseousness, and nausea. High-threshold receptors detect distention or contraction beyond a set threshold and perceive painful stimuli, eliciting acute, sharp visceral pain. Actuation of both low- and high-threshold receptors contributes to the range of symptoms that are felt along the gastrointestinal tract.21,22,44,47 In the setting of inflammation or ischemia, chronic pain can develop from sensitization of both types of receptors and activation of silent receptors (notable only in pathologic states). Vagal afferents are primarily

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SECTION 3  Common Clinical Problems

implicated in the emetic response, and spinal afferents are primarily implicated in the sensation of nausea.44,47

Enteric Nervous System Relationship to the Spinal Cord and Brain Sensory information from vagal afferents in the ENS is relayed to the nodose ganglia (caudal ganglion of the vagus) and consequently to the nucleus tractus solitarius (NTS) and area postrema in the medullary area of the brainstem. The NTS and the area postrema send signals to the rostral centers in the brain.123,126 The brain processes the data and projects descending connections to the dorsal vagal complex. The brain also participates in vago-vagal reflex circuits that continuously monitor and promptly modify responses to changes in the chemical, thermal, and mechanical environment in the whole gut (mostly in the esophagus, stomach, duodenum, gallbladder, and pancreas). Sensory stimulation through this vagal circuit does not appear to reach the level of consciousness.123,126 Besides making connections with the NTS and the area postrema in the brainstem, vagal afferents synapse with the dorsal motor nucleus of the vagus and the nucleus ambiguus, creating the dorsal vagal complex. The incoming sensory information is integrated and shared with the forebrain and brainstem by the dorsal vagal complex. Brain coordination and influences (conscious and nonconscious) are translated to the dorsal vagal complex, where the dorsal motor nucleus of the vagus and nucleus ambiguus represent the efferent arm of the reflex pathway. It is the final common pathway from the brain responsible for precise control of muscular, glandular and circulatory responses of the gastrointestinal tract.123,124,126 Multiple neurotransmitters are involved in the intricate conduction of impulses between the neuronal circuits in the dorsal vagal complex. Approximately 30 are identified and include acetylcholine, biogenic amines, amino acids, nitric oxide, and peptides.123,126 Spinal afferents (splanchnic and pelvic) send sensory impulses to the dorsal root ganglia (or prevertebral sympathetic ganglia) that are then conducted to the dorsal horn (laminae I, II, V, X) of the spinal cord and the dorsal column nuclei.47,88 The dorsal column is thought to play a greater role in nociceptive transmission of messages from the gut than the spinothalamic or spinoreticular tracts. The conscious perception of pain in the digestive tract is largely mediated through spinal afferents. The spinal cord modulates the conduction of neural messages (both nociceptive and nonnociceptive) to the higher brain.47 Other somatic and visceral sensory stimuli from the vagina, uterus, bladder, colon, and rectum are conveyed through the dorsal horn and dorsal column in the spinal cord as well. Likewise, somatic afferents supply sensory input from the muscles of the pelvic floor through the pudendal nerve to the sacral region of the spinal cord.10,47,88,89 Brain centers modulate the nociceptive impulses from the bowel that are relayed to the dorsal horn of the spinal cord. These descending pathways are facilitatory, inhibitory, or both, based on the visceral stimulus, and can alter the perception

of pain in the digestive tract.47,97 The neurotransmitters serotonin, noradrenalin, and dopamine are released by these descending pathways as they synapse with the spinal cord.126 The secondary somatosensory cortex and, to a lesser extent, the paralimbic and limbic areas (anterior insular, anterior and posterior cingulate, prefrontal and orbitofrontal cortices) mediate emotional, volitional, and psychologic responses to sensory input from the gut. These are manifested by abdominal pain, anorexia, nausea, vomiting, hyperphagia, constipation, or diarrhea.47,73,104 The somatosensory cortex regulates the awareness and recognition of pain, and the paralimbic and limbic areas contribute to the cognitive and affective aspects of pain.47,104,126 Data from the brain and descending vagal pathways are conducted to the spinal cord, and then with the preganglionic neurons in the thoracolumbar area (modulates the sympathetic response) and the sacral area (modulates the parasympathetic response). Sympathetic or parasympathetic output is translated to the neurons in the ENS circuitry, which can be excitatory or inhibitory to motor neurons, gastric or digestive glands, and secretory mechanisms.47,126

Gastrointestinal Neuromotor System The muscles of the gastrointestinal tract carry out essential functions throughout the gut, including propulsion, grinding, mixing, absorption, storage, and disposal. These muscles are composed of “self-excitable” smooth muscles that contract in an all-in-one manner. These smooth muscles spontaneously responds to stretch and can be independent of neural or endocrine control. The interstitial cells of Cajal act like a pacemaker and allow propagation of electrical slow waves into the circular muscle layer, which generates spreading muscle contraction. These smooth muscles act like an electrical syncytium where action potentials are conducted in three dimensions from one smooth muscle fiber to another through gap junctions.47,126 The gastrointestinal tract muscles respond to influences of the vagal efferents and the ENS microcircuitry based on excitatory or inhibitory innervation of motor neurons. Contraction is mediated by the release of excitatory neurotransmitters by vagal afferents at the neuromuscular junctions, acetylcholine (at the muscarinic receptor), and substance P (at the neurokinin-1 receptor).26,47,82,126 Conversely, the release of nitric oxide, ATP, and vasoactive intestinal peptide from the inhibitory motor neurons (which express the serotonergic 5-HT1 receptor) impedes contractile activity and facilitates relaxation. The aboral direction of propulsive activity throughout the digestive tract is achieved by segmental inactivation of inhibitory motor neurons distally.15,16,47,58,126 Contraction can only occur in the segments where the inhibitory motor neurons are inactivated. With passing of the food bolus or stool, the esophageal and internal anal sphincters (smooth muscle sphincters), and inhibitory motor neurons are usually shut off and are inactivated. During vomiting, however, the inhibitory motor neurons are deactivated in the opposite direction.47,126 The sympathetic and parasympathetic nervous systems seem to modulate the ENS, rather than directly controlling the smooth muscles of the bowel.121 The smooth muscles

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

of the bowel also have their own electromechanical automaticity, which is directly modulated by the inhibitory control of the ENS.24,46 Sympathetic nervous system stimulation tends to promote the storage function by enhancing anal tone and inhibiting colonic contractions, although little clinical deficit occurs from bilateral sympathectomy.32 Parasympathetic activity enhances colonic motility, and its loss is often associated with DWE, including impactions and functional obstructions, such as Ogilvie’s pseudo­ obstructive syndrome.32 The ENS and sympathetic postganglionic neurons transmit excitatory or inhibitory messages to secretomotor neurons. These secretomotor neurons release acetylcholine and vasoactive intestinal polypeptide when there is excitatory activation from paracrine stimulation by mucosal and submucosal cells such as enterochromaffin cells, mast cells, and other immune and inflammatory cells. Acetylcholine and vasoactive intestinal polypeptide are released at the neuroepithelial and neurovascular junctions. This promotes secretion into the gut of water, sodium chloride, bicarbonate, and mucus drawn from the intestinal glands. In addition, dilatation and an increase in blood flow occur with the release of nitric oxide from the vascular endothelium.6,13,47 The inhibitory influence reduces neuronal firing from secretomotor neurons by hyperpolarization of membranes. Sympathetic release of norepinephrine from nerve endings of the α2-noradrenergic receptors inhibits secretomotor actuation, preventing the release of excitatory neurotransmitters. As a result, there is a decrease in secretion of water and electrolytes into the lumen and a congruent shunting of blood from the splanchnic to systemic circulation.47,76,91

Gastric Motility Based on its motility pattern the stomach is divided into an upper and lower portion. The upper portion (fundus) has sustained, low-frequency contractions and has a tonic pattern. The lower portion (antrum) has intermittent, powerful contractions and has a phasic pattern. The fundus acts as reservoir and accommodates incoming food, which inhibits contraction and allows the stomach to stretch without a significant increase in pressure. The antrum is a mixer that generates propulsive waves that accelerate as food is propagated towards the pylorus. The amount and consistency of food in the fundus regulates excitatory and inhibitory influences and adjustments to volume and pressure.47,69

Intestinal Motility The ENS is designed to control the various patterns of motility in the intestinal tract. The interdigestive migrating motor complex pattern occurs during fasting in the stomach and the small intestine.47,120 It seems to be influenced by the hormone motilin, and is responsible for removal of waste from the intestinal lumen throughout the fasting period.47,77 When a meal is ingested, the postprandial segmentation (“mixing”) pattern of motility commences as digestion transpires. The brainstem sends signals that are transmitted to vagal efferents, which convert migrating motor complex motility to segmentation motility with the increase in bulk and nutrients, especially lipids

623

(medium-chain triglycerides). This subsequently becomes peristaltic motility, which is propagated through brief segments of intestine at a time.30,47 Peristaltic activity gradually evolves into powerful contractions sustained through long portions of circular muscle along the small and large bowel. These “giant migratory contractions” (GMCs) propel waste through the lumen, particularly in the large intestine.47,59,99

Motility of the Anus, Rectum, and Pelvic Floor Normal defecation and maintenance of fecal continence entail a highly coordinated mechanism that involves the levator ani, puborectalis, and the external (EAS) and internal anal sphincter (IAS) muscles. The pelvic floor is composed of the levator ani, the underlying sheets of which form a sling. The levator ani, puborectalis, and EAS are skeletal muscles that constantly maintain tone and sustain pelvic organs in place against the forces of gravity.35,47 Simultaneous contraction of these muscles prevents the involuntary loss of stool and helps maintain the regular pattern of defecation.41,47

Physiology of Normal Defecation The colon is a reservoir for food waste until it is convenient for elimination. It also acts as a storage device as long as the colonic pressure is less than that of the anal sphincter mechanism. Fecal elimination occurs when colonic pressure exceeds that of the anal sphincter mechanism. Other functions of the colon are to reabsorb fluids (up to 30 L/ day can be reabsorbed from the large and small bowel walls, with typically only 100 mL of water loss in feces) and gases (90% of the 7 to 10 L of gases produced by intracolonic fermentation is absorbed rather than expelled). The colon also provides an environment for the growth of bacteria needed to assist in digestion, and serves to absorb certain bacterial breakdown products as well.48 The layers of the colon wall are depicted in Figure 29-3. The rectum is usually empty until just before defecation. Perception of rectal contents and pressures105 is essential for signaling voluntary contraction of the anal sphincter. Normal defecation begins with reflexes triggered by rectosigmoid distention produced by approximately 200 mL of feces (Figure 29-4).94 A rectorectal reflex occurs in which the bowel proximal to the distending bolus contracts and the bowel wall distally relaxes, serving to propel the bolus further caudad. Reflex relaxation of the IAS also occurs, which is enhanced by, but does not require, an extrinsic nerve supply. This relaxation, called the r­ ectoanal inhibitory reflex, correlates with the urge labeled “the call to stool.”121 One can then volitionally contract the levator ani to open the proximal anal canal and relax the EAS and puborectalis muscles. This allows a straighter, shorter, and more open anorectal passage (see Figure 29-4), which permits the bolus to pass. Increasing the intraabdominal pressure by squatting and by Valsalva’s maneuver assists bolus elimination. For 90% of normal individuals, only the contents of the rectum are expulsed, whereas 10% will clear the entire contents of the left side of the colon from the splenic flexure distally.33

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SECTION 3  Common Clinical Problems

One can elect to defer defecation, however, by volitionally contracting the puborectalis muscle and EAS. The reflexive IAS relaxation subsequently fades, usually within 15 seconds, and the urge resolves until the IAS relaxation is again triggered. The rectal wall accommodates to the bolus by decreasing its wall tension with time, resulting in less Subserosal plexus

Adrenergic neuron

Serosa

Myenteric plexus (Auerbach)

Longitudinal layer

Deep muscular plexus

Circular layer

Submucous plexus (Meissner)

Muscularis mucosae

Artery Mucosal plexus

Mucosa FIGURE 29-3  A transverse section of the gut, showing the enteric plexus and the distribution of adrenergic neurons. Note the ganglionic plexuses of Auerbach and Meissner. The deep muscular plexus contains a few ganglia, the subserosal contains an occasional ganglion, and the mucosal plexus shows none. The adrenergic fibers are all extrinsic and arise from the prevertebral sympathetic ganglia. The adrenergic fibers are distributed largely to the mesenteric, submucous, and mucosal plexus and to blood vessels. (From Goyal RK, Crist, JR: Neurology of the gut. In: Sleisenger MH, Fordtram JS, editors: Gastrointestinal disease, Philadelphia, 1989, WB Saunders, with permission.)

A

Holding • Puborectalis, external and internal anal sphincters contracted

B

sensory input and less reflex triggering from that particular accommodated bolus. This continence and reflex process is somewhat analogous to the function of the striated external urethral sphincter in volitional control of urinary voiding (see Chapter 28). The EAS generally tenses in response to small rectal distentions via a spinal reflex, although reflexive relaxation of the EAS occurs in the presence of greater distentions.105 These spinal cord reflexes are centered in the conus medullaris and are augmented and modulated by higher cortical influences. When cortical control is disrupted, as by SCI, the EAS reflexes usually persist and allow spontaneous defection. During sleep the colonic activity, anal tone, and protective responses to abdominal pressure elevations are all decreased, while rectal tone increases.24,121 The gastrocolonic response or gastrocolic reflex refers to the increased colonic activity (GMCs and mass movements) in the first 30 to 60 minutes after a meal. This increased colonic activity appears to be modulated both by hormonal effects, from release of peptides from the upper gastrointestinal tract (gastrin, motilin, cholecystokinin) that increase the contractility of the colonic smooth musculature, and by a reduction in the threshold for spinal cord–mediated vesicovesical reflexes.24 Upper gastrointestinal receptor stimulation also results in increased activity in the colon, possibly because of reflexively increased parasympathetic efferent activity to the colon. The possibility of a purely ENS-mediated activation exists, although the small bowel and colon motor activities do not seem to be synchronized. In persons with SCI the measured increase in colonic activity after a meal is blunted as compared with that in normal subjects.24 The gastrocolonic response is often used therapeutically, even in patients with SCI, to enhance bowel evacuation during this

Initiation • Puborectalis and external anal sphincter relax • Levator ani, abdominals, and diaphragm contract

C

Completion • Internal and external anal sphincters relax • Rectum contracts

FIGURE 29-4  A, Defecation is prevented by a statically increased tone of the internal anal sphincter (IAS) and puborectalis, as well as by the mechanical effects of the acute anorectal angle. Dynamic responses of the external anal sphincter (EAS) and puborectalis to rectal distention reflexes or increased intraabdominal pressures further impede defecation. B, To initiate defecation, the puborectalis muscle and EAS relax while intraabdominal pressure is increased by Valsalva’s maneuver, which is facilitated by squatting. The levator ani helps reduce the acute anorectal angle to open the distal anal canal to receive the stool bolus. C, Intrarectal reflexes result in continued IAS relaxation and rectal propulsive contractions, which help expel the bolus through the open canal. (Modified from Schiller LR: Fecal incontinence. In: Sleisenger MH, Fordtran JS, editors: Gastrointestinal disease, Philadelphia, 1993,  WB Saunders.)

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

30- to 60-minute postprandial time frame.1,34 Occasionally certain foods can serve as trigger foods that are especially likely to induce bowel evacuation shortly after consumption. The resting anal canal pressure is largely determined by the angulation and pressure at the anorectal junction by the puborectalis sling and smooth muscle IAS tone. Continence is maintained by the anal sphincter mechanism,81,107 which consists of the IAS, EAS, and puborectalis muscle.81 Only about 20% of the anal canal pressure is due to the static contraction of the somatically innervated striated EAS.9 The EAS and puborectalis muscle are the only striated skeletal muscles whose normal resting state is tonic contraction, and these muscles consist mainly of slowtwitch, fatigue-resistant type I fibers (unlike the situation in nonupright animals such as the cat or dog, in which these muscles consist of predominately type II fibers).9 Anal pressure can be increased volitionally by contracting the EAS and puborectalis muscles. Maximum volitional squeeze pressures, however, are not as high as can be generated reflexively against Valsalva pressure. The EAS is physically larger than the IAS, and its contraction is under both reflex and volitional control. The volitional control is learned during the course of normal maturation. Normal baseline reflex action of the anorectal mechanism allows spontaneous stool elimination.102 The EAS is innervated by the S2 through S4 nerve roots via the pudendal nerve, and the puborectalis muscle is innervated by direct branches from the S1 to S5 roots (see Figures 29-1 and 29-2).92 The remarkable degree of learned EAS coordination allows the selective discrete passage of gas while juggling a variable mixture of solids, liquids, and gases.

Pathophysiology of Gastrointestinal Dysfunction A whole range of neurologic diseases affecting central, peripheral, and intrinsic enteric nervous innervation can cause disorders that affect various segments of the bowel. These are predominantly characterized by disturbances in gastroesophageal, small or large intestinal motility and by disturbances in sensation. Symptoms of dysphagia, vomiting, bloating, abdominal discomfort and pain, constipation, and incontinence have been described in individuals with neurologic ailments.5,18,19,93 Exact and detailed pathophysiologic mechanisms of gastrointestinal dysfunction in the various neurologic diseases are not very well understood. Recent studies, however, have been able to identify various mechanisms of symptom production that might facilitate therapeutic strategies.

Nausea,Vomiting, and Bloating The syndrome of nausea, vomiting, bloating, and early satiety in the setting of neurologic conditions without mechanical obstruction can herald motility problems in the gastrointestinal tract. Neurologic dysfunction that affects the inhibitory motor neurons in the ENS at any level of the neural axis from the brain, spinal cord, afferent nerves, or efferent nerves can lead to spasticity of the gastric or intestinal and colonic musculature. The digestive muscles perform as an electrical syncytium. Inhibitory

625

motor neurons allow propagation of contractile activity in an organized, segmental, and aboral pattern. When inhibitory motor neurons are inactivated or destroyed by disease, the circular muscles contract continuously and nonsystematically. These contractions are incapable of forward propulsion, causing functional obstruction.123,125 This can be manifested as dysphagia, gastroparesis, or chronic intestinal or colonic pseudoobstruction, which might be associated with anorexia, abdominal pain, and diarrhea and constipation (these symptoms can occur together). Inhibitory motor neurons can be affected by autonomic neuropathy, dysfunction of neurons in the myenteric plexus, or degeneration of smooth muscle.*

Abdominal Pain and Discomfort Abdominal pain and discomfort arise from gastrointestinal tract distention and powerful contractions. High-threshold and silent mechanoreceptors sense severe distention and intense contractions when there is ischemia, injury, or inflammation. Mechanical and chemical irritants stimulate mechanoreceptors in the ENS and translate signals to the brain and spinal cord from muscle stretching and contractions.11,89,125 The presence and persistence of ischemia, injury, and inflammation can elicit abdominal pain from the following mechanisms: 1. The spinal afferent nerves express receptors for inflammatory mediators. Release of bradykinin, ATP, adenosine, prostaglandins, leukotrienes, histamine, and mast cell proteases heighten the sensitivity of the spinal sensory endings.125 2. Amplified levels of 5-HT3 released from hyperactive 5-HT3 receptors at the vagal and spinal nerve endings facilitate production of pain. On the other hand, there can be an excessive induction of serotonergic receptors by 5-HT3 because of a defective serotonin transporter.56,70,125 3. Central sensitization occurs in the spinal cord from constant stimulation of the C fibers in the dorsal horn and dorsal column nuclei. Neurons become hypersensitive and are persistently activated. The “wind-up” phenomenon develops with the actuation of N-methyl-d-­aspartate (NMDA) receptors from the release of ­glutamate from C fibers. The reactive state of dorsal horn and dorsal column neurons becomes a memory imprint in the spinal cord.3,4,125 4. Mechanoreceptors in the gut wall can receive a deluge of signals from mechanical irritation. This barrage of impulses conducted to the brain can be inferred as nociceptive because of the overwhelming stimulation.125,126 5. The descending facilitative modulation of the brain through the dorsal horn can promote recognition of ordinary sensory input as innocuous. The brain misreads normal nonconscious signals relayed from mechanoreceptors as noxious.97,125

Diarrhea Neurologic dysfunction can present with frequent passage of watery stools. Diarrhea occurs when there is overstimulation of secretomotor neurons by histamine from *References 7, 27, 54, 55, 106, 116, 125.

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SECTION 3  Common Clinical Problems

inflammatory and immune-mediated cells in the mucosa and submucosa, or overstimulation by vasoactive intestinal peptide and serotonin from mucosal enterochromaffin cells, or overstimulation by all three substances. Moreover, these substances influence presynaptic inhibitory receptors to block the release of norepinephrine from the postganglionic sympathetic fibers that inhibit secretomotor neurons.124,125 Bacterial overgrowth in the gut can be a factor in chronic inflammatory states presenting with diarrhea.7,27

Defecation Dysfunction Constipation Constipation can be a huge enigma in neurologic states. Infrequent, incomplete emptying of hard stools is due to decreased water and electrolyte secretion into the lumen, resulting from reduced excitation of the secretomotor neurons in the ENS. Norepinephrine released by sympathetic stimulation inhibits the firing of secretomotor neurons by hyperpolarization. Release of excitatory neurotransmitters is reduced in the secretory epithelium, decreasing the secretion of water and electrolytes.125,126 A lack of rectal sensation and a decreased urge to defecate can be strongly associated with constipation in various conditions that present with lesions in the brain, spinal cord, sacral nerves, and hypogastric and pudendal nerves. Outlet obstruction can ensue because of delayed colonic transit times and lack of perineal and rectoanal sensation.125 Fecal Incontinence True FI, described as an unconscious loss of stool, often occurs in neurologic conditions with lesions affecting the lumbar spinal cord, cauda equina, S2–S4 nerves, pudendal nerve, and pelvic floor nerves. Denervation leads to impaired perineal and rectoanal sensation, aberrant contraction, loss of tone, and weakening of the pelvic floor muscles and the EAS. These contribute to unexpected loss of stool and abnormal defecation, and diminished support for pelvic structures.25,47 Parasympathetic augmentation can occur and might further complicate matters, since it contributes to weakness in the IAS and increases the risk for incontinence. It is always important to rule out overflow incontinence resulting from constipation.

Upper Motor Neurogenic Bowel Any destructive CNS process above the conus, from SCI to dementia, can lead to the upper motor neurogenic bowel (UMNB) pattern of dysfunction. Spinal cortical sensory pathway deficits lead to a decreased ability to sense the urge to defecate. Most persons with SCI, however, sense a vague discomfort when excessive rectal or colonic distention occurs. It has been reported that 43% of persons with SCI have chronic complaints of a vague discomfort caused by abdominal distention that eases with bowel evacuation.80,110 These sensations might be mediated by autonomic nervous system afferent fibers bypassing the zone of SCI via the paraspinal sympathetic chain, or by means of vagal parasympathetic afferents.

Colonic compliance and sphincter tone102 have been experimentally evaluated in subjects with SCI. Studies of colonic compliance in response to a continuous infusion of saline initially suggested rapid pressure rises and a ­hyperreflexic response.87,117 More recent studies have demonstrated normal colonic compliances in subjects with SCI who have UMNB.79,90 Passive filling of the rectum leads to increases in the resting sphincter tone.114 These increases are associated with increased EAS pressure development resulting from sacral reflexes that can be abolished by pudendal block.9 This form of rectal sphincter ­dyssynergia has unfortunately been labeled decreased colonic compliance, even though intermittent or slow filling in the rectum appears to be associated with normal bolus accommodation and pressure relaxation.79,100 This contrasts with “true” decreased rectal wall compliance caused by fibrosis resulting from ischemia or inflammation, where there is no accomodation and relaxation of the rectal wall regardless of flow rates. Colonic motility and stool propulsion are known to be affected by SCI. De Looze et al.29 used a questionnaire method to study subjects with SCI levels above L2, and found 58% of subjects with chronic SCI had constipation (defined as two or less bowel movements per week or the requirement for digital evacuation). Only 30% (p = 0.002) of patients with paraplegia below T10 and above L2, however, were prone to constipation. Actual stool propulsion was studied later by Krogh et al.71 using swallowed markers and serial radiographs. In subjects with chronic SCI with supraconal lesions, transit times were significantly prolonged in the ascending, transverse, and descending colon and rectosigmoid. Total gastrointestinal transit time averaged 3.93 days (control subjects, 1.76 days) for chronic complete SCI above the conus. In an attempt to demonstrate a difference that might have been conferred by sympathetic innervation, mean total gastrointestinal transit times were compared in patients with lesions above T9 (2.92 ± 2.41 days) and in those with lesions from T10 to L2 (2.84 ± 1.93 days). No significant differences could be found even with comparison of transit times for individual colonic segments. Subjects with SCI who had complete upper motor neuron bowel lesions were studied during the acute phase (5 to 21 days) after SCI. These same patients were reevaluated 6 to 14 months later. Total gastrointestinal transit time was longer during the acute rather than the chronic phase. The upper motor neuron neurogenic colon tended to have slower transit throughout the colon, with less severe rectosigmoid dysfunction.71 Patients with UMNB have spared reflex arc control of the rectosigmoid and pelvic floor. IAS relaxation on rectal distention occurs in persons with SCI as well as in neurologically intact persons. Sufficient rectal distention might cause the EAS to completely relax, resulting in expulsion of the fecal bolus. Rectal sphincter dyssynergia does not necessarily correlate with bladder sphincter dyssynergia, but it often results in DWE.92 The protective vesicorectal reflex, in which the EAS pressure increases in response to increased intraabdominal pressure, is usually intact (Table 29-1).9 Patients with UMNB also have normal or increased anal sphincter tone, intact anocutaneous (or “anal wink”) and bulbocavernosus reflexes,107 a palpable puborectalis muscle sling, and normal anal verge appearance (Figure 29-5).

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

627

Table 29-1 Features of Colorectal Function in Normal Subjects and in Those With UMNB, UMNB With Posterior Rhizotomy, and LMNB UMNB and Posterior Rhizotomy

Normal

UMNB

LMNB

Bowel dysfunction

Normal colon activity and defecation

Chronic intractable constipation, fecal impaction, reflex defecation with or without incontinence

Chronic constipation; no reflex defecation

Chronic constipation; fecal impaction maximal in the rectum

Transit time (cecum to anus)

12-48 hr

Prolonged >72 hr

Very prolonged unless sacral nerve stimulator used

Prolonged >6 days, especially left side of colon

Colonic motility at rest

GMCs approximately 4 per 24 hr

GMCs might be reduced in frequency

Reduced GMCs

Reduced GMCs

Colonic motility in response to stimuli

GMCs facilitated by defecation, exercise, and food ingestion

Less GMC facilitation by defecation, exercise, or food ingestion

Less GMC facilitation by defecation, exercise, or food ingestion

Less GMC facilitation by defecation, exercise, or food ingestion

Resting tone

>30

>30

Normal

Reduced

Volitional squeeze

>30 (up to 1800)

Absent

Absent

Absent

Rectal compliance

Normal

Normal but sigmoid compliance decreased

Normal or increased

Rectum dilated; increased distention volume; increased compliance

Effect on IAS

Normal rectoanal inhibitory reflex

Normal rectoanal inhibitory reflex

Normal rectoanal inhibitory reflex

Normal rectoanal inhibitory reflex

Effect on EAS

Causes contraction

Causes contraction

No contraction

No contraction

Sensory perception threshold

50 mm Hg)

Present

Absent

Absent

Reflex defecation

Yes

Yes

Impaired

lmpaired

Perianal sensation (cutaneous sensation of touch, pinprick)

Normal

No sensory perception

No sensory perception

Loss of perianal and buttock sensation resulting from injury to sacral nerves

Anocutaneous reflex (“anal wink”)

Present

Present; might be increased

Absent

Absent because of injury to afferent or efferent sacral pathways

Bulbocavernosus reflex

Present

Present; might be increased

Absent

Absent

Anal appearance

Normal

Normal

Normal

Flattened, scalloped, because of loss of EAS bulk

Anal Sphincter Pressure (mm Hg)

Rectal balloon distention

Valsalva Protective Reflex

Modified from Banwell JG, Creasey GH, Aggarwal AM, et al: Management of the neurogenic bowel in patients with spinal cord injury. Urol Clin North Am 20(3):517-526, 1993; and Schiller LR: Fecal incontinence. In: Sleisenger MH, Fordtran JS, editors. Gastrointestinal disease, Philadelphia, 1993, WB Saunders. EAS, External anal sphincter; GMCs, giant migratory contractions; IAS, internal anal sphincter; LMNB, lower motor neurogenic bowel; UMNB, upper motor neurogenic bowel.

Lower Motor Neurogenic Bowel Polyneuropathy, conus medullaris or cauda equina lesions, pelvic surgery, vaginal delivery, or even chronic straining during defecation can impair the somatic innervation of the anal sphincter mechanism. Persons with benign joint hypermobility syndrome might be more predisposed to these lesions.84 These conditions can also produce sympathetic and parasympathetic innervation deficits. If an

isolated pudendal insult has occurred, colonic transit times are normal and FI predominates. Distal colonic sluggishness can occur as a result of loss of parasympathetic supply. Segmental stool transit studies demonstrate prolonged transit through the rectosigmoid segments resulting from the lack of direct innervation from the conus.71 The addition of constipation and DWE to FI compounds

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SECTION 3  Common Clinical Problems

B

Gastrointestinal Dysfunction in Common Neurologic Disorders Brain Disorders

A

D

C FIGURE 29-5  Upper motor neurogenic bowel presents an appearance similar to normal (A, rear view; B, profile from above). Anal contour of the lower motor neurogenic bowel (C, rear view; D, profile from above), with its atrophic external anal sphincter, shows a flattened, scalloped-appearing anal area.

difficulties. This is an especially problematic combination because the accumulation of a large amount of hard stool that can result from such colonic inertia can overstretch the weakened anal mechanism. This can result in a gaping, patulous, incompetent anal orifice, often with associated rectal prolapse. The denervation, atrophy, and overstretching of the EAS and IAS lead to loss of the protective IAS tone, which can result in stool soilage from the increased abdominal pressures associated with everyday activities. Rectal distention leads to the expected IAS relaxation, but attenuated or absent EAS protective contractions can result in FI or fecal smearing whenever boluses are present at the rectum. The presence of a large bolus in the rectal vault can further compromise the rectoanal angulation at the pelvic floor and contribute to paradoxical liquid incontinence around a low impaction, called the ball-valve effect.9,112,127 Patients with lower motor neurogenic bowel (LMNB) dysfunction have decreased anal tone because of the smooth muscle that makes up the IAS. If no tone is found initially on inserting the examining finger, the examiner should wait up to 15 seconds to allow IAS reflex relaxation to recover and restore tone. Chronic overstretching has probably occurred if tone does not return. The anal-to-buttock contour typically appears flattened and “scalloped” (see Figure 29-5) because of atrophy of the pudendal-innervated pelvic floor muscles and EAS.9 The anocutaneous reflex is absent or decreased (depending on the completeness of the lesion). The bulbocavernosus reflex is also weak if present (see Table  29-1). The anal canal is shortened (as compared with the normal 2.5- to 4.5-cm length), and the puborectalis muscle ridge might not be palpable. Excessive perineal descent and even rectal prolapse can occur with Valsalva’s maneuver.

Strokes (ischemic or hemorrhagic), cerebral trauma, masses, infections, and other lesions cause a whole range of neurologic damage and complications to many areas of the brain. These disorders commonly present with dysphagia, delays in gastric emptying and ileus (intestinal pseudoobstruction), constipation, and FI. Brainstem or cranial nerve involvement often causes dysphagia. Studies report that dysphagia occurs in approximately 45% of patients with stroke during the acute phase. Cerebral edema and increased intracranial pressure play a role in gastrointestinal ulceration, gastroparesis, and ileus through unknown mechanisms. Depending on the severity of the cerebral or brainstem involvement, dysphagia and ileus progressively improve. About 23% of patients with stroke were shown to have FI in stroke research, and constipation has been observed to be very common in clinical practice.5,19,53,93

Parkinson’s Disease and Parkinson’s-Plus Diseases Parkinson’s disease and Parkinson’s-plus diseases (multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration) are neurodegenerative diseases that affect various parts of the nervous system including the cerebral cortex, basal ganglia, brainstem, cerebral cortex, cerebellum, and spinal cord. They are characterized by dementia, muscle rigidity, bradykinesia, resting tremor, dystonia, shuffling gait, and dysphagia. They also have dysautonomia, which is manifested as orthostatic hypotension, sexual incompetence, gastric dysmotility, and constipation (see Chapter 51). Up to 50% of persons with Parkinson’s disease have been found to have dysphagia and problems with defecation in a study of 98 persons. In this group, 52.1% had dysphagia, 28.7% had constipation, and 65% had problems with defecation. These gastrointestinal problems can be severe enough to compromise nutrition and cause severe morbidity.25,36-38,72,95

Multiple Sclerosis Multiple sclerosis is a demyelinating disease caused by an autoimmune process that involves different regions of the brain and spinal cord (see Chapter 52). Presentation can be any neurologic sign or symptom, which can consist of paresis, spasticity, ataxia, paresthesias, visual problems, cognitive deficits, mood disorders, dysphagia, gut dysmotility, urinary incontinence or retention, FI, diarrhea, or constipation. In a study of patients with multiple sclerosis, 68% were reported to have gastrointestinal problems, with 43% having constipation and 53% having FI. The bowel and bladder problems in multiple sclerosis are believed to be caused by supraspinal or spinal lesions associated with autonomic sympathetic and parasympathetic system impairment.19,25,42,118

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

Spinal Cord Disorders Trauma, masses, infection, hemorrhage, or ischemia involving the spinal cord and causing tetraplegia or paraplegia, primarily affects colonic motility and perineal and anorectal sensation and function during the acute and chronic phases (see Chapter 55). Upper gastrointestinal tract problems resulting from disorders of the spinal cord, however, are increasingly being recognized. Depending on the level of the injury, brain and autonomic modulation of the ENS is impaired. The bowel dysfunction is principally one of motility rather than secretion or absorption. The upper digestive tract is more involved in persons with tetraplegia rather than with paraplegia, and is characterized by gastroparesis, impaired gastric emptying, and delayed gastrointestinal times. Dysphagia is common in persons with cervical cord lesions during the acute phase, and often eventually resolves. Gastric and duodenal ulcerations have been prevalent as well in persons with myelopathy. Across all levels of injury, there is a loss of voluntary control over bowel movements, with a scenario of constipation or FI. For lesions occurring above the conus medullaris (above T12), rectoanal reflexes are preserved with the sphincters being spastic. This is usually called the UMNB. Lesions below the conus medullaris (below T12) display flaccidity of the sphincters with loss of reflexes. This is referred to as the lower motor neuron bowel (LMNB).*

Peripheral Neuropathy Peripheral neuropathy has multiple causes including metabolic, viral, traumatic, toxic, metastatic, and genetic (see chapter 47). Sensory and motor deficits are associated with autonomic involvement. Disturbances in gastrointestinal transit are most often caused by peripheral neuropathies. Motility problems might result in diarrhea (from bacterial overgrowth) or in constipation. Well-known complications of diabetes include gastroparesis and decreased intestinal motility primarily from autonomic dysfunction. In paraneoplastic syndromes caused by small cell carcinoma of the lung or pulmonary carcinoid, immunoglobulin G antibody against enteric neurons has been found to be responsible for esophageal dysmotility, gastroparesis, and constipation. Injury to the pudendal nerve (from childbirth or persistent and protracted straining), S2–S4 nerve root lesions, or cauda equina compromise under FI and abnormal defecation.5,18,24,86

Comprehensive Evaluation History A comprehensive investigation for nausea, vomiting, bloating, early satiety, abdominal pain, diarrhea, constipation, and FI must be completed.27,50,109 The gastrointestinal history should not only review for cardinal symptoms, but should also address the patient’s general neuromuscular and gastrointestinal function. A detailed review of the *References 5, 12, 19, 23, 62, 123.

629

patient’s bowel program includes an assessment of fluids, diet, activity, medications, and aspects of bowel care.65 Careful consideration must be given to drugs that seriously decrease gastrointestinal motility such as opiates, anticholinergics, tricyclics, antihistamines, calcium channel blockers, and phenothiazines.27,50,109 A review of the technique and outcome of bowel care should include a description of schedule, initiation method (chemical or mechanical stimulation), facilitative techniques, time requirements, and characteristics of stool results.107 The history should include premorbid bowel pattern information such as defecation frequency, typical time(s) of the day, associated predefecatory activities, bowel medications and techniques or trigger foods, and stool consistency. It is important to elicit any history of premorbid gastrointestinal disease or dysfunction. The presence of gastrointestinal sensations or pain, warning sensations for defecation, a sense of urgency, and an ability to prevent stool loss during Valsalva activities such as laughing, sneezing, coughing, or transfers should be noted. Excessively large-caliber, hard stool can be ascertained by a history of toilet plugging.86 The patient’s goals and willingness to alter prior bowel patterns or management need to be established.63 The approach to the problems associated with neurogenic bowel is the same as for all issues that confront the patient in the rehabilitation process. All aspects of impairment and disability that limit a person’s ability to maintain continence and volitionally defecate must be assessed within the perspective of the entire person. This includes an appraisal of the patient’s activity level, bowel pattern, and dietary habits. All aspects of personal performance should be addressed in person-centered rehabilitation, with the overall goal of maximizing independence in bowel management or direction of a bowel program.98,100

Physical Examination The physical examination should include the gastrointestinal system and the associated parts of the musculoskeletal and nervous systems required for independent management of the bowel program. The examination should be completed at the onset and then annually for SCI.65 The purpose of the examination is to detect functional changes, screen for complications, and identify any new masses or lesions. The abdomen should be inspected for distention, hernias, and other abnormalities. Careful assessment for the presence or absence of bowel sounds should be done. Percussion and auscultation should precede palpation for masses and tenderness. With the abdomen relaxed, the examiner transabdominally palpates the colon for hard stool. Palpable hard stool should not be present on the right side of the abdomen (ascending colon). Gastroparesis and intestinal pseudoobstruction present with a distended abdomen that is tympanitic with hypoactive bowel sounds, and with generalized abdominal tenderness (which can be accompanied by autonomic dysreflexia in persons with SCI). The patient can show signs of malnutrition and dehydration, including loss of weight, pale skin, dry mucous membranes, poor skin turgor, orthostatic hypotension, and tachycardia.33,65,117

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SECTION 3  Common Clinical Problems

trauma secondary to bowel care.107 A flat plate radiograph of the abdomen can be helpful to rule out impaction,127 megacolon, obstruction, and a perforated viscus.

The rehabilitation evaluation should be interdisciplinary in approach and include assessment not only of colon and pelvic floor dysfunction, but also of impairments of other organs or systems that could affect rehabilitative strategies to make bowel care independent or prevent unplanned bowel movements. Physical examination continues with inspection of the anus. A patulous, gaping orifice suggests a history of overdistention and trauma by a previous regimen. A normal anal-buttock contour (see Figure 29-5) suggests an intact EAS muscle mass, whereas its loss results in a flattened, fanned-out, scalloped-appearing anal region. The patient should perform a Valsalva maneuver while the examiner observes the anus and perineum for excessive descent.113 Perianal cutaneous sharp stimulation normally results in an externally visible anal sphincter reflexive contraction. This is the anocutaneous reflex, mediated by the inferior hemorrhoidal branch of the pudendal nerve (S2–S5). Sensation to pinprick is tested at the same time. The tone and voluntary squeeze strength of the EAS and tone of the IAS should be assessed. Integrity of the pelvic floor muscles can be examined by the ability to contract and relax. The length of the anus, where pressure is sensed, is normally 2.5 to 4.5 cm. The point where the pressure decreases marks the anorectal junction. Along the posterior wall, 1.5 to 2.5 cm from the anal verge, the puborectalis muscular sling can be palpated as a ridge that will push the finger forward as the subject resists defecation. No palpable ridge or push suggests puborectalis atrophy or dysfunction. A shortened length of anal pressure zone suggests EAS muscle atrophy. With the examiner’s finger in place, the bulbocavernosus reflex can be elicited by rapidly tapping or squeezing the clitoris or glans penis. The response can be delayed up to a few seconds in pathologic conditions. A consistent response to the stimulus indicates an intact bulbocavernosus reflex, although the reflex extinguishes when repeatedly elicited. Insertion of the finger in the anal canal occasionally triggers IAS relaxation, but more often triggers a tightening squeeze that is efferently equivalent to the bulbocavernosus reflex. Ask the patient to volitionally squeeze the anus before removing the finger (“resist defecation”) to check for volitional EAS and puborectalis tone and control. In addition, ask the patient to bear down and relax alternately to evaluate contraction, relaxation, and coordination of the pelvic muscles.

Nausea, vomiting, bloating, and early satiety typically indicate gastroparesis or a small intestinal or colonic pseudoobstruction in persons with neurologic disease. Acute or chronic episodes of subocclusion can occur. During episodes of acuity, there are findings of distended bowel loops and air-fluid levels requiring gastrointestinal decompression with nasogastric and rectal tubes. The patient must be placed on bowel rest and take nothing by mouth. Nutritional, fluid, and electrolyte support must be provided with an intravenous infusion. Drugs such as opiates, anticholinergics, tricyclics, antihistamines, calcium channel blockers, and phenothiazines (all of which profoundly diminish motility) must be discontinued or minimized. Once decompression is achieved, feeding is slowly advanced to a general diet. Prokinetic agents such as metoclopramide and domperidone (dopamine antagonists) and erythromycin (macrolide antibiotic, motilin receptor agonist) have been found to be beneficial in facilitating gastric emptying and intestinal motility and improving symptoms. Bethanechol and neostigmine have been shown to have limited success. Effects of tegaserod (Zelnorm) and cisapride (Propulsid), 5-HT4 receptor agonists, were more favorable, but these drugs were pulled out of the U.S. market because of serious cardiovascular adverse events, including myocardial ischemia, acute angina, arrhythmias, and stroke.* For chronic subocclusive states, enteral nutrition is preferred in patients with satisfactory digestive function. Meals should be small; frequent; liquid; contain polypeptide and hydrolyzed protein; be low in fat, fiber, and lactose; and contain multivitamins (iron, folate, calcium, vitamins D, K, and B12). If oral intake is not tolerated, enterostomies can be helpful to optimize nutrition. Total parenteral nutrition to satisfy nutritional requirements should be reserved for very severe cases. It generates various complications such as pancreatitis, glomerulonephritis, liver abnormalities, and septicemia or thrombosis from long-term catheter use.†

Diagnostic Testing

Management of Diarrhea

The history and physical examination provide most of the necessary information. The clinical cause of neurogenic bowel dysfunction in most patients who are referred to physiatrists is readily apparent. Additional objective laboratory testing can be helpful when the cause of FI or DWE is obscure, the history appears doubtful, conservative interventions fail, or surgical interventions are contemplated. Table 29-2 lists some of the many tests available. Basic laboratory tests complement the physical examination. A stool guaiac test is helpful to rule out the presence of blood in the stool. False-positive results are common after SCI because of hemorrhoids, as well as from anal

Occurrence of diarrhea in neurologic disease is commonly caused by bacterial overgrowth. Treatment with 4 weeks of antibiotics is helpful in relieving diarrhea, thus preventing malnutrition. Alternating 1-week courses (for a period of 2 to 4 weeks) of various antibiotics, including metronidazole, co-trimoxazole, ciprofloxacin, doxycycline, and amoxicillin-clavulanate, is recommended. Broad-spectrum antibiotics have been shown to be effective in a limited number of patients.7,33,117

Management Management of Nausea,Vomiting, Bloating, and Early Satiety

*References 7, 10, 33, 60, 65, 117, 129. †References 7, 33, 60, 65, 117, 129.

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

Table 29-2 Diagnostic Tests for Gastrointestinal Dysfunction Techniques for Delivery of Gastrointestinal Tract Sensory Stimulation Category of Stimulus

Experimental Technique

Mechanical* (pressure or volume)

Intraluminal balloon or bag distention with air Intraluminal gas perfusion (e.g., nitrogen/carbon dioxide/oxygen with nonabsorbable marker) Fluid loading (e.g., water or nutrient drink test)

Chemical*

Oral, intraluminal, and intravenous delivery of macronutrients, specific dietary components, and so forth

Pharmacologic*

Oral, intraluminal, intravenous, inhaled, and transcutaneous delivery of drugs, peptides, and so forth

Electrical

Transmucosal electrical stimulation

Thermal

Intraluminal bags with recirculated warm or cold water

Invasive Techniques for Measurement of Gastrointestinal Tract Motility Category of Technique

Physiologic Measure

Manometry*

Contractile activity

Main Region (Application)

(intraluminal pressure) Water perfused

All regions

Solid state

All regions

Barostat*

Tone or compliance

All regions

Tensostat

Wall tension

All regions

Electromyography

Myoelectric activity

Intraluminal or needle

Stomach Anal sphincter (pelvic floor)

Intraluminal gas perfusion

Gas transit

Small bowel and colon

Intraluminal impedance

Bolus transit

Esophagus, antropyloroduodenum

(multichannel)

Esophageal reflux (liquid, gas)

Noninvasive Techniques for Measurement of Gastrointestinal Tract Motility Category of Technique

Physiologic Measure

Imaging

Transit, wall motion, volume

Main Region (Application)

Scintigraphy*

All regions

Barium radiopaque markers and radiography*

Colon (transit)

Videofluoroscopy*

Esophagus (transit or bolus movement) Anorectum (defecography)

Ultrasonography

Gastroduodenum (wall motion) Antrum or proximal stomach (area or volume)

MRI

Stomach (wall motion)

SPECT

Stomach (volume or accommodation)

Other marker techniques

Transit

C-substrate breath tests

Stomach (gastric emptying)

Acetaminophen (plasma)

Stomach (gastric emptying)

Lactulose breath test

Small bowel (orocecal transit)

Sulfasalazine (plasma) Elecytromyography

Small bowel (orocecal transit) Myoelectric activity

Surface Modified from Kellow JE: Principles of motility and sensation testing, Gastroenterol Clin North Am 32:733-750, 2003 MRI, Magnetic resonance imaging; SPECT, three-dimensional single photon emission computed tomography. *Most commonly used techniques.

Stomach

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SECTION 3  Common Clinical Problems

Management of Defecation Dysfunction: Constipation and Fecal Incontinence A bowel program is a comprehensive, individualized patientcentered treatment plan focused on preventing incontinence, achieving effective and efficient colonic evacuation, and preventing the complications of neurogenic bowel dysfunction.107 The subcomponents of a bowel program address diet, fluids, exercise, medications, and scheduled bowel care. Bowel care is the individually developed and prescribed procedure for defecation that is carried out by the patient or attendant.107 Neurogenic bowel dysfunction results in problems with fecal storage and elimination. Inability to volitionally inhibit spontaneous defecations leads to incontinence, whereas the inability to adequately empty leads to constipation and impactions. Paradoxically, impactions can result in diarrhea and incontinence. Providing adequate, timely emptying must be combined with the inhibition of spontaneous defecations, except at desired times, to achieve social continence. The role of the individual that occurs after the acute rehabilitation process is complete determines the timing and content of the bowel care schedule. The demands of life activities, the duration of bowel care, and the needs of other members of the household should all be considered in scheduling the bowel program.

Goals of the Bowel Program It is essential to outline the goals of the bowel program. Each person responds differently to various techniques and medications used to treat constipation and FI. Regular bowel emptying is recommended as the primary means for enhancing both elimination and decreasing incontinence between stooling. The goals of the bowel program should include the following: 1. Regular passage of stool on a daily or every-other-day basis 2. Bowel evacuation at a consistent time of day (am or pm) 3. Complete emptying of the rectal vault with every bowel program 4. Stools that are soft, formed, and bulky 5. Completion of the bowel program within half an hour (at most within 1 hour) Fully appreciating an individual’s premorbid “normal” bowel function is important in the planning and goal setting for a new neurogenic bowel program. A wide range of “normal” bowel patterns exist. Ninety-five percent of individuals have a frequency of between three times per day and three times per week.33,96 Stool consistencies vary from liquid to pudding, pasty, semisolid, soft-formed, mediumformed, and hard-formed. The choice of the frequency and specific timing of bowel care to induce adequate colonic emptying can be based on previous elimination patterns. It is best, however, to plan for everyday or every-other-day bowel movements to avoid episodes of fecal impaction. Waiting more than 2 days to have a bowel movement increases episodes of constipation and incomplete emptying of the rectum. Establishing a consistent schedule for the bowel program facilitates predictability and planning. Ensuring complete emptying

of the rectum decreases incontinence or multiple stooling during the course of the day. Incontinence is reduced by less stool accumulation, because stool is not presented to the rectum between desired defecation times. Adequate emptying is accomplished by making stools easier to move by means of softening, adding bowel stimulant medication if needed, and triggering the defecatory reflex at consistent, desired times to promote habituation. If the defecatory reflex cannot be used, mechanical means should be used to clean out stools. Bowel programs and techniques for bowel care training can be more effectively pursued during inpatient rehabilitation. Some patients need attendants to help with bowel care, and the attendants must also be well trained.108,109 The burden of care for persons with neurogenic bowel is much higher if continence is not achieved or if bowel care evacuation times are excessive.118,127 It is crucial that the patient takes a decisive leadership role in designing a bowel program that includes a convenient bowel care schedule. Educating patients about their altered neurogenic bowel physiology empowers them with options and techniques to construct a bowel care regimen compatible with their daily routine. Making them independent with their bowel care is an important aspect of the overall rehabilitation process.

Dietary Considerations Food and fluid choices are important when colonic transit time is prolonged, as in SCI, where the transit time is often 96 hours versus the 30 hours typically found in normal subjects.9,12,95 The main goal of dietary choices is to achieve soft but well-formed, bulky stools. Excessive fluid resorption can result in stool hardening and subsequent constipation. Gases and liquids are propelled 30 to 100 times faster than solids by the colon. Stools that have lost their plasticity might not be kneaded and folded properly by the haustra, impeding the transit time. Stool softeners, both docusate and food fiber, have been used to maintain a more fluid content. Fiber increases stool bulk and plasticity, especially the more physically coarse forms of fiber, which also tend to decrease colonic pressures.9 Control of excessive stool hardness requires higher fiber foods in preference to lower residual foods. It is important to remember, however, that sufficient intake of fluids (preferably water) is imperative when consuming a high-fiber diet. Drinking at least 2 to 3 L of fluids per day is recommended. Otherwise, a high-fiber diet with insufficient intake of fluids can promote constipation. It should also be remembered that highly caffeinated fluids such as coffee, tea, and energy drinks can lead to dehydration from diuresis. A diet that contains at least 15 g of fiber daily is recommended.65 Aside from fiber from vegetables, fruits, and grains, artificial fiber products such as psyllium (Metamucil, Fiberall), calcium polycarbophil (Fibercon), and methylcellulose (Citrucel) can be used. Increases in the fiber content of the diets of persons with SCI do not decrease colonic transit time,17 but enhance the rectoanal inhibitory reflex.33 The effects of fiber intake on stool consistency, frequency, and efficacy of evacuation should be evaluated in each individual patient, and fiber intake should be titrated accordingly. High pressures involved in moving solid feces

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

probably contribute to the 90% incidence of hemorrhoids in Americans, and to premature diverticula formation and hemorrhoidal complications in more than 70% of patients with SCI.110 Constant straining at stool can contribute to peripheral neuropathic deficits in the anal sphincteric musculature.33 Acceptance of softer stools from a higher fiber diet might help reduce these complications and is often recommended for their treatment.

Treatment Approaches and Rationale To select the best treatment approach, the UMNB must be delineated from the LMNB. Brain disease and spinal cord disorders above T12 present with UMNB, and peripheral neuropathy and spinal cord disorders below T12 present with LMNB. Colonic transit time and fecal elimination are enhanced by softer stool. If the stool becomes too liquid, however, the protective angle provided by the puborectalis becomes less effective, and greater EAS pressures are required to maintain continence. Neurogenic bowel resting anal pressures are usually normal to slightly decreased, but are unable to develop the protective increases in EAS tone needed to control more liquid stool.9 Some degree of stool firmness must be tolerated to prevent incontinence. To avoid incontinence on straining, more firmness (mediumformed) is required for the weaker anal sphincter mechanism of the LMNB than for the UMNB (semiformed to soft-formed). Docusate is often used to try to increase fluid content and plasticity of the stool, although its clinical efficacy should be individually monitored. Fiber more consistently softens stool but also adds bulk. Bulkier stools can help stimulate the defecatory response more easily in LMNB, although less stimulus is needed in UMNB.41,83 The presentation of stool to the rectum, triggering defecation, can be associated with GMCs and mass movements more than with the slow accumulation of sufficient rectal stool to trigger reflex defecation. The GMC might be what is actually habituated.100 Choosing long intervals between elimination allows more fluid reabsorption, resulting in harder stools, which can worsen DWE. Because 95% of unimpaired persons defecate three or more times per week, choosing a frequency of at least as often as every other day would seem more physiologic and less likely to contribute to constipation.40,71,105 One study of patients with well-managed SCI found frequencies of bowel care to be chosen as daily by 24%, every other day by 46%, and more often than three times a week by 85%.67 The desire to avoid the unpleasant task of stool elimination leads some to elect longer intervals between bowel care sessions, but this carries the attendant risk for impaction or sphincter damage caused by rectal distention by larger-caliber, harder stools. Management of Upper Motor Neuron Defecatory Dysfunction In the UMNB the defecatory reflex is intact, so that triggering of defecation can be accomplished by digital stimulation, rectal stimulant medications, enemas, or electrical stimulation. All of these cause reflex relaxation of the IAS, and if strong enough can reflexly relax the EAS as well. This initiates the rectorectal reflex that helps to eliminate any

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stool that is present. The GMC and mass movement associated with the “call to stool” for many intact persons often occurs at consistent times, which can be trainable. Digital rectal stimulation is done by inserting a gloved, lubricated finger into the rectum and stimulating the rectal wall with gentle circular movements. This should be done for 20 seconds and repeated every 5 to 10 minutes until the bowel program is completed and the rectal vault is emptied. Various rectally administered medications are used to trigger and sustain reflex defecation. These are usually inserted into the rectum approximately 30 minutes before the intended bowel program, followed by digital rectal stimulation. The rationale for this prescription is to use the least irritating and most easily inserted and retained medication. Suppositories that are typically used include glycerine, vegetable oil–based bisacodyl (Dulcolax), and polyethylene glycol–based (PGB) bisacodyl (Magic Bullet). Options for minienema-triggered bowel care include small-volume phospho-soda enema, bisacodyl enema, and Enemeez. Clinical efficacy studies have been conducted in attempts to measure efficiency and effectiveness of bowel care using various rectally administered triggering medications. In a randomized blinded study, hydrogenated vegetable oil–based (HVB) bisacodyl suppositories were compared with PGB suppositories and the Therevac minienema.57 Subjects with UMNB dysfunction were studied with the events and intervals of bowel care.57 Bowel care trials with PGB suppositories showed an average time to defection of approximately 22 minutes, and a total bowel care time of 50 minutes. This was much shorter than the average time to defecation of 40 minutes and total bowel care time of 85 minutes observed with HVB bisacodyl suppository trials. The use of minienemas had an efficiency similar to that of PGB suppositories and have been since replaced by Enemeez. Results vary in individual patients, and the use of digital stimulation alone is efficient for many SCI persons with UMNB. In the UMNB, digital stimulation to induce defecatory reflexes should be favored over manual disimpaction, because the latter can easily result in inadvertent overstretching of the insensate and more delicate anal mechanisms of the neurogenic bowel. Local rectal stimulant suppositories and minienemas with bisacodyl or glycerin do not carry the same risk as oral stimulant medications and do not appear to lead to chronic inflammatory changes of the rectal mucosa. Oral bowel stimulants can be used, however, when digital rectal stimulation and rectal medications are not sufficient to achieve the goals of the bowel program. Senna (Senokot), bisacodyl, polyethylene glycol (Miralax), and magnesium derivatives (Milk of Magnesia, magnesium citrate) are commonly used. Determining the most appropriate oral medication is usually done by trial and error based on type, dosage, quantity, and duration of efficacy. Constantly being aware of the goals of the bowel program assists with titration, revision, and timing of intake of oral medications. Judicious use of these medications is warranted because certain stimulants, especially in the anthraquinone family (senna, cascara, aloes), have been shown to damage myenteric neurons with chronic use and can cause

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SECTION 3  Common Clinical Problems

atonic “cathartic bowel” syndrome.35,116 It has not been definitively established whether late complications from chronic use of oral bowel stimulant medications occur in those with neurogenic bowel dysfunction. Approaches that appear effective initially need longer-term studies to verify their continued benefits, especially because there is a high incidence of late gastrointestinal problems reported in an initially successfully managed SCI population.110 Management of Lower Motor Neuron Defecatory Dysfunction In the LMNB the bowel is areflexic, and the most effective way of completely emptying the rectum is through manual disimpaction or the use of cleansing enemas (water, soapsuds, mineral oil) that are done daily or twice a day. Sphincter and pelvic floor muscle tone is lost, increasing the likelihood of FI. Consequently it is imperative to keep the stools well formed and bulky, and to empty the rectal vault more regularly. Use of oral medications as outlined for the UMNB might likewise be warranted if stool is not efficiently reaching the rectum in a timely manner. One approach to initiating neurogenic bowel training is outlined in Box 29-1. Each step is added only after 2 weeks’ consistent trial of the previous step has been ineffective. In this stepwise approach, obtaining elimination at the desired time is emphasized as the first step, and usually precedes development of complete continence by several weeks. This regimen is designed to enhance responsiveness and emptying at the habituated time, with less stool presentation between bowel care sessions. Intrinsic loss of the ENS in any segment, or surgical reanastomosis, can result in loss of the rectoanal inhibitory reflex, causing DWE. Oral laxative abuse can cause dysfunction of the ENS.35,116 If bowel training is not accomplishing defecation at the desired times, or if repeated involuntary incontinence occurs, further diagnostic evaluation might be indicated (see Table 29-2). When neurogenic bowel deficits are incomplete and some degree of control and sensation is present, biofeedback might offer a means of enhancing the patient’s residual sensory and motor abilities. Improved sensory awareness after biofeedback training is an indicator of success. This typically requires only a few sessions, and most patients improve after just one session.100 Among more severely impaired nonselected children with myelomeningocele, biofeedback and behavioral training are equally effective in restoring continence.100 For selected individuals with some degree of volitional EAS activation and some degree of anorectal sensation, biofeedback can be a tool to help restore not just social continence, but also normal defecatory control.

Surgical Options Gastric Electrical Stimulation Treatment of gastroparesis with electrical pacemakers has been studied. The most promising device was surgically implanted in nine subjects with gastroparesis in whom conservative pharmacologic treatment had been unsuccessful. The causes of gastroparesis were diabetes in 5 subjects, idiopathic causes in 3, and postoperative complications in

BOX 29-1

Protocol for Progressive Steps in Bowel Habituation Program 1. Perform bowel cleanout if stool is present in the rectal vault or palpable proximal to the descending colon, by multiple enemas or oral cathartic. 2. Titrate to soft stool consistency with diet and bulking agents (fiber) and stool softeners (docusate). 3. Trigger defecation with a glycerin suppository or by digital stimulation 20 to 30 minutes after a meal; 10 minutes later, have the patient attempt defecation on the toilet, limited to less than 40 minutes, and relieving skin pressure every 10 minutes. 4. If defecation is not initiated, a trial of a bisacodyl suppository per rectum is initiated. 5. Digital stimulation. Start 20 minutes after suppository placement and repeat every 5 minutes. 6. Timed oral medications. Administer casanthranol– docusate sodium (Peri-Colace), senna (Senokot), or bisacodyl (Dulcolax) tablets timed so that bowel movement would otherwise result 30 minutes to 1 hour after anticipated triggered bowel timing. 7. If defecation occurs in less than 10 minutes after suppository insertion, transition to digital stimulation technique only. Once the patient is well habituated, straining alone may rarely trigger defecations at a desired time.

  Note: Steps 1 through 3 are initial interventions and are always followed, with steps 4 through 6 incorporated only as needed. At least 2 weeks trial with proper technique is pursued before advancing to the next step.

1 subject. This device delivered high-energy electric pulses at a frequency higher than normal slow-wave impulses. Results showed improvement in gastric emptying and discontinuation of enterostomal feedings. Unfortunately, the device was too large to be implanted and was impractical for long-term use. Research is ongoing for a more feasible device.60,62,129 Gastrostomies and Enterostomies Optimization of nutrition via gastrostomies and enterostomies has been found to be beneficial in patients with gastroparesis or intestinal or colonic pseudoobstruction. It not only helps prevent malnutrition, it also alleviates discomfort from nausea, vomiting, and abdominal distention. For persons receiving parenteral nutrition, a venting enterostomy provides symptomatic relief from gaseous distention and bloating.* Surgeries for Chronic Intestinal or Colonic Pseudoobstruction During acute subocclusive episodes, colonoscopic decompression is successful in 75% to 90% of cases where nasogastric or rectal tubes were ineffective. A colonic decompression tube with suctioning can be used for those requiring repeated decompression. Decompression of the gastrointestinal tract also improves forward motility and coordinated propulsion. For cases in which conservative treatment has been unsuccessful, subtotal colectomy with *References 7, 33, 60, 62, 65, 129.

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation

ileorectostomy has been found to be the most effective treatment for chronic colonic pseudoobstruction. Intestinal transplantation is another option for patients with complete small intestinal failure who cannot receive total parenteral nutrition. Intestinal transplantation is often accompanied by liver transplantation for patients with liver failure that developed because of total parenteral nutrition. These patients have to receive lifelong immunosuppressive therapy. Survival rates have improved with the use of tacrolimus (FK506) rather than cyclosporine for immunosuppressive therapy.7,33,65,117 Pelvic Floor Sling Sacral nerve deficits interfere with the action of the puborectalis, levator ani, and EAS (see Figure 29-2). The resulting pelvic floor descent impairs the protective puborectalis sling angle and decreases the efficacy of protective EAS contractions. Some patients have benefited from transposition of innervated gracilis, adductor longus, gluteus maximus, or free muscle graft palmaris longus to replace puborectalis function and restore the acute anorectal junction angle that this sling provides. Chronic electrical stimulation to enhance development of fatigue resistance is used with these transplants. Sensory deficits are not improved, but continence is somewhat restored with the ability to inhibit defecation if some degree of sensation remains.88,110 Internal Anal Sphincter and Partial External Anal Sphincter Myotomy Incomplete EAS relaxation during defecation (dyssynergia) results in a functional outlet obstruction and DWE. A prolonged descending colon transit time occurs, which improves with an IAS and partial EAS myotomy.32 This procedure relieves constipation in 62% of patients, but results in FI in 16%. As a consequence of the FI complication, it has not become a popular option.85 Electroprosthesis Stimulation of anterior sacral roots S2, S3, and S4 by trans­ rectal electric stimulation or via a stimulator surgically placed for micturition has been performed.17,27,50,86 Stimulation of S2 tends to promote nonperistaltic, low-pressure colorectal motor activity. Stimulation of S3 causes occasional high-pressure peristaltic waves, especially with repetitive stimulation. Stimulation of S4 increases both rectal and anal tone.86,128 Electrodefecation has been obtainable by sacral root stimulation in up to 50% of patients, but remains unpredictable.8,17,27,29 A reliable electroprosthesis for defecation remains an elusive goal.8,50 An electroprosthesis for both bowel and bladder control has been found to be cost-effective in suprasacral spinal cord–injured persons, although it is unclear how much of this benefit was from improved bowel control.28 Artificial anal sphincters with a subcutaneous pump reservoir similar to urinary artificial sphincters have high complication rates and poor outcomes, and their use has only been investigative.81 Antegrade Continence Enema The options of the antegrade continence enema should be considered in clinical scenarios of prolonged bowel care time, recurrent fecal impactions, or poor or intermittent response to rectal medications to initiate bowel

635

care.29,76,91,125 This is an alternative method of antegrade enema delivery that requires the surgical construction of a catheterizable appendicocecostomy stoma. The appendix and the right side of the colon are mobilized through a horizontal right lower quadrant incision and brought against the abdominal wall. The tip of the appendix is then amputated, and the opening into the appendix lumen is modified into a catheterizable stoma on the abdominal wall. This procedure can now also be performed laparoscopically.60 This stoma can be catheterized and infused with 200 to 600 mL of tap water to trigger a propulsive colonic peristalsis and defecation within 10 to 20 minutes.128 Bowel care can then be additionally facilitated with digital stimulation in the usual fashion. Colostomy Colostomy has been shown to reduce bowel care time, especially when offered to those with chronic DWE.107,122 It can be indicated in four general scenarios: 1. When conservative medical measures and training have failed71,118 2. When intrinsic bowel deficits exist, such as in Hirschsprung’s disease, Chagas’ disease, and “cathartic colon” 3. When pressure ulcers or other skin lesions occur that cannot be effectively healed because of frequent soiling 4. When recurrent urinary tract seeding by repetitive bowel impactions occurs38,107,122 Although diversion for pressure ulcer healing is usually anticipated to be reversed, those with neurogenic bowel often elect to maintain the colostomy even after the pressure ulcer has healed.99,111 Colostomy carries a surgical risk, is cosmetically disfiguring, and is seldom necessary to achieve adequate social continence. It remains as a procedure of last resort for the treatment of FI or DWE.8,31,65,107,110

Complications For persons with gastroparesis or intestinal pseudoobstruction, the primary complications are chronic malnutrition, dehydration, and electrolyte imbalance. It is important to optimize nutrition and hydration, and monitor weight, vitamin, and electrolyte levels regularly. Oral and enteral feedings must provide adequate calories, protein, electrolytes, and vitamins despite being liquid in consistency; low in fat, fiber, and lactose; high in polypeptides and hydrolyzed protein; and received in small, frequent amounts.33,62,117,129 In acute subocclusive episodes of colonic pseudoobstruction, it is important to achieve decompression as soon as possible. Failure to do so can result in progressive distention and cecal ischemia, causing perforation. The risk for perforation is increased when cecal diameters are 12 cm or greater. Colonic perforation requires emergent exploratory laparotomy and intestinal resection. The mortality rate is approximately 36% to 44% and is determined by age, diameter of the cecum, delay of decompression, and comorbidities.10,109 Significant bowel complications requiring medical treatment or lifestyle alterations are reported by 27% of persons with SCI by 5 years or greater beyond their injury, even if

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SECTION 3  Common Clinical Problems

bowel management was satisfactory during the first 5 years. More than 80% of persons with SCI reported bowel impactions, and 20% had chronic bowel impaction and DWE problems.110 Impactions have been reported to be complicated by perforation or even death.127 Impactions have a morbidity rate ranging up to 6% in the “normal” population, being higher in the cognitively impaired elderly.127 Other late gastrointestinal complications reported by patients with SCI include gastroesophageal reflux, premature diverticulosis, and autonomic dysreflexia.45,68,110 Morbidity from colonic perforation by enema use has also been reported.75 Hemorrhoids are more symptomatic when patients have intact sensation, but in one study, rectal bleeding caused by hemorrhoids was reported by 74% of patients with SCI.110 Hemorrhoids develop because of frequent high pressures in the anorectal marginal veins and are associated with constipated hard stool passage. Stool softening is the best preventive and chronic treatment measure, but it should be balanced with the requirement to modulate stool consistency to maintain continence. An overstretched, patulous, noncompetent sphincter associated with rectal prolapse often is the end result of chronic passage of very large, hard stools through a weakened anorectal mechanism in LMNB. Overdistention of the weakened neurogenic anal mechanism should be avoided by use of stool softening and gentle care to dilate the sphincter whenever manual disimpaction is required, to minimize trauma to these denervated structures. Although the anus can be significantly dilated to accommodate two fingers for breaking up low impactions, anorectal overdistention has been hypothesized to lead to atonic segments similar to bladder overdistention. The bowel, however, cannot be as easily decompressed and rested to allow recovery as can the bladder. The IAS is smooth muscle that will shorten and remodel to eventually regain competent closure if the overstretching can be eliminated. Unfortunately, this might require months of incontinent, liquid to soft pasty stools, which is seldom tolerated.50,67 Should the patient require a temporary colostomy for some other disease process, it might be possible after many months to then train toward social continence with the decompressed and restored IAS. Such patients have usually had long courses of constant soiling, however, and often prefer to keep their colostomy and continence rather than pursue surgical reversal and training.98,111 Autonomic dysreflexia occurs in patients with SCI who have lesions at or above the midthoracic region. FI is a common and potentially dangerous cause of autonomic dysreflexia because of the substantial time that can be required for its clearance (see Chapter 55).12 If manual disimpaction is required, lubrication with lidocaine gel is recommended to decrease additional nociceptive sensory input from the richly innervated anal region. Bloating and abdominal distention are common complaints of patients with neurogenic bowel dysfunction.40,54 These complaints can be reduced in patients with SCI by increasing the frequency of bowel care. This complaint can be especially severe in those with hyperactive EAS protective responses to rectal distention, which can preclude the passing of flatus. Digital release of flatus might be required, in addition to diet modification to eliminate

foods that produce excessive gases. The workup should also include assessment for any contributing aerophagia (air swallowing).

Treatment Outcomes Bowel habituation training in children with myelomeningocele by means of suppositories, digital stimulation, or both, resulted in 83% of compliant patients having less than one incontinent stool per month.64 The continence catheter enema, which has a distal rectal balloon to avoid immediate enema expulsion, when used daily or every other day, reduced FI to fewer than three episodes per month in children with myelomeningocele.39,103 Nursing home residents with FI and dementia evaluated to have UMNB were treated by medically constipating them (with codeine) and giving biweekly enemas. Those with diagnosed LMNB had their stools softened with lactulose and received weekly enemas. Fecal continence was restored in 80% of those who were consistently treated with these protocols.115 Although all patients with complete SCI have episodic FI,80 this is a chronic problem for only 2%.108 DWE appears to be a progressive problem that develops 5 years or more after SCI. This is rarely reported after training in the first 4 years but occurs in 20% by a mean of 17 years after injury.108 Gastrointestinal problems in SCI are not merely nuisances, because they also account for 10% of SCI late mortality.45 Patients with multiple sclerosis, Parkinson’s disease, or muscular dystrophy have also been helped by methods to enhance bowel storage or elimination in the setting of deteriorating neuromuscular and anorectal function.8,20,119 Colostomy can also provide a means of achieving social continence in these patients. As noted above, colostomy complications include embarrassing gas problems, appliance loosening and leakage, and cosmetic difficulties. Patients who develop social bowel continence are able to venture into public without fear of malodorous embarrassment and unpredictable social disasters that humiliate as well as require substantial cleanup time. When fear of such adverse events persists, full social and vocational reintegration is impeded. A major hurdle that many patients with neuromuscular compromise can overcome is control of the seemingly automatic neurogenic functions of defecation and bowel elimination. Such patients should not needlessly suffer because inadequate attention has been paid by care providers to this potentially functionally impairing and socially disabling deficit. Many solutions are yet to come for the large number of persons who cope with neurogenic bowel dysfunction. The colon will continue to be a fertile area for research.107 REFERENCES 1. Aaronson MJ, Freed MM, Burakoff R: Colonic myoelectric activity in persons with spinal cord injury, Dig Dis Sci 30(4):295-300, 1985. 2. Abercrombie JF, Rogers J, Swash M: Faecal incontinence in myotonic dystrophy, J Neurol Neurosurg Psychiatry 64(1):128-130, 1998. 3. Al-Chaer ED, Kawasaki M, Pasricha PJ: A new model of chronic visceral hypersensitivity in adult rats induced by colon irritation during postnatal development, Gastroenterology 119(5):1276-1285, 2000.

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation 4. Al-Chaer ED, Westlund KN, Willis WD: Sensitization of postsynaptic dorsal column neuronal responses by colon inflammation, Neuroreport 8(15):3267-3273, 1997. 5. Altaf MA, Sood MR: The nervous system and gastrointestinal function, Dev Disabil Res Rev 14(2):87-95, 2008. 6. Andriantsitohaina R, Surprenant A: Acetylcholine released from guinea-pig submucosal neurones dilates arterioles by releasing nitric oxide from endothelium, J Physiol 453:493-502, 1992. 7. Antonucci A, Fronzoni L, Cogliandro L, et al: Chronic intestinal pseudo-obstruction, World J Gastroenterol 14(19):2953-2961, 2008. 8. Banwell JG, Creasey GH, Aggarwal AM, et al: Management of the neurogenic bowel in patients with spinal cord injury, Urol Clin North Am 20(3):517-526, 1993. 9. Bartolo DC, Read NW, Jarratt JA, et al: Differences in anal sphincter function and clinical presentation in patients with pelvic floor descent, Gastroenterology 85(1):68-75, 1983. 10. Berkley KJ, Hubscher CH, Wall PD: Neuronal responses to stimulation of the cervix, uterus, colon, and skin in the rat spinal cord, J Neurophysiol 69(2):545-556, 1993. 11 Beyak MJ, Bulmer DCE, Jiang CD, et al: Extrinsic sensory afferent nerves innervating the gastrointestinal tract. In Johnson LR, Barrett KE, Ghishan FK, et al: Physiology of the gastrointestinal tract, ed 4, San Diego, 2006, Academic Press. 12. Bittinger M, Barnert J, Wienbeck M: Autonomic dysfunction and the gastrointestinal tract, Clin Auton Res 9(2):75-81, 1999. 13. Bornstein JC, Furness JB: Correlated electrophysiological and histochemical studies of submucous neurons and their contribution to understanding enteric neural circuits, J Auton Nerv Syst 25(1):1-13, 1988. 14. Boss BJ, Pecanty L, McFarland SM, et al: Self-care competence among persons with spinal cord injury, SCI Nurs 12(2):48-53, 1995. 15. Burnstock G: Physiology and pathophysiology of purinergic neurotransmission, Physiol Rev 87(2):659-797, 2007. 16. Burnstock G: The journey to establish purinergic signalling in the gut, Neurogastroenterol Motil 20(suppl 1):8-19, 2008. 17. Cameron KJ, Nyulasi IB, Collier GR, et al: Assessment of the effect of increased dietary fibre intake on bowel function in patients with spinal cord injury, Spinal Cord 34(5):277-283, 1996. 18. Camilleri M: Disorders of gastrointestinal motility in neurologic diseases, Mayo Clin Proc 65(6):825-846, 1990. 19. Camilleri M, Bharucha AE: Gastrointestinal dysfunction in neurologic disease, Semin Neurol 16(3):203-216, 1996. 20. Caroscio JT: Amyotrophic lateral sclerosis: a guide to patient care, New York, 1986, Thieme, 126. 21. Cervero F, Janig W: Visceral nociceptors: a new world order? Trends Neurosci 15(10):374-378, 1992. 22. Cervero F, Laird JM: Visceral pain, Lancet 353(9170):2145-2148, 1999. 23. Chelimsky G, Wszolek Z, Chelimsky TC: Gastrointestinal dysfunction in autonomic neuropathy, Semin Neurol 16(3):259-268, 1996. 24. Christensen J: The motor function of the colon. In Yamada T, editor: Textbook of gastroenterology, Philadelphia, 1991, JB Lippincott. 25. Coggrave M, Wiesel PH, Norton C: Management of faecal incontinence and constipation in adults with central neurological diseases, Cochrane Database Syst Rev (2):CD002115, 2006. 26. Cooke HJ: Role of the “little brain” in the gut in water and electrolyte homeostasis, FASEB J 3(2):127-138, 1989. 27. Coulie B, Camilleri M: Intestinal pseudo-obstruction, Annu Rev Med 50:37-55, 1999. 28. Creasey GH, Dahlberg JE: Economic consequences of an implanted neuroprosthesis for bladder and bowel management, Arch Phys Med Rehabil 82(11):1520-1525, 2001. 29. De Looze D, Van Laere M, De Muynck M, et al: Constipation and other chronic gastrointestinal problems in spinal cord injury patients, Spinal Cord 36(1):63-66, 1998. 30. De Wever I, Eeckhout C, Vantrappen G, et al: Disruptive effect of test meals on interdigestive motor complex in dogs, Am J Physiol 235(6):E661-E665, 1978. 31. Deshmukh GR, Barkel DC, Sevo D, et al: Use or misuse of colostomy to heal pressure ulcers, Dis Colon Rectum 39(7):737-738, 1996. 32. Devroede G, Lamarche J: Functional importance of extrinsic parasympathetic innervation to the distal colon and rectum in man, Gastroenterology 66(2):273-280, 1974. 33. Devroede G, Lamarche J, editors: Constipation. In Sleisenger MH, Fordtran JS, editors: Gastrointestinal disease, Philadelphia, 1993, WB Saunders.

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34. Doughty DB, Jackson DB: Gastrointestinal disorders, St Louis, 1993, Mosby-Year Book. 35. Dubrovsky B, Filipini D: Neurobiological aspects of the pelvic floor muscles involved in defecation, Neurosci Biobehav Rev 14(2):157-168, 1990. 36. Edwards LL, Pfeiffer RF, Quigley EM: Gastrointestinal symptoms in Parkinson’s disease, Mov Disord 6(2):151-156, 1991. 37. Edwards LL, Quigley EM, Harned RK, et al: Characterization of swallowing and defecation in Parkinson’s disease, Am J Gastroenterol 89(1):15-25, 1994. 38. Edwards LL, Quigley EM, Pfeiffer RF: Gastrointestinal dysfunction in Parkinson’s disease: frequency and pathophysiology, Neurology 42(4):726-732, 1992. 39. Eire PF, Cives RV, Gago MC: Faecal incontinence in children with spina bifida: the best conservative treatment, Spinal Cord 36(11):774776, 1998. 40. Fealey RD, Szurszewski JH, Merritt JL, et al: Effect of traumatic spinal cord transection on human upper gastrointestinal motility and gastric emptying, Gastroenterology 87(1):69-75, 1984. 41. Filipini DL, Dubrovsky B: Pelvic floor muscles response to graded rectal distension and cutaneous stimulation, Dig Dis Sci 36(12):17611767, 1991. 42. Fowler CJ, Henry MM: Gastrointestinal dysfunction in multiple sclerosis, Semin Neurol 16(3):277-279, 1996. 43. Fox EA, Phillips RJ, Martinson FA, et al: Vagal afferent innervation of smooth muscle in the stomach and duodenum of the mouse: morphology and topography, J Comp Neurol 428(3):558-576, 2000. 44. Gebhart GF: Pathobiology of visceral pain: molecular mechanisms and therapeutic implications IV. Visceral afferent contributions to the pathobiology of visceral pain, Am J Physiol Gastrointest Liver Physiol 278(6):G834-G838, 2000. 45. Gore RM, Mintzer RA, Calenoff L: Gastrointestinal complications of spinal cord injury, Spine (Phila Pa 1976) 6(6):538-544, 1981. 46. Goyal RK, Crist JR: Neurology of the gut. In Sleisenger MH, Fordtram JS, editors: Gastrointestinal disease, Philadelphia, 1989, WB Saunders. 47. Grundy D, Al-Chaer ED, Aziz Q, et al: Fundamentals of neurogastroenterology: basic science, Gastroenterology 130(5):1391-1411, 2006. 48. Guyton AC: Textbook of medical physiology, ed 8, Philadelphia, 1991, WB Saunders. 49. Hammond MC, Umlauf RL, Matteson B, et al: Yes you can! A guide to self-care for persons with spinal cord injury, Washington, DC, 1989, Paralyzed Veterans of America, 361. 50. Han TR, Kim JH, Kwon BS: Chronic gastrointestinal problems and bowel dysfunction in patients with spinal cord injury, Spinal Cord 36(7):485-490, 1998. 51. Hanson RW, Franklin MR: Sexual loss in relation to other functional losses for spinal cord injured males, Arch Phys Med Rehabil 57(6):291293, 1976. 52. Harari D, Minaker KL: Megacolon in patients with chronic spinal cord injury, Spinal Cord 38(6):331-339, 2000. 53. Harari D, Norton C, Lockwood L, et al: Treatment of constipation and fecal incontinence in stroke patients: randomized controlled trial, Stroke 35(11):2549-2555, 2004. 54. Hasler WL: Gastroparesis: symptoms, evaluation, and treatment, Gastroenterol Clin North Am 36(3):619-647, ix 2007. 55. Hasler WL: Gastroparesis: current concepts and considerations, Medscape J Med 10(1):16, 2008. 56. Hillsley K, Kirkup AJ, Grundy D: Direct and indirect actions of 5-hydroxytryptamine on the discharge of mesenteric afferent fibres innervating the rat jejunum, J Physiol 506(pt 2):551-561, 1998. 57. House JG, Stiens SA: Pharmacologically initiated defecation for persons with spinal cord injury: effectiveness of three agents, Arch Phys Med Rehabil 78(10):1062-1065, 1997. 58. Jin JG, Murthy KS, Grider JR, et al: Stoichiometry of neurally induced VIP release, NO formation, and relaxation in rabbit and rat gastric muscle, Am J Physiol 271(2 pt 1):G357-G369, 1996. 59. Kamath PS, Phillips SF, O’Connor MK, et al: Colonic capacitance and transit in man: modulation by luminal contents and drugs, Gut 31(4):443-449, 1990. 60. Kaname A, Kakizaki H, Machino R, et al: Laparoscopic antegrade continence enema procedure for fecal incontinence in a patient with spina bifida, Int J Urol 10:401-403, 2003. 61. Kerr TP, Robb SA, Clayden GS: Lower gastrointestinal tract disturbance in congenital myotonic dystrophy, Eur J Pediatr 161(8):468469, 2002.

638

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62. Kiba T: Relationships between the autonomic nervous system, humoral factors and immune functions in the intestine, Digestion 74(3-4):215-227, 2006. 63. King JC, Currie DM, Wright E: Bowel training in spina bifida: importance of education, patient compliance, age, and anal reflexes, Arch Phys Med Rehabil 75(3):243-247, 1994. 64. King JC, Nelson R, Tuturro T, et al: Prescriptions, referrals, and the rehabilitation team. In DeLisa JA, editor: Rehabilitation medicine principles and practice, ed 3, Philadelphia, 1998, JB Lippincott. 65. King R, Biddle A, Braunschweig C, et al: Neurogenic bowel management in adults with spinal cord injury, J Spinal Cord Med 21:248-293, 1998. 66. Kirkup AJ, Brunsden AM, Grundy D: Receptors and transmission in the brain-gut axis: potential for novel therapies. I. Receptors on visceral afferents, Am J Physiol Gastrointest Liver Physiol 280(5):G787G794, 2001. 67. Kirshblum SC, Gulati M, O’Connor KC, et al: Bowel care practices in chronic spinal cord injury patients, Arch Phys Med Rehabil 79(1): 20-23, 1998. 68. Kirshblum SC, House JG, O’Connor KC: Silent autonomic dysreflexia during a routine bowel program in persons with traumatic spinal cord injury: a preliminary study, Arch Phys Med Rehabil 83(12):17741776, 2002. 69. Koch KL, Hong SP, Xu L: Reproducibility of gastric myoelectrical activity and the water load test in patients with dysmotility-like dyspepsia symptoms and in control subjects, J Clin Gastroenterol 31(2):125-129, 2000. 70. Kozlowski CM, Green A, Grundy D, et al: The 5-HT(3) receptor antagonist alosetron inhibits the colorectal distention induced depressor response and spinal c-fos expression in the anaesthetised rat, Gut 46(4):474-480, 2000. 71. Krogh K, Mosdal C, Laurberg S: Gastrointestinal and segmental colonic transit times in patients with acute and chronic spinal cord lesions, Spinal Cord 38(10):615-621, 2000. 72. Krogh K, Ostergaard K, Sabroe S, et al: Clinical aspects of bowel symptoms in Parkinson’s disease, Acta Neurol Scand 117(1):60-64, 2008. 73. Ladabaum U, Minoshima S, Hasler WL, et al: Gastric distention correlates with activation of multiple cortical and subcortical regions, Gastroenterology 120(2):369-376, 2001. 74. Levi R, Hultling C, Nash MS, et al: The Stockholm Spinal Cord Injury Study: 1. Medical problems in a regional SCI population, Paraplegia 33(6):308-315, 1995. 75. Liptak GS, Revell GM: Management of bowel dysfunction in children with spinal cord disease or injury by means of the enema continence catheter, J Pediatr 120(2 pt 1):190-194, 1992. 76. Liu S, Xia Y, Hu H, et al: Histamine H3 receptor-mediated suppression of inhibitory synaptic transmission in the submucous plexus of guinea-pig small intestine, Eur J Pharmacol 397(1):49-54, 2000. 77. Luiking YC, Akkermans LM, Peeters TL, et al: Effects of motilin on human interdigestive gastrointestinal and gallbladder motility, and involvement of 5HT3 receptors, Neurogastroenterol Motil 14(2):151159, 2002. 78. Lynn P, Zagorodnyuk V, Hennig G, et al: Mechanical activation of rectal intraganglionic laminar endings in the guinea pig distal gut, J Physiol 564(Pt 2):589-601, 2005. 79. MacDonagh R, Sun WM, Thomas DG, et al: Anorectal function in patients with complete supraconal spinal cord lesions, Gut 33(11):1532-1538, 1992. 80. MacDonagh RP, Sun WM, Smallwood R, et al: Control of defecation in patients with spinal injuries by stimulation of sacral anterior nerve roots, BMJ 300(6738):1494-1497, 1990. 81. Madoff RD, Parker SC, Varma MG, et al: Faecal incontinence in adults, Lancet 364(9434):621-632, 2004. 82. Maggi CA, Catalioto RM, Criscuoli M, et al: Tachykinin receptors and intestinal motility, Can J Physiol Pharmacol 75(6):696-703, 1997. 83. Maggi CA, Meli A: The sensory-efferent function of capsaicin-sensitive sensory neurons, Gen Pharmacol 19(1):1-43, 1988. 84. Manning J, Korda A, Benness C, et al: The association of obstructive defecation, lower urinary tract dysfunction and the benign joint hypermobility syndrome: a case-control study, Int Urogynecol J Pelvic Floor Dysfunct 14(2):128-132, 2003. 85. Martelli H, Devroede G, Arhan P, et al: Mechanisms of idiopathic constipation: outlet obstruction, Gastroenterology 75(4):623-631, 1978. 86. Martelli H, Devroede G, Arhan P, et al: Some parameters of large bowel motility in normal man, Gastroenterology 75(4):612-618, 1978.

87. Meshkinpour H, Nowroozi F, Glick ME: Colonic compliance in patients with spinal cord injury, Arch Phys Med Rehabil 64(3):111112, 1983. 88. Ness TJ, Gebhart GF: Visceral pain: a review of experimental studies, Pain 41(2):167-234, 1990. 89. Ness TJ, Gebhart GF: Acute inflammation differentially alters the activity of two classes of rat spinal visceral nociceptive neurons, Neurosci Lett 281(2-3):131-134, 2000. 90. Nino-Murcia M, Stone JM, Chang PJ, et al: Colonic transit in spinal cord-injured patients, Invest Radiol 25(2):109-112, 1990. 91. North RA, Surprenant A: Inhibitory synaptic potentials resulting from alpha 2-adrenoceptor activation in guinea-pig submucous plexus neurones, J Physiol 358:17-33, 1985. 92. Pedersen E: Regulation of bladder and colon–rectum in patients with spinal lesions, J Auton Nerv Syst 7(3-4):329-338, 1983. 93. Perkin GD, Murray-Lyon I: Neurology and the gastrointestinal system, J Neurol Neurosurg Psychiatry 65(3):291-300, 1998. 94. Pierce E, Cowan P, Stokes M: Managing faecal retention and incontinence in neurodisability, Br J Nurs 10(9):592-601, 2001. 95. Quigley EM: Gastrointestinal dysfunction in Parkinson’s disease, Semin Neurol 16(3):245-250, 1996. 96. Rendtorff RC, Kashgarian M: Stool patterns of healthy adult males, Dis Colon Rectum 10(3):222-228, 1967. 97. Saab CY, Park YC, Al-Chaer ED: Thalamic modulation of visceral nociceptive processing in adult rats with neonatal colon irritation, Brain Res 1008(2):186-192, 2004. 98. Saltzstein RJ, Romano J: The efficacy of colostomy as a bowel management alternative in selected spinal cord injury patients, J Am Paraplegia Soc 13(2):9-13, 1990. 99. Sarna SK: Giant migrating contractions and their myoelectric correlates in the small intestine, Am J Physiol 253(5 pt 1):G697-G705, 1987. 100. Schiller LR: Fecal incontinence. In Sleisenger MH, Fordtran JS, ­editors: Gastrointestinal disease, Philadelphia, 1993, WB Saunders. 101. Sengupta JN, Gebhart GF: Gastrointestinal afferent fibers and sensation. In Johnson LR, Alpers DH, Christensen J, et al, editors: Physiology of the gastrointestinal tract, ed 3, New York, 1994, Raven Press. 102. Shafik A, Shafik AA, Ahmed I: Role of positive anorectal feedback in rectal evacuation: the concept of a second defecation reflex: the anorectal reflex, J Spinal Cord Med 26(4):380-383, 2003. 103. Shandling B, Gilmour RF: The enema continence catheter in spina bifida: successful bowel management, J Pediatr Surg 22(3):271-273, 1987. 104. Silverman DH, Munakata JA, Ennes H, et al: Regional cerebral activity in normal and pathological perception of visceral pain, Gastroenterology 112(1):64-72, 1997. 105. Siproudhis L, Bellissant E, Juguet F, et al: Perception of and adaptation to rectal isobaric distension in patients with faecal incontinence, Gut 44(5):687-692, 1999. 106. Stanghellini V, Cogliandro RF, de Giorgio R, et al: Chronic intestinal pseudo-obstruction: manifestations, natural history and management, Neurogastroenterol Motil 19(6):440-452, 2007. 107. Stiens SA, Bergman SB, Goetz LL: Neurogenic bowel dysfunction after spinal cord injury: clinical evaluation and rehabilitative management, Arch Phys Med Rehabil 78(suppl 3):S86-S102, 1997. 108. Stiens SA, Braunschweig C, Cowel F, et al: Neurogenic bowel: what you should know. A guide for people with spinal cord injury (Vol 1999), Washington, DC, 1997, Consortium for Spinal Cord Medicine, 53. 109. Stiens SA, Pidde T, Veland B, et al: Accidents stink! Bowel care 202 [video], Washington, DC, 2001, Paralyzed Veterans of America Education and Training Foundation. 110. Stone JM, Nino-Murcia M, Wolfe VA, et al: Chronic gastrointestinal problems in spinal cord injury patients: a prospective analysis, Am J Gastroenterol 85(9):1114-1119, 1990. 111. Stone JM, Wolfe VA, Nino-Murcia M, et al: Colostomy as treatment for complications of spinal cord injury, Arch Phys Med Rehabil 71(7):514-518, 1990. 112. Suckling PV: The ball-valve rectum due to impacted faeces, Lancet 2(7266):1147, 1962. 113. Swash M: New concepts in the prevention of incontinence, Practitioner 229(1408):895-899, 1985. 114. Tjandra JJ, Ooi BS, Han WR: Anorectal physiologic testing for bowel dysfunction in patients with spinal cord lesions, Dis Colon Rectum 43(7):927-931, 2000.

CHAPTER 29  Neurogenic Bowel: Dysfunction and Rehabilitation 115. Tobin GW, Brocklehurst JC: Faecal incontinence in residential homes for the elderly: prevalence, aetiology and management, Age Ageing 15(1):41-46, 1986. 116. Waseem S, Moshiree B, Draganov PV: Gastroparesis: current diagnostic challenges and management considerations, World J Gastroenterol 15(1):25-37, 2009. 117. White JC, Verlot MG, Ehrentheil O: Neurogenic disturbances of the colon and their investigation by the colon metrogram: a preliminary report, Ann Surg 112(6):1042-1057, 1940. 118. Wiesel PH, Norton C, Glickman S, et al: Pathophysiology and management of bowel dysfunction in multiple sclerosis, Eur J Gastroenterol Hepatol 13(4):441-448, 2001. 119. Wiesel PH, Norton C, Roy AJ, et al: Gut focused behavioural treatment (biofeedback) for constipation and faecal incontinence in multiple sclerosis, J Neurol Neurosurg Psychiatry 69(2):240-243, 2000. 120. Wingate DL: Backwards and forwards with the migrating complex, Dig Dis Sci 26(7):641-666, 1981. 121. Wingate DL, Ewart WR: The brain–gut axis. In Yamada T, editor: Textbook of gastroenterology, Philadelphia, 1991, JB Lippincott.

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CHAPTER 30 SPASTICITY MANAGEMENT Patricia W. Nance, Lalith Satkunam, and Karen Ethans

Spasticity is a common sequela to an insult to the upper motor neuron (UMN) in the central nervous system. The definition of spasticity is most commonly cited as follows135: Spasticity is a motor disorder that is characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome. American Academy of Neurology (1990)2

The specific behavioral features of the UMN syndrome can vary depending on the underlying cause, for example spinal cord injury (SCI) versus cerebral vascular damage. Spinal interneurons, sensory afferents, and modulatory and motor efferent pathways normally interact to control, coordinate, and modulate spinal motor neuronal activation. The medical literature supports the notion that insufficient descending inhibition results in structural and physiologic reorganization of segmental circuits following injury or dysfunction within the UMN pathways, such as alterations of intrinsic and extrinsic properties of motor neurons and interneurons. From a clinical standpoint, it is important to distinguish between the positive symptoms related to the UMN syndrome (e.g., spastic dystonia, flexor spasms, exaggerated cutaneous reflexes, and autonomic hyperreflexia) and the negative symptoms (e.g., paresis, loss of fine dexterity, and fatigability).245 This difference relates directly to the expectations of outcome following treatment for a positive symptom of spasticity, without necessarily worsening the negative symptom of weakness.246 The successful management of spasticity can be a therapeutic challenge. When severe, spastic muscular movements can be violent and uncontrolled, resulting in severe complications such as chronic pain, contractures, long bone fracture, joint dislocations, and chronic skin ulceration. Undesirable complications such as these can be anticipated, prevented, and treated with appropriate management. The effects of spasticity, however, might not always be negative. For example, spasticity can assist weakened legs, allowing the person to stand or transfer and have improved bed mobility. This review focuses on a rehabilitative approach to spasticity treatment. One must first establish whether there is a functional problem caused by the spasticity and what are the related goals of treatment. All spasticity-aggravating factors must be treated, and the medical therapy must be matched to the specific needs of the patient. Finally, one must reevaluate the patient to ensure that the goal of therapy has been met.

Causes of Spasticity Like the UMN syndrome, spasticity can accompany diffuse or localized cerebral or spinal pathology. Anoxic, toxic, or metabolic encephalopathies can cause diffuse cerebral abnormalities,2 whereas localized cerebral injury can occur with tumor, abscess, cyst, vascular malformations, infarction, hemorrhage, or trauma. Trauma, inflammation, demyelinating disease, and degenerative and familial disorders, as well as compression by a mass (e.g., neoplasm, infection, or cyst) are examples of spinal cord disorders. An example of a combination of UMN and lower motor neuron pathology is amyotrophic lateral sclerosis, where spasticity can be the dominant feature in some patients. Spasticity is often cited as a significant problem in multiple sclerosis (see Chapter 52), traumatic brain injury (see Chapter 49), cerebral palsy (see Chapter 53), SCI (see Chapter 55), and stroke (see Chapter 50). Problematic spasticity occurs in 40% to 60% of patients with SCI and multiple sclerosis, which results in a significant impact on activities of daily living and patient independence. Almost two thirds of patients with cerebral palsy present with “spastic diplegia.”* Changes in the characteristics of a person’s regular spasticity can help to alert those affected and caregivers of problems in parts of the body where the patient no longer has voluntary movement or sensory appreciation; for example, an increase in spasm frequency in a person with complete tetraplegia who has developed an otherwise asymptomatic urinary tract infection. In neurolathyrism, a rare disorder, spasticity can be the main presenting symptom.166 Physiatrists are often asked to evaluate the patient who presents with the sudden worsening of spasticity, possibly a result of the onset of a new pathologic process, such as a urinary tract infection, urolithiasis, stool implication, pressure sore, fracture, dislocation, ingrown toe nail, excessively restrictive clothing, irritating condom drainage appliance, or even thyrotoxicosis.208 If there is a remediable cause of spasticity, it must be discovered and treated. If problematic spasticity persists in the absence of a remediable cause, then it is appropriate to pursue treatment until a therapeutic response is obtained. Inevitable complications are the natural history of suboptimal treatment of severe spasticity. These complications include skin breakdown, infection, bone fracture or dislocation, and more frequent inpatient hospitalization.17,180 *References 28,

36, 155, 192, 245, 246. 641

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SECTION 3  Common Clinical Problems

Evaluation and Measurement Of the many clinical monitoring tools described in the literature to assess the severity of spasticity, most researchers agree that assessment tools should be tailored to meet the individual characteristics of a given patient. A number of spasticity-measuring tools are used, which range from simple questionnaires and goniometry evaluations to more technologically complicated electromyographic and biomechanical analysis of limb resistance to mechanical displacement, and even video monitoring assessments of joint mobility.32,43,98,186 The Ashworth Scale,10,73,139 Oswestry Scale of Grading,91 and Degree of Adductor Muscle Tone224 are some of the tone intensity scales used to assess spasticity in SCI. As proposed originally, the Ashworth Scale is a simple five-point Likert scale in which the observer’s subjective opinion of the subject’s resting muscle tone ranges from “normal” at the lowest grade to “rigid” at the highest10 (Table 30-1). The original scale was modified by adjusting the lowest number from 0 to 1 and the highest scale from 4 to 5. Another modification from the original scoring scheme was the addition of a point between 1 and 2, where 1 was a “catch” at the end of joint motion range and 1+ was a catch earlier in the joint motion range nearer to midpoint.24 The Ashworth Scale has the advantage of ease of use in the clinical setting. This asset has been used in a number of pharmaceutical trials of antispasticity medications in which a simple measurement tool can be used easily by the participating clinicians to assess the efficacy of the intervention. A recent comprehensive review of engineering and medical literature concluded that the Ashworth Scale is in common use and has significant interrater agreement and good reliability, but it is not a functional outcome measure and can be biased by evaluator subjectivity.73 A monitoring test should be able not only to assess the change in spasticity during therapy but also to assess the functional effects of interventions. Such a test should have a well-defined scoring system, be reliable and sensitive to change, and have standard instructions.186 Another method of observing the spasticity phenomenon is to assess the number of episodic spasms as reported by the patient. The Penn Spasm Frequency Score195 is an ordinal ranking of the frequency of leg spasms per day and per hour. One problem with this scale is that patients usually report that the number of spasms occurring per hour is often affected by their activity at the time. For example, they tend to report few spasms if resting comfortably or more if physically active. The duration of each spasm is also not considered. The casual observation of the free swing of the knee in the “pendulum test” was formalized and provided objective data by the use of videomotion analysis. The advantages of videomotion analysis of the pendulum test include the ability to do the analysis anywhere a video recorder is available, freedom from the attachment of cumbersome recording devices to the patient, and processing by a nonbiased “blinded” observer who has had no contact with the patient.105,179 Pain can be assessed, whether or not it is associated with spasticity, by a self-administered test such as the Pain Intensity Descriptor Scale95 or by using a 10-cm visual

Table 30-1 The Ashworth Scale Score

Definition

0

No increase in muscle tone

1

Slight increase in muscle tone, manifested by a catch and release

2

More marked increase in muscle tone through most of the range of motion, but affected limb is easily moved

3

Considerable increase in muscle tone—passive movement difficult

4

Limb rigid in flexion or extension

F orm Ashworth B: Preliminary trial of carisoprodol in multiple sclerosis, Practitioner 192:540-542, 1964.

analog scale.40,117 It is important to decipher whether the pain is from the spasticity itself or caused by other factors such as with neuropathic pain in SCI or multiple sclerosis, thalamic pain syndromes, or frozen shoulder in stroke. Standardized assessments of functional ability or caregiver burden might or might not be sensitive to changes in relative levels of spasticity. These include the Sickness Impact Profile,22 the 36-Item Short-Form Health Survey,6 the functional independence measure (FIM),5 and the Caregiver Dependency Scale.4 The Canadian Occupational Performance Measure (COPM)200 and the Goal Attainment Scale (GAS) have been shown to be sensitive to detect changes following intervention in cerebral palsy.49 The GAS has been shown to have potential of detecting functional changes.9 A multicenter trial of intrathecal baclofen with 138 patients reported improvement in both the performance and satisfaction scores on the COPM.101

Physiologic Mechanisms No single pathophysiologic mechanism accounts for all the observable aspects of spasticity. Dysfunction within the central nervous system of descending pathways to and within the spinal cord causes a UMN syndrome that is often associated with exaggerated reflexes and spasticity, which includes velocity-dependent increased muscle tone.135 Although enhanced reflexes are sufficiently common and associated with the spasticity phenomenon to be part of its definition, measurement of the reflex amplitude in some patients (such as patients with stroke or neurologically complete SCI) has shown reductions compared with that in able-bodied subjects.176,178,207 Although the spinal α-motor neuron is considered to be the final common pathway for expression of spasticity, one should consider the more complex motor pathways involved in the disordered movements of spastic braininjured patients. Spastic hypertonia encompasses a variety of conditions, including dystonia, rigidity, myoclonus, muscle spasm, clonus, cocontraction, posturing, and spasticity.109,158,174 The following sections briefly review the physiology of segmental reflexes.

The Monosynaptic Reflex The physiologic components involved in the spinal stretch reflex response include the muscle spindle stretch receptor, the myelinated sensory neuron, the synapse, the

CHAPTER 30  Spasticity Management MUSCLE SPINDLE EFFERENTS

MUSCLE SPINDLE AFFERENTS

Static γ motor neuron Dynamic γ motor neuron

Group la fiber Group lI fiber

muscle contraction. They are innervated by special motor neurons known as the γ-motor neurons. α motor neuron

Nuclear bag fiber

Intrafusal muscle fiber

643

Nuclear chain fiber

cle fiber Extrafusal mus

Group la afferents ← Primary endings Group II afferents ← Secondary endings Static γ motor neurons → Trail endings (in nuclear chain fiber) Dynamic γ motor neurons → Plate endings (in nuclear bag fiber) FIGURE 30-1  Nuclear bag and nuclear chair fibers of the muscle spindle.

homonymous α-motor neuron, and the muscle it innervates. As originally described in the decerebrate cat model, the stretch reflex shows a dramatic increase in extensor muscle tone on passive flexion of the extended hindlimbs. This stretch reflex has two components: a brisk, short-­acting phasic component that responds to the initial dynamic change in length, and a weaker, longer-acting tonic component that responds to the steady stretch of the muscle at a new length.144 A change in muscle length can evoke a stretch reflex. Modified muscle fibers (intrafusal receptor organs) that detect changes in muscle length are called muscle spindles. Nuclear bag fibers and nuclear chain fibers are two types of specialized muscle spindle fibers (Figure 30-1). Nuclear bag fibers are further subdivided into dynamic and static nuclear bag fibers. Dynamic nuclear bag fibers are highly sensitive to the rate of change in muscle length, providing velocity sensitivity to muscle stretch.151 Static nuclear bag fibers and nuclear chain fibers are more sensitive to the steady-state, static or tonic, muscle length. The structural differences between these fibers are responsible for the physiologic differences in their sensitivities and for the two different components, phasic and tonic, of the stretch reflex. Intracellular muscle fibers are observed to undergo changes as a result of spasticity, as does the extracellular matrix.145 Group Ia and group II fibers are two types of myelinated sensory afferent fibers that innervate intrafusal fibers. Group Ia, or primary sensory, afferents convey both phasic and tonic stretch information. Group II fibers innervate static nuclear bag and nuclear chain fibers and convey information on the tonic or static change in muscle length. Contained within the muscle spindle unit are contractile elements that stiffen the region of the nuclear bag fibers. These contractile elements maintain spindle sensitivity during skeletal

The Inverse Stretch Reflex The Golgi tendon organ is sensitive to intramuscular tension and is innervated by myelinated Ib sensory afferents. The Golgi tendon organ is particularly sensitive to muscle tension created by active muscle contraction but has a high threshold for detecting passive stretch. Stimulation of Ib afferents leads to inhibition of the homonymous α-motor neuron and of its synergists. The excitation of its antagonistic motor neurons also stimulates Ib afferents. This behavior has been called the inverse myotactic reflex because its actions oppose those of the stretch (myotactic) reflex. It is also called Ib nonreciprocal inhibition. It should be noted that this reflex is stimulated by muscle tension, whereas the stretch reflex is stimulated by a change in muscle length. The Golgi tendon organ has been hypothesized to function as part of a muscle tension feedback system.137

Elevated Reflex Activity The stretch reflex can be viewed as a feedback system with muscle length as the regulated variable. Normally the gain, or input–output relationship, of the stretch reflex to a given change in muscle length is kept low by descending influences when the individual is at rest. The gain is enhanced when physical demand for performance is needed. Hyperreflexia is an example of segmental reflex dysregulation associated with an upper motor lesion. Hyperreflexia can theoretically result from a number of mechanisms, including decreased spinal inhibitory mechanisms from brain centers, hyperexcitability of α-motor neurons, peripheral nerve sprouting, and increased γ-fiber activity. Long-term reductions in inhibition can contribute to hyperreflexia. Examples of inhibition types are as follows: recurrent Renshaw inhibition, reciprocal Ia inhibition, presynaptic inhibition, nonreciprocal Ib inhibition, and inhibition from group II afferents. Various lines of research have supported deficient presynaptic and nonreciprocal inhibition as significant contributors to spasticity. The supportive evidence for it being caused by deficient group II afferent-related and Renshaw inhibition is lacking.153 Presynaptic inhibition is mediated via a γ-aminobutyric acid (GABA)ergic mechanism that decreases the efficacy of Ia afferent transmitter release. Inhibitory interneurons synapse with the presynaptic terminal of the Ia afferent via an axoaxonic synapse where GABA is the neurotransmitter. Inhibitory interneurons involved in presynaptic inhibition are modulated by descending pathways. The loss or reduction of rostral control can reduce tonic levels of descending facilitation on inhibitory interneurons, leading to increased α-motor response to normal Ia afferent input.245 The Ia afferent presynaptic inhibitory interneurons are normally controlled by descending excitatory pathways. Reciprocal Ia inhibition decreases the chance for cocontraction of antagonistic and agonistic muscles during the stretch reflex or during voluntary movement. Evidence exists for decreased excitability of the inhibitory neurons after rostral lesions of the central nervous system. This dysfunction could lead to an increased cocontraction and

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SECTION 3  Common Clinical Problems

–

+ – –

Axoaxonic synapse Golgi tendon organ

+

Muscle spindle

Group Ia and II sensory neurons Group Ib sensory neuron Inhibitory interneuron Alpha motor neuron Renshaw cell FIGURE 30-2  Influences on the stretch reflex. (Redrawn from Satkunam LE: Rehabilitation medicine. 3. Management of adult spasticity, CMAJ 169:1173-1179, 2003.)

weakness of voluntary movement.44 Nonreciprocal Ib inhibition has been found to be decreased or even replaced by facilitation in patients with spastic paresis and spastic dystonia, in this case both stroke and SCI subjects, but not in subjects without spastic dytonia.59 Patients with spastic paresis from SCI show increased rather than decreased levels of recurrent Renshaw inhibition. Renshaw cells are inhibitory neurons that are stimulated by collateral axons from α-motor neurons. When an α-motor neuron fires, it stimulates a Renshaw cell that in turn inhibits the initiating motor neuron and its synergists. The Renshaw cell also inhibits the IIa afferents presynaptic inhibitory interneuron associated with the initiating motor neuron. Because the Renshaw cell inhibits the inhibitory interneurons as well as agonist α-motor neurons, increased Renshaw cell activity might contribute to spasticity by decreasing reciprocal Ia inhibition.211 Hyperexcitability of α-motor neurons might contribute to spasticity. Examples of primary changes in membrane properties that would be expected to produce increased α-motor neuron discharge include a reduction in the area of dendritic membranes, deafferentation dendritic hyperexcitability, and an increase in the number of excitatory synaptic inputs as a result of sprouting (Figure 30-2).245

Multisynaptic Segmental Connections The majority of spinal segmental connections are polysynaptic. In addition to the muscle spindle afferents making direct contact with the α-motor neuron of the agonist muscle, interposed interneurons connect these afferents and antagonistic α-motor neurons to opposing muscle groups, resulting in a polysynaptic connection. As mentioned above, the Golgi tendon organ contributes to this via Ib nonreciprocal inhibition. These reflex pathways coordinate muscle action around the joint. Interneurons also receive

excitatory and inhibitory signals from descending pathways. Supraspinal centers can control joint stiffness through the modulation of excitatory and inhibitory input to segmental interneurons and interneuronal networks.41,108 The interneurons that mediate Ib nonreciprocal inhibition connect inhibitory agonist and excitatory antagonistic motor neurons. At rest, Ib nonreciprocal inhibition opposes the actions of the stretch reflex. Convergent input from Ia spindle afferents is received by Ib interneurons, along with low-threshold cutaneous afferents and joint afferents and excitatory and inhibitory inputs from descending pathways. The Golgi tendon organ afferents make polysynaptic connections via the Ib inhibitory interneuron with the homonymous α-motor neurons and via other interneurons with the antagonist motor neurons. Because of Golgi tendon organ sensitivity to active muscle tension and the short-latency convergent input from Ia spindle afferents that Ib interneurons receive, cutaneous afferents, joint afferents, modulating descending pathways, and spinal interneuronal networks are likely to play an important role in exploratory movements of the limbs. A functional example of this network organization would be the reduction of muscle contraction if a limb encountered an unexpected obstacle. The interneuron receiving Ib afferent information would mediate the inhibition of the agonist, which would reduce the force against the impediment. Ib inhibition could also function to decrease muscle contraction at the extreme range of joint motion. The net effect of Ib inhibition during volitional activity depends on inputs from multiple sources. Recurrent Renshaw inhibition takes place via polysynaptic connections to α-motor neurons. Renshaw cells not only directly inhibit the homonymous α-motor neuron but also disinhibit the antagonist α-motor neuron via Ia inhibitory interneurons. The Renshaw cells are also influenced by the descending pathways. These polysynaptic connections also help to coordinate the action of muscles around a joint. The majority of group II afferent connections are polysynaptic and involve several classes of interneurons. These interneurons typically arise from muscle spindles, but some afferents originate as free nerve endings or in other types of receptors. Their activation tends to activate flexor synergistic muscles and inhibit physiologic extensors. Unopposed, group II-mediated activity produces tonic activation of physiologic limb flexors. Group III (Aδ fibers) and IV (C fibers) afferents originate from deep muscle and cutaneous receptors. Group III fibers are thinly myelinated. Group IV fibers are small-diameter afferents, often unmyelinated, and originate as free nerve endings serving nociceptive and thermoregulatory functions. Both types of fibers convey impulses generated by extreme pressure, heat, and cold. Similar to type II responses, the reflex responses to these stimuli are bilateral flexion predominantly and are typically proportionate to the stimulus intensity. The afferent fibers that produce generalized reflexive flexor movements have become known collectively as flexor reflex afferents. Interestingly, the response to cutaneous stimuli is not always one of generalized flexion. The vestibulocollic and cervicocollic reflexes produce patterns of coordinated ipsilateral limb flexion accompanied by contralateral limb extension with activation of group

CHAPTER 30  Spasticity Management

II and III fibers to either keep the head level during body tilt or to oppose a fall. Different modalities of stimuli can have differential effects, particularly evident after a neurologic injury. For example, after certain neurologic lesions, pressure applied to the plantar surface of the foot produces a marked extension of the leg, known as extensor thrust. In contrast, a pinprick in the same area leads to flexion withdrawal of the limb. The spinal circuits responsible for ipsilateral flexion and crossed limb extension also receive descending inputs and coordinate voluntary limb movements. A cutaneous stimulus can modulate the activity of particular motor neurons. Touching an area of skin can cause a reflex contraction of specific muscles, usually those beneath the area of stimulation. This is an example of an exteroceptive response. Cutaneous stimuli might not always produce observable contractions. They can have subthreshold or facilitative effects. Proprioceptive information is transmitted from muscle spindles and Golgi tendon organs via group Ia, II, and Ib afferents. Finally, there are indications that pathway connectivity and neurotransmitter distribution might account for differential responses comparing the upper limbs with the lower limbs.159

Goal Setting Because spasticity results from neurologic dysfunction within several regions in the central nervous system, the associated loss of voluntary motor function can be highly variable among patients with symptomatic spasticity. Prediction of the functional impact resulting from the presence of spasticity consequently can be challenging. Compare an individual with C4 tetraplegia who uses a mouth stick or suck and puff actuator to operate a computer, telephone, and numerous adapted electronic devices, as well as a head controller to operate an electric wheelchair, for example, with a person with T10 paraplegia. The presence of mild to moderate spasticity can alter the sitting position so that the control over the adaptive devices is lost for the person with tetraplegia, whereas the paraplegic person does not experience the same functional impact to that level of spasticity intensity. The functional goal for spasticity treatment should be one within the ability of the patient when the performance of the function is limited mainly by spasticity. Common examples of spasticity-limited functional goals are to improve speed and safety of wheelchair transfers, to improve the performance of activities of daily living such as dressing, and to facilitate perineal hygiene by reducing thigh adductor or pectoral muscle spasticity, thus facilitating ease of caregiver assistance. One must consider also the extent to which the spasticity helps the individual functionally; therefore the goal of functional improvement must consider the balance of treatment effects. Spasticity can be protective against skeletal muscle atrophy and indirectly affect functional independence, ambulation, and incidence of fracture.93 Spasticity has been reported to increase glucose uptake and thereby reduce the risk for diabetes in those with SCI.20 One potential functional goal might be the improvement of gait. Although patients with spasticity are reported to have disturbances of gait speed, timing, kinematics, and

645

electromyographic patterns, the relative impact of spasticity on gait remains controversial.76,78,133,196 Although it seems logical that knee extensor muscle torque should correlate with the speed of “comfortable” walking, by experimental measurement it accounts for only 30% of the variance in gait speed in spastic stroke patients.23 Young244 concluded that not all abnormalities underlying “spastic gait” are caused by spasticity, and consequently are not affected by antispasticity drug treatment. Pain and fatigue are examples of other factors that can contribute to functional limitations. Spasticity can be caused or exacerbated by pain. The presence of pain is widely acknowledged as a significant negative contributor to the quality of life. The time and energy required to complete a task also could change more with the presence of spasticity and its treatment than with the actual ability or inability to complete the task. Spasticity can significantly disturb sleep, contributing even more to fatigue. If there are treatable goals such as improving function, hygiene, ease of care, and seating and positioning, as well as decreasing pain, contractures, or sleep disturbance, then treatment options can be offered as follows.

Nonpharmacologic Treatments A regular exercise routine that includes daily range of motion exercise must be done, with a focus on muscle stretching. This can be accomplished with assistance from a therapist in the short term, but in the long term the exercise should be taught to be done by self or caregivers.31,102,197 Immediate reduction in spasticity can be seen objectively from passive movements or from stretch.187,220 Any spasticity-aggravating factors (e.g., urinary tract infection, constipation, skin ulceration, ingrown nails, and fractures) must be identified and treated. A number of other helpful physical treatments can be used. Casting a joint with the muscle in a lengthened position can help maintain muscle length, with serial casting allowing for progressive improvement in joint range. With this treatment, however, one must be extremely vigilant not to cause skin breakdown from pressure points in the insensate limb. Externally applied repetitive cycling movements to the lower limbs using a motorized exercise bicycle has allowed some subjective improvements but no objective changes in torque resistance response to movement.121 Another approach to spasticity reduction is hippotherapy, which involves the rhythmic movements associated with riding a horse to regulate muscle tone. The short-term effect of hippotherapy has been shown in decreasing spasticity of the lower limb as noted by the Ashworth Scale and self-reported spasticity with a small crossover randomized clinical trial.138 In a recent review of the literature pertaining to randomized trials of antispasticity treatments for amyotrophic lateral sclerosis, the recommended treatment included individualized, moderate-intensity, endurancetype exercises for the trunk and limbs.11 Electrical stimulation of the spinal cord has been reported to result in reduction of spasticity,15,103 although the measurement of spasticity in these studies has been questioned.61 Several investigators have shown that electrical stimulation of the peripheral nerves can decrease spasticity in patients

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SECTION 3  Common Clinical Problems

with SCI, stroke, or traumatic brain injury.* Other physical modalities that have been reported to ameliorate spasticity include application of tendon pressure,140 cold, warmth, vibration, splinting, bandaging, massage, low-power laser, and acupuncture.90,96 Some success has also been reported with magnetic stimulation over the thoracic spinal cord185 and topical application of 20% benzocaine,206 although these are not mainstays of therapy at this point.

decreased excitatory transmitter release, and subsequently reduced motor neuron firing. For this reason, presynaptic inhibition of the afferent neuronal terminal reduces motor neuron output without direct inhibition of motor neuron excitability. Because GABA does not cross the blood-brain barrier, it would not be useful as an oral antispasticity agent.

Pharmacologic Treatments

The main inhibitory neurotransmitters in the central nervous system are GABA and glycine. The physiologic action of GABA on the Ia-mediated spinal reflex is by presynaptic inhibition, as was shown in the 1940s by Sir John Eccles. GABA-containing cells are typically small interneurons. Localized ischemia is a common experimental methodology for eliminating these small GABA-containing interneurons while leaving long tracts intact. A spinal transection, on the other hand, disrupts long tract function but does not decrease the number of GABA interneurons or the concentration of GABA in spinal tissue below the level of transection. Once GABA is released by GABAergic interneurons, free GABA is released to bind to receptors on the postsynaptic membrane. The classic GABAA receptor has been characterized as having a number of cell membrane protein subunits: α, β, and γ. GABA binding activates the receptor, which stimulates the chloride ionophore channel, resulting in membrane hyperpolarization. When an axonal connection exists between a GABAergic interneuron and the terminal of a Ia afferent, then hyperpolarization of that membrane will result in decreased excitability,

Baclofen (Lioresal). Baclofen is β-4-chlorophenyl GABA, which binds to and activates the bicuculline-insensitive GABAB receptors. Bicuculline is a toxin that antagonizes the inhibitory effects of endogenous GABA at GABAA receptors, which cause treated animals to convulse. Once a presynaptic GABAB receptor is activated, potassium conductance is altered, resulting in a net membrane hyperpolarization and a reduction in endogenous transmitter release.53,112 For example, in a presynaptic sensory neuron, release of GABA by a local interneuron and binding at the receptor on the sensory neuron produce inhibition of the primary afferent terminal, and result in a decrease in excitatory neurotransmitter release. Baclofen activation of receptors postsynaptically inhibits calcium conductance and causes inhibition of γ-motor neuron activity, reduced drive to intrafusal muscle fibers, and reduced muscle spindle sensitivity.234 The overall inhibitory effect of baclofen administration at the spinal cord level reduces sensory and motor neuron activation. It also reduces the activation of monosynaptic spinal reflexes and, to a lesser extent, polysynaptic spinal reflexes. Numerous clinical reports note the antispasticity effects of oral baclofen for patients with multiple sclerosis or SCI.* Orally delivered baclofen has recently been studied in patients with cerebral disorders and was found to have selective efficacy on lower limb spasticity but not on spasticity in the upper limbs.159 Short-term studies with multiple sclerosis patients suggest that gait enhancement is observable with effective spasticity treatment in selected patients.189,222 Baclofen absorption after oral administration occurs mainly in the proximal small intestine. This probably involves two different amino acid transporter systems as a result of competitive inhibition of absorption by the neutral and β amino acids. The kidney normally excretes the baclofen essentially unchanged, but the liver can metabolize as much as 15% of a given dose. This is why periodic liver function testing is advisable during baclofen treatment, and the dosage should be reduced in patients with impaired renal function. The average therapeutic half-life of baclofen is 3.5 hours but ranges from 2 to 6 hours. Baclofen dosing is usually initiated as 5 mg three times per day and increased gradually to a therapeutic level. The recommended maximum dosage is 80 mg/day in four divided doses.127 Reports of improved therapeutic effects with higher dosages have been published.1,128,222 Because baclofen treatment can produce sedation, patients should be cautioned regarding the operation of automobiles or other dangerous machinery and activities made hazardous by decreased alertness. Baclofen is excreted by the kidneys, so patients with renal impairment will likely require

*References 12, 63, 141, 142, 204, 205, 213, 243.

*References 1, 66, 77, 113, 118, 120, 128, 194, 215, 216.

The first treatment that usually springs to mind for spasticity is pharmacologic. It is hoped that, after reading the preceding paragraphs, what also comes to mind is excellent medical management, treatment of aggravating factors, and use of physical modalities. Nevertheless, pharmacologic treatment is often required in the management of spasticity, and it is important to have a thorough understanding of the various effects of the medications in this class of therapeutics. The specific pharmacologic effects can be directed toward alteration of transmitters or neuromodulators by suppression of excitation (glutamate), enhancement of inhibition (GABA or glycine), a combination of noradrenaline (norepinephrine), serotonin, adenosine, and various neuropeptides, or action on peripheral neuromuscular sites. Although numerous substances have potential antispasticity effects, the USA Food and Drug Administration (FDA) has approved only four prescription pharmaceuticals for the treatment of spasticity related to central nervous system disorder. These are baclofen, tizanidine, dantrolene sodium, and diazepam. These four agents will be discussed first, followed by other pharmaceuticals with similar pharmacologic actions but without an FDA-approved antispasticity indication.

Enhancement of Segmental Inhibition via GABA

Medications With GABA-Mimetic and GABA-Like Actions

CHAPTER 30  Spasticity Management

a lower dosage. The effects of chronic baclofen treatment during human pregnancy are largely unknown. In some patients, seizure control has been lost during treatment with baclofen.131 Abrupt discontinuation of baclofen can produce seizures, confusion, hallucinations, and rebound muscle spasticity with fever.231 Oral baclofen is a widely prescribed pharmaceutical in North America, and there are few reports of major toxicity. Massive overdose with oral baclofen has been reported, however, including a case report of a 57-year-old woman who ingested 2 g of baclofen, causing coma and hypoventilation. She was given naloxone, 50% dextrose, and activated charcoal. Initially her blood pressure was low, and later systolic hypertension was noted, followed 16 hours later by bradycardia and hypotension. Her pupils were small and unresponsive, and muscle stretch reflexes were absent. Plasma baclofen concentrations over time showed first-order elimination kinetics and a half-life of 8 hours.89

Modulating the Monoamines

647

Tizanidine is well absorbed after an oral dose, with extensive first-pass hepatic metabolism to inactive compounds that are subsequently eliminated in the urine. Therefore tizanidine should be used with caution in patients with known liver abnormality. Because the most common side effects reported during the clinical trials with tizanidine include dizziness and drowsiness, it is recommended that tizanidine therapy begin with a single dose of 2 to 4 mg at bedtime. The titration of tizanidine should be tailored to the patient. The maintenance dosage is the one at which the therapeutic goals have been met with the fewest side effects. The scored tizanidine tablets contain 4 mg. Dosage increases of 2 to 4 mg every 2 to 4 days are recommended; most clinicians experienced with tizanidine, however, recommend a slower and more gradual upward titration. This is particularly the case for patients with multiple sclerosis, who tend to experience side effects at lower dosages. The maximum recommended dosage is 36 mg/day. All trials, including those in people with SCI, multiple sclerosis, or cerebral disorders, have reported somnolence consistently in 42% to 46% of the patients.162,179,221

Tizanidine (Zanaflex) Tizanidine is an imidazoline derivative and agonist that binds to α2-receptor sites both spinally and supraspinally,46,210 similar to the α2-adrenergic agonist clonidine (see description following). The medical literature supports the notion that the pharmacologic effects include the restoration or enhancement of presynaptic inhibitory modulation of spinal reflexes in patients with spasticity.57,175,182,227 Tizanidine has been shown to decrease reflex activity, especially polysynaptic reflex activity.54,55,227 Tizanidine also has an antinociceptive effect as shown in animal models.54-56,122 Several European and American studies have shown that tizanidine is equal in effectiveness to baclofen and diazepam but with a more favorable tolerability profile. The main advantage appears to be fewer complaints of treatment-related weakness. Furthermore, two clinical trials demonstrated that patients with spasticity improved muscle strength during tizanidine treatment.129,162 Gelber et al.87 describe a statistically significant improvement in upper limb spasticity, pain intensity, and quality of life in stroke patients by titrating dosages in 2-mg intervals, mindful of withdrawal rebound effects. Tizanidine has been tested in a number of clinical trials in Europe and has been found to be safe, well tolerated, and beneficial in treating spasticity of various etiologies.74 Tizanidine is an α2 agonist like clonidine but has a much reduced potency and does not consistently induce a reduction in blood pressure or pulse, as clonidine does.33 Symptomatic hypotension has been reported when tizanidine is taken with an antihypertensive drug; thus the concomitant administration of tizanidine and antihypertensive drugs should be avoided. An important drug interaction between ciprofloxacin, an antibiotic, and tizanidine has prompted the USA FDA to approve safety labeling. As a result of ­ciprofloxacin-induced inhibition of cytochrome P450 1A2, hepatic metabolism of tizanidine is decreased. The resulting increase in tizanidine plasma concentration and clinically significant adverse events is a contraindication to the coadministration of tizanidine, taken orally, and ciprofloxacin, given intravenously.

Alteration of Ion Channels Dantrolene Sodium (Dantrium) Dantrolene sodium is a hydantoin derivative whose primary pharmacologic effect is to reduce calcium flux across the sarcoplasmic reticulum of skeletal muscle. This action uncouples motor nerve excitation and skeletal muscle contraction.71,238 It is indicated for use in chronic disorders characterized by skeletal muscle spasticity, such as SCI, stroke, cerebral palsy, and multiple sclerosis. The oral formulation is prepared as a hydrated sodium salt to enhance absorption (approximately 70%), which occurs primarily in the small intestine. After a dose of 100 mg, the peak blood concentration of the free acid, dantrolene, occurs in 3 to 6 hours. The compound is hydroxylated, and the active metabolite, 5-hydroxydantrolene, peaks in 4 to 8 hours. Dantrolene sodium has been shown to produce a dose-dependent decrease in the stretch reflex109 and a percentage decrease of grip strength.79 Dantrolene is lipophilic and crosses cell membranes well, achieving wide distribution and significant placental concentration in the pregnant patient. Liver metabolism by mixed function oxidase and cytochrome P450 produces a 5-hydroxylation of the hydantoin ring and reduction of the nitro group to an amine, which is then acetylated. Urinary elimination of 15% to 25% of the unmetabolized drug is followed by urinary excretion of the metabolites after oral administration of the drug. The median elimination half-life is 15.5 hours after an oral dose and 12.1 hours after an intravenous dose. The majority of placebo-controlled clinical trials of dantrolene have shown a reduction of muscle tone, stretch reflexes, and increased passive motion. The most consistent finding has been a reduction of clonus in patients with clonus.198 Mixed conclusions have been drawn regarding the effects of dantrolene sodium on gross motor performance and strength. In comparative trials with spasticity of different etiologies, some have suggested that the best responders to dantrolene sodium are those with stroke and cerebral palsy, and that patients with SCI improve the least, if at

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SECTION 3  Common Clinical Problems

all. Most investigators agree, however, that patients with multiple sclerosis do not generally benefit from dantrolene treatment.148 In four trials of children with cerebral palsy, dantrolene sodium was found to be superior to placebo. The degree of improvement appeared greater in children than in adults. One study found dantrolene to be superior to baclofen, and another suggested equal efficacy to diazepam. In addition to its antispasticity effects, dantrolene has been used in the treatment of malignant hyperthermia and the neuroleptic malignant syndrome.231 Dantrolene has also been reported to be useful in the treatment of hyperthermia following abrupt baclofen withdrawal.126,148 At least 13 clinical reports of overt hepatotoxicity appear in the literature, five of which report hepatonecrosis. The overall incidence of hepatotoxicity in a large group of patients receiving dantrolene sodium for more than 2 months is reported to be 1.8%, with symptomatic hepatitis occurring in 0.6% and fatal hepatitis in 0.3%. The greatest risk was in women older than 30 years who were taking more than 300 mg/day for more than 60 days. Initiation of antispasticity treatment with dantrolene sodium should begin with 25 mg once daily, increasing every 4 to 7 days by 25-mg increments to 100 mg four times per day. The dosage at which the anticipated therapeutic response occurs with the fewest side effects should be the maintenance dose. Benzodiazepines The pharmacologic and antispasticity effects of benzodiazepines are generally mediated by a functionally coupled benzodiazepine–GABA receptor chloride ionophore complex.45,188,212 As described above, the GABAA receptor supramolecular structure is envisioned as a heteropentameric glycoprotein of about 275 kDa, whose subunits react with GABA, benzodiazepines, steroids, barbiturates, and picrotoxin-like convulsants.146 More specifically, the duration of action is related to the receptor and pharmacodynamics; certain benzodiazepine subunits are either highaffinity or low-affinity receptors, as well as long-acting and short-acting benzodiazepines. Benzodiazepines enhance GABAA receptor current, which increases the opening frequency of the chloride ionophore without altering channel conductance or open duration.228 The relative length of action is also related to the duration of activity and rate of metabolism of the pharmacologically active metabolites. Examples of long-acting benzodiazepines are diazepam, chlordiazepoxide, and clonazepam. Oxazepam, alprazo­ lam, and lorazepam are considered to be short acting without significant production of active metabolites. Benzodiazepines cross the placental barrier and are secreted into breast milk. Microsomal enzymes of the liver metabolize the benzodiazepines extensively. Diazepam (Valium). Diazepam is a benzodiazepine that is sedating, reducing agitation and anxiety. It decreases polysynaptic reflexes and has muscle relaxant, sedation, and antispasticity effects.58,148,193 Long used as a treatment for stiff person syndrome, its effects diminish over time, requiring alternative treatment such as intravenous propafol.107 Diazepam is usually started with a bedtime dose of 5 mg, increased to 10 mg as needed for adults, but is found to be effective when given 0.1 to 0.05 mg/kg and excessively sedating in children when given in excess

of 1 mg/kg.150 Diazepam is well absorbed after an oral dose, with the peak blood level occurring typically in 1 hour. Diazepam is metabolized to the active compound ­N-desmethyldiazepam (nordiazepam) and then to oxazepam. The half-life of diazepam and its active metabolites is 20 to 80 hours, and it is 98% to 99% protein-bound. In patients with low serum albumin and lower protein-binding capacity, such as is often the case in patients with SCI or stroke, the incidence of undesirable sedation is increased. Daytime therapy is initiated with 2 mg and increased as needed; a clinical trial of children with cerebral palsy, however, suggests that a single bedtime dose was sufficient to improve passive stretching exercises throughout the day with the additional benefit of being a relatively lowcost pharmaceutical.150 Intravenous diazepam is reported to have been effective in the attenuation of intrathecal baclofen withdrawal.48 Diazepam intoxication causes a range of symptoms from somnolence to coma. Although it is generally regarded as having a wide margin of safety, treatment of patients with myelopathy has been linked to increased body weight.84 Benzodiazepine poisoning also has been reported.214 Near-term infants born with benzodiazepine intoxication are at risk. A case report notes a young mother at term who consumed a diazepam overdose of 250 to 300 mg and became drowsy but responsive. The fetal heart rate showed decreased variability and absence of accelerations. The benzodiazepine antagonist flumazenil, 0.3 mg, was given to the mother intravenously. Within 5 minutes, behavioral arousal in the mother and improved fetal heart rate variability were observed.225 Typical symptoms of patients in withdrawal from high-dose diazepam (>40 mg/day) are anxiety and agitation; restlessness; irritability; tremor; muscle fasciculation; twitching; nausea; hypersensitivity to touch, taste, smell, light, and sound; insomnia; nightmares; seizures; hyperpyrexia; and psychosis. The intensity of the symptoms and risk for death are related to the prewithdrawal dose. Symptoms of withdrawal from low-dose benzodiazepine (T6 level), insensitivity, denervation atrophy, spasticity, contractures, bowel/bladder alterations78

Elderly

Reduced skin elasticity and altered skin microcirculation,199 co-morbidities, reduced healing rate noted clinically and in animal models90

Diabetes

Insensitivity, microangiopathy and altered inflammatory response,139 foot deformities (intrinsic minus, Charcot), blunted reactive hyperemia, reduced incision breaking strength,154 and contraction92 in animal models

Malnutrition

Negative nitrogen balance, cachexia, ­immunosuppression

Anemia

Local hypoxia

Arteriosclerosis

Local hypoxia

End-stage renal disease

Transient dialysis-related hypoperfusion, ­arteriosclerosis, microangiopathy

Steroid ­medications

Reduced healing rate in animal models, ­immunosuppression

Transplant ­recipients

Immunosuppression

Smoking

Hypoxia, vasoconstriction, increased blood viscosity

Parkinson disease

Immobility

Osteoporosis

Bony prominences

Upper motor neuron disease

Immobility, contractures, bowel/bladder alterations

Dementia

Immobility, malnutrition, contractures, bowel/ bladder alterations

Acutely ill ­(intensive care unit related)

Hypotension, immobility, bowel/bladder alteration, malnutrition, increased metabolic demands

Noncompliance, abuse and neglect

Multifactorial

Clinical Wound Assessment Wound Area and Volume Assessment Assessments are performed weekly or biweekly to document the effectiveness of therapy, make changes in treatment if necessary, and support the overall treatment plan. Wound Area The most straightforward technique is to document the wound’s perpendicular linear dimensions (typically in centimeters); the maximum distance is length, and perpendicular distance is width.2 Although linear dimensions can be performed rapidly, they have limited sensitivity to change in wound size, limited information about shape, and overestimate the wound area by up to 25%.88 Because of these concerns, serial wound outlines are often performed. Manual tracing, a useful and inexpensive technique, involves drawing the wound outline on clear plastic (e.g., acetate

687

sheet for transparencies) with an indelible marker. Counting the number of squares inside the wound periphery on the acetate sheet gives an estimate of wound area.2 These drawings then become part of the patient’s permanent record. Inspection allows immediate appraisal of progress, and if the wound has increased in size, the clinician can modify the treatment without delay. Wound Volume For a first approximation of volume, area is multiplied by depth to find volume. The volume of a rectangular solid calculated in this manner overestimates the volume of pressure ulcers. Computing volume of a spheroid is more accurate.88 By either calculation, using depth is most accurate for deep cavities and least accurate for shallow, irregularly shaped wounds. Wound Appearance To describe wound appearance, the red–yellow–black system is often used (wounds classically transform from black, to yellow, to red as they heal; Figure 32-1). One method is to classify a wound as the least advantageous of the three colors that it displays.123 This method has been criticized as simplistic. The color of the wound surface can be alternatively described as a relative percentage of the three colors. Digital photography makes it convenient to serially classify with wound color. Computerized Assessment of Wound Geometry Computerized systems have been developed for more accurate and automated assessment of wound geometries. Digital planimetry enables automatic calculation of the wound area once the wound edge is traced manually or digitally.95 Excellent interrater and intrarater reliabilities and concurrent validity have been reported for computerized planimetry compared with other methods of wound area determination.83,116,216 Stereophotographic systems use multiple cameras to reconstruct the three-dimensional shape of the wound (Figure 32-2). This gives the most exhaustive representation of the geometry of the wound surface because virtually no loss of information is involved. To assess the volume and depth of the wound, the geometry of the original intact skin overlying the wound is required. The wound volume is the volume of the region enclosed by the recorded wound surface and the surface of the original intact skin. Because the original skin surface has already been destroyed, it is reconstructed computationally by interpolating the normal skin neighboring the wound. Regions of fast and slow healing (e.g., via granulation tissue induction) can also be tracked by following the geometry of the wound surface (Figure 32-3). In summary, wound measurement techniques need to be accurate, reliable, and reproducible. When used for clinical and research purposes, any measurement technique must possess a high level of sensitivity and specificity. Measurement techniques must also be easy to use. Volumetric wound assessment is paramount for the refinement and advancement of modern wound measurement techniques., The current state-of-the-art stereographic volumetric systems, however, are not yet readily available to the clinician.

688

SECTION 3  Common Clinical Problems

10

Area (cm2)

8 6 4 2 0

0

20

40

60

80

100

120

140

Time (days) FIGURE 32-1  Illustrated is the transformation of wound bed from black eschar, to yellow slough, to beefy red granulating base. As the wound bed granulates, area (determined by serial outlines) first increases, then stabilizes, then decreases as epithelialization commences over a granulating wound base. Of the 16 weeks spent in healing this wound, almost half was devoted to wound bed preparation and half to epithelialization. Patient is a 38-year-old man with type 1 diabetes and “small vessel disease,” which is often associated with black eschar. Lines connect the wound photographs to corresponding time points. (From Goldman R, Salcido R: More than one way to measure a wound: an overview of tools and techniques, Adv Skin Wound Care 15:236-243, 2002.)

compression might cause pressure necrosis; and (2) the degree of perfusion is predictive of wound closure. Macrocirculation Macrocirculation refers to blood flow through named anatomic arteries, such as the iliac, femoral, posterior tibial, and plantar arteries.

FIGURE 32-2 The three-dimensional geometry of a wound reconstructed by a stereophotographic wound measurement system (MAVIS-II). (Courtesy Dr. Peter Plassmann, University of Glamorgan, Pontypridd, U.K.)

Perfusion Assessment It is exceedingly rare that large vessel disease contributes to the formation of pressure ulcers of the trunk, occiput, hips, or buttocks. As a result, perfusion is more commonly assessed on distal wounds of the leg and foot. It is very important to have a regional assessment of perfusion because (1) in the setting of poor perfusion, therapeutic

Ankle–Brachial Index and Pulse Volume Recording. Ankle–brachial index (ABI) is the ratio of systolic blood pressure of the ankle to that of the arm (brachium).88 Normal ABI is 0.8 to 1.3 and can be determined by a portable Doppler instrument and a blood pressure cuff. A series of cuffs can be used to obtain a pulse volume recording (PVR), which is continuous monitoring of pressure within cuffs applied to the thigh, calf, and ankle. These segmental pressure traces are checked for bilateral symmetry and waveform morphology. Pulse pressure curves of normal arteries resemble steep isosceles triangles. Flattened pulse pressure waveforms or asymmetric indices suggest proximal flow compromise from arteriosclerosis. For patients with diabetes, calcinosis of the tunica media often falsely elevates ABI. Because calcinosis is less likely to involve foot arteries, it is often helpful to determine toe pressures. To determine toe pressure, a tiny cuff fits over the hallux and a Doppler probe records systolic pressure. A pressure greater than 40 mm Hg is a good prognostic indicator of healing a foot ulcer. Toe pressure and ABI determination use a portable Doppler instrument and do not require a dedicated vascular laboratory.23

CHAPTER 32  Prevention and Management of Chronic Wounds

Reference is tag1

8-7-04 Red labeled reference surface

tag1 tag2 tag3

– 4.00 mm

tag4

– 3.00 mm

tag5

– 2.00 mm

Surface area (selected/not selected) jahnke03zu 0.00 cm2/146.50 cm2 tag1 58.89 cm2/181.45 cm2 tag2 57.46 cm2/193.82 cm2 tag3 57.20 cm2/167.87 cm2 tag4 57.52 cm2/223.50 cm2 tag5 57.05 cm2/178.20 cm2

689

11-7-04

– 1.00 mm – 0.00 mm – –1.00 mm

14-7-04

20-7-04

29-7-04

– –2.00 mm – –3.00 mm

Relative volumes to tag1 tag2 9.30 cm3 tag3 10.50 cm3 tag4 12.31 cm3 tag5 19.61 cm3

– –4.00 mm

FIGURE 32-3  Monitoring the change in the elevation/depression of the wound geometry (from baseline) using a stereophotographic wound measurement system (DigiSkin). (Modified with permission from Körber A, Reitkötter J, Grabbe S, et al:  Three-dimensional documentation of wound healing: first results of a new objective method for measurement, J Dtsch Dermatol Ges 4:848-854, 2006.)

Angiography. Angiography typically involves injecting radiopaque dye into the proximal arterial tree. Conventional dye angiography is the gold standard for imaging macrovessels. It is an accurate prognosticator of limb salvage based on burden of arteriosclerosis visualized in the lower extremity.64 A noninvasive alternative to conventional angiography is magnetic resonance angiography, which requires no contrast dye and is superior to conventional angiography in visualizing arteries of the ankle and foot.129 Microcirculation In the skin, blood flows through arterioles, capillaries, and venules in the papillary and reticular dermis.32 A direct and absolute measure of microcirculation is transcutaneous oxygen (Tcpo2). Tcpo2 is in essence a “blood gas” of the skin. The normal Tcpo2 is greater than 50 mm Hg, with the ischemic level less than 20 mm Hg.152 A typical pattern of electrode placement is the upper leg, foot dorsum, and periwound (Figure 32-4). Tcpo2 prognosticates the healing rate of neuropathic and ischemic ulcers. Its predictive value is uniquely strong for patients with diabetes who typically have distal arterial calcinosis.152 For this population, Tcpo2 is more accurate than toe pressures to prognosticate healing.110 The surgical literature reports that Tcpo2 also prognosticates success of incisional healing at the transtibial level170 and foot level.156 A disadvantage of Tcpo2 is that the technique gives values that are inaccurately low over areas of callus and transiently low in the setting of infection80 and in the immediate postoperative situation. Tcpo2 measuring instruments are expensive ($2500 to $5000 per channel) and time-consuming (20 minutes to 1  hour to obtain a reading).

The most complete picture of lower extremity perfusion comes from combining Tcpo22 and segmental pressures. For example, very low distal segmental pressures (i.e., ABI 30% TBSA

Laserskin

Chronic wounds, deep partial- and full-thickness burns >30% TBSA

AlloDerm

Deep partial- and full-thickness burns

Cellular dermal allograft

TransCyte

Superficial partial-thickness wounds not requiring skin grafts, deep wounds requiring subsequent skin grafts

Composite allograft

Apligraf

Chronic wounds, excision sites, epidermolysis bullosa

OrCel

Skin graft donor sites, chronic wounds, epidermolysis bullosa

Synthetic monolayer substitute

Suprathel

Split-thickness skin graft donor sites, partial-thickness burns

Synthetic bilayer substitute

Biobrane

Superficial partial thickness burns, temporary coverage of excised wounds, split-thickness skin graft donor sites

Integra

Coverage after excision of deep burns, chronic wounds, traumatic wounds, draining wounds

Autograft

Cultured autologous skin

Allograft

Acellular dermal allograft

TBSA, Total body surface area.

stage IV pressure ulcers, bone, tendon, or muscle is exposed. Full-thickness lesions with wound bed covered with slough or eschar are called “unstageable.” Recently added to the staging system is suspected deep tissue injury (DTI), where the skin is intact but discolored. DTI can also be present when a blood-filled blister is present as a result of damage of underlying soft tissue. DTIs are lesions confined to the deep tissues but with intact skin. They arise in deep muscle layers covering bony prominences as a result of high tissue stresses adjacent to the prominences and are aggravated by muscle stiffening caused by prolonged compression.81,82 The vulnerability of skeletal muscles to ischemia/hypoxia as described previously is an etiologic factor of DTI. The pressure ulcer staging system is illustrated in Figure 32-6. Decubitus ulcer and bed sore are terms used interchangeably with pressure ulcers. These terms, however, have a connotation of describing pressure ulcers arising in bedridden patients only and consequently are not recommended. Patients with intact sensorimotor function can use periodic movements to relieve noxious mechanical stimuli prone to cause pressure ulcers. However, patients who are comatose, severely demented, or who are insensate (e.g., patients with SCI) are at increased risk. Spasticity, contractures, immobility, incontinence, cachexia, diabetes, and advanced age also increase risk. It has been suggested that patients with darkly pigmented skin are at higher risk because nonblanching erythema of stage I pressure ulcers might not be readily visible on casual inspection.187 The most common sites of pressure ulcer formation are ischium (28%), sacrum (17% to 27%), trochanter (12% to 19%), and heel (9% to 18%). A case history of a sacral pressure ulcer on a geriatric patient is provided in Figure 32-5. Sacral and trochanteric pressure ulcers are also common in patients with SCI. For more information regarding the staging systems, there are two excellent guidelines for pressure ulcer assessment and treatment,18,78 the more recent focusing on pressure ulcers in the setting of SCI. Pressure ulcers in children often occur in the setting of severe illnesses or neurologic impairments.12,145,215 Pediatric pressure ulcers also frequently result from the use of

equipment and devices.208 Potential locations for skin breakdown are points of contact with objects such as wheelchairs, orthoses, prostheses, traction boots, casts, identification bands, blood pressure cuffs, continuous positive airway pressure equipment, nasogastric and orogastric tubes, and tracheostomy plates.208 In neonates pressure ulcers are more prevalent in the head area (31%) because of the disproportionately large head compared with the rest of the developing body. In neonates the buttock/ sacral area and foot area account for only 20% and 19%, respectively.12,136,184 Treatment The mainstay of pressure ulcer treatment is evidenced-based medical and nursing care, including continence care. In the long-term care setting or at home, the debilitated or partially dependent patient with a pressure ulcer should be turned at a minimum every 2 hours.169 The side-lying position should be avoided as much as possible, however, because of high pressures against the trochanteric region. Much lower pressures are recorded for the 30-degree side-lying positions, between which patients should be transferred during position changes.53 Wound area, depth, undermining, and appearance should be assessed at least weekly, and treatment should be modified as necessary to maintain healing rate. Nutritional management is a critical issue for patients with pressure ulcers (see discussion of nutrition in this chapter). Total enteral nutrition should be considered if oral intake is inadequate and likely to remain so. Pressure ulcers with necrosis or fibrin must be periodically debrided (e.g., sharp, mechanical, or enzymatic). Deep wounds should be irrigated. Irrigation can also be done at the bedside with normal saline using a 50-mL syringe with a 19-gauge flexible catheter. After irrigation, all “dead space” should be loosely packed. Significant drainage is managed with foams, alginates, or specialty absorptives at an adequate change schedule, so that the dressing can be moist (but not soaked). Hydrogels are appropriate once drainage has diminished and is minimal to moderate, and the wound is completely granulating. Without an underlying absorptive layer, hydrocolloids (e.g., Duoderm)

696

SECTION 3  Common Clinical Problems Stage I

Stage II

Stage III

Stage IV

redistribute pressure and are referred to as “static” types of devices. Pressure-relieving devices can also be “dynamic” (i.e., they require an energy source to redistribute pressure). An example of a dynamic system is a low air loss (e.g., the SAR Low Air Loss Mattress System). Pressurerelieving, dynamic systems are required for high-risk patients (e.g., those with complete SCI) who cannot turn themselves off the ulcerated surface (i.e., they need assistance for bed mobility). Seating systems for wheelchairs are prescribed to many patients who lack protective sensation. Examples include air-filled villous cushions (e.g., Roho), contoured foam with a gel insert (e.g., Jay), or contoured foam on a solidseat wheelchair (e.g., polyurethane). For patients who cannot perform weight shifts, mechanical weight shift devices (i.e., tilt-in-space) are appropriate. “Doughnuttype” devices should be avoided because they might be more likely to cause pressure ulcers than prevent them.50 In a comprehensive study including 19,889 elderly residents in 51 nursing homes, 28% of stage III and 20% of stage IV ulcers were healed using optimal treatment strategies after 3 months of treatment, with the majority healed within 1 year.28,201 This report illustrates that pressure ulcers are challenging to heal. The report also indicates that healing is possible with careful attention to wound bed preparation, pressure relief, moisture balance, and nutrition (all elements of conservative, nonsurgical standard care). Recent studies on adjunctive treatments have the goal of improving these outcomes. Those therapies that are commercially available and are supported by prospective randomized controlled clinical trials include electric stimulation70,79,94 and normal temperature therapy.205 The use of growth factor therapy PDGF-BB for pressure ulcers, although supported by several randomized clinical trials,166 remains controversial.85,150 The increased use of negative pressure wound therapy and the strength of evidence for its clinical use is evolving.73,203 Prevention

FIGURE 32-5  Pressure ulcer staging system. Although there is no consensus on generalizing the Shea Index to leg ulcer types, for reimbursement purposes, practitioners are frequently asked to describe stasis or neuropathic wounds according to the Shea Index. (Modified with permission of the National Pressure Ulcer Advisory Panel, Washington, DC.)

are appropriate by themselves for stage II ulcers or small, clean stage III wounds. Pressure relief in bed includes placing pillows or other cushioning between trochanteric prominences and bed surface for side-lying, keeping the bed as horizontal as possible, and using heel protectors. The efficiency of pressure and shear stress relief correlates positively with cost (Table 32-4). The most expensive systems are called “pressure relieving” because they theoretically maintain tissue interface pressure below capillary closing pressure of 32 mm Hg. Those systems with peak pressures more than 32 mm Hg but that are better than hospital mattresses are called “pressure reducing.” Pressure-reducing surfaces work by using air, gel, water, or foam to passively

A good argument can be made that some pressure ulcers cannot be avoided, especially on moribund patients.210 One large hospital-based cohort study found that having a DNR order was a significant risk factor for pressure ulcer formation.147 Formation of multiple stage III and IV pressure ulcers near the end of life has been termed “skin failure.”210 For patients with advanced age and with a reasonable chance of long-term survival, education, inspection, and continued pressure and shear stress optimization are the keys to prevent the first or recurrent ulcerations. In the long-term care setting, assessments by the Norton147 or Braden19 Scales are reliable and valid. The Braden Scale might be more cost-effective21 and is widely used in the United States. It comprises six subscales that reflect sensory perception, skin moisture, activity, mobility, shear force, and nutritional status. A score of 12 or less indicates high risk necessitating aggressive inspection, nutritional, and support surface interventions. For the assessment of pressure ulcer risk in the pediatric population, Braden Q Scale, Neonatal Skin Risk Assessment Scale, and Glamorgan Scale have been clinically validated in terms of efficacy and reliability.12

CHAPTER 32  Prevention and Management of Chronic Wounds

A

B

C

D

697

FIGURE 32-6 The course toward healing for a 66-year-old woman with type 2 diabetes mellitus who developed a stage III sacral pressure ulcer during a prolonged acute hospitalization for bilateral iliofemoral bypass complicated by congestive heart failure. On initial evaluation, 2 months postoperatively, the wound had a foul odor and was covered with yellow-green eschar laterally. Wound size was 4 × 8 cm and 2.5 cm deep (A). The patient received a pressure-relieving surface, nutritional interventions, two sharps debridements, and saline/dilute Betadine (1:100) wet to dry. B, Wound 3 weeks after initial evaluation, after the second sharps debridement. After this, topical treatment included papain-urea-chlorophyllin copper complex (Panafil) with a specialty adsorptive (ABD) and overlying composite (Alldress), changed daily at first. Nine weeks later the wound is actively contracting (C). With contraction, wound reached 95% closure 28 weeks after initial evaluation but took an additional 12 weeks to achieve full closure (D).

Surgery of greater than 4 hours duration is associated with the development of pressure ulcers that involve the heels and sacrum.176 A program of risk assessment, pressure ulcer grading, pressure-reducing mattress, and an educational awareness program reduces pressure ulcer incidence by 50%.105 Another high-risk group is patients with SCI. An incidence of pressure ulcers ranging from 23% to 30% in patients with SCI and a cumulative prevalence of 85.7% in patients with paraplegia have been observed.78,192 An SCI consensus panel advocates education, daily skin inspection, frequent weight shifts, and pressure-reducing or pressure-relieving support surfaces for prophylaxis.78

a pressure ulcer. The disadvantage of this test is its limited use in patients with dark skin color in whom redness is often difficult to observe. This might be a contributing cause of the high proportion of patients developing stage III and IV pressure ulcers in African-American and Hispanic populations.120,138 A multitude of screening tools drawing on various technologies are being developed to detect stage I pressure ulcers irrespective of the patient’s skin tone, although none are yet ready to be used in the clinical setting. These technologies purport to detect substantive biophysical changes in skin tissue that accompany ulcerations.

Screening of Pressure Ulcers Detection of early-stage pressure ulcers is an important goal because in stage I pressure ulcers the skin is still intact and recovery is typically easier than in later stages. The early detection of pressure ulcers has recently become even more crucial in light of the Inpatient Prospective Payment System of the Centers for Medicare & Medicaid Services (CMS). The Hospital-Acquired Conditions provision in the regulation requires hospitals to identify whether certain specified diagnoses such as pressure ulcer are present when the patient is admitted. For discharges occurring on or after October 1, 2008, CMS full reimbursement might not be available to hospitals to cover for the extra cost incurred in the treatment of stage III or IV pressure ulcers that had not been documented on admission.2 The clinical procedure for identifying a stage I pressure ulcer is the manual blanch test. A stage I pressure ulcer is diagnosed when redness persists after the release of pressure exerted by the finger on that area suspected of having

Uncomplicated Chronic Venous Ulcers Presentation Patients with chronic venous ulcers usually have a history of previous venous ulcer, dependent edema, previous deep venous thrombosis, pelvic surgery, vein stripping, or vein harvest for coronary artery bypass graft. Peripheral pulses are typically intact (although it is sometimes difficult to palpate pulses through edematous skin). A well-granulating ulcer with irregular borders positioned about the medial malleolus is typical of saphenous vein dysfunction. Although the “gator area” (i.e., lower third of the leg) is typical, venous ulcers can be located anywhere on the lower leg, ankle, or edematous foot dorsum. Frequently associated with the venous ulcer are lower leg hyperpigmentation and a “knobby” induration of subcutaneous tissue called lipidermosclerosis.66 Edema of the leg is a hallmark of venous stasis disease, and stasis

698

SECTION 3  Common Clinical Problems

Table 32-4  Advantages and Disadvantages of Support Surfaces Surface

Advantages

Disadvantages

Low maintenance

Can be punctured

Inexpensive

Requires proper inflation

Static overlays Air

Multipatient use Durable Gel

Low maintenance

Heavy

Easy to clean

Expensive

Multipatient use

Little research

Resists puncture Foam

Water

Lightweight

Retains heat

Resists puncture

Retains moisture

No maintenance

Limited life

Readily available in the community

Requires heater

Easy to clean

Transfers are difficult Can leak Heavy Difficult maintenance Procedures difficult

Dynamic overlays

Easy to clean Moisture control Deflates for transfers Reusable pump

Replacement mattresses

Noisy Assembly required Requires power

Reduced staff time

High initial cost

Multipatient use

May not control ­moisture

Easy to clean Low maintenance Low air loss

Can be damaged by sharp objects

Head and foot of bed can be raised Less frequent turning required

Loses effectiveness Noisy Difficulty with transfers Requires energy source

Expensive

Restricts mobility

Pressure relieving

Skilled setup required

Reduces shear and friction

Rental charge

Moisture control Air-fluidized

Reduces shear and friction

Expensive

Lowest interface pressure

Noisy

Low moisture

Heavy

Less frequent ­turning required

Dehydration can occur Electrolyte imbalances can occur May cause disorientation Difficulty with transfers Hot

From Bryant R: Acute and chronic wounds: nursing management, St Louis, 1992, Mosby Yearbook.

ulceration is the end result of longstanding venous congestion (Figure 32-7). Normally the contraction of skeletal muscles in the lower limb results in the compression of deep veins and cephalad propulsion of blood in the deep venous system. This muscle pump is powered by the contraction mainly of calf muscles within an unyielding leg fascial envelope, creating cyclic pressure peaks, which can reach 100 mm Hg.119 During muscle relaxation, blood in the superficial venous system drains into deep veins through perforator veins, which are aided by valves in the perforator veins that resist blood flow from deep to superficial veins. This siphoning effect lowers the superficial venous pressure in the lower limb during standing. The valves in deep venous system and perforator veins can become incompetent, however, because of the presence of an old clot or proximal vein occlusion (e.g., from organized clot, pelvic mass, or fibrosis). The ensuing superficial venous hypertension during standing in turn is transmitted to dermal exchange vessels. The venoarteriolar reflex (which is arteriolar constriction in response to an increase in precapillary pressure) also is often abnormal in cases of severe chronic venous insufficiency. This results in failure to prevent the increased arterial pressure during standing from being transmitted to dermal capillaries.132 The increased hydrostatic pressure in the superficial microvasculature results in fluid filtration and extravasation of plasma proteins into extracellular matrix, which can overwhelm the lymphatic drainage system and cause protein-rich edema that limits nutrient delivery. Extravasated fibrinogen molecules aided by suboptimal fibrinolytic activity form fibrin cuffs around dermal capillaries. The microenvironment in the edematous region can also induce fibroblast dysfunction and can impede wound healing.52 Furthermore, capillary plugging by white blood cells reduces the number of perfused capillaries and can cause epithelial injury and inflammation. This further decreases tissue nutritional support and aggravates edema. The differential diagnosis of venous stasis ulcers includes ulcers related to congestive heart failure, lymphedema, or sickle cell anemia. Other diagnoses requiring alternative treatment approaches include squamous or basal cell carcinoma, cutaneous T-cell lymphoma, Kaposi sarcoma,197 cutaneous tuberculosis, vasculitis (such as in the setting of rheumatoid arthritis), and pyoderma granulosum. If a wound does not respond within 4 to 6 weeks or occurs on an unusual location (i.e., popliteal fossa, foot dorsum), a biopsy might be indicated (Figure 32-8).156 Diagnostic Tests The centerpiece of a recent venous leg ulcer guideline is pretreatment determination of ABI.134 For a normal ABI, standard care including compression (see later discussion) works well for most stasis ulcers. If arterial disease is suspected, segmental studies (e.g., pulse volume recordings or arterial Doppler studies) are useful to ensure that therapeutic compression is safe. Measurement of Tcpo2 is considered when the ABI is less than 0.8 or where microcirculation might be impaired (e.g., diabetes mellitus or end-stage renal disease). If the presentation warrants, venous studies including Doppler and venogram are useful to rule out acute venous thrombosis on an urgent basis. A venous duplex study might confirm venous insufficiency or postphlebitic syndrome.

CHAPTER 32  Prevention and Management of Chronic Wounds

A

B

C

D

699

FIGURE 32-7 The course of healing a venous stasis ulcer of 1 year duration and area greater than 100 cm2 on a 81-year-old woman with good blood flow (ABI = 1.2). On initial presentation, pain was significant (20 mg hydrocodone/day) as was edema (+4 pitting). Dramatic edema is also evident in the initial appearance (A). Initial care included a course of systemic antibiotics for wound infection without systemic signs (amoxicillin/clavulanate). Topical care included silver sulfadiazine to the wound with rolled gauze (Kerlex) and loose long-stretch compression bandaging toe to knee (Coban), with substantial reduction of edema by week 4 of treatment (B). Over the first 4 weeks, to decrease eschar burden there were twice per week curettage debridements, with daily dressing changes because of significant drainage.Also at 4 weeks and with a moderately red base, silver sulfadiazine was changed to a hydrocolloid with an overlying specialty absorptive dressing. Compression was tapered up to 1.5 rolls of Coban/leg at 4 weeks and 2 rolls at 8 weeks of treatment. The wound at week 12 is illustrated (C). Opiate intake continued to decrease: At 12 weeks she consumed hydrocodone 5 to 10 mg per day, and at 16 weeks, 5 mg/week. With pain decrease, drainage also decreased, resulting in need for dressing changes twice per week by week 20 and once per week by week 23. The wound closed by week 26 (D).

Treatment Compression therapy has emerged over time as the standard of care for venous stasis ulcers. Edema reduction typically results in pain reduction and wound healing. A common denominator for applying compression is application from toe to knee (distal to proximal). Two major types of compression are used: elastic and nonelastic (using long-stretch and nonstretch bandaging, respectively). Nonelastic nonstretch compression, classically the Unna paste boot, is effective.119 Edema is reduced by the inelastic dressing, which serves as a “fascial envelope” against which calf muscles can increase pressure during ambulation and reestablish a venous ankle pump. Ambulators obtain the best edema reduction. Elastic compression provides compression of 30 to 40  mm Hg continuously, depending on the elastic compression brand. Because of the “high” static pressure, elastic dressings typically have three layers to increase tolerability: (1) a primary dressing over the wound; (2) a secondary layer of padding from toe to knee, applied distal to proximal (e.g., bulky 4-inch Kerlex); and (3) an overlying long-stretch compression layer (e.g., Coban). The entire three-layer system can be purchased as a unit (e.g., Profore). Over-the-counter elastic wraps (e.g., ACE) tend not to supply an adequate and uniform compression needed to heal venous ulcers, unless the patient can adhere to a most-of-the-day schedule of waist-level leg elevation. A common error in the treatment of venous ulcers is inadequate attention to drainage management, such as in

the presence of infection. If infection is suspected and is being treated, compression therapy can be used with frequent dressing changes and debridements, or with primary dressings that are more efficient at collecting or “wicking away” drainage. Frequent dressing changes are also required for draining wounds to prevent maceration of surrounding tissues and shear stress. Inadequate drainage management is a likely common reason for failure of the weekly applied Unna boot. Although the Unna boot is durable, a disadvantage is that it requires training to apply. The Unna boot increases interstitial leg pressure during the toe-off phase of the gait cycle as a substitute for the leg’s natural ankle pump, which facilitates the flow of venous blood back to the central circulation. Because of the cyclic rather than constant pressure, the Unna boot could be the most appropriate method for mixed venous–arterial ulcers. Elastic compression is, in contrast, relatively easy to apply by caregivers in the home setting (with training). Elastic compression is best for those who are nonambulators. McGuckin et al.135 have incorporated the above set of treatments into a guideline that demonstrates efficacy; if the guideline is not used, the healing time is 4 times longer and costs 6 times more. With treatment consistent with this guideline, approximately 50% of ulcers heal after 12 weeks of treatment, and another 35% heal after 24 weeks.122 Wounds that do not close typically have these characteristics in common: ulcer size greater than 10 cm2, wound present more than 12 months, and ABI less than 0.8.

700

SECTION 3  Common Clinical Problems

A

B FIGURE 32-8  Differential diagnosis of venous stasis ulceration: basal cell carcinoma established by 3-mm punch biopsy for stasis-like ulcer on posterior leg of an elderly man with chronic obstructive pulmonary disease (A); Kaposi sarcoma (by wedge biopsy) on a 45-year-old man with epidemic AIDS, on medial ankle (B). Both lesions were unresponsive to compression therapy.

For intractable wounds for which the wound bed is optimally prepared,65 bioengineered skin substitutes can be applied beneath compressive dressings with a bolster and without suturing.59 Because of their high cost, prudence dictates that skin substitutes should be reserved for venous ulcers that remain open for an extended period despite the best conservative treatment outlined above. Prevention: Compression Stockings Once venous ulcers heal, the patient remains at risk for recurrence because the underlying venous or fascial anatomic defect remains. Compression must be a lifelong practice. Compression garments (e.g., Jobst and Juzo) look and feel like stiff stockings and come in many sizes, colors, and pressures. Most patients do well with 20 to 30 mm Hg pressure. If an adherent patient ulcerates at the 20 to 30 mm Hg level, they are then prescribed the 30 to 40 mm Hg level. Using this stepwise approach, only a few patients will require 40 to 50 mm Hg compression. Most garments are off the shelf, and only very obese patients or those with unusual-shaped legs (e.g., posttrauma) require custom-fitted stockings. Several pairs of stockings should be purchased to allow washing and rotation, and stockings should be replaced at 6-month intervals. Patient education

and “buy-in” are key to long-term ulcer prevention, and follow-up evaluation at 6-month intervals can maximize adherence.

Uncomplicated Neuropathic Ulcers Presentation Neuropathic or “insensate” foot ulcers can occur as a result of neuropathy of any cause (e.g., diabetes, leprosy45) or congenital sensory neuropathy (e.g., heredity sensory motor neuropathy type 2, lumbar meningomyelocele). The most common type in the United States, however, is neuropathy secondary to diabetes mellitus (Figure 32-9). The sensorimotor neuropathy of diabetes is a “dying back” distal neuropathy leading to preferential denervation atrophy of intrinsic foot muscles (intrinsic minus foot). This results in an unbalanced pull of long flexors and extensors leading to pes cavus, claw toes, and subluxation of the metatarsal heads. This “intrinsic minus” deformity increases the pressure on bony prominences of already insensate feet. Insensitivity most often affects the plantar forefoot first, so neuropathic ulcers commonly affect plantar toes, hallux, or metatarsal heads. Neurotrophic osteoarthropathy, or

CHAPTER 32  Prevention and Management of Chronic Wounds

A

B

C

D

701

FIGURE 32-9  Presentations of neuropathic ulceration as circular or ovoid granular wounds surrounded by callus on weight-bearing bony prominences. For each example, weight bearing is excessive because of foot deformity such as claw toe (A), subluxation of first metatarsal head (B), and Charcot foot with calcaneal bony prominence (C). These patients have diabetes mellitus with peripheral neuropathy and local insensitivity to the 5.07 monofilament. D, A 31-year-old with lumbar meningomyelocele with a left medial malleolar “fat pad” as an adaptation to ambulation on pronated feet as a child.  As an adult he no longer ambulates, but a neuropathic ulcer has occurred on this prominence as a result of repetitive trauma.

Charcot foot, frequently causes midfoot collapse and plantar-grade subluxation of the navicular or cuboid, leading to especially problematic neuropathic midfoot ulcers.95 The physical examination of an uncomplicated foot ulcer typically shows peripheral pulses to be intact, but sensation is diminished or absent in the vicinity of the ulcer, as measured by the Semmes 5.07 monofilament. Ulcers most frequently are located on bony prominences of the plantar metatarsals, midfoot, or heel. Ulcers can also be associated with digital abnormalities such as claw toes or hallux rigidus. Ulcers usually have regular borders and exuberant surrounding callus formation (see Figure 32-9 for examples of neuropathic ulcers). Sensory neuropathy and high plantar pressures (>6 kg/cm2) are independently associated with ulceration in a diverse diabetic population.74 Diagnostic Tests Segmental arterial pressures, including toe pressures, are often used to assess perfusion. If these are equivocal, Tcpo2 can prognosticate healing as long as hyperkeratotic skin is avoided (e.g., the plantar foot). If there is clinical suspicion of osteomyelitis, magnetic resonance imaging (MRI) or combined indium-leukocyte bone scan is useful before initiating conservative treatment.

Treatment Treatment strategies involve “off-weighting” the ulcer; which promotes healing by reducing mechanical irritation, inflammation, and edema. Neuropathic patients might not feel pain on ambulation, making it challenging to adhere to weight-bearing restrictions. Limited weight bearing must be implemented after a complete physiatric assessment. This assessment should result in prescriptions for orthoses, assistive devices, weight-relief shoes, physical therapy, and limited weight bearing. Local care of neuropathic ulcers follows general “good wound care” principles. The moist wound environment can be maintained by antibiotic ointments, such as mupirocin (Bactroban), or a hydrogel. Debridement (i.e., “saucerization”) is also used on a weekly or biweekly basis (see Debridement section in this chapter). Using standard methods, about 24% of neuropathic wounds are healed at 12 weeks and 31% to 47% at 20  weeks.128 Factors positively associated with healing are wound areas less than 2 cm2 and duration at time of presentation of less than 2 months.124 The disappointing results with standard care have prompted many clinicians to seek adjunctive and complementary treatment strategies for their patients with neuropathic wounds.

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SECTION 3  Common Clinical Problems

A very popular and effective treatment for recalcitrant neuropathic ulcers with good circulation is total contact casting (TCC), which many consider to be the “gold standard” of care.45,144 TCC uses very little padding, usually only around the toes, the malleoli, and the tibial crest. In contrast to a conventional orthopedic cast for fractures, TCC is lightweight and is mainly designed for protection, immobility, and uniform pressure application. Pressure concentration is avoided by virtue of the custom contour of the set plaster, and there is minimal shear stress because of negligible amount of space inside the cast to allow movement. TCC is contraindicated where Tcpo2 is less than 35 mm Hg or ABI is less than 0.45 in the affected leg.101 The effectiveness of TCC has been documented in clinical trials. An open-labeled, controlled trial revealed that in the casting group 90% of neuropathic ulcers healed during 12 weeks of observation. This is in contrast to a conventional treatment group, wherein only 26% (p 30 kg/m2). Increasing numbers of children are overweight. Currently 22% of African American children are overweight.196 Childhood obesity is linked to a greater risk for adult mortality from CVD. Overweight is associated with 300,000 deaths annually from all causes.4 Obesity is also related to increased morbidity and poorer QOL.65,67 Overweight contributes to hypertension, dyslipidemia, diabetes, and the metabolic syndrome. A 10-lb weight gain increases the risk for CVD and mortality.134 Conversely, a weight loss of 10% reduces risk factors for CAD.154 Direct economic costs of obesity-related CAD, diabetes, and hypertension approach $43 billion. Indirect costs total $31 billion, approximately 9.4% of the U.S. health care expenditure.48 Strong evidence for the positive effect of training has been established on pathogenesis, diagnosis-specific symptoms, physical fitness and strength, and QOL in obesity.166

716

SECTION 3  Common Clinical Problems

Table 33-2   Classification of Dyslipidemia

Optimal Near optimal

Total Cholesterol (mg/dL)

Low-Density Lipoprotein (mg/dL)

500

—

Table 33-3   Dietary Guidelines for Lipid Management Calorie Source

BOX 33-3

Total Daily Calories (%)

Total fat

30

Polyunsaturated fat

10

Monounsaturated fat

20

Saturated fat

88 cm (women) 2. Triglycerides >150 mg/dL 3. High-density lipoprotein 110 mg/dL 6. Proinflammatory state 7. Prothrombotic state

Metabolic Syndrome Key components of the metabolic syndrome are noted in Box 33-3. Three or more of components 1 through 5 must be present for diagnosis.153 Approximately 47 million people in the United States have metabolic syndrome. Prevalence increases with age. It is noted in nearly 45% of people older than 60 years and in one third of overweight or obese people.66 Metabolic syndrome is an independent risk factor for CAD89 and predisposes to diabetes and increased mortality.116 Treatment focuses on management of underlying risk factors including overweight, physical inactivity, and poor diet. Medications for dyslipidemia, hypertension, hyperglycemia, and thrombosis are considered to optimize control. There is strong evidence that in the metabolic syndrome, the pathogenesis of insulin resistance, specific symptoms, physical fitness, strength, and QOL are all affected by exercise.166

Emerging Risk Factors Other emerging factors associated with CAD risk are summarized in Table 33-4.

Nonmodifiable Risk Factors The risk for CAD increases with age, and men have higher rates of CAD at any age than those of women. Women lag about 10 to 15 years behind men in the incidence of CAD.245 A previous personal history of CAD, peripheral vascular disease (PVD), and CVD increases the chance of a future cardiac event. Family history also correlates with risk for CAD, although the influence of genetic predisposition is not easily separated from environmental factors and learned behaviors.187 Men and postmenopausal women are more likely to develop CAD, as are many minorities, partly because of higher rates of hypertension, obesity, and diabetes in these populations.

CHAPTER 33  Cardiac Rehabilitation

Table 33-4   Emerging Risk Factors for the Development of Coronary Artery Disease Risk Factor Lipoprotein

Carbonic acid is rapidly converted to water (H2O) and carbon dioxide (CO2):

Treatment

(a)52

Homocysteine239 Prothrombotic

717

states144

High-sensitivity C-reactive protein114

Nicotinic acid9

H2 CO3 carbonic acid dehydrogenase → H2 O + CO2

Folic acid, vitamins B6 and B12132 Aspirin101 Statins147,160,175

Exercise Physiology Adenosine triphosphate (ATP) is used to power all organ function, and is produced by one of two metabolic pathways: the aerobic and the anaerobic. Unlike anaerobic metabolism, aerobic metabolism is dependent on oxygen to drive the process.

Energy Substrates Energy substrates are the fuels used in metabolic pathways (Table 33-5). Carbohydrates and fats are the primary sources of metabolic fuel. Protein and amino acids are used as an energy source only with severe caloric deprivation, starvation dieting, or “overexercising.” Oxygen is required to maximize energy production from carbohydrates and fats. At intense external “work rates,” the body’s physiologic mechanisms cannot provide oxygen at the rate it is required by the metabolizing tissues. Aerobic pathways are limited, and anaerobic pathways take over. Muscles store energy in the form of ATP and phosphocreatine in sufficient quantities to support short bursts (10 seconds) of intense activity. Use of stored ATP and phosphocreatine is considered anaerobic metabolism. After burst activity, restoration of these stores occurs through aerobic pathways. The production of pyruvate from any substrate does not require oxygen and is also considered anaerobic metabolism. Transport of pyruvate into the mitochondria is oxygen dependent. The anaerobic conversion of pyruvate to lactic acid by lactate dehydrogenase also occurs, but has a very limited capacity to produce ATP. The accumulation of lactic acid is associated with impairment of cellular metabolic pathways, muscle soreness, fatigue, significant respiratory stimulation, and a “forced” decrement or cessation of exercise. Cardiac arrhythmias are more likely to occur under anaerobic conditions. To limit lactic acid accumulation, at least two mechanisms exist to increase its degradation. First is the Cori cycle, where lactate is transported to the liver, converted back into pyruvate and then into glucose, and released for further muscle metabolism. Second are buffering systems that are important in the energy process. With the production of lactic acid the pH of the local milieu is lowered, activating buffering mechanisms. Sodium bicarbonate (NaHCO3) is the most abundant and active buffering system for lactic acid, with the production of sodium lactate and carbonic acid (H2CO3): Lactic acid + NaHCO3 → Sodium lactate + H2 CO3

Sodium lactate is converted back to lactic acid and then to pyruvate when aerobic conditions are restored.  co2) with Detection of a spike in CO2 production ( V a metabolic gas analysis identifies the transition from aerobic to predominantly anaerobic metabolism. Dur 2 ing exercise testing the intensity of exercise when Vco  exceeds oxygen consumption ( Vo2) is considered the anaerobic threshold. Anaerobic threshold is one of the key determinants of functional and exercise performance. Because patients with HD do not feel well under anaerobic conditions, exercise intensities should be set below anaerobic threshold.

Oxygen Consumption  o2 is measured using a metabolic cart, and is the volV ume of oxygen consumed at any level of activity. Under controlled conditions, at rest, an average 70-kg man consumes 3.5 mL of oxygen per minute for every kilogram of body weight. The unit of oxygen consumption at resting, or “basal metabolic rate,” is referred to as one metabolic equivalent (1 MET). Any increment in activity will produce greater oxygen consumption, or METs. Many tables exist of the MET level equivalent for varying intensities of exercise and different activities, such as in Table 33-6. For any given level of aerobic training, as exercise intensity increases past a critical point, the ability of physiologic systems to provide oxygen is outstripped by the body’s oxygen requirements. This represents anaerobic threshold, and using metabolic gas analysis, no further  o2 is seen (Figure 33-1). A rate of maximal increase in V   o2max, or aerobic capacity). If Vo2 has been reached ( V further exercise is done after this point, anaerobic mechanisms produce the energy required. Because of lactic acid accumulation, only a short duration of further exercise is possible.

The Fick Equation Complex multicellular organisms use organ systems to transport oxygen from the atmosphere to the site of energy production. The efficiency of these systems at any given  o2max and the level of aerobic fitness determines the V maximal functional capacity. The Fick equation links the significant organ systems involved in the transportation of oxygen—lungs, cardiovascular, and muscle—and is the central theme underlying the enhanced function achieved with aerobic exercise training: Oxygen consumption = Cardiac output ¥ Arteriovenous oxygen difference Cardiac output at any degree of aerobic training is a product of the heart rate (HR) and stroke volume (SV; the volume of blood expelled by the left ventricle during one contraction). The major determinant of SV is the diastolic

718

SECTION 3  Common Clinical Problems

Table 33-5   Substrates Used in Metabolic Pathways Stored as

Circulating as

Converted to

Metabolic Pathways

Net ATP Produced

Carbohydrate

Glycogen: liver, muscle

Glucose

Pyruvate, acetyl coenzyme A

Citric acid cycle in mitochondria

36

Fat

Triglycerides: adipose tissue

Free fatty acids, glycerol

Acetyl coenzyme A, glucose

β-Oxidation, citric acid cycle

460

Protein

Muscle

Amino acids

Pyruvate or acetyl coenzyme A

Deamination

—

ATP, Adenosine triphosphate.

Table 33-6 The Metabolic Equivalent Energy Expenditure of Varying Intensity Activities Level

Self-care

Household

Recreational

Vocational

Light (1-3 METS)

Sponge bathing Shaving Dressing or undressing

Preparing light meals Setting table Dusting

Walking 2 mph Writing Reading Playing piano

Typing Light machine work Lifting 10 mm Hg from baseline, despite an increase in workload, with ischemia • Moderate to severe angina • Increasing nervous system symptoms (e.g., ataxia, dizziness, or near-syncope) • Signs of poor perfusion (cyanosis or pallor) • Technical difficulties in monitoring electrocardiogram or SBP • Subject’s desire to stop • Sustained VT • ST elevation >1.0 mm in leads without diagnostic Q waves (other than V1 or aVR) Relative • Drop in SBP of >10 mm Hg from baseline, despite an increase in workload, without ischemia • ST or QRS changes such as excessive ST depression >2 mm of horizontal, or downsloping ST-segment depression or marked axis shift • Arrhythmias other than sustained VT, including multifocal premature ventricular contractions, triplets, or supraventricular tachycardia, heart block, or bradyarrhythmias • Fatigue, shortness of breath, wheezing, leg cramps, claudication • Development of bundle branch block or intraventricular conduction delay that cannot be distinguished from VT • Increasing chest pain • Hypertensive response: Systolic blood pressure >250 mm Hg and/or diastolic blood pressure >115 mm Hg

Table33-8   Exercise Stress Test Findings Associated With Poor Prognosis Exercise Stress Test Finding

Associated Outcome(s)

Post–myocardial infarction, exercise-induced angina ­symptoms

Stable angina within 1 year53,207

Achieving 40) and found that although absolute Vo2max (mL O2/min) was similar to controls, walk/run distance was approximately 60% of the control average. Although obese adults with COPD might have greater fatigue, functional impairment, and significantly lower 6-minute walk distance compared with normal-weight individuals with COPD, similar relative improvements in walk distance are seen after pulmonary rehabilitation.58

Spinal Cord Injury and Pulmonary Dysfunction In SCI, there is diminished cardiopulmonary and circulatory function, as well as lower limb muscle atrophy and bone mass reduction. Patients with high cervical cord injuries, including children as young as 3 years, can learn neck breathing28 or GPB as forms of voluntary respiration. This allows some time off the ventilator. In GPB (or frog breathing), air is pumped into the lungs by the patient using the tongue as a piston (Figure 34-9). This technique is known as glottic press to speech pathologists. They teach it to patients who have had a laryngectomy, to pump air into the esophagus for esophageal speech. GPB can be used for a number of purposes in addition to being an alternative form of breathing. GPB can improve vocal volume and flow of speech to allow the patient to call for help, and to provide the deep breath needed for an assisted cough.

751

Many patients are now surviving significant illness only to become chronically ventilator-dependent. The number of long-term care hospitals in the United States has increased to more than 250 in the past 15 years to care for these patients. Acute lung injury survivors weaned from the ventilator have been studied 1 year after hospital discharge.19 Thirty percent still have generalized cognitive dysfunction, and 78% have decrements in attention, memory, concentration, and/ or mental-processing speed. Many also have musculoskeletal complications such as weakness and numbness resulting from critical illness neuropathy and steroid-induced myopathy. Acute respiratory distress syndrome survivors weaned from the ventilator have been studied 1 year after hospital discharge.19 Emotional dysfunction included the presence of depression, anxiety, and posttraumatic stress disorder. Long-term outcomes of diaphragm paralysis after acute SCI have been reported.51 Over a 16-year period, 107 patients required assisted ventilation in the acute phase of injury. Of this group, 31% (33 patients) with a level of injury between C1 and C4 (scale A in the American Spinal Injury Association impairment scale) had diaphragmatic paralysis at the time of respiratory failure. Twenty-one percent of the 33 patients were able to breathe independently after 4 to 14 months, with a vital capacity greater than 15 mL/kg. Another 15% (five patients) had some recovery that took more time and for whom the vital capacity remained less than 10 mL/kg. Bach3 has described in detail the long-term outcomes of NIPPV in neuromuscular disease. No patient with DMD has been tracheostomized since 1983 at the Center for Ventilator Management Alternatives and Pulmonary Rehabilitation of the University Hospital in Newark, New Jersey. Some have been using 24-hour mechanical ventilation for up to 15 to 25 years. Cardiomyopathy has become the limiting factor for survival in this population as respiratory deaths are being avoided. Wijkstra et al.79 reported the long-term outcomes of inpatients with chronic assisted ventilatory care over 15 years. Thirty-six percent of their 50 patients left the hospital to enter a more independent community-based environment. Better outcomes were seen among patients with SCI and neuromuscular disease than in patients with COPD and thoracic restriction. Gonzalez et al.30 studied long-term NIPPV in kyphoscoliotic ventilatory insufficiency (thoracic restriction) over 3 years. Patients showed improved blood gas levels and respiratory muscle performance and reduced hypoventilation-­ based symptoms and number of hospital days.

Long-Term Results for Lung Volume Reduction Surgery Naunheim et al.46 provided evidence that the distribution of emphysematic changes in lung parenchyma (measured by high-resolution computed tomography) and measures

752

SECTION 3  Common Clinical Problems

5200

5200

5L

5L

4800

4800

4600

4600

4400

4400

4200

4200

4L

4L

3800

3800

3600

3600 12 s GPB VE f Vt Gulp

= 8.9 L =4 = 2.2 L = 76 cc

1 min PFTs without GPB VE = 5.3 L f = 17 Vt = 0.31 L

VC Pred. VC % VC ERV

= 0.52 L = 2.19 L = 24% = 56 cc

FIGURE 34-9  Glossopharyngeal breathing (GPB) tracing and results compared with pulmonary function tests without GPB in a tetraplegic ventilator user with postpolio syndrome. ERV, Expiratory reserve volume; f, frequency; gulp, volume or single GPB stroke; VE, minute ventilation; Vt, tidal volume.

of exercise capacity after rehabilitation are important factors in predicting the long-term effects of LVRS. Patients who received LVRS and had emphysema predominantly in the upper lobes with lower levels of exercise capacity continued to have improved survival rates after 4 years, improved function after 3 years, and improved dyspnea after 5 years. Patients with upper lobe involvement and high levels of exercise capacity after rehabilitation continued to have symptomatic improvements when assessed after 4 years. Patients with non– upper lobe emphysema and low exercise capacity primarily experienced improvements in health-related quality of life that became insignificant after 3 years. Patients with non– upper lobe emphysema and high exercise capacity did not experience significant benefits from LVRS, and actually experienced a higher mortality rate during the first 3 years. Improvements in all groups were no longer significant after 5 years.

Long-Term Results in Lung Transplant Survival rates for all lung transplants from 1994 through mid-2005 were 78% at 1 year, 50% at 5 years, and 26% at 10 years, with the highest mortality rate occurring during the first year.73 Although perioperative mortality rates are not significantly different for all age-groups, patients older than 50 years tend to experience a lower survival rate beyond the first year.73 Sepsis and bronchiolitis obliterans remain the two most common causes of death. These results, however, should be tempered with the knowledge that the mortality rate for those on the transplant wait list is also high. For example, the 3-year survival rate for those in the sickest category of the COPD BODE Index (Body mass index, Degree of airflow Obstruction, functional Dyspnea, Exercise capacity) is only 50%.15

CHAPTER 34  Pulmonary Rehabilitation

Summary To practice pulmonary rehabilitation, physiatrists need a basic knowledge of the anatomy and pathophysiology of the cardiovascular and respiratory systems, as well as of exercise physiology. Patient assessment skills include proficiency in the electromyography of the respiratory muscles and an understanding of the rapidly expanding field of cardiopulmonary imaging. The practice of pulmonary rehabilitation can be in a setting limited to this subspecialty but more commonly is practiced as a component of general rehabilitation, where patients have pulmonary dysfunction as a complication of their neurologic or musculoskeletal disabilities or as a medical comorbidity. General rehabilitative therapeutic approaches apply in either setting. Health policy, legislation, and regulations, including current health care delivery systems, must take into account the need for pulmonary rehabilitation at all ages in society. An informed public can facilitate change in this regard. The public is more informed now because of the development of online interest groups, Internet bulletin boards, and almost 350,000 articles pertaining to pulmonary rehabilitation on the Internet. REFERENCES 1. Ambrosino N, Strambi S: New strategies to improve exercise tolerance in chronic obstructive pulmonary disease, Eur Respir J 24:313-322, 2004. 2. Aniwidyaningsih W, Varraso R, Cano N, et al: Impact of nutritional status on body functioning in chronic obstructive pulmonary disease and how to intervene, Curr Opin Clin Nutr Metab Care 11:435-442, 2008. 3. Bach JR: Management of patients with neuromuscular disease, Philadelphia, 2004, Hanley & Belfus. 4. Bach JR, Smith WH, Michaels J, et al: Airway secretion clearance by mechanical exsufflation for post-poliomyelitis ventilator-assisted individuals, Arch Phys Med Rehabil 74:170-177, 1993. 5. Barreiro E, Gea J, Sanjuás C, et al: Dyspnoea at rest and at the end of different exercises in patients with near-fatal asthma, Eur Respir J 24:219-225, 2004. 6. Benditt JO: Full-time noninvasive ventilation: possible and desirable, Respir Care 51:1005-1012, 2006. 7. Blau H, Mussaffi-Georgy H, Fink G, et al: Effects of an intensive 4-week summer camp on cystic fibrosis: pulmonary function, exercise tolerance, and nutrition, Chest 121:1117-1122, 2002. 8. Broekhuizen R, Creutzberg EC, Weling-Scheepers CAPM, et al: Optimizing oral nutritional drink supplementation in patients with chronic obstructive pulmonary disease, Br J Nutr 93:965-971, 2005. 9. Brug J, Schols A, Mesters I: Dietary change, nutrition education and chronic obstructive pulmonary disease, Patient Educ Couns 52:249257, 2004. 10. California Pulmonary Rehabilitation Collaborative Group: Effects of pulmonary rehabilitation on dyspnea, quality of life, and healthcare costs in California, J Cardiopulm Rehabil 24:52-62, 2004. 11. Casaburi R: Principles of exercise training, Chest 101:263S-267S, 1992. 12. Casaburi R, Patessio A, Ioli F, et al: Reductions in exercise lactic acidosis and ventilation as a result of exercise training in patients with obstructive lung disease, Am Rev Respir Dis 143:9-18, 1991. 13. Celli BR. Pulmonary rehabilitation in COPD. UpToDate. Online. Available at: http://www.uptodate.com. Accessed May 29, 2009. 14. Celli BR: Update on the management of COPD, Chest 134:892, 2008. 15. Celli BR, Cote CG, Marin JM, et al: The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease, N Engl J Med 350:1005-1012, 2004. 16. Celli BR, Thomas NE, Anderson JA, et al: Effect of pharmacotherapy on rate of decline of lung function in chronic obstructive pulmonary disease: results from the TORCH study, Am J Respir Crit Care Med 178:332-338, 2008.

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SECTION 3  Common Clinical Problems

42. McCool FD, Rosen MJ: Nonpharmacologic airway clearance therapies: ACCP evidence-based clinical practice guidelines, Chest 129:250S259S, 2006. 43. Mota S, Güell R, Barreiro E, et al: Clinical outcomes of expiratory muscle training in severe COPD patients, Respir Med 101:516-524, 2007. 44. Murugan AT, Sharma G: Obesity and respiratory diseases, Chron Respir Dis 5:233-242, 2008. 45. National Emphysema Treatment Trial Research Group: A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema, N Engl J Med 348:2059-2073, 2003. 46. Naunheim KS, Wood DE, Mohsenifar Z, et al: Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the National Emphysema Treatment Trial Research Group, Ann Thorac Surg 82:431-443, 2006. 47. Naylor JM, McLean A, Chow CM, et al: A modified postural drainage position produces less cardiovascular stress than a head-down position in patients with severe heart disease: a quasi-experimental study, Aust J Physiother 52:201-209, 2006. 48. Nici L, Donner C, Wouters E, et al: American thoracic society/European respiratory society statement on pulmonary rehabilitation, Am J Respir Crit Care Med 173:1390-1413, 2006. 49. Norman AC, Drinkard B, McDuffie JR, et al: Influence of excess adiposity on exercise fitness and performance in overweight children and adolescents, Pediatrics 115:e690-e696, 2005. 50. Ogden CL, Carroll MD, Curtin LR, et al: Prevalence of overweight and obesity in the United States, 1999-2004, JAMA 295:1549-1555, 2006. 51. Oo T, Watt J, Soni BM, et al: Delayed diaphragm recovery in 12 patients after high cervical spinal cord injury: a retrospective review of the diaphragm status of 107 patients ventilated after acute spinal cord injury, Spinal Cord 37:117-122, 1999. 52. Otani K, Kanazawa H, Fujiwara H, et al: Determinants of the severity of exercise-induced bronchoconstriction in patients with asthma, J Asthma 41:271-278, 2004. 53. Pastva A, Estell K, Schoeb TR, et al: Aerobic exercise attenuates airway inflammatory responses in a mouse model of atopic asthma, J Immunol 172:4520-4526, 2004. 54. Patel NJ, Jorgensen C, Kuhn J, et al: Concurrent laryngeal abnormalities in patients with paradoxical vocal fold dysfunction, Otolaryngol Head Neck Surg 130:686-689, 2004. 55. Patessio A, Carone M, Ioli F, et al: Ventilatory and metabolic changes as a result of exercise training in COPD patients, Chest 101:274S278S, 1992. 56. Pierson DJ: Translating new understanding into better care for the patient with chronic obstructive pulmonary disease, Respir Care 49:99-109, 2004. 57. Planas M, Álvarez J, García-Peris PA, et al: Nutritional support and quality of life in stable chronic obstructive pulmonary disease (COPD) patients, Clin Nutr 24:433-441, 2005. 58. Ramachandran K, McCusker C, Connors M, et al: The influence of obesity on pulmonary rehabilitation outcomes in patients with COPD, Chron Respir Dis 5:205-209, 2008. 59. Ries AL: Pulmonary rehabilitation: summary of an evidence-based guideline, Respir Care 53:1203-1207, 2008. 60. Ries AL, Bauldoff GS, Carlin BW, et al: Pulmonary rehabilitation: Joint ACCP/AACVPR evidence-based clinical practice guidelines, Chest 131:4S-42S, 2007. 61. Ries AL, Make BJ, Lee SM, et al: The effects of pulmonary rehabilitation in the National Emphysema Treatment Trial, Chest 128:37993809, 2005.

62. Rubin BK, Van Der Schans CP, Kishioka C, et al: Mucus and muco­ active therapy in chronic bronchitis, Clin Pulm Med 5:1-14, 1998. 63. Rundell KW, Anderson SD, Spiering BA, et al: Field exercise vs laboratory eucapnic voluntary hyperventilation to identify airway hyperresponsiveness in elite cold weather athletes, Chest 125:909-915, 2004. 64. Rutten EPA, Franssen FME, Engelen MPKJ, et al: Greater whole-body myofibrillar protein breakdown in cachectic patients with chronic obstructive pulmonary disease, Am J Clin Nutr 83:829-834, 2006. 65. Shaul DB, Danielson PD, McComb JG, et al: Thoracoscopic placement of phrenic nerve electrodes for diaphragmatic pacing in children, J Pediatr Surg 37:974-978, 2002. 66. Soriano JB, Davis KJ, Coleman B, et al: The proportional venn diagram of obstructive lung disease: Two approximations from the United States and the United Kingdom, Chest 124:474-481, 2003. 67. Spruit MA, Troosters T, Trappenburg JCA, et al: Exercise training during rehabilitation of patients with COPD: a current perspective, Patient Educ Couns 52:243-248, 2004. 68. Steiner MC, Barton RL, Singh SJ, et al: Nutritional enhancement of exercise performance in chronic obstructive pulmonary disease: a randomised controlled trial, Thorax 58:745-751, 2003. 69. Takaoka ST, Weinacker AB: The value of preoperative pulmonary rehabilitation, Thorac Surg Clin 15:203-211, 2005. 70. Tang NLS, Chung ML, Elia M, et al: Total daily energy expenditure in wasted chronic obstructive pulmonary disease patients, Eur J Clin Nutr 56:282-287, 2002. 71. Thomson CC, Clark S, Camargo CA Jr: Body mass index and asthma severity among adults presenting to the emergency department, Chest 124:795-802, 2003. 72. Toder DS: Respiratory problems in the adolescent with developmental delay, Adolesc Med 11:617-631, 2000. 73. Trulock EP, Christie JD, Edwards LB, et al: Registry of the International Society for Heart and Lung Transplantation: Twenty-fourth official adult lung and heart-lung transplantation Report-2007, J Heart Lung Transplant 26:782-795, 2007. 74. Vlahakis NE, Patel AM, Maragos NE, et al: Diagnosis of vocal cord dysfunction: the utility of spirometry and plethysmography, Chest 122:2246-2249, 2002. 75. Wadell K, Sundelin G, Henriksson-Larsén K, et al: High intensity physical group training in water: an effective training modality for patients with COPD, Respir Med 98:428-438, 2004. 76. Warburton DE, Nicol CW, Bredin SS: Prescribing exercise as preventive therapy, CMAJ 174:961-974, 2006. 77. Weisman IM, Marciniuk D, Martinez FJ, et al: II. Indications for cardiopulmonary exercise testing. ATS/ACCP statement on cardiopulmonary exercise testing, Am J Respir Crit Care Med 167:211-277, 2003. 78. Whaley MH, Brubaker PH, Otto RM, editors: ACSM’s guidelines for exercise testing and prescription ed 7, Philadelphia, 2006, Lippincott Williams & Wilkins. 79. Wijkstra PJ, Avendaño MA, Goldstein RS: Inpatient chronic assisted ventilatory care: a 15-year experience, Chest 124:850-856, 2003. 80. Yankaskas JR, Marshall BC, Sufian B, et al: Cystic fibrosis adult care: consensus conference report, Chest 125:1S-39S, 2004. 81. Zeitoun M, Wilk B, Matsuzaka A, et al: Facial cooling enhances exercise-induced bronchoconstriction in asthmatic children, Med Sci Sports Exerc 36:767-771, 2004. 82. Zu Wallack RL, Patel K, Reardon JZ, et al: Predictors of improvement in the 12-minute walking distance following a six-week outpatient pulmonary rehabilitation program, Chest 99:805-808, 1991.

CHAPTER 35 EMPLOYMENT OF PERSONS WITH DISABILITIES Heidi Klingbeil and Kevin Sperber

Disability is a significant public health and social issue in the United States. The number of Americans who experience disability, activity limitations secondary to chronic illnesses, or impairments has increased, whereas mortality has decreased. A U.S. Census Bureau report found in 2005 that of a total population of 291.1 million, approximately 54.4 million (18.7%) individuals reported some degree of mental or physical disability.40 This represents an increase from the 51.2 million who reported a disability in 2002.40 In the 2005 report, 35 million people—or 12% of U.S. residents—were classified as severely disabled.40 Given these findings, disability ranks as the nation’s largest public health problem.* The growing numbers of Americans with disabilities present new medical, social, and political challenges. The major activity limitations found in those with disabilities include an inability to manage personal care, the inability to work and be financially self-supporting, and the inability to integrate socially and enjoy leisure.38 These limitations have medical, behavioral, social, and economic implications. To help those with disabilities restore functional capacity, prevent further deterioration in functioning, and maintain or improve their quality of life, programs of any type should emphasize rehabilitation and prevention of secondary conditions.30 These programs must respect disability as multifaceted and foster an interdisciplinary approach to treatment. Within the medical arena, the specialty of physical medicine and rehabilitation has been concerned with the establishment of physiologic, psychologic, and social equilibrium for persons with disabilities.19 According to Rusk, “A rehabilitation program is designed to take a disabled person from his bed back to his job, fitting him for the best life possible commensurate with his disability and more importantly with his ability.”33 To help all persons with disabilities achieve their maximum level of independence, avert further deterioration in functioning, and maintain or improve their quality of life, the physiatrist and the medical rehabilitation team must appreciate the multifaceted character of disability. We must accept the responsibility to initiate appropriate referrals to other collaborating programs that can support these goals beyond the medical arena. One such program is vocational rehabilitation. In this chapter, we examine the subject of employment of people with disabilities. Specifically, we: • Discuss the concept of disability • Review national data on disability and employment • Consider the economic impact of disability *References 8, 21, 22, 25, 30, 33, 40, 52.

• Review policies supporting employment of persons with disabilities • Discuss economic assistance strategies • Discuss vocational rehabilitation strategies • Enumerate the incentives and disincentives for returning to work • Postulate that vocational rehabilitation serves as a rehabilitation treatment and disability prevention strategy for people with disabilities

The Concept of Disability Disability itself is not always quantifiable. In the Americans with Disabilities Act of 1990 an individual with a disability is defined as a person who has a physical or mental impairment that substantially limits one or more major life activities.40 The concept of disability differs among persons who consider themselves to have a disability, professionals who study disability, and the general public.22 This lack of agreement is an obstacle to all studies of disability, as well as to the equitable and effective administration of programs and policies intended for people with disabilities.12,13,22,28,30 The World Health Organization (WHO) has a mandate to develop a global common health language— one that is understood to include physical, mental, and social well-being. The International Classification of Impairments, Disabilities, and Handicaps (ICIDH-2) was developed by WHO as a tool for classification of the “consequences of disease.” The ICIDH-2 reflects the biopsychosocial model of disablement, viewing disablement and functioning as outcomes of an interaction between a person’s physical or mental condition and the social and physical environment. Human functioning is characterized at three levels: the body or body part, the whole person, and the whole person in social context. Disablements are the dimensions of dysfunctioning that result for an individual at these three levels; these include impairment, losses, or abnormalities of bodily function and structure; limitations of activities; and restrictions of participation. This biopsychosocial model regards functioning and disablement as outcomes of interactions between health conditions (disorders or diseases) and conceptual factors such as social and physical environmental factors and personal factors. The interactions in this paradigm are dynamic, complex, and bidirectional (Figure 35-1). 755

756

SECTION 3  Common Clinical Problems

Table 35-1  Conditions With the Highest Prevalence of Activity Limitation

Health condition

Main Cause

Impairment

Activity

Participation

Conceptual factors FIGURE 35-1  Biopsychosocial model of disablement.

Dimensions of dysfunctioning are defined as follows. • Impairment is the loss or abnormality of body structure or of a physiologic or psychologic function. • Activity is the nature and extent of functioning at the level of the person. • Participation is the nature and extent of a person’s involvement in life situations in relation to impairment, activities, health conditions, and contextual factors, and can be restricted in nature, duration, and quality.46 The concept of disability or disablement continues to be one about which there are many interpretations and opinions. This lack of agreement about the concept of disablement affects epidemiologic studies of disablement and the development of effective treatment and prevention strategies. The biopsychosocial model and the common language of the ICIDH-2 helped to define the need for health care and related services; define health outcomes in terms of body, person, and social functioning; provide a common framework for research, clinical work, and social policy; ensure the cost-effective provision and management of health care and related services; and characterize physical, mental, social, economic, and environmental interventions that would improve lives and levels of functioning.51 The 2001 World Health Assembly subsequently endorsed a revised system, the International Classification of Functioning, Disability and Health (ICF). This is a classification of health and health-related domains, which are classified from body, individual, and societal perspectives using a list of body functions and structure, as well as a list of domains of activity and participation. The ICF also includes a list of environmental factors to provide context for the disability.53 The ICF provides a common transcultural language across health care systems and is intended to allow comparison of international data and the measurement of health outcomes, quality, and cost, as well as health disparities.

Data: Impairment and Disability The U.S. Census Bureau provides extensive information on the number and characteristics of people with disabilities. Data from the Americans with Disabilities Report of 2005 indicate that 54.4 million people, or 18.7% of the U.S. population,40 have some level of disability. Among those

Percentage

Orthopedic impairments

16.0

Arthritis

12.3

Heart disease

22.5

Visual impairments

  4.4

Intervertebral disk disorders

  4.4

Asthma

  4.3

Nervous disorders

  4.0

Mental disorders

  3.9

Hypertension

  3.8

Mental retardation

  2.9

Diabetes

  2.7

Hearing impairments

  2.5

Emphysema

  2.0

Cerebrovascular disease

  1.9

Osteomyelitis or bone disorders

  1.1

All Causes Orthopedic impairments

21.5

Arthritis

18.8

Heart disease

17.1

Hypertension

10.8

Visual impairments

  8.9

Diabetes

  6.5

Mental disorders

  5.6

Asthma

  5.5

Intervertebral disk disorders

  5.2

Nervous disorders

  4.9

Hearing impairments

  4.3

Mental retardation

  3.2

Emphysema

  3.1

Cerebrovascular disease

  2.9

Abdominal hernia

  1.8

From La Plante MP: The demographics of disability, Milbank Q 69:55-77, 1991, with permission.

15 years or older, inability to walk without an assistive device was reported by 10.2 million individuals, and 3.3 million individuals required a wheelchair. Requiring help with one or more activities of daily living was reported by 4.1 million.40 Impairments resulting from chronic disease have become increasingly significant risk factors of disability.8,22 Table 35-1 lists the 15 conditions with the highest prevalence of functional compromise or disability.22 The prevalence of disability with these conditions appears to be due to the prevalence of the condition itself and the chance that the condition will cause a disability. Table 35-2 shows the ranking of persons, by percentage of specific conditions, who have functional limitations secondary to that condition.22 In general, many of the conditions that are significant risk factors for disability are low in prevalence.

757

CHAPTER 35  Employment of Persons With Disabilities

Table 35-2  Conditions With the Highest Risk for Disability Rank

Causes Major Activity Limitation (%)

Rank

Causes Need for Help in Basic Life Activities (%)

Mental retardation

1202

84.1

1

80.0

1

19.91*

9

Absence of leg(s)*

289

83.3

2

73.1

2

39.0*

2

Lung or bronchial cancer

200

74.8

3

63.5

3

34.5*

4 1

Chronic Condition

Number of Conditions (in 1000s)

Causes Activity Limitation (%)

Rank

Multiple sclerosis*

171

70.6

4

63.3

4

40.7*

Cerebral palsy*

274

69.7

5

62.2

5

22.8*

8

Blind in both eyes

396

64.5

6

58.8

6

38.1*

3

Partial paralysis in extremity*

578

59.6

7

47.2

7

27.5*

5

Other orthopedic impairments*

316

58.7

8

42.6

8

14.3†

12

Complete paralysis in extremity*

617

52.7

9

45.5

9

26.1*

6

Rheumatoid arthritis*

1223

51.0

10

39.4

12

14.9*

11

Intervertebral disk disorders*

3987

48.7

11

38.2

14

5.3*

—

247

47.8

12

43.7

10

14.1†

13

4708

46.9

13

35.1

15

13.6*

14

228

45.3

14

40.3

11

15.9†

15

2074

43.6

15

29.8

—

9.6*

15

84

43.1

—

39.0

13

4.1*

—

2599

38.2

—

33.3

—

22.9*

7

Paralysis in other sites (complete or partial)* Other heart disease disorders‡ Cancer of digestive tract Emphysema Absence of arm(s) or hand(s)* Cerebrovascular disease*

From La Plante MP: The demographics of disability, Milbank Q 69:55-77, 1991, with permission. *Conditions frequently managed by physiatrists. †Figure has low statistical reliability or precision (relative standard error >39%). ‡Heart failure (9.8%), valve disorders (15.3%), congenital disorders (15.0%), other ill-defined heart conditions (59.9%).

For example, multiple sclerosis has a low overall prevalence but is a significant risk factor for disability. Examination of this ranking shows 7 of the top 10 disabling conditions are conditions frequently managed by the physiatrist and the rehabilitation team. These conditions or diseases are typically chronic, requiring a lifetime of rehabilitative management to have an effect on the disabling process, prevent secondary conditions, and maintain quality of life.

Socioeconomic Effect of Disability Disablement has significant socioeconomic consequences for the individual with disabilities and for society. When a person is unable to participate in her or his social role as a worker or homemaker because of a physical or mental condition, that person is said to have a work disability or a work participation restriction.7,54 Work participation restriction results in dependency and loss of productivity for that person. Society, in turn, incurs direct and indirect costs. Direct expenditures include those for medical and personal care, architectural modification, assistive technology, and institutional care, as well as income support for the person with a disability. For the individual, these expenses contribute to impoverishment.6,49 Society’s response to the expenditures related to disablement includes disability-­ related programs such as Social Security Disability Insurance (SSDI), Supplemental Security Income (SSI), Medicare, and Medicaid. In 2002, federal and federal–state programs for working-aged people with disabilities were

estimated to cost $276 billion, or 2.7% of the gross domestic product (GDP) of the United States.11 Disablement is costly to the individual and to society because of the loss of productivity. People with disabilities are more likely to be unemployed or underemployed and have lower average salaries than their nondisabled peers (Table 35-3). The indirect monetary costs for the individual are reckoned in terms of losses in earnings and homemaker services.55 A 2006 study by researchers at the University of California, using 1997 as an example year, found that people with disabilities were estimated to spend an average of 4.5 times as much on medical expenses55 and that the overall net salary loss associated with disability was $115.3 billion, or 1.4% of the 1997 GDP.55 Disablement is associated with poverty. In 2007, 21% of disabled people 5 years and older were below the poverty level as opposed to only 10.9% of those without a disability.41 In 2005, people 21 to 64 years of age without a disability had median monthly earnings of $2539. Those with a nonsevere disability had $2250 median monthly earnings, and those with a severe disability had $1458 median monthly earnings (Table 35-3).40 The indirect monetary cost to society is loss from the labor force.6 For example, in 1996, spinal cord injury alone was estimated to have cost the U.S. economy $9.73 billion, including $2.6 billion in lost productivity.24 Disablement imposes indirect nonmonetary costs to the individual and to society. Fifty-seven percent of persons with disabilities believed their disability prevented them from reaching their full potential.14 Restriction in work participation, in particular, places the individual in

758

SECTION 3  Common Clinical Problems

Table 35-4  Disability-Related Programs

Table 35-3  Employment and Earnings Employment Rate of People 21-64 Years Old (%)

Median Monthly Earnings 21-64 Years Old ($)

Median Monthly Family Income 21-64 Years Old ($)

No disability

83.5

2539

4669

Any disability

45.6

Nonsevere disability

75.2

2250

3801

Severe disability

30.9

1458

2182

Type of Program

Specific Programs

Cash transfer

Social insurance: Social Security Disability Insurance Private insurance Indemnity compensation

From U.S. Census Bureau:  Americans with disabilities: 2005 report, issued December 2008.

Income support: Supplemental Security Income, veterans’ pensions,  Aid to Families with Dependent Children

Medical care

Medicare Private disability insurance

a position of dependency on insurance payments or government benefits for income support and medical care. Dependency affects people’s feelings about themselves and their overall satisfaction with life. Pressure from various customers, and especially the third-party payers, for accountability in medical care focuses attention on outcome and cost-effectiveness. Interventions directed at disablement should be assessed with measures of both outcome and cost-effectiveness. Disablement is more than a medical phenomenon: It is a complex socioeconomic process. Assessment of the outcome and cost-effectiveness of an intervention should take into consideration the quality of life and indirect monetary costs, as well as direct expenditures. Vocational rehabilitation is an intervention that can limit restrictions in work participation. In 1993, the Social Security Administration estimated that for every dollar spent on vocational rehabilitation services, five dollars in future direct expenditures was saved.23 A 2006 analysis of spending by the New Mexico Division of Vocational Rehabilitation found a total benefit/cost ratio of 5.63.29 Although employment is the expected outcome of vocational rehabilitation, the impact of this intervention goes beyond simple employment and saving of direct expenditures. The positive effects of working are demonstrated when the characteristics of working and nonworking persons with disabilities are compared. Those who work are better educated, have more money, are less likely to consider themselves disabled, and in general are more satisfied with life.14 Comprehensive rehabilitation of persons with disabilities should include strategies that reduce work restrictions, such as vocational rehabilitation. The outcomes include increased independence and increased productivity. The cost-effectiveness of comprehensive rehabilitation should be measured in direct and indirect monetary and nonmonetary costs over the lifetime of the individual.3

Disability-Related Programs and Policies Programs A plethora of disability-related programs and policies exist. Each program and policy has its own definition of disablement and disability, and differs in the eligibility and

Veterans’ programs Workers’ compensation Tort settlements Medicaid Direct services

Rehabilitation and vocational education veterans’ programs Services for persons with specific impairments General funded programs (e.g., food stamps, developmental disabilities, blind, mentally ill) Employment assistance programs (i.e., comprehensive employment training program)

From Berkowitz M, Hill MA: Disability and the labor market: an overview. In Berkowitz M, Hill MA, editors: Disability and the labor market: economic problems, policies, and programs, New York, 1989, ILR Press, with permission.

application criteria. The programs can be characterized as ameliorative or corrective.16 Ameliorative programs provide payment for income support and medical care. Corrective programs facilitate the individual’s ability to return to work and to reduce or remove the disablement. Whether ameliorative or corrective, all programs influence the biopsychosocial model of disablement. Disability-related programs can be categorized into three basic types: cash transfers, medical care programs, and direct service programs. Table 35-4 presents specific programs within these three basic types.7 Estimates of the expenditures of these disability-related programs provide insight into expenditure trends. In 1970, 61.4% of the disability dollar went for cash transfers, 33% for medical care, and 5.4% for direct services. By 1986, the proportion of the disability dollar for direct services had decreased to 2.1%, while the proportion for medical care had increased.7 In 2002, of the estimated $276 billion spent, 41.9% went to income maintenance, 54.2% went to health care programs, 2% went to housing and food, and 1.5% for education training and employment.11 The trend toward ameliorative programs’ capturing more of the resources is a concern. Studies of the socioeconomic consequences of disability support the utility of rehabilitating people with disabilities, allowing them to enter the labor market and thereby decrease their dependency and loss of productivity. The physiatrist has an important supportive role in initiating referrals to the corrective programs. These programs are in keeping with the philosophy of rehabilitation, which is to maximize individual functioning and lessen disability.

CHAPTER 35  Employment of Persons With Disabilities

Public Disability Policies Public policy in the United States has begun to recognize that many barriers to integration faced by persons with disabilities are the result of discriminatory policy and practices. Some also have the view that disability is an interaction between an individual and the environment. This has played a fundamental role in shaping public policy toward disability during the past 20 years. Since the late 1960s, Congress has passed a series of laws aimed at enhancing the quality of life for persons with disabilities. These laws have mandated that housing and transportation be accessible, that education for children with disabilities be appropriate, and that employment practices be nondiscriminatory.1,10,47 Three legislative actions deserve to be highlighted. The Rehabilitation Act of 1973 extended civil rights protection to persons with disabilities. This legislation included antidiscrimination and affirmative action in employment. The Rehabilitation Act Amendments of 1978 broadened the responsibility of the Rehabilitation Services Administration to include independent living programs, and created the National Council of the Handicapped (the National Council of the Handicapped became the National Council on Disability in January 1989). The capstone of this legislative tradition is the Americans with Disabilities Act (ADA) of 1990. This legislation established a clear and comprehensive prohibition of discrimination based on disability.10,45,47,50 More recent legislation, such as the Workforce Investment Act and the Ticket to Work and Work Incentives Improvement Acts of 1998, continue to attempt to eliminate the barriers that prevent disabled individuals from working. Table 35-5 reviews the prominent federal disability laws.

Vocational Rehabilitation The objective of vocational rehabilitation is to allow persons with physical disabilities to engage in gainful employment. Historically, formal vocational rehabilitation services were instituted to provide returning World War II veterans with disabilities assistance in obtaining suitable occupations.47 Before the 1970s, jobs earmarked for persons with disabilities were provided through government-subsidized sheltered workshops. The Comprehensive Employment Training Act of 1973 (CETA) provided public service jobs for persons with disabilities and for the disadvantaged, along with training programs for this population. At its peak in 1980, CETA and sheltered workshops provided more than 1 million jobs for a broadly defined “disabled” population. The CETA program lasted from 1973 to 1982, when the federal government subsequently returned to state-run vocational rehabilitation agencies for provision of these services to persons with disabilities. The Rehabilitation Act of 1973 authorized federal funding for state rehabilitation agencies to provide a variety of services to qualified persons with disabilities. The federal government supplies 80% of the funding for state vocational rehabilitation agencies, whereas the states must provide the remaining 20%. State agencies administer the

759

Table 35-5  Federal Disability Laws Americans with Disabilities Act of 1990

Prohibits discrimination on the basis of disability in employment, state and local government, public accommodations, commercial facilities, transportation, and telecommunications

Telecommunications Act of 1996

Require manufacturers of telecommunications equipment and providers of telecommunications services to ensure that such equipment and services are accessible to and usable by persons with disabilities, if readily achievable

Fair Housing Amendments Act of 1988

Prohibits housing discrimination on the basis of race, color, religion, sex, disability, familial status, and national origin

Air Carrier Access Act of 1986

Prohibits discrimination in air transportation by domestic and foreign air carriers against individuals with physical or mental impairments

Voting Accessibility for the Elderly and Handicapped Act of 1984

Attempts to ensure polling places across the United States to be physically accessible to people with disabilities for federal elections; this law also requires states to make available registration and voting aids for disabled and elderly voters

National Voter Registration Act of 1993 (Motor Voter Act)

Attempts to improve the low registration rates of minorities and persons with disabilities that have resulted from discrimination; all offices of state-funded programs that are primarily engaged in providing services to persons with disabilities are required to provide all program applicants with voter registration forms, assistance in completing the forms, and to transmit completed forms to the appropriate state official

Civil Rights of Institutionalized Persons Act

Authorizes the U.S. Attorney General to investigate conditions of confinement at state and local government institutions such as prisons, jails, pretrial detention centers, juvenile correctional facilities, publicly operated nursing homes, and institutions for people with psychiatric or developmental disabilities

Individuals with Disabilities Education Act

Requires public schools to make available to children with disabilities a free appropriate public education in the least restrictive environment appropriate to their individual needs

Rehabilitation Act of 1973

The Rehabilitation Act prohibits discrimination on the basis of disability in programs conducted by federal agencies, in programs receiving federal financial assistance, in federal employment, and in the employment practices of federal contractors

Architectural Barriers Act of 1968

Requires that buildings and facilities that are designed, constructed, or altered with federal funds, or leased by a federal agency, comply with federal standards for physical accessibility

From U.S. Department of Justice Civil Rights Division:  A guide to disability rights laws, September 2005.

programs under the Rehabilitation Services Administration in the Department of Education. The intent of the Rehabilitation Act was to provide services to persons with disabilities, with emphasis placed on serving those with more severe disabilities (General Accounting Office testimony).46 State agencies are usually located in the state division or bureau of vocational rehabilitation. The state division provides direct services and also refers individuals to private rehabilitation agencies and training programs when indicated.

760

SECTION 3  Common Clinical Problems

BOX 35-1

Services Provided by Vocational Rehabilitation Specialists Diagnosis and evaluation • Counseling and guidance • Restoration* • Transportation • College or university training • Income maintenance Adjustment training • Business or vocational training • Miscellaneous training • Placement • Referrals • On-the-job training

  *Includes medical treatment, prosthetic devices, or medically necessary services to correct or modify a physical or mental disorder.

Traditional Approaches to Vocational Rehabilitation A variety of approaches to vocational rehabilitation have been developed over the years. The traditional approach begins with referral of a person with a disability to a vocational rehabilitation counselor. This referral can be generated by the person with a disability, a physician, a social worker, or a case manager. The initial referral includes medical records, documentation of disabilities and capabilities, and neuropsychologic testing (if available). The initial interview between the counselor and the client (person with a disability) establishes rapport and provides background information about previous job skills and experiences. The interview also provides information about the individual’s educational level, motivation, perceived abilities and disabilities, and areas of interest. If the client was employed before the onset of disability, there is often potential for placement with the former employer. This previous employer should be contacted to learn of employment opportunities for the person with a disability. The vocational rehabilitation counselor also assesses the skills the person had premorbidly and the skills needed before placement in a suitable position. If no positions are available, vocational testing is performed.

Aptitude Matching Versus Work Sample Vocational testing is performed to assess the client’s level of general intelligence, achievement, aptitudes, interests, and work skills. Formal testing consists of administering a battery of paper-and-pencil standardized tests, examples of which are listed in Table 35-6. This type of approach is known as aptitude matching. It determines the client’s aptitudes or traits in the areas of general intelligence, visuospatial perception, eye–hand coordination, motor coordination, and dexterity. Performance on the tests is compared against a list of essential aptitudes, grouped by occupation, in the Dictionary of Occupational Titles published by the Department of Labor.26 When a client’s aptitudes match a particular occupation, a job search is undertaken by the counselor.

Table 35-6 Tests Administered by Vocational Rehabilitation Counselors or Neuropsychologists Test

Type

Wechsler Adult Intelligence Scale—Revised

Intelligence

General Aptitude Test Battery

Aptitude

Differential Aptitude Test

Aptitude

Wide Range Achievement Test

Achievement

Strong–Campbell Interest Inventory

Interest

Career Assessment Inventory

Interest

Minnesota Multiphasic Personality Inventory

Personality

Halstead–Reitan

Cognitive evaluation

Luria–Nebraska

Cognitive evaluation

A work sample approach is often used in conjunction with aptitude batteries. The work sample approach measures general characteristics such as size discrimination, multilevel sorting, eye–hand–foot coordination, and dexterity. The Valpar Component Work Sample Series (VCWSS) is a good example of the work sample approach. The VCWSS uses complex work apparatus to measure almost exclusively motor responses. Less focus is applied to general intelligence, aptitude, and academic performance. Work samples can also evaluate the type of “work group” in which the client is most skilled. This simulated work requires performance of a series of tasks, such as drill press operation or circuit board or bench assembly.26 Once the client’s skills have been evaluated and interests explored, a vocational goal is developed. The requirements of the potential position must first be determined. This is accomplished by performing a job analysis of the position, then identifying the physical and mental requirements and any necessary job site modifications (e.g., adaptive equipment). If training is proposed, it must be accessible and available to the client. Transportation should be arranged and can be paid for by the vocational rehabilitation agency. Tuition, books, and adaptive equipment to allow performance of the position can also be provided by the agency. Training programs vary in length depending on the potential vocational goal. They can last from a few weeks to several years. Training can be conducted at a trade school, college, university, or on the job with state vocational rehabilitation agency funding. On-the-job training requires job development. The counselor or the client explores community business resources to develop suitable positions. Tax incentives for potential employers can help convince industry to offer training. Sliding-scale wages can be arranged to assist in developing positions. For example, the state rehabilitation agency might fund 100% of salary for 3 to 6 months. The employer gradually assumes that responsibility over the next 3 to 6 months as the new employee becomes trained. Many employers want to keep the employees they have trained, but some prefer to act in the capacity of trainers for a series of persons with disabilities. In this case, the counselor still has the task of placing the newly trained people.

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Once an individual has completed training and has been placed for 60 days, the state vocational rehabilitation agency considers the case a “success” and closes its file. No follow-up evaluation is typically provided.

Sheltered Workshops One of the problems with the traditional approach of the vocational rehabilitation agency has been its poor record of success, especially for persons with severe disabilities. Fortyfive percent fewer people were successfully vocationally rehabilitated in 1988 than in 1974, despite increased financial support and larger numbers of persons with disabilities.47 A 1987 General Accounting Office survey found that of SSDI recipients receiving vocational rehabilitation, less than 1% left the SSDI rolls.37 Although now a bit better, these numbers remain small. A 2007 General Accounting Office report to Congress noted that by 2005 an average of 7% of Social Security Administration (SSA) beneficiaries had left the roles after vocational rehabilitation. The International Center for the Disabled (ICD) survey reported that although 60% of persons with disabilities knew about vocational rehabilitation services, only 10% took advantage of those services. Of those using the services, more than 50% believed they were not useful in securing gainful employment.14 As a result of the poor placement record, alternative strategies have been developed for enabling persons with disabilities to obtain gainful employment. These include sheltered workshops, day programs, transitional and supported employment, Projects with Industry, independent living center (ILC)–directed employment, and others. Funding for these programs has come from public, nonprofit, and private industry, state and federal social service programs, religious entities, corporate and foundation contributions, and individual donations. A sheltered workshop is a “public non-profit organization certified by the U.S. Department of Labor to pay ‘subminimum’ wages to persons with diminished earning capacity.”17 More than 5000 of these workshops exist, including Goodwill, Inc., serving approximately 250,000 persons with disabilities. This form of employment serves persons with severe disabilities, including limited vision, mental illness, mental retardation, and alcoholism. Although sheltered workshops provide job experience and income, critics report that sheltered workshops rarely lead to competitive, integrated employment. People with severe disabilities can be competitively employed in the community through the use of some modern strategies, as outlined below.

Day Programs Day programs have existed since before the 1970s and are meant to provide supervised vocational activity for persons with severe disabilities, usually those with mental retardation or mental illness. These programs are funded by private and corporate sponsors, as well as by state and federal agencies. They are not designed as a transition into competitive employment, nor do they allow community integration. They are geared toward providing supervised day activities while the caretakers of these persons work or perform their own daily routines. Activities are performed in facilities that serve only persons with disabilities.

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Home-Based Programs Another more traditional method for assisting persons with severe disabilities to obtain employment is the home-based program. Home-based programs can be funded by state vocational rehabilitation, insurance carriers, foundations, and societies, or by other agencies. The person with a disability can perform a variety of jobs, including telephone solicitation, typing, or computer-assisted occupations. Some examples include graphics, accounting, or drafting. Of these programs—sheltered workshops, day ­programs, and homebound programs—none emphasizes gainful employment in a nonsheltered integrated setting. It was the failure of these programs to reintegrate their clients into competitive community employment that resulted in the emergence of transitional and supported employment models.

Other Programs for Employment Projects with Industry Projects with Industry is a federally sponsored collaborative program established by the Vocational Rehabilitation Act. Employers design and provide training projects for specific job skills in cooperation with rehabilitation agencies. The goal of Projects with Industry is competitive employment for the participants. Job fairs have been somewhat successful in matching vacant positions with capable individuals with disabilities. Businesses in a community spend 1 day interviewing applicants with disabilities who have been prescreened by a participating placement agency. The placement agency might provide further services, such as transportation for the potential employee, and make recommendations for work accommodations to the potential employer. Transitional and Supported Employment Two newer strategies for returning disabled persons to competitive, integrated gainful employment are transitional and supported employment. Transitional employment consists of providing the job placement, training, and support services necessary to help persons move into independent or supported employment.39 Independent employment provides at least a minimum wage to the employee and requires no job subsidy or ongoing support. Transitional employment is a short-term provision of services for a period not to exceed 18 months, and culminates in an independent or supported employment position. Supported employment has been used as a successful strategy for placing or returning the most severely disabled individuals to competitive, integrated community employment. It requires ongoing support after placement, including counseling for the employee and co-workers, and assistance with transportation, housing, and other non–work-related activities. It began as an alternative to sheltered workshops and day programs and has grown to have modest federal funding and broad community support. This support comes from groups of persons with disabilities, state vocational rehabilitation agencies, and state departments for the developmentally disabled. This concept became a permanent part of the Rehabilitation Act of

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BOX 35-2

Critical Criteria for Supported Employment • Interventions provided at the job site • Assistance long term or permanent • Programs serve only the severely disabled • Real pay for real work • Work performed in an integrated setting

  From Wehman P, Sherron P, Kregel J, et al: Return to work for persons following severe traumatic brain injury: supported employment outcomes after five years, Am J Phys Med Rehabil 72:355-363, 1993, with permission.

1973 with the passage of the 1986 amendments and additional regulations published in June 1992.51 Supported employment is meant to provide ongoing support for persons with severe disabilities. According to Wehman et al.,51 it must meet five critical criteria (Box 35-2). The first is that all interventions, including training, placement, and counseling, be provided at the job site rather than in a therapy room or vocational school. Second, the intervention and services are provided on a permanent or long-term basis as the individual requires them. Third, these programs are intended to serve only those individuals with the most severe disabilities who have been unable to enter the competitive labor market with their disability in the past. Fourth, the work provided is real and meaningful for the employee, and compensation is received equal to that of an able-bodied co-worker for the same duties. Fifth, work must occur in an integrated setting allowing interaction with co-workers without disabilities.51 The Department of Education’s operational definition of supported employment requires that employees be paid for working an average of at least 20 hours per week in a position that provides interactions with persons who are not disabled and are not paid caregivers. There must be eight or fewer people with disabilities working together at the job site, and there must be ongoing public funding for providing intervention directly related to sustaining employment. Supportive employment defines the type and level of support needed by an individual to be employable now, not after a nonintegrated training program. Four models of supported employment have been developed. The enclave model consists of a small group of persons with disabilities working together at an integrated job site. The mobile work crew model uses a small group of workers who travel from job to job and offer contractual services under the direction of a supervisor. The small business or entrepreneurial model creates a new small business that produces goods or services using both workers with disabilities and those without them. The most frequently used model is the job coach with individual placement.17 The job coach, or employment specialist, is an employee of the agency providing supported employment services. The coach works with an individual at the job site to provide interpersonal and coping skills, as well as job skills. The coach performs job development before placement. Once placement occurs, job training and ongoing job retention services are provided. Job coaches might initially be required to complete the duties not yet mastered by the worker with a disability.

Depending on the disability, behavior modification or cognitive training might be required to enable learning of vital skills. These become the responsibility of the job coach. The job coach should be able to evaluate the ecology of the job site, including attitudes of co-workers, accessibility of the job site, and the necessity for adaptive equipment. The job coach should then be able to educate co-workers and ensure implementation of appropriate accommodations for the person with a disability. Job coach intervention time can be very significant (almost 8 hr/day) initially. Wehman et al.51 conducted a 5-year study of supported employment for persons with traumatic brain injury. They documented an average requirement of 249.1 hr/person of job coach time over 6 months. The job coach’s intervention time decreased steadily with time on the job to an average of less than 3 hr/wk/person after 30 weeks of employment. Some persons require continued significant intervention to assist them in meeting difficulties that arise from changes at the job site; that is, new job duties or changes in personnel or goods produced. Some workers are able to depend on support from employers and co-workers, however, and require little or no further direct job coach support. Supportive employment has been highly successful in allowing persons with severe disabilities to participate competitively in the job market and improve their quality of life and economic situation. Independent Living Centers The ILC movement has traditionally provided a core of nonvocational services such as housing, independent living skills, advocacy, and peer counseling. Just as supported employment has broadened its scope, so has the ILC movement. Both provide a combination of nonvocational and vocational services to persons with severe disabilities. ILCs often employ workers with disabilities as peer counselors and program administrators. The small business approach of supported employment has been successfully implemented by ILCs to place their clients in competitive community employment. As these two philosophies continue to merge and provide similar services to persons with severe disabilities, cooperative ventures between them allow persons with severe disabilities to fully achieve their maximum level of independence. Provision of vocational rehabilitation services to persons with disabilities requires a diversity of strategies. The more severe the disability, the more intensive the support and services have to be. Full participation in society is a right of all people. This participation includes being employed in a meaningful job that gives satisfaction to the worker and contributes to society as a whole. The methods for returning persons with disabilities to work vary, but creative strategies have proved significantly more successful than noncreative strategies.

Disincentives for Vocational Rehabilitation Public and political opinion has changed in recent years regarding the ability of persons with disabilities to work. Both persons with disabilities and policy makers have

CHAPTER 35  Employment of Persons With Disabilities

demonstrated a desire to return persons with disabilities to gainful employment. Statements of past presidents of the United States reflect the change of opinion. In 1973, Richard M. Nixon spoke concerning the Rehabilitation Act of 1973, saying it “would cruelly raise the hopes of the handicapped [for gainful employment] in a way that we could never hope to fulfill.”17 Advocacy by groups for the rights of persons with disabilities has achieved significant policy changes, as reflected by Ronald Reagan’s November 1983 proclamation of the Decade of Disabled Persons, in which the economic independence of all people with disabilities was to become a “clear national goal.”39 With the passage of the ADA in July 1990, George H. W. Bush proclaimed the “end to the unjustified segregation and exclusion of people with disabilities from the mainstream of American life.”17 Despite the obvious changes in public and political policies and attitudes, disincentives to entering “the mainstream” abound for persons with disabilities. To become eligible for cash and medical benefits through SSI and SSDI, persons with disabilities must prove that they have total and permanent or long-term disability and must meet strict eligibility criteria. Before meeting those criteria, the individual and the family typically must have suffered a series of indignities, including exhausting all personal resources and submitting to significant bureaucratic red tape. “Red tape” means completing substantial paperwork, obtaining medical reports verifying disability, and enduring long waiting periods for commencement of benefits. This is usually a long and arduous process. Once the person with a disability finally achieves a modest degree of security, an “opportunity” to give it all up and enter the workforce is made available. Naturally, the person with a disability is suspicious about the assurance that benefits will be preserved and eligibility will not be taken away because of returning to or entering the job market. Stereotypes about persons with disabilities being unproductive in society are pervasive. Individuals with disabilities often come to view themselves as totally dependent and unable to work. After all, they are placed in a position to prove their dependency and inability to be productive. The government disability entitlement policies state that if you are unable to work, the government will take care of you. In fact, many government policy makers believe that the person with a disability cannot and should not be expected to work. Some even believe that sending a person with a disability a check is much simpler than implementing the provisions of the ADA. Employers’ attitudes serve as another disincentive. Obstacles to qualified applicants with disabilities who want to participate in the workforce include employers’ ignorance about the capabilities of a potential employee with a disability, inaccessible work sites, transportation inaccessibility, and discrimination in hiring. The ADA is instrumental in changing much of this behavior and removing some of these disincentives. As disabled employees take their places, employers and co-workers will become educated and attitudes will change. The physiatrist and other physicians can also provide disincentives for persons with disabilities by labeling them as “totally and permanently disabled” or by restricting their activities. Emphasis should be on the capabilities of persons with disabilities and documentation of their functional abilities, both mental and physical.

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Table 35-7  Summary of Incentives for the Individual Receiving Benefits to Enter Work Activities Incentive

Details

Social Security ­Disability ­Insurance (SSDI)

Disability benefits program based on medical disability and a worker’s earnings covered by social security (Title II—Social Security Act)

Supplemental Security Income (SSI)

Disability benefits program based on medical disability and the amount of income a person receives (Title XVI—Social Security Act)

Trial work period (TWP)

Allows trial return to work to test work ability without affecting benefits (SSDI)

Substantial gainful activity (SGA)

Performance of significant and productive physical or mental work for pay or profit (>$700/ month for nonblind [SSDI and SSI] and $810/ month for blind recipients [SSDI only])

Extended period of eligibility

Allows reinstatement of cash benefits without a waiting period if the worker’s earnings fall below SGA level within 36 months after TWP (SSDI)

Impairment-related work expenses

Allows costs for certain items to be deducted from earnings when figuring SGA level (SSI and SSDI)

Earned income exclusion

Allows exclusion of a portion of earned income when figuring an individual’s monthly benefit (SSI)

Blind work expenses

Allows work-related expenses when figuring benefits (SSI)

Incentives for Vocational Rehabilitation In an effort to overcome disincentives, government policy makers have created incentives for persons with disabilities and for potential employers. These incentives often have a long list of requirements and are very specific in wording to prevent abuse.

Incentives for the Individual Since the inception of the SSI program in 1974, only a small number of beneficiaries have been employed. Social Security bulletins note that in 1976 approximately 71,000 beneficiaries were working. By 2006, that number had increased to 349,000. During the same years, the Supplemental Security Income (SSI) blind and disabled caseload increased from 2 million to 6.1 million. It appears that in 2006 about 6% of those who received an SSI payment were employed. Because these low numbers have been believed to reflect actual disincentives built into the current SSI payment system, a number of incentive programs have been implemented.20 Incentive programs are applicable depending on whether the person with a disability receives SSDI or SSI benefits, or both. SSDI work incentives are discussed first. Table 35-7 presents a summary of the terminology and abbreviations for easy reference. Additional references are given here for those wanting more detailed information.* The initial incentive toward return to work involves a trial work period (TWP). The TWP lets people test their ability to work or run a business without affecting their *References 27, 31, 32, 35, 37, 42, 43.

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benefits. This TWP maintains cash benefits for 9 months (not necessarily consecutive) of trial work in a 60-month period. During this period, beneficiaries can earn up to $530 per month.4 On completion of the TWP and continued employment at or above the substantial gainful activity (SGA) level, benefits continue to be paid for an additional 3 months and are then terminated.27,42,43 Any earnings from work below the monetary limit of the SGA level described in Table 35-7 are excluded when figuring monthly benefit amounts. The SGA dollar amount was increased in 1999 from $500 to $700, and a formula was adopted to link this amount in the future to the national average wage index.4 The extended period of eligibility (EPE) is a period of 36 consecutive months during which cash benefits can be reinstated if, during that period, the individual’s earnings fall below the SGA level. If the individual is unable to maintain earnings at the SGA level, benefits resume automatically and no waiting periods are required. Benefits cease at the end of the EPE, but Medicare continues for an additional 3 months.27,42,43 The elimination of a second waiting period for both cash benefits and Medicare benefits is also an incentive to perform a trial of work. Under certain circumstances, the person might be able to participate in a Medicare “buy-in.” The client must have completed both the TWP and the EPE. In addition, the extended 3 months of Medicare benefits must have passed. Once these conditions are met, Medicare A and B coverage can be purchased. This medical coverage is for those who cannot otherwise obtain health insurance because of preexisting conditions.27 In March of 2010, President Obama signed the Affordable Care Act. This law includes the PreExisting Insurance Plan. When implemented, this plan is inteded to provide a new coverage option to individuals who have been uninsured for at least 6 months because of preexisting condition. Another major incentive program for those receiving SSDI or SSI is for impairment-related work expenses. This allows the cost of certain items and services to be deducted from earnings when determining the SGA level. Examples include attendant care, medical devices, equipment, and prostheses.27 For those persons with disabilities receiving SSI benefits, a different, but often similar, set of incentives applies. These incentives provide SSI recipients with assurances that working will not disadvantage them. Section 1619 of the Social Security Act was made permanent by the Employment Opportunities for Disabled Americans Act passed in November 1986. The incentive of Section 1619 allows receipt of SSI cash benefits, even though earned income exceeds the SGA level. Cash benefits are calculated using the earned income exclusion discussed below. Medicaid benefits continue as an additional incentive even after wages become high enough to cause cessation of SSI cash benefits, provided their continuation is needed to allow the recipient to maintain employment.27,42,43 The earned income exclusion allows most of a recipient’s earned income to be excluded, including pay received from a sheltered workshop or day activity center, when figuring the SSI monthly amount.37 “Blind” work expenses is an incentive that allows a person who has visual impairment to pay for work expenses, such as visual aids, guide

dogs, or Braille translations. These allowable expenses are then excluded when calculating benefit amounts. In an effort to prevent work disincentives, benefit caps have been implemented to decrease excessively generous benefits. These caps use various formulas to reduce or limit maximum benefits paid by social security. These formulas take into account other sources of income, such as workers’ compensation benefits, but do not exclude veterans’ benefits or disability pensions from government jobs. Another incentive program, Plans for Achieving SelfSupport, allows an SSI recipient to set aside income and resources necessary to achieve a work goal.31,42,43 Incentives for Industry Government policy makers have made various attempts to offer tax incentives to business and industry. These incentives have mainly been directed at making the workplace accessible. Section 190 of the Internal Revenue Code, enacted in 1976 and revised by the Revenue Reconciliation Act of 1990, allows a set amount per year to be deductible for any expenses incurred in barrier removal (making a business or public transportation accessible).34 The Revenue Reconciliation Act of 1990 (which was passed 3 months after the ADA) allows an “access” tax credit with Section 44 of the Internal Revenue Code for small businesses. It allows credit against income taxes for eligible expenditures (auxiliary services for the disabled employee and aids are covered). This access credit is allowed only for expenses incurred for the purpose of enabling a business to comply with the ADA.34 Tax credits have also been used as incentives to encourage hiring of target groups, including the “hard core” unemployed: persons with disabilities and the homeless. The Targeted Jobs Tax Credit (TJTC), originally enacted in 1978, is meant to encourage employers to hire members of these groups. It provides a tax credit for targeted persons, including those persons receiving SSI benefits and vocational rehabilitation referrals (both groups containing large numbers of persons with disabilities). This credit only provides benefits to an employer for 1 year per employee. Many employers use the credit as a windfall; that is, hiring anyone they want and later checking to see whether the new employee falls into a targeted group. This practice is called “retroactive certification.”34 The TJTC has, unfortunately, not been particularly useful in increasing the number of disabled people hired. In fact, legislative incentives in general have not been very successful in achieving the goal of vocationally rehabilitating persons with disabilities. Ongoing efforts in Congress, however, are working to improve the incentives for persons with disabilities to return to work. For example, the Work Incentives Improvement Act of 1999 (S.331) provides adequate and affordable health insurance when a person on SSI or SSDI goes to work by expanding Medicaid options for states and by continuing access to Medicare after returning to work. It encourages SSDI beneficiaries to return to work by ensuring that cash benefits remain available if employment proves unsuccessful. An expedited eligibility process is proposed for SSDI beneficiaries who lose benefits because of work and need reinstatement of benefits later. A “ticket” program would provide a new payment system for SSDI and SSI beneficiaries for employment services. It reimburses vocational

CHAPTER 35  Employment of Persons With Disabilities

rehabilitation, training, and employment service providers a portion of benefit payments saved when the beneficiary earns more than the SGA level, currently $700 per month ($1000 for blind beneficiaries).4,19 This program originally called for sanctions (deductions against social security benefits or suspension of SSI benefits) for refusal of vocational rehabilitation, but this was eliminated as of January 1, 2001.5 Approximately 80% of SSI recipients work before applying for SSI, and 20% work after they start receiving payments.35 Scott Muller of the Social Security Administration performed a retrospective analysis of a cohort of more than 4000 people who were initially entitled to benefits.27 Approximately 10% worked during the initial period of entitlement. Of those, 84% were granted a TWP, and of that group, more than 70% completed the TWP. More than 50% did not leave the rolls as a result of their efforts. Less than 3% had benefits terminated as a result of return to work.24 It is clear from the research conducted by the Social Security Administration that legislating incentives is not the complete answer to rehabilitating persons with work disability. Potential employers and persons with disabilities alike must take the initiative. But the search for feasible means to return work-disabled persons to work is well worth it. The General Accounting Office estimates that removing even 1% of disabled beneficiaries from the SSDI and SSI programs each year would result in estimated lifetime savings of $3 billion.36

Disability Prevention With disability ranking as the nation’s largest public health problem, it seems reasonable to interface the public health model of prevention with the ICIDH-2 model of disablement. The public health model defines three categories of prevention: primary, secondary, and tertiary. Primary prevention is intended for healthy persons, helping them to avoid the onset of a pathologic condition. In persons with disabilities, primary prevention comprises efforts toward preventing a worsening of impairments. Secondary prevention is aimed at early identification and treatment of a pathologic condition and reduction of risk factors for disablement. For persons with disabilities, there are many opportunities for preventing impairment from limiting one or more activities. The ameliorative and corrective programs discussed above, including vocational rehabilitation strategies, are aimed at reducing activity limitation. These programs have been effective not only in returning the unemployed person to work, but also in preventing job loss in those workers with a disability.2 Interventions in medical rehabilitation focused on the enhancement of activity, such as provision of assistive technology, can be considered secondary prevention. The General Accounting Office has studied return-towork strategies used by Germany and Sweden, and recommends that intervention occur as soon as possible after an actual or potentially disabling event to promote and facilitate return to work. Because the current SSI benefit structure in the United States includes a lengthy application process, and then benefits linked to full, permanent disability only, intervention often is only offered long after an applicant has been removed from the workforce—a situation

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numerous studies have shown to significantly decrease the chance of a successful return to the workforce.36 Tertiary prevention focuses on arresting the progression of a pathologic condition and on limiting further disablement. For people with disabilities, tertiary prevention is designed to limit the restriction of a person’s participation in some area by the provision of a facilitator or the removal of a barrier.54 Environmental modifications, provision of services, removal of physical barriers, changes in social attitudes, and reform in legislation and policy are tertiary prevention strategies. Medical rehabilitation is traditionally considered a tertiary prevention strategy. The public disability policies, such as the ADA, are also efforts to reduce environmental and social barriers to participation.30,48,54 Considering functioning and disablement as outcomes of interactions between health conditions (disorders or diseases) and conceptual factors (social, environmental, and personal), there are many opportunities for the physiatrist and the medical rehabilitation team to intervene. Rehabilitation interventions aimed at prevention of activity limitation or prevention of participation restriction are secondary and tertiary prevention strategies that push the dynamic model of disablement in the direction of function. Some physiatrists feel a responsibility to be actively involved in therapeutic and public health management of disablement to develop and support policies that encourage improved function.18

Conclusion Comprehensive rehabilitation is an intervention directed at human functioning. The desired outcome is to maximize the physical, mental, social, and economic function of the individual with disabilities. The physiatrist as team leader has the responsibility of encouraging the team to take a holistic approach to the person with disabilities. The holistic approach includes collaboration with professionals outside the traditional medical rehabilitation team, such as those who can facilitate vocational rehabilitation for persons with disabilities. Vocational rehabilitation is an intervention aimed at preventing impairment from limiting activities and limiting participation in work. Limitation in work participation has significant socioeconomic consequences for the individual and for society. Employment of persons with disabilities supports a better quality of life and promotes function. Even for people with severe disabilities, vocational rehabilitation strategies have been successful in facilitation of work participation. Disability is the largest public health problem in the United States. The demands of this public health issue have captured the attention of public policy makers. This has resulted in implementation of significant federal disability laws. The nation’s public policies on disability reflect the policy makers’ acceptance of disability as a complex process. Disablement is considered to be the result of a dynamic, complex, and bidirectional interaction between health conditions and conceptual factors for each individual. The physiatrist is positioned to serve a primary role in the functioning and disablement paradigm. As persons

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SECTION 3  Common Clinical Problems

with disabilities become a greater segment of our society, the opportunities for physiatrists’ involvement are expanded. It is the physiatrist’s responsibility to be active in disability prevention, in care and advocacy for persons with disabilities, and in the development of public policy on disablement. REFERENCES 1. Adams PF, Benson V: Current estimates for the National Health Interview Survey, 1988, Vital Health Stat 10(173):1-250, 1989. 2. Allaire S, Li W, LaValley M: Reduction of job loss in persons with rheumatic diseases receiving vocational rehabilitation: a randomized controlled trial, Arthritis Rheum 48:3212-3218, 2003. 3. Anderson TP: Quality of life of the individual with a disability, Arch Phys Med Rehabil 63:55, 1982. 4. [Anonymous]: Federal Register: rules and regulations 65(251): 82905-82912, 2000. 5. [Anonymous]: Federal Register: rules and regulations 68(129):40119-40125, 2003. 6. Berkowitz M: The socioeconomic consequences of SCI, Paraplegic News 1994, pp18-23. 7. Berkowitz M, Hill MA: Disability and the labor market: an overview. In Berkowitz M, Hill MA, editors: Disability and the labor market: economic problems, policies, and programs, New York, 1989, ILR Press. 8. Colvez A, Blanche M: Disability trends in the United States population 1966–76: analysis of reported causes, Am J Public Health 71: 464-471, 1981. 9. Dean, DH, and Honeycutt, T. Evaluating the Long-Term Employment Outcomes of Vocational Rehabilitation Participants using Survey and Administrative Data. Final Technical Report May 26, 2005. Disability Research Institute, University of Illinois at Urbana-Champaign. 10. DeJong G, Lifchez R: Physical disability and public policy, Sci Am 248:40-50, 1983. 11. Goodman N, Stapleton DC: Program expenditures for working-age people with disabilities in a time of fiscal restraint, Washington, DC, November 2005, Cornell University Institute for Policy Research. 12. Haber LD: Identifying the disabled: concepts and methods in the measurement of disability, Soc Secur Bull 51:11-28, 1988. 13. Haber LD: Issues in the definition of disability and the use of disability survey data. In Daniel LB, Aitter M, Ingram L, editors: Disability statistics, an assessment: report of a workshop, Washington, DC, 1990, National Academy Press. 14. Harris L: The ICD survey of disabled Americans: bringing disabled Americans into the mainstream, New York, 1986, Louis Harris and Associates. 15. Harvey C: The business of employment: employment after traumatic SCI, Paraplegic News 1993, pp10-14. 16. Haveman RH, Halberstandt V, Burkhauser RV, editors: Public policy toward disabled workers: cross-national analyses of economic impacts, New York, 1984, Cornell University Press. 17. Hearne PG: Employment strategies for people with disabilities: a prescription for change, Milbank Q 69:111-128, 1991. 18. Joe TC: Professionalism: a new challenge for rehabilitation, Arch Phys Med Rehabil 62:245-250, 1981. 19. Kennedy EM, Jeffonds J, Moynahan DP, et al: The Work Incentives Improvement Act of 1999, Senate Bill 331, Feb 1999. 20. Kenney L: Earning histories of SSI beneficiaries working in December 1997, Soc Secur Bull 63(3):34-46, 2000. 21. Kraus LE, Stoddard S, Gilmartin D: Chartbook on disability in the United States, Washington, 1996, US Department of Education, National Institute on Disability and Rehabilitation Research. 22. La Plante MP: The demographics of disability, Milbank Q 69:55-77, 1991. 23. La Plante MP, Kennedy J, Kaye S, et al: Disability and employment, no. 11. Disability statistics abstract series, San Francisco, 1997, University of California. 24. Lin VW, Cardenas DD: Spinal cord medicine: principles and practice New York, 2003, Demos Medical Publishing. 25. McNeil JM: Current population reports, household economic studies, series P70-61. Washington, US Department of Commerce, Bureau of the Census, 1994–1995. 26. Menchetti BM, Flynn CC: Vocational evaluation. In Rusch FR, editor: Supported employment, Sycamore, IL, 1990, Sycamore.

27. Muller LS: Disability beneficiaries who work and their experience under program work incentives, Soc Secur Bull 55:2-19, 1992. 28. Nagi SZ: Disability concepts revisited: implication to prevention, appendix A. In Pope AM, Tarlov AR, editors: Disability in America: toward a national agenda for prevention, Washington, 1991, National Academy Press. 29. New Mexico Division of Vocational Rehabilitation: The Economic Impact of the New Mexico Division of Vocational Rehabilitation, September 2006, New Mexico Division of Vocational Rehabilitation Departmental website. Available at: http://www.dvetsjobs.com/Documents/ EconInpRep 2006.pdf. Accessed August 8, 2010. 30. Pope AM, Tarlov AR, editors: Disability in America: toward a national agenda for prevention, Washington, 1991, National Academy Press. 31. Rigby DE: SSI work incentive participants, Soc Secur Bull 54:22-29, 1991. 32. Rocklin SG, Mattson DR: The Employment Opportunities for Disabled Americans Act: legislative history and summary of provisions, Soc Secur Bull 50:25-35, 1987. 33. Rusk HA: The growth and development of rehabilitation medicine, Arch Phys Med Rehabil 50:463-466, 1969. 34. Schaffer DC: Tax incentives, Milbank Q 69:293-312, 1991. 35. Scott CG: Disabled SSI recipients who work, Soc Secur Bull 55:26-36, 1992. 36. Sim J: Improving return-to-work strategies in the United States disability programs, with analysis of program practices in Germany and Sweden, Soc Secur Bull 59(3):41-50, 1999. 37. Social Security Administration: Report of Disability Advisory Council: executive summary, Soc Secur Bull 51:13-17, 1988. 38. Symington DC: The goals of rehabilitation, Arch Phys Med Rehabil 65:427-430, 1984. 39. Thornton C, Maynard R: The economics of transitional employment and supported employment. In Berkowitz M, Hill MA, editors: Disability and the labor market: economic problems, policies, and programs, New York, 1989, ILR Press. 40. U.S. Census Bureau: Americans with Disabilities: 2005 Report, Issued, December 2008. Available at: http://www.census.gov/prod/ 2008pups/p70-117.pdf. Accessed August 1, 2010. 41. U.S. Census Bureau: 2007 American Community Survey 1-Year Estimates. S1801. Available at: http://factfinder.census.gov/servlet/ DatamainPageServlet?-program= DEC&_submenuId=datasets 42. U.S. Department of Health and Human Services: Social Security Administration: redbook on work incentives, Washington, DC, 1992, Government Printing Office. 43. U.S. Department of Health and Human Services: Social Security Administration. Social Security handbook, ed 13, Washington, DC, 1997, Government Printing Office. 44. U.S. Department of Justice: Civil Rights Division, A Guide to Disability Rights Laws, September 2005. 45. U.S. Equal Employment Opportunity Commission: U.S. Department of Justice: Americans with Disabilities Act handbook (EEOC-BK-19), Washington, DC, 1991, Government Printing Office. 46. U.S. General Accounting Office: Report to Congressional Requestors: vocational rehabilitation: improved information and practices may enhance state agency earnings outcomes for SSA beneficiaries, Washington, DC, May 2007, Government Printing Office. 47. U.S. General Accounting Office: Testimony before the Subcommittee on Select Education, Committee on Education and Labor, House of Representatives. Vocational rehabilitation program: client characteristics, services received, and employment outcomes, Washington, DC, 1991, Government Printing Office. 48. Vachon RA: Employing the disabled. Issues Sci Technol 1989-1990; winter:44-50. Available at: http://www.ada.gov/guide.htm. Accessed August 8, 2010 49. Vachon RA: Employment assistance and vocational rehabilitation for people with HIV or AIDS: policy, practice, and prospects. In O’Dell MW, editor: HIV-related disability: assessment and management: physical medicine and rehabilitation: state of the art reviews, Philadelphia, 1993, Hanley & Belfus. 50. Vachon RA: Inventing a future for individuals with work disabilities: the challenge of writing national disability policies. In Woods DE, Vandergoot D, editors: The changing nature of work, society and disability: the impact on rehabilitation policy, New York, 1987, World Rehabilitation Fund.

CHAPTER 35  Employment of Persons With Disabilities 51. Verville R: The rehabilitation amendments of 1978: what do they mean for comprehensive rehabilitation? Arch Phys Med Rehabil 60:141-144, 1979. 52. Wehman P, Sherron P, Kregel J, et al: Return to work for persons following severe traumatic brain injury: supported employment outcomes after five years, Am J Phys Med Rehabil 72:355-363, 1993. 53. Wilson RW: Do health indicators indicate health? Am J Public Health 71:461-463, 1981. 54. World Health Organization: International Classification of Functioning, Geneva, WHO, 2001, Disability and Health.

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55. World Health Organization: Towards a common language for functioning and disablement: ICIDH-2, the International Classification of Impairments, Activities, and Participation, Geneva, 1998, World Health Organization. 56. Yelin EH, Cisternas M, Trupin L: The economic impact of disability in the U.S., 1997: total and incremental estimates (2006). Avai­lable at http://papers.ssrn.com/Sol3/papers.cfm?/abstract id=899927. Accessed August 8, 2010.

CHAPTER 36 RHEUMATIC DISEASES Santiago D. Toledo, Kathleen Trapani, and Elizabeth Feldbruegge

General Introduction to Rheumatic Diseases Rheumatic diseases are among the oldest diseases recognized, and more than 100 diverse disorders affect the muscles, bony joints, and supporting structures of the musculoskeletal system (Table 36-1). The classification of rheumatic diseases is often difficult because of their unknown etiology and heterogeneity in their clinical presentation. Some of them are relatively more common, whereas many other conditions are rare (e.g., connective tissue diseases and disorders of collagen metabolism). This chapter focuses on the rheumatic diseases most likely to be seen by a physiatrist, in particular osteoarthritis (OA) and rheumatoid arthritis (RA). Both conditions are variable in manifestation, chronic in status, widespread in nature, and often take a progressive course. Other disorders, such as fibromyalgia, complex regional pain syndrome, and osteoporosis, are described in other chapters in this textbook. OA and RA are the two most common rheumatic diseases and account for a large proportion of disability worldwide. Impairment to the musculoskeletal organ systems as a result of rheumatic conditions is the primary cause of functional limitations in the adult population. OA has been estimated to be the eighth leading cause of disability in the world and accounts for 2.8% of the total number of years of living with a disability. RA affects up to 1% of the adult population in developed countries, with 10% of these patients having severe disability. The prevalence of overall disability has been estimated at 20% of the adult and aging population. The physical impairments, functional decline or lack of ability, decreased quality of life, lost productivity, and staggering costs of health care for rheumatic diseases such as OA and RA affect both the individual and society. The economic and social burden of these diseases can be overwhelming. This overall impact can be expected to increase with the incremental pace of aging of our world’s population. One of the many challenges in studying rheumatic diseases is deriving epidemiologic data that can be used to better understand the factors that contribute to the initiation and progression of these diseases. With these data, significant progress can be made in the clinical diagnosis, medical management, surgical interventions, and rehabilitative care of patients. The goal of this chapter is to describe the fundamental concepts and basic principles that a physiatrist needs to know to effectively address the impairments and disability that are associated with rheumatic diseases. We recommend that the rehabilitation-centered approach to these

chronic and progressive illnesses include the following: (1) patient-defined problems are identified along with clinical and functional problems diagnosed by clinicians; (2) patients and providers focus on a specific problem, set realistic objectives, and develop an action plan for attaining these objectives in the context of patient preferences and readiness; (3) patients have access to educational services that teach the skills needed to carry out medical regimens, guide health behavior changes, and provide emotional and psychologic support; and (4) patients are contacted at specified intervals to monitor health status, identify potential complications, and check and reinforce progress in implementing the care plan. The rehabilitation of patients with rheumatic diseases demands an appropriately reasonable, systematically organized, and comprehensively coordinated approach that is both multidisciplinary and collaborative.

Kinesiology: T   he Structure and Function of Joints Kinesiology is a significant part of the foundation for the practice of physical medicine and rehabilitation. It involves knowledge from anatomy, biomechanics, and physiology. The human body is composed of more than 200 joints, each with different shapes and functions. Joints are links between bones in the human body that control the movement of bony segments and provide stability. The knee joint, for example, joins the femur and tibia and allows the lower leg to swing freely. It also allows it to be stable during the stance phase of gait. Some joints provide the body with stability, whereas others provide with mobility. Most joints provide both mobility and stability. All the joints in the human body can be affected by rheumatic diseases. For this chapter, we will divide joints into three classifications: diarthrosis, amphiarthrosis, and synarthrosis. A diarthrosis joint, also known as a synovial joint, consists of two reciprocally shaped bony articular surfaces and is a freely movable joint. The knee joint is an example of a diarthrosis joint. The ends of the adjoining bones are covered with a thin cartilaginous sheet, and the bones are linked by a ligament lined with synovial membrane. The synovial membrane secretes synovial fluid. Synovial fluid lubricates and smoothes the tendon movement. The amphiarthrosis joint, sometimes called a fibrocartilaginous joint, is a junction between bones that is formed primarily by a fibrocartilage or hyaline cartilage. The interbody joint in the spine is an example. The amphiarthrosis joint is only slightly movable, allowing relatively restrained movements. It can also transmit and disperse 769

770

SECTION 3  Common Clinical Problems

Table 36-1 The Main Types of Rheumatic Diseases Disease Group

Description

Examples

Degenerative and overuse syndromes

Diseases in which the predominant feature is repetitive trauma and/or “wear and tear” of cartilage or periarticular tissues, with minor secondary inflammation

Osteoarthritis Tendonitis Bursitis

Inflammatory ­arthropathies

Diseases characterized by chronic or recurrent joint inflammation of unknown cause; ­classified according to the pattern of joint involvement and associated features

Rheumatoid arthritis Psoriatic arthritis Spondyloarthropathies

Extraarticular rheumatism

Poorly understood disorders characterized by chronic or recurrent pain with no evidence of inflammation; primary pathology might be in the perception of pain rather than in the soft tissues

Fibromyalgia Nonspecific neck pain Nonspecific back pain

Connective tissue diseases

Autoimmune diseases of unknown etiology characterized by multisystem inflammation and damage

Systemic lupus erythematosus Polymyositis or dermatomyositis Scleroderma Vasculitis

Inherited disorders of ­connective tissue

Rare diseases caused by genetic abnormalities affecting the synthesis of structural ­molecules of the bone and connective tissues

Collagenopathies Mucopolysaccharidoses Osteogenesis imperfecta Ehlers-Danlos syndrome

Crystal-associated ­arthropathies

Diseases characterized by acute or recurrent inflammation caused by deposition of ­crystals in or around the joints

Gout Calcium pyrophosphate crystals Hydroxyapatite crystals

Infectious arthropathies

Diseases caused by invasion of joint tissues by microorganisms

Viral Bacterial Tuberculosis and fungi

Postinfectious ­arthropathies

Diseases triggered by previous exposure to infectious agents

Poststreptococcal Postchlamydial Postviral

forces between the bones separated by the fibrocartilage or hyaline cartilage. The synarthrosis, or synarthodial, joint functions primarily to allow forces to be dispersed across a relatively large area of contact, thereby reducing the possibility of injury. The interosseous membrane of the radial–ulnar and tibial–fibular joints is a good example. OA is a rheumatic disease that can affect one or multiple joints in the human body. OA is commonly seen in diarthrosis and amphiarthrosis joints, such as the hand, hip, knee, shoulder, and spine. The predominant feature of OA is the causal relationship between repetitive trauma, the “wear and tear” of the cartilage and periarticular tissues, with minor secondary inflammation. RA is usually seen in multiple joints and presents symmetrically. RA is one of the rheumatic diseases that are characterized by chronic or recurrent joint inflammation of unknown cause. Similar to OA, RA is seen in all types of joints. Joints of the human body can be affected by injury, increased demand, immobilization, or long-term bed rest. Diseases such as OA and RA also affect joints. Injury can occur if a large stress or load is placed on a joint. Constant excessive loading, repetitive over time, can also change the joint structure, leading to breakdown. Immobilization or long-term bed rest causes muscles around the joints to atrophy and weaken. It is just as important to understand that joints and articular surfaces need some load, such as gravity, to maintain proper integrity. If a load is not present, over time articular surfaces will progressively weaken and degenerate because of a lack of stimulus. Inflammatory disease processes can also disrupt the integrity of the

joint. The above problems can affect and impair joint structure and eventually disrupt functions such as standing and walking. Severely advanced or progressive joint degradation can lead to disability.

An Overview of Common Rheumatic Diseases Osteoarthritis OA is the most common form of arthritis and affects nearly 21 million people in the United States. OA is the leading cause of chronic disability. The number of people diagnosed with OA is increasing steadily. The aging of the population, the increase in obesity, and the sports-related injuries of active baby boomers can be attributed to this increase. OA is a disease that involves degeneration in various structures of the joint, including cartilage, bone, synovium, muscles, and ligaments. This can result in stiffness, loss of mobility, swelling, and pain. In contrast to RA, OA is primarily a noninflammatory disorder, but inflammation eventually occurs and is progressive. OA generally occurs in weight-bearing joints, such as hips, knees, and the lower back. It also commonly occurs in the neck, the fingers, the base of the thumb, and the great toe. It rarely occurs elsewhere in the absence of stress or injury. No single known cause of OA exists. Factors that might contribute to a diagnosis of OA include genetic disposition, age, injury, weight, stress on the joint, and previous surgery involving the joint. Age is the most commonly identified risk factor for OA of all joints. The prevalence

CHAPTER 36  Rheumatic Diseases

of OA increases sharply for women after age 40 years and after age 50 for men. OA of the hand is more prevalent in women, whereas men are slightly more likely to have hip OA. Genetics is likely to contribute to the development of primary OA. Inhibited bone abnormalities or inherited traits (e.g., dysplasia, malalignment) that subject the joint to unusual stress increase the likelihood of its development. No standard definition of OA is used by researchers and clinicians. A review of the literature showed the validity of the various definitions of hip OA has been barely investigated. Despite precise and extensive development, the American College of Rheumatology (ACR) criteria showed poor reliability and cross-validity in a primary care setting. No agreed criteria exist for knee OA in population studies. The radiographic scoring system of Kellgren and Lawrence15 (Table 36-2) has been most used in the past. Although other methods have been developed, comparisons have not been performed. Data suggest that the presence or absence of a definite osteophyte read on a weight-bearing radiograph is the best method of defining knee OA for epidemiologic studies. Assessment of joint space narrowing might be better used in evaluating the disease severity. The typical progression of OA involves the following events: (1) loss of cartilage matrix, which makes the joint more susceptible to further injury; (2) alterations to underlying bone associated with wear on the cartilage, with the development of osteophytes at the periphery of the affected joint; (3) release of debris of cartilage or bone fragments into the joint; (4) cartilage breakdown associated with synovial inflammation, which can lead to release of cytokines and enzymes that exacerbate the cartilage damage. Some examples of OA in different joints can be seen in Figure 36-1. Goals of OA therapy are to decrease pain, increase function in activities of daily living (ADL) and mobility, prevent and correct deformity, and slow disease progression. The treatment approach varies because of lack of inflammation and the influence of degeneration in joint integrity. Many pharmacologic options can be used for the treatment of OA. Conditioning muscles around joints with physical therapy and weight loss have been shown to improve symptoms and ADL. Application of heat and cold therapy and use of assistive devices have specific benefits. If OA progresses where conservative measures are not successful, joint replacement surgery is an option. Box 36-1 lists the criteria for classification of OA of the hand, hip, and knee.

Rheumatoid Arthritis RA is defined as an autoimmune disease in which the joint lining and occasionally other tissues become inflamed as a result of overactivity of the body’s immune system.5,7 RA is a chronic, systemic, inflammatory disorder of unknown etiology that primarily involves the joints. RA begins insidiously with generalized weakness, anorexia, fatigue, and vague musculoskeletal symptoms before the appearance of synovitis. RA affects about 1% of the adult population but causes more than 250,000 hospitalizations annually. RA is one of the most serious and disabling types of arthritic diseases and affects women 2 to 3 times more often than men.

771

Table 36-2  Kellgren-Lawrence Radiographic Grading Scale for Osteoarthritis of the Tibiofemoral Joint Grade of Osteoarthritis

Description

0

No radiographic findings of osteoarthritis

1

Minute osteophytes of doubtful clinical significance

2

Definite osteophytes with unimpaired joint space

3

Definite osteophytes with moderate joint space narrowing

4

Definite osteophytes with severe joint space ­narrowing and subchondral sclerosis

Like OA, RA encompasses a combination of events or a pattern of reactions that can result in joint injury.26 Although RA is universal and found in all populations, prevalence and incidence rates vary in different ethnic groups. A low prevalence is found among African blacks, and a high prevalence is seen in rural Germany. Prevalence rates are influenced according to which set of criteria is used to diagnose RA and whether the RA is definite or probable. Genetic studies of RA show that there is a limited concordance of the disease in twins. No specific pattern of inheritance exists, although there is a twofold increase among first-degree relatives of patients with RA. Some examples of its effects on the hands and feet are shown in Figure 36-2. Review of the literature presents various quantitative measures to assess RA in research trials and clinical care. No single “gold standard” is used to assess and monitor the status of patients with RA. Different measures have been used in research and clinical care, including laboratory tests, radiographic scores, formal joint counts, physical measures of functional status, global measures, and patient self-report questionnaires. These measures or assessment tools can address the activity of the disease, damage to the joint, both activity and damage, or long-term outcomes. Measures of disease activity (e.g., joint swelling) are reversible and can be improved over time, whereas measures of joint damage (e.g., radiographic scores) indicate disease progression.22,23 In evaluating new therapies for RA, randomized controlled trials provide the optimal method by comparing a therapy with a placebo or another therapy without selecting patients for specific therapies. Randomized trials in chronic diseases have important limitations. Examples of these limitations include relatively short observation, patient selection for inclusion and exclusion criteria, inflexible dosage schedules, influence of the design on results despite a control group, emphasis on group data instead of individual variations in treatment responses, and nonstandardized interpretation of adverse effects. Clinical trials in RA must be supplemented by long-term observational studies to assess the results of therapy in regard to long-term outcomes. Long-term outcomes include work disability, joint replacement surgery, and premature mortality. The patient self-report questionnaire is the most simple and effective method of collecting important long-term data from patients in routine clinical care. Goals of RA therapy are to prevent or control joint damage, prevent loss of function, and decrease pain. Treatment

772

SECTION 3  Common Clinical Problems

OA of the spine Sclerosis of facet joints

Spondylolisthesis

Anterior osteophyte Loss of intervertebral space

A

Heberden and Bouchard nodes

Osteophytes

Loss of articular space

Heberden in distal interphalangeal joint

Bouchard in proximal interphalangeal joint

B OA of the hip

Subchondral cysts Osteophytes of acetabulum and femoral head

Sclerosis of roof of acetabulum Asymmetric loss of articular space

C OA of the knee

Sclerosis of medial femoral condyle Subchondral cysts

Asymmetic loss of articular space

D FIGURE 36-1 Typical deformities and x-ray findings in osteoarthritis of the spine (A), hands (B), hip (C), and knee (D).

CHAPTER 36  Rheumatic Diseases

773

BOX 36-1

The American College of Rheumatology Criteria for the Classification of Osteoarthritis of the Hand, Hip, and Knee Classification criteria for osteoarthritis of the hand, traditional format Hand pain, aching, or stiffness, and at least three of the following: • Hard tissue enlargement of 2 or more of 10 selected joints • Hard tissue enlargement of 2 or more DIP joints • Fewer than 3 swollen MCP joints • Deformity of at least 1 of 10 selected joints Classification criteria for osteoarthritis of the hip, traditional format Hip pain and at least two of the following: • ESR (Westergren) 50 yr • Stiffness 50 yr

0.84

0.61

Age >70 yr

0.22

0.96

Corticosteroid use

0.66

0.99

Sciatica

0.95

0.88

From Nachemson A, Vingard E: Assessment of patients with neck and back pain: A bestevidence synthesis. In Nachemson AL, Johnsson B, editors: Neck and back pain: the scientific evidence of causes, diagnosis, and treatment, Philadelphia, 2001, Lippincott Williams & Wilkins. *The sensitivity of “fever.”

Besides determining a diagnosis, a purpose of the history is to explore the patient’s perspective and illness experience. Certain psychosocial factors are valuable in determining prognosis (Box 40-3). Factors such as poor job satisfaction, catastrophic thinking patterns about pain, the presence of depression, and excessive rest or downtime are much more common in patients in whom back pain becomes disabling. These are called yellow flags because the clinician should proceed with caution, and further psychologic evaluation or treatment should be considered if they are present. Some of these psychosocial factors are addressed by specific questions, and some become evident through statements that patients make during the history as they describe their illness experience. Questions about, for example, what patients believe is causing the pain, their fear and feelings surrounding this belief, their expectations about the pain and its treatment, and how back pain is affecting their lives (including work and home life) can yield valuable information. Many of these yellow flags are better prognostic indicators than the more traditional medical diagnoses.235

Observation Observation should include a survey of the skin, muscle mass, and bony structures, as well as observation of overall posture (Figures 40-13 and 40-14), and the position of the lumbar spine in particular. Gait should also be observed for clues regarding etiology and contributing factors. Palpation Palpation should begin superficially and progress to deeper tissues. It can be done with the patient standing. To ensure that the back muscles (Figure 40-15) are fully relaxed, palpation is often done with the patient lying prone, perhaps with a pillow under the abdomen to slightly flex the spine into a position of comfort. It should proceed systematically to determine what structures are tender to palpation. Range of Motion Quantity of Range of Motion. Several methods can be used to measure spinal range of motion (ROM). These include using a single or double inclinometer; measuring the distance of fingertips to floor; and, for forward flexion, the Schober test (measuring distraction between two marks on the skin during forward flexion). Of these methods, the double inclinometer has been shown to correlate the closest to measurements on radiographs.77,210 Fingertip to floor has good interrater and intrarater reliability, but this takes into account the movement of the pelvis and is affected by structures outside the spine, such as tight hamstrings.168 The Schober test is commonly used to assess a decrease in forward flexion in ankylosing spondylitis. It is sensitive for this condition but is not specific. General figures for normal ROM are forward flexion, 40 to 60 degrees; extension, 20 to 35 degrees; lateral flexion, 15 to 20 degrees; and rotation, 3 to 18 degrees. Studies to determine normal ROM in asymptomatic adults have found large variations within the normal range.165 It is unclear what the significance of decreased ROM is in patients with back pain because many people without back pain also have limited range. ROM

CHAPTER 40  Low Back Pain

881

Table 40-2 Physical Examination for Low Back Pain Examination Component

Specific Activity

Reason for This Part of the Examination

Observation

Observation of overall posture

Determine whether structural abnormality or muscle imbalances are ­present

Observation of lumbar spine

Further define muscle imbalance and habitual posture

Observation of the skin

Search for diagnoses such as psoriasis, shingles, or vascular disease as cause of the pain

Observation of gait

Screen the kinetic chain and determine whether muscular, neurologic, or joint problems are contributing to symptoms

Bones

Search for bony problems such as infection or fracture

Facet joints

Identify whether specific levels are tender

Ligaments and intradiskal spaces

Determine whether these are tender

Muscles

Search for trigger points, muscle spasms, muscle atrophy

Forward flexion

Amount, quality if painful

Palpation

Active range of motion

Extension Side bending

— Same, also side to side differences

Rotation Neurologic examination

Orthopedic special tests

—

Manual muscle testing of L1–S1 myotomes

Determine weakness

Pinprick and light touch sensation, L1–S1 dermatomes

Determine sensory loss

Reflexes: patellar, hamstring, Achilles

Test injury to L4, L5, or S1 roots if diminished, upper motor neuron disease if brisk

Balance and coordination testing

Signs of upper motor neuron disease

Plantar responses

Same

Straight leg raise

Neural tension at L5 or S1

Femoral nerve arch

Neural tension at L3 or L4

Abdominal muscle strength

Determines weakness and deconditioning

Pelvis stabilizer strength, i.e., gluteus medius, maximus, etc.

Determines weakness and deconditioning

Tightness or stiffness of hamstrings

Determines areas of poor flexibility

Tightness or stiffness of hip flexors

—

Tightness or stiffness of hip rotators Prone instability test

can also change depending on the time of day, the effort the patient expends, and many other factors.255 Quality of Range of Motion. The examiner should record whether there are abnormalities in the patient’s movement pattern during ROM, such as a “catch” in the range or whether it causes pain. This might give clues to the diagnosis. For example, pain with forward flexion can signify disk disease, and pain with extension can indicate spondylolisthesis, zygapophyseal joint disease, or spinal stenosis. The Neurologic Examination The neurologic examination of the lower limbs can rule out clinically significant nerve root impingement and other neurologic causes of leg pain (Tables 40-3 and 40-4). The physical examination should logically proceed to discover whether a particular root level is affected by combining the findings of weakness, sensory loss, diminished or absent reflexes, and special tests such as straight leg-raising sign. Upper motor neuron abnormalities should also be ruled

— Signs of instability

out. The accuracy of the neurologic examination in diagnosing herniated disk is moderate. The accuracy can be increased considerably, however, with combinations of findings.50 The sensitivity and specificity of different findings for lumbar radiculopathy have been well studied (Table 40-5). Orthopedic Special Tests to Assess for Relative Strength and Flexibility Back pain can be caused by deconditioning, poor endurance, and muscle imbalances. This makes it important to identify any inefficient or abnormal movement patterns of muscles that control the movement of the spine and the position of the pelvis. Because of their stabilizing effect on the spine, abdominal muscle strength and endurance is important. Several different ways can be used to measure abdominal muscle strength and control (Figures 40-16 and 40-17). One grading system assesses whether the patient is able to maintain a neutral spine position while adding increasingly more challenging leg movements (Figure 40-18).

882

SECTION 4  Issues in Specific Diagnoses

A

A

B

C

B

C

D

D

FIGURE 40-13 The four types of postural alignment: Ideal alignment (A), kyphosis–lordosis posture (B), flat back posture (C), and sway-back posture (D). (Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Williams & Wilkins.)

Besides determining the strength of the abdominals, strength testing of the back muscles and pelvic stabilizers, such as the hip abductors, can be useful. Assessing for areas of relative inflexibility is also important. Commonly performed tests are hip flexor flexibility, hamstring flexibility, other hip extensors’ length, and gastrocnemius/ soleus length. Balance challenges, such as the ability to maintain single-footed stance, the ability to lunge or squat, and other functional tests are also helpful to determine a patient’s baseline status. Orthopedic Special Tests for Lumbar Segmental Instability Many clinicians and researchers believe that one cause of mechanical low back pain is segmental instability that responds to specific stabilization treatments. Therefore accurately identifying this group from other forms of low back pain could be important. These special tests include passive intervertebral motion testing and the prone instability test. Passive Intervertebral Motion Testing. The patient lies prone. The examiner applies a firm steady pressure over the spinous process anteriorly and assesses the amount of vertebral motion and whether pain is provoked.90 Prone Instability Test. The patient lies prone, with the torso on the examining table and the legs over the edge of the table with the feet resting on the floor. The examiner performs passive intervertebral motion testing at each level and notes provocation of pain. Then the patient lifts the legs off the floor, and the painful levels are repeated. A positive test is when the pain disappears when the legs are lifted off the table. This is

30°

G

FIGURE 40-14  Faulty pelvic alignment as a result of weak and long abdominal muscles (A), short and stiff hip flexors (B), apparent anterior tilt (C), and posterior tilt (D). The effect of pelvic tilting on the inclination of the base of the sacrum to the transverse plane (sacral angle) during upright standing is shown. E, Tilting the pelvis backward reduces the sacral angle and flattens the lumbar spine. F, During relaxed standing, the sacral angle is about 30 degrees. G, Tilting the pelvis forward increases the sacral angle and accentuates the lumbar spine. (Modified from Sahrmann SA: Movement impairment syndromes of the lumbar spine: diagnosis and treatment of movement impairment syndromes, St Louis, 2002, Mosby.)

because the extensors are able to stabilize the spine in this position.90,138 Examining the Area Above and Below the Lumbar Spine Generally in musculoskeletal medicine, the joint above and the joint below the painful area should be assessed to make sure nothing is missed. This is a good idea for the examination of the lumbar spine as well. ROM of the hip joints should be assessed, and a quick screen of the knee and ankle joint can determine whether pathology in these areas is contributing to the back problem. The thoracic spine can be quickly screened as well during ROM and palpation.

CHAPTER 40  Low Back Pain

Erector spinae muscles

L4–5 intervertebral joint

Iliac crest

Sacroiliac joint

FIGURE 40-15  Anatomy of the low back surface anatomy.

Table 40-3 Factors That Affect Posture Reason for Abnormality

Clinical Example

Bone structure

Compression fractures Scheuermann disease

Ligamentous laxity

Hyperextension of the knees, elbows

Muscle and fascial length

Tight hamstrings that cause a posterior pelvic tilt Weak and long abdominal muscles that allow an anterior pelvic tilt

Body habitus

Obesity or pregnancy causes changes in force and increased lumbar lordosis

Neurologic disease

Spasticity causes an extension pattern of the lower limb

Mood

Depression causes forward slumped shoulders

Habit

Long-distance cyclists have increased thoracic kyphosis and flat spine from prolonged positioning while riding

Illness Behavior and Nonorganic Signs Seen on Physical Examination Multiple reasons can explain why patients with back pain might display symptoms out of proportion to injury. Illness behaviors are learned behaviors and are responses that some patients use to convey their distress. Several studies have found that patients with chronic low back pain and chronic pain syndrome experience significant anxiety during the physical examination, even to the level experienced during panic attacks. This complicates the assessment by altering the clinical presentation of the condition. This anxiety is generally manifest as avoidance behavior, such as decreased ROM or poor effort with muscle testing.81 Other reasons for illness behavior include a desire to prove to physicians how disabling the pain is and malingering. One way to assess for illness behavior on physical

883

examination is to perform parts of the examination to search for Waddell’s signs. Waddell’s signs are forms of illness behavior.234 They are nonorganic findings on physical examination that correlate with psychologic distress. They are as follows: • Inappropriate tenderness that is widespread or superficial • Pain on testing that only simulates loading the spine, such as light pressure applied to the top of the head, which reproduces back pain, or rotating the hips and shoulders together to simulate twisting without actually moving the spine, which reproduces back pain • Inconsistent performance when testing the same thing in different positions, such as a difference in outcome of the straight leg-raising test with the patient supine versus sitting • Regional deficits in strength or sensation that do not have an anatomic basis • Overreaction during the physical examination Findings in three of these five categories suggest psychologic distress and also suggest that other parts of the physical exam that require patient effort or reporting of symptoms might be inaccurate.

Clinical Evaluation: Diagnostics Imaging Studies Imaging of the lumbar spine should be used in the evaluation of low back pain if specific pathology needs to be confirmed after a thorough history and physical examination. Plain Radiography Conventional radiographs are indicated in trauma to evaluate for fracture and to look for bony lesions such as tumor when red flags are present in the history. As an initial screening tool for lumbar spine pathology, however, they have very low sensitivity and specificity.73 Anterior–posterior and lateral views are the two commonly obtained views. Oblique views can be obtained to examine for a spondylolysis by visualizing the pars interarticularis and the “Scottie dog” appearance of the lumbar spine (Figure 40-19). Lateral flexion–extension views are obtained to check for dynamic instability, although the literature does not support their usefulness.55 They are potentially most helpful from a surgical screening perspective when evaluating a spondylolisthesis. They are commonly obtained in posttrauma and postsurgical patients. Magnetic Resonance Imaging MRI is the preeminent imaging method for evaluating degenerative disk disease, disk herniations, and radiculopathy (Figure 40-20) (see also Chapter 7). On T2-weighted imaging, the annulus can be differentiated from the internal nucleus, and annular tears can be seen as high-intensity zones. These zones are of unclear clinical significance but are thought to be potential pain generators. Adding gadolinium contrast enhancement helps to identify structures with increased vascularity. Contrast is always indicated in evaluating for tumor or infection or to determine scar tissue (vascular) versus recurrent disk

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SECTION 4  Issues in Specific Diagnoses

Table 40-4 Lumbar Root Syndromes Root

Dermatome

Muscle Weakness

Reflexes or Special Tests Affected

L1

Back, over trochanter, groin

None

None

Paresthesias Groin, after holding posture, which causes pain

L2

Back, front of thigh to knee

Psoas, hip abductor

None

Occasionally front of thigh

L3

Back, upper buttock, front of thigh and knee, medial lower leg

Psoas, quadriceps–thigh wasting

Knee jerks sluggish, protein kinase B-positive, pain on full straight leg raise

Inner knee, anterior lower leg

L4

Inner buttock, outer thigh, inside of leg, dorsum of foot, big toe

Tibialis anterior, extensor hallucis

Straight leg raise limited, neck flexion pain, weak knee jerk, side flexion limited

Medial aspect of calf and ankle

L5

Buttock, back and side of thigh, lateral aspect of leg, dorsum of foot, inner half of sole, and first, second, and third toes

Extensor hallucis, peroneals, gluteus medius, ankle ­dorsiflexors, hamstrings–calf wasting

Straight leg raise limited to one side, neck flexion pain, ankle jerk decreased, crossed ­leg-raising pain

Lateral aspect of leg, medial three toes

S1

Buttock, back of thigh, and lower leg

Calf and hamstrings, wasting of gluteals, peroneals, plantar flexor

Straight leg raise limited

Lateral two toes, lateral foot, lateral leg to knee, plantar aspect of foot

S2

Same as S1

Same as S1, except peroneals

Same as S1

Lateral leg, knee, heel

S3

Groin, inner thigh to knee

None

None

None

S4

Perineum: genitals, lower sacrum

Bladder, rectum

None

Saddle area, genitals, anus, ­impotence

From Maguire JH: Osteomyelitis. In Braunwald E, Fauci AS, Kasper DL, et al, editors: Harrison’s principles of internal medicine, ed 15, New York, 2001, McGraw-Hill.

Table 40-5 Lumbosacral Radiculopathy in Patients With Sciatica* Finding†

Sensitivity (%)

Specificity (%)

Positive Lumbrosacral Radiculopathy

Negative Lumbrosacral Radiculopathy

Motor examination Weak ankle dorsiflexion

54

89

4.9

0.5

Ipsilateral calf wasting

29

94

5.2

0.8

16

86

NS

NS

48

89

4.3

0.6

Straight leg-raising maneuver

73-98

11-61

NS

0.2

Crossed straight leg-raising maneuver

23-43

88-98

4.3

0.8

Sensory examination Leg sensation abnormal Reflex examination Abnormal ankle jerk Other tests

From McGee SR: Evidence-based physical diagnosis, Philadelphia, 2001, Saunders. NS, Not significant. *Diagnostic standard: for lumbosacral radiculopathy, surgical finding of disk herniation compressing the nerve root. †Definition of findings: for ipsilateral calf wasting, maximum calf circumference at least 1 cm smaller than on contralateral side; for straight leg-raising maneuvers, flexion at hip of supine patient’s leg, extended at the knee, causes radiating pain in affected leg (pain confined to back or hip is a negative response); for crossed straight leg-raising maneuver, raising contralateral leg provokes pain in the affected leg.

herniation (avascular) in postsurgical patients with recurrent radicular symptoms. The downside of MRI is that, although it is a very sensitive test, it is not very specific in determining a definite source of pain. It is well established that many people without back pain have degenerative changes, disk bulges, and protrusions on MRI. Boden et al.21 demonstrated that one third of 67 asymptomatic subjects were found to have a “substantial abnormality” on MRI of the lumbar spine. Of the subjects younger than 60 years, 20% had a disk herniation, and 36% of those older than 60 had a disk herniation and 21% had spinal stenosis. Bulging and degenerative disks were even more commonly found. In another study

of lumbar MRI findings in people without back pain, Jensen et al.97 demonstrated that only 36% of 98 patients had normal disks. They found that bulges and protrusions were very common in asymptomatic subjects, but that extrusions were not. In a more recent study in 2001, Jarvik confirmed these findings.96 Computed Tomography Because of the resolution of anatomic structures in MRI, it has essentially replaced computed tomography (CT) scanning as the imaging study of choice for low back pain and radiculopathy. CT scanning is still more useful than MRI, however, in evaluating bony lesions. CT scans are

CHAPTER 40  Low Back Pain

60%

80%

45

°

75°

70%

60 °

90°

50%

885

°

90%

30

A

15°

100%

0°

B

A

C FIGURE 40-16 Trunk raising forward: grading. The curl trunk sit-up is performed with the patient lying supine and with the leg extended. The patient posteriorly tilts the pelvis and flexes the spine, and slowly completes a curled trunk sit-up. Kendall states that the “crucial point in the test for the abdominal muscle strength is at the moment the hip flexors come into strong action. The abdominal muscle at this point must be able to oppose the force of the hip flexors in addition to maintain the trunk curl.” At the point where the hip flexors strongly contract, patients with weak abdominal muscles will tilt the pelvis anteriorly and extend the low back. A, A 100% or normal grade is the ability to maintain spinal flexion and come into the sitting position with the hands clasped behind the head. B, An 80% or good grade is the ability to do this with the forearms folded across the chest. C, A 60% or fair grade is the ability to do this with the forearms extended forward. A 50% or fair grade is the ability to begin flexion but not maintain spinal flexion with the forearms extended forward. (Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Williams and Wilkins.)

also useful in the postsurgical patient with excessive hardware that can obscure MRIs, and in patients with implants (aneurysm clips or pacemakers) that preclude MRI. Myelography In myelography, contrast dye is injected into the dural sac and plain radiographs are performed to produce images of the borders and contents of the dural sac (Figure 40-21). CT images can also be obtained after contrast injection to produce axial cross-sectional images of the spine that enhance the distinction between the dural sac and its surrounding structures. This is typically reserved as a potential presurgical screening tool but has been used less with the advancement of MRI. Scintigraphy Radionuclear bone scanning is a fairly sensitive but not specific imaging modality that can be used to detect occult fractures, bony metastases, and infections. To

B

C FIGURE 40-17  Leg lowering: grading. In the second test, the patient raises the legs one at a time to a right angle, and then flattens them back on the table. The patient slowly lowers the legs while holding the back flat. A 100% or normal grade is the ability to hold the low back flat on the table as the legs are lowered to the fully extended position. An 80% or good grade is the ability to hold the low back flat and lower the legs to a 30-degree angle. A, A 60% or fair plus grade is the ability to lower the legs to 60 degrees with the low back flat. B, The pelvis tilted anteriorly and the low back arched as the legs were lowered. C, The final position. Kendall notes that this second test is more important than the first (see Figure 40-16) in grading muscles essential to proper posture, and that often patients who do well on the first test do poorly on the second. (Modified from Kendall FP, McCreary EK: Trunk muscles in muscle testing and function, Philadelphia, 1983, Williams and Wilkins.)

increase anatomic specificity, single-photon emission computed tomography (SPECT) bone scanning is used to obtain bone scans with axial slices. This allows the diagnostician to differentiate uptake in the posterior elements from more anterior structures of the spine. The diagnostic use of this study with regard to altering clinical decision-making is controversial. Studies have been published demonstrating that the use of SPECT can help identify patients with low back pain who might benefit from Z-joint injections.172

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SECTION 4  Issues in Specific Diagnoses

A

B

C

D

E

FIGURE 40-18  Abdominal strength grading. A, The patient lies supine with the knees bent (supine crook lying). The physician cues the patient to activate the transversus abdominis (“Pull your belly button toward your backbone”), and a very slight lumbar lordosis is maintained in a neutral position in which the spine is neither flexed nor extended. The ability to maintain the neutral spine is progressively challenged by loading the spine via lower extremity movements. Grading is as follows. B, Grade 1:The patient is able to maintain a neutral spine while extending one leg by dragging the heel along the table; the other leg remains in the starting position. C, Grade 2: The patient is able to maintain a neutral spine while holding both legs flexed 90 degrees at the hip and 90 degrees at the knee, and touching one foot to the mat and then the other. D, Grade 3: The patient is able to maintain a neutral spine while extending one leg by dragging the heel along the table. The other leg is off the mat and flexed 90 degrees at the hip and 90 degrees at the knee. E, Grade 4: The patient is able to maintain a neutral spine while extending one leg hovered an inch or two above the table, while the other leg is off the mat and flexed 90 degrees at the hip and 90 degrees at the knee. Grade 5: The patient is able to extend both legs a few inches off the mat and back again while maintaining the spine in neutral. Superior articular process (ear of Scottie dog)

truly physiologically significant.181 See Chapters 9 through 11 for further details.

Transverse process (nose)

Laboratory Studies

Pedicle (eye) Defect at pars interarticularis (collar or broken neck) Inferior articular process (foot) FIGURE 40-19  Oblique drawing of the lumbosacral junction, outlining the “Scottie dog” and the area of spondylolysis.

Electromyography Electromyography is useful in evaluating radiculopathy because it provides a physiologic measure for detecting neurogenic changes and denervation with good sensitivity and high specificity. It can help to provide information as to which anatomic lesions found in imaging studies are

Blood tests are rarely used in isolation as a diagnostic strategy for low back pain. Some blood tests are helpful as an adjunct in diagnosing inflammatory disease of the spine (with such markers of inflammation as sedimentation rates and C-reactive proteins), as well as some neoplastic disorders, such as multiple myeloma with a serum protein electrophoresis and urine protein electrophoresis.

Differential Diagnosis and Treatment: T   he Prototype of Back Pain Greater Than Leg Pain Mechanical Low Back Pain Nearly 85% of those who seek medical care for low back pain do not receive a specific diagnosis.50 The majority of these patients most probably have a multifactorial cause for back pain, which includes deconditioning; poor muscle

CHAPTER 40  Low Back Pain

A

B

887

C

FIGURE 40-20  Disk extrusion in a 48-year-old woman with back and left leg pain. A and B, Sagittal T2- and T1-weighted magnetic resonance image (MRI) showing L5–S1 disk extrusion with caudal extension. C, Axial T2-weighted MRI showing the extrusion is left paracentral in the lateral recess, occupying the space where the S1 root resides.

A

B

FIGURE 40-21  Anteroposterior (A) and lateral (B) myelograms of a 59-year-old woman with severe L4–L5 central stenosis caused by a large left L4–L5 zygapophyseal joint synovial cyst. Note the obvious filling defect at the L4–L5 level. She had symptoms of cauda equina syndrome and regained full neurologic function after decompression surgery.

recruitment; emotional stress; and changes associated with aging and injury such as disk degeneration, arthritis, and ligamentous hypertrophy. This type of back pain can be given many names; simple backache, nonspecific low back pain, lumbar strain, and spinal degeneration are a few of the common names for this condition. The name given to a condition sends certain messages to the patient who receives the diagnosis. The term simple backache might cause a patient to think that the physician misunderstands because, from the patient’s perspective, the pain is not simple if it has not resolved in a few days. The label nonspecific low back pain can cause the patient to continue to seek care from multiple providers to receive a specific diagnosis. Lumbar strain suggests that the condition was caused by overactivity, which is often not the case, and that further physical activity would cause it to recur, which is not true. Spinal degeneration sends the message that the changes are permanent and will probably worsen.235 The term mechanical low back pain is perhaps the best term for this multifactorial axial backache. It suggests the mechanism of injury better than terms such as strain or sprain, and it does not imply permanence. The biomechanics of the spine are not unlike the biomechanics of other systems, in that longevity of the components and efficiency of the system depend on precise

movements of each segment. In the spine, this means both an alignment in sustained postures and movement patterns that reduce tissue strain and allow for efficient muscle action without trauma to the joints or soft tissue.189 Clinicians and researchers alike theorize that when alignment and movement patterns deviate from the ideal, degeneration and tissue overload is more likely. This is analogous to the abnormal tire wear that occurs on a car when the wheels are out of alignment. Unlike machinery, the body can adapt over the course of time to stress on the segments. This adaptation can be the healthy response of tissue to loading (as is seen with exercise), such as muscle hypertrophy or increased bone density. It can also, however, begin a cycle of microtrauma that can lead to macrotrauma.125,140,189 The theoretic model for this approach is strong, and research is beginning to validate many of these concepts, although this is not easy given the complex nature of the system. History, Physical Examination, and Diagnostic Tests in Mechanical Low Back Pain The history and physical examination in mechanical low back pain are variable. No specific diagnostic tests exist for mechanical low back pain. Tests and imaging are used to exclude other diagnoses. Treatment of Low Back Pain Most studies of the various treatments for low back pain, particularly chronic low back pain, unfortunately have shown limited efficacy. Even the most commonly prescribed treatments, such as medications, exercise, and manipulation, in large trials tend to show improvements of only 10 to 20 points on a 100-point pain visual analogue scale. For this reason, most clinicians use multiple treatments on a particular patient in the hope that their cumulative effect will provide sufficient pain relief and an improvement in symptoms. The most common treatments for low back pain are discussed below. Reassurance and Patient Education. Education should include providing as much of an explanation as patients need in terms they can understand. The physician should also provide empathy and support and impart a positive

888

SECTION 4  Issues in Specific Diagnoses

message. Reassurance that there is no serious underlying pathology, that the prognosis is good, and that the patient can stay active and get on with life despite the pain can help counter negative thoughts and misinformation that the patient might have about back pain.235 Strong evidence from systematic reviews indicates that the advice to continue ordinary activity as normally as possible fosters faster recovery and can lead to less disability than the advice to rest and “let pain be your guide.”236 It is controversial whether patients with low back pain fare better with a specific diagnosis or not. Education and explanations, however, should be adequate. As Waddell states in his book The Back Pain Revolution, “Simply saying that ‘I can’t find anything wrong’ might imply that you are not sure and make patients worry more!”235 On the other hand, some diagnoses carry negative messages to patients that suggest permanent damage and the need to “get fixed,” such as degenerative disk disease or arthritis.235 Mechanical low back pain is a useful diagnostic term because it implies the mechanism of the pain and the way it is best treated without suggesting permanence. Beyond a diagnosis, there is other information that patients want about low back pain. In a study of patients who presented with low back pain to their primary care doctors in a health maintenance organization setting, the information that patients wanted from their doctor included the likely course of their back pain, how to manage their pain, how to return to usual activity quickly, and how to minimize the frequency and severity of recurrences. They ranked each of these areas of education a higher priority than finding a cause or receiving a diagnosis for their pain.235 Providing this information in an amount and in a way that patients can understand helps build a therapeutic doctor–patient relationship and, it is hoped, helps reduce anxiety and speed recovery. Back Schools. The term back school is generally used for group classes that provide education about back pain. The content and length of these classes varies a great deal, but generally they include information about the anatomy and function of the spine, common sources of low back pain, proper lifting technique and ergonomic training, and sometimes advice about exercise and remaining active. Studies have generally found back schools to be effective in reducing disability and pain for those with chronic low back pain.224 Exercise. No well-controlled studies show that exercise is effective for the treatment of acute low back pain. Many practitioners believe that exercise for patients with acute low back pain is appropriate to prevent deconditioning, to reduce the chance of recurrence of symptoms, and to reduce the risk of the development of chronic pain and disability. This is consistent with rehabilitation principles for other acute injuries, such as sports-related injuries or rehabilitation after joint replacement surgery.239 This principle is not yet supported by scientific research, perhaps because of problems with long-term exercise compliance, the overall favorable prognosis for each episode of acute back pain, or the outcome measures used. Multiple high-quality studies have found, however, that exercise results in positive outcomes in the treatment of

chronic low back pain.226 This includes pain relief (although this relief is modest, with a recent metaanalysis of 43 trials showing a mean difference of 10 points on a 100-point scale), improvement in function, and slightly reduced sick leave.43,87 It appears that the most effective exercise for low back pain includes an individualized regimen learned and performed under supervision that includes stretching and strengthening.87 This is not surprising because it is generally believed that the purpose of exercises for the treatment of low back pain is to strengthen and increase endurance of muscles that support the spine and improve flexibility in areas where this is lacking. This is combined with motor retraining to establish normal patterns of muscle activity, and treatment of deficits of the kinetic chain that interfere with biomechanical efficiency. One reason that studies have not been able to determine what exercises are best for patients with low back pain could be that multiple forms of exercise can achieve the goal of restoring function and regaining physical fitness.116,225,239 The exact dose of exercise, how much exercises should be advanced, and the ideal length of supervised treatment is not known. Because endurance is a significant problem with many patients with persistent back pain, activity levels should be increased in planned, fixed increments based on realistic goals rather than on symptoms. This is because it is normal in the course of low back pain that there will be temporary exacerbations of pain along the way. Beyond the physiologic benefits of exercise, increasing activity has positive effects on beliefs and behaviors about pain. Small doses of exercise that are not sufficient to cause physiologic change have been found to increase function and decrease pain. When specifically studied, this appeared to be from decreased fear-avoidance beliefs and reduced anxiety. By exposing fearful patients to physical activity through gradually increasing activity levels despite pain, they receive positive reinforcement by meeting goals, and personal experience can reduce fear of movement, reinjury, and catastrophizing.22 Adverse effects of exercise for low back pain are rarely reported, so it is generally a very safe form of treatment. Specific Exercise Treatment for Low Back Pain. ­Exercise prescriptions for mechanical low back pain generally begin with the goal of improving alignment and posture. Although researchers have not been able to consistently identify which specific postural faults are associated with chronic low back pain,56 the correction of posture could be important for at least two reasons. One is that exercises are more effective if they are done from a position of proper alignment that promotes optimal joint function and movement patterns. The second is that, for virtually all patients, much more time will be spent in habitual postures such as sitting and standing than will ever be spent exercising. If these habitual postures can reduce abnormal tissue strains, there is a better chance of reducing pain and promoting healing.188 Research on measuring posture, especially in regard to what is “normal” posture and whether exercise can influence posture, is difficult to conduct, and there are few studies to guide us in this area. In general, posture is evaluated in both sitting and standing positions, and an attempt to correct faulty posture is made. Some of these postural faults

CHAPTER 40  Low Back Pain

889

are habitual and can be improved with education, cuing, and practice. Some postural faults are structural problems that do not change with exercise, such as the kyphosis of Scheuermann disease or idiopathic scoliosis, and should be addressed with aids such as higher armrests or a chair with increased lumbar support. Many postural faults begin as habitual, and then become structural as tight muscles and tendons do not allow immediate correction with cuing, and weak muscles cannot maintain the proper position even if it can be reached. This is what is seen with typical postural faults such as long-standing lordosis, in which hip flexors and lumbar paraspinals become tight from prolonged positioning in lordosis, and abdominal muscles become long and weak from disuse and their prolonged lengthened position. These types of faults can be addressed with the proper exercises to stretch tight areas and strengthen weak areas. This is harder, however, to achieve in patients with persistent back pain. Multiple studies have shown that subjects with chronic low back pain have deficits in spinal proprioception and make repositioning errors. For example, in a study in which asymptomatic patients were compared with patients with chronic low back pain in an activity in which participants were assisted into neutral spine posture and then asked to reproduce this position after periods of relaxed full lumbar flexion, the group with back pain had significantly more repositioning errors.157 This has important implications for treatment because those with back pain might need extensive training by a physical therapist to change their posture, rather than just education regarding posture or a few simple demonstrations. Lumbar stabilization and core strengthening exercises that strengthen the muscles that support the spine are the most common exercises used to treat low back pain. A wide range of exercises can be used to strengthen these tissues. Because of research that shows that the deep stabilizers, such as the multifidi and transversus abdominus, do not function as well in those with low back pain, some programs emphasize beginning training of these muscles in the treatment of low back pain. Typically the exercise program is then progressed to include more complex dynamic and functional tasks. These are sometimes called motor control exercises because of the emphasis on precision of movement, rather than simply gaining global strength or flexibility. Multiple randomized controlled trials have shown that lumbar stabilization exercises, core strengthening, and motor control exercises are beneficial in reducing pain and improving function in patients with persistent low back pain. It is not clear whether these types of exercises are superior to other types.121

extending the arms and legs causes more than 6000 N of compression to the spine and might be much too intense for those with back injuries. The quadruped position with the leg extended, however, also activates spinal extensors but causes less than half the amount of spinal compression if done properly with the abdominal muscles engaged and the spine in neutral.138 These examples show how modification of exercises can reduce spinal forces and increase exercise tolerance. Some patients, especially those with persistent pain, can have high fear-avoidant behavior and develop kinesophobia (a fear of movement and a belief that movement will increase pain or cause them to be injured). This fear of pain, rather than forces on the spine or spinal pathology, leads to poor exercise tolerance. If this is the reason for poor exercise tolerance, it can be addressed by graded reactivation and gradual increases in activity. A positive experience with this might decrease fears. For more severe cases, a multidisciplinary approach that includes psychologic counseling to explore these dysfunctional thought processes might be needed. The physician should emphasize to patients that exercise needs to become a daily habit. Lack of compliance is one of the main reasons why exercise treatments fail. The health benefits of the exercise program beyond pain relief should be discussed, and patients should be reminded that exercising needs to continue even after symptoms decrease or resolve.

Modifications for Those in Whom Exercises ­Aggravate Pain. McGill138 has done extensive research evaluating spinal forces generated during exercise. For example, sit-ups cause more than 3000 N of compressive loads on the spine because of psoas activity, about the same as moderately heavy lifting. Leg raises also cause relatively high compressive forces. Curl-ups cause lower forces on the spine, so they are a better choice for anterior abdominal strengthening in the early stages of rehabilitation, or in those who have increased pain and cannot tolerate exercises with increased spinal loading. Lying prone and extending the spine while

Aerobic Activity. Increasing aerobic activity is a cornerstone of most exercise programs for low back pain. Studies in this area are often difficult to interpret because, both in the clinical and research settings, aerobic activity is usually combined with strengthening and flexibility exercise. Studies have shown that group classes that combine low-impact aerobics with strengthening and stretching floor exercises can be as effective in reducing pain and decreasing disability as individualized physical therapy and strengthening with weight machines.128 Many clinicians have found that patients with chronic low back pain tend to have very

Flexion Exercises for Low Back Pain. Once popular for the treatment of acute low back pain, using a series of flexion exercises has not been found to be more helpful for acute low back pain than other interventions, such as spinal manipulation, in several studies. No research has been done on the effectiveness of flexion exercises for chronic low back pain.223 Extension Exercises for Low Back Pain. Still commonly used by therapists in the treatment of low back pain, and in particular back pain accompanied by radicular leg pain, extension-based exercises are often done using the principles of the McKenzie method of physical therapy. This therapy approach divides the diagnosis for back pain into three categories: derangement, dysfunction, and postural syndrome. The most common of these are derangements, and exercises are chosen that centralize the pain, that is, move the pain from the leg or buttock into the low back. Although early studies were very promising, later studies have found this type of physical therapy to be helpful for low back pain but no more effective than other types of exercise.40,223

890

SECTION 4  Issues in Specific Diagnoses

low fitness levels, but research in this area has had conflicting results. For example, in one study in which prediction equations to estimated Vo2max (a measure of aerobic fitness) in patients with chronic low back pain were compared with normal values, the values for chronic low back pain patients did not differ from age-matched normal values for sedentary men and women.250,251 This could be because those who agreed to participate in the study were not representative of all patients with chronic low back pain, or it might simply demonstrate the poor aerobic fitness of sedentary people in general. Perhaps this poor fitness level is related more to lifestyle than to back pain. No particular type of aerobic activity has been found to be more effective for gaining fitness or decreasing pain than another for patients with back pain. A willingness to regularly participate in the activity at an intensity level to improve fitness is a more important factor than the specific type of exercise. One small study that compared symptomlimited exercise tests performed on the treadmill, stationary bicycle, or upper extremity ergometer by patients with low back pain found that pain scores were higher at the end of the treadmill test than the tests on the other two pieces of equipment. This appeared to occur because patients prematurely stopped the bicycle and arm ergometer tests because of muscular fatigue, and patients were able to reach significantly higher heart rates and peak Vo2 on the treadmill test despite pain complaints.251 If increasing aerobic fitness in a commonly used activity is the goal, then walking might be the best way to achieve this, despite pain complaints in patients with back pain. Patients with chronic low back pain tend to walk slower during gait analysis than those without pain. This is linked more with fear of pain and high scores on fear-avoidance and catastrophic thinking scales than with pain ratings.3 Interestingly, a slow stroll reduces spine motion and causes almost static loading of tissues, overall higher spine loading, and therefore more pain than faster walking with arm swings. Faster walking causes cyclic loading of tissues and results in lower spine torques, muscle activity, and loading. Swinging the arms facilitates efficient storage and use of elastic energy, which reduces the need for concentric muscle contractions with each step.140 Fast walking has been shown to be therapeutic for low back pain, as has other aerobic activity.140,195 Aquatic Exercises for Mechanical Low Back Pain. Patients who have not tolerated land-based exercises are often able to participate in pool exercises. Exercising in water has several benefits. One is buoyancy and reduction of gravitational stress. The greater the amount of the body that is submerged, the greater the effect. For example, there is a 90% reduction in gravitational stresses when exercising in the vertical position when the patient is immersed to the neck.110 Water can also decrease pain via the gate theory, in which the sensory input from the water temperature, hydrostatic pressure, and turbulence cause the patient to feel less pain. Muscle guarding and muscle overactivity might also be decreased in warm water. For those patients fearful of movement and reinjury, moving in the pool can increase their confidence as they see that they can progress without pain. The same principles for progressing therapy apply to aquatic exercise as to land-based exercise. Patients

can learn neutral position, stabilizing, and other strengthening exercise, and by walking, jogging (these can be done in deep water using a buoyancy belt or vest), or swimming can add an aerobic component.110 Multiple studies have found a beneficial effect on pain and function for patients with low back pain who exercise in the water.11,110,241 Exercise After Spine Surgery. Most of the research in this area has been done on patients who have undergone lumbar disk surgery. One systematic review of this subject found no evidence that exercising after disk surgery increases injury rate or need to reoperate.160 Overall, exercise appears effective in decreasing pain and increasing return to work rates. Those who used high-intensity exercise compared with low-intensity exercise resulted in significantly better short-term pain relief, functional status, and faster return to work. No difference was found, however, between the high- and low-intensity groups at 1-year follow-up evaluation, perhaps because of long-term compliance issues with the high-intensity exercises. Another study found home exercise programs equally effective to a supervised exercise program when all patients are given the same exercises.160 Exercise has generally been found to be one of the most effective treatments for decreasing pain and increasing function in chronic low back pain. The many other health benefits of exercise, along with the low risk of causing harm, make it a first-line treatment for mechanical low back pain. Medication Nonsteroidal Antiinflammatory Drugs. Multiple studies provide strong evidence that nonsteroidal antiinflammatory drugs (NSAIDs) prescribed at regular intervals provide pain relief for both acute and chronic low back pain. Studies comparing the effectiveness of NSAIDs have not found any particular NSAID to be superior to others.225,229 NSAIDs are associated with some risk, including gastrointestinal bleeding, decreased hemostasis, and renal dysfunction or failure in patients with abnormal renal function or hypovolemia.16 The cardiovascular risks of NSAIDs are also becoming more evident. Data on the long-term benefits and side effects associated with NSAIDs for low back pain are lacking. For example, of 51 trials included in the Cochrane Review on NSAIDs and low back pain, the longest trial evaluated only 6 weeks of therapy.43 Muscle Relaxants. The use of muscle relaxants remains controversial. One reason is that it is unclear what role muscle “spasms” play in mechanical low back pain. Some object to the term muscle spasm for skeletal muscle because only smooth muscles have the syncytial innervation pattern needed to actually spasm. They prefer the term muscle guarding. Other experts do not believe that pain in the low back is generally caused by muscles. Despite this controversy, 35% of patients who visit a primary care physician for low back pain are prescribed muscle relaxants.228 These medications fall into three classes of drug: the benzodiazepines, the nonbenzodiazepines that are antispasmodics, and antispasticity medication. The mechanism of action for benzodiazepines is the enhancement of γ-aminobutyric acid (GABA) inhibitory activity. The limited research done on this class of

CHAPTER 40  Low Back Pain

medication has found them to be effective for both acute and chronic low back pain for short-term pain relief (trials generally lasted from 5 to 14 days). They have significant adverse effects, however, such as sedation, dizziness, and mood disturbances. Rapid withdrawal can cause seizures. These medications have serious abuse and addiction potential, and they are not recommended for mechanical low back pain except in unusual cases for a short time.44,228 No evidence exists to support that they are more effective than other muscle relaxants such as cyclobenzaprine.43,154 Nonbenzodiazapine antispasmodics include medications with multiple mechanisms of action. Cyclobenzaprine has a structure similar to that of tricyclic antidepressants and is believed to act in the brain stem. Carisoprodol blocks interneuronal activity in the spinal cord and descending reticular formation. The mechanism of action of methocarbamol is not known but could be due to central nervous system depression.8 Multiple highquality studies show that these medications are effective for patients with acute low back pain for short-term pain relief (usually 2 to 4 days’ duration). The most common side effects are drowsiness and dizziness. Currently no evidence shows that one is more efficacious than another. Carisoprodol is metabolized to meprobamate, an antianxiety agent. It has significant potential for abuse and can result in psychologic and physical dependence.228 Because of this risk, and the fact that it is not more efficacious than other muscle relaxants, it should not be used except in rare cases. Little literature exists on the use of muscle relaxants for chronic pain. The drug manufacturers in this class state that they are not for long-term use.44,170 Antispasticity medication has also been used to treat low back pain. Baclofen is a GABA derivative that inhibits transmission at the spinal level and brain. One study has shown this medication to be effective for short-term pain relief in those with acute low back pain. Dantrolene works on the muscle, blockading the sarcoplasmic reticulum calcium channels. A small study of 20 patients found it to be effective for acute low back pain. It does not have the drowsiness side effect of the other muscle relaxants, but there is a risk of severe hepatotoxicity.228 Tizanidine, a centrally acting α2 agonist developed to treat spasticity. has been shown to be effective for acute low back pain in multiple trials. No studies support its use for chronic low back pain.43 Antidepressants. Tricyclic antidepressants are an effective treatment for many painful conditions, such as diabetic neuropathy, postherpetic neuralgia, fibromyalgia, and headaches. No adequate studies show whether they are effective for the treatment of acute low back pain. Multiple studies and reviews have shown their effectiveness, however, for chronic low back pain. Staiger et al.206 did a best evidence synthesis of randomized, placebo-controlled trials on this topic, which included 440 patients. They found that the tricyclics and tetracyclics had significant effects in reducing pain. These reductions were seen in studies in which depressed patients were excluded, so the mechanism is independent of any treatment of underlying depression. The doses used in almost all these studies were within the Agency for Health Care Policy and Research guidelines for treatment of depression. The most common

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side effects seen with the use of tricyclic antidepressants are dry mouth, blurry vision, constipation, dizziness, tremors, and urinary disturbances. The selective serotonin reuptake inhibitors and trazodone are not effective in treating chronic low back pain, which is consistent with the findings in studies for other painful conditions, such as diabetic neuropathy.206 Opioids. Many providers use short-acting opioids to treat acute low back pain. The use of opioids for chronic nonmalignant pain is much more controversial. Opioid use for chronic back pain varies a great deal by treatment setting, ranging from 3% to 66%, with the highest numbers in specialty treatment centers.132 Studies regarding the efficacy of opioids for chronic low back pain have not demonstrated that they are significantly better than placebo or other nonopioid medications.48,132 Studies also have not been able to demonstrate improvements in function with opioid use for chronic low back pain.132 Opiate side effects are substantial, and in many studies occur in more than half the participants. These effects include nausea, constipation, somnolence, dizziness, and pruritus.17 In studies that have compared long-acting with short-acting opioids, the long-acting medications appear to generally give better pain relief, are better tolerated, and are thought to have less abuse potential. Because of side effects, abuse potential, tolerance, unknown long-term effects on pain and neuronal functioning, and questionable efficacy, opioid medications are generally avoided, and a more global approach to mechanical low back pain is used. As with other treatments, long-term opioid treatment should be used only after careful analysis of the positive and negative impacts on function and quality of life. Outcomes beyond simple pain reduction should be used, and a rational endpoint of treatment and criteria for tapering and discontinuing the medications should be determined. Opioid medications should not be used without regular follow-up evaluation (see Chapter 42).16,17 Anticonvulsants. The anticonvulsants, particularly gabapentin and pregabalin, are widely used for neuropathic pain. Large randomized, controlled trials have not yet been conducted with these medications for the treatment of low back pain. One study of topiramate showed small improvement in chronic low back pain. Side effects include sedation and diarrhea.106,147 Tramadol. One study has shown it to be helpful for short-term treatment of chronic low back pain with a low rate of side effects.192 Systemic Steroids. Multiple studies have found them not to be effective for low back pain.43 Herbal Medicines for Low Back Pain. Several herbal medicines are used in the treatment of low back pain. Literature studies in this area tend to be of low quality, but several herbal preparations seem to reduce pain more than placebo, including Capsicum frutescens (cayenne) in a topical preparation, Salix albab (white willow bark), and Harpagophytum procumbens (devil’s claw). More research in this area is necessary.69 Topical Treatments. Lidocaine (lignocaine) patches have been found effective by some patients for the treatment of back pain. No large studies have proved or disproved its efficacy. A variety of creams and lotions are used by patients, including irritants and antiinflammatory

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SECTION 4  Issues in Specific Diagnoses

creams. Some people find them effective, but they have not been subjected to extensive research. These treatments carry little risk and have a low incidence of side effects. Injections and Needle Therapy for Mechanical Low Back Pain Myofascial Pain and Trigger Point Injections. The ­theory that irritable foci in skeletal muscle can cause both local and referred pain is generally accepted, although some physicians doubt the diagnosis of myofascial pain because, in general, the research supporting the biochemical and mechanical basis of trigger points is inconclusive (see Chapter 43). In regard to mechanical low back pain, it is thought that acute trauma or overload, chronic overwork and fatigue, or altered neurologic input causes trigger points to develop. They are treated by a combination of techniques, which include reducing biomechanical stress in the area by avoiding tissue overload, making postural changes, ischemic compression, stretching, and injections.217,218 The injection component has been the most studied. A Cochrane review of injection therapy for low back pain pooled the results of multiple studies that have found injections of trigger points to be effective in the treatment of low back pain. These included studies that evaluated dry needling, lidocaine (lignocaine) alone, and lidocaine with steroid injections. The reviewers concluded that trigger point injections are better than placebo injections for long-term pain relief based on these studies.152 Acupuncture. Acupuncture has been used for the treatment of pain conditions for thousands of years. From a Western medicine perspective, it appears to have multiple mechanisms of action, including effects on the endogenous opioid peptide system, an effect on the sympathetic nervous system, and alterations in pain processing in the spinal cord and brain.89 The efficacy of acupuncture in the treatment of low back pain is difficult to determine. Like other physical treatments, it is difficult to perform blinded studies. When comparing acupuncture with other standard treatments for low back pain, such as exercise, the results are difficult to interpret because the placebo effect is thought to increase with more invasive procedures. Great variations exist in the diagnosis and treatment of low back pain by acupuncturists. Much like other treatments for low back pain, such as physical therapy and medication regimens, treatments are patient- and provider-specific, and acupuncture treatments vary from one another by the points chosen, what type of needle stimulation is done, and the duration of the treatment.92,99 Despite these difficulties, the effectiveness of acupuncture to treat low back pain is increasingly being studied. It has also been the subject of multiple systematic reviews and metaanalyses. Most of these reviews comment primarily on the quality of studies done, and most studies are considered to be of poor quality; therefore only limited conclusions on the efficacy of acupuncture can be made. There seems to be general consensus in multiple reviews, however, that the evidence for acupuncture in relieving low back pain is either positive or inconclusive. For example, the British Medical Association’s rigorous analysis in 2002 of acupuncture found it to be effective for low back pain, whereas the Canadian/Alberta Health Authorities report’s

rigorous analysis done the same year found the results inconclusive for low back pain.20 More recent systematic reviews have also yielded mixed results with the consensus being that acupuncture can be a useful supplement to other forms of treatment, but it is unclear whether sham acupuncture can be as effective as true acupuncture.254 More high-quality definitive studies and clinical experience are obviously needed to reach a final conclusion in this area. Acupuncture is safe for the treatment of low back pain, with very low complication rates and few side effects. The most common side effects are bruising and pain at the site of needle insertion.20 Experimental Injection Procedures. Botulinum toxin injections are increasingly being used to treat low back pain. The mechanism of action could be through changes in sympathetic tone, reduction of muscle spasms, or another unknown mechanism. Studies in this area are currently small, and the results are inconclusive as to whether this will be an effective treatment for back pain. Prolotherapy is another controversial procedure gaining popularity in certain parts of the country. It consists of a series of injections into spinal ligaments to cause inflammation and thickening of the ligaments. Based on the scientific literature, the ability of this procedure to treat low back pain has not yet been validated. Steroid Injections and Other Spinal Procedures. See Chapter 25 for other specific spinal procedures used in the treatment of low back pain. Manual Mobilization or Manipulation. Historical references to manual medicine go back more than 4000 years. In the nineteenth century, an increased interest in manual medicine began in Great Britain and the United States. Multiple theories exist as to how manual medicine works. One theory is that it restores normal motion to restricted segments. Another is that it changes neurologic control via reflex mechanisms, especially the interaction between the autonomic nervous system and the spinal cord.76 Multiple randomized controlled trials and systematic reviews have been done to assess the efficacy of manual therapy. In most countries with national guidelines for the treatment of low back pain, spinal manipulation is recommended for acute low back pain,237,238 although this is not universal. The recommendations for chronic back pain are much more varied. Assendelft et al.12 performed a metaanalysis of the effectiveness of this treatment for low back pain and found many high-quality studies. This metaanalysis had weaknesses common to all metaanalyses, including the variety in quality of the studies, the possibility of publication bias, and statistical issues. Its strengths were the size of the patient pool, thoroughness, and inclusion of the most recent available data up to 2002. The metaanalysis included a total of 5486 patients. For both acute and chronic low back pain, the authors found spinal manipulation more effective than placebo (which was either sham manipulation or treatments judged to be ineffective) for short-term pain relief. An improvement in function was noted, but this did not reach statistical significance. When spinal manipulation was compared with other treatments known to be effective, such as analgesics, exercise, and physical therapy, the authors could find no statistically significant benefits

CHAPTER 40  Low Back Pain

compared with other therapies. Results did not change when they looked at studies in which only manipulation and not mobilization was used. They also could not identify any particular subgroup of patients for whom manipulation was particularly effective, although they theorized that if such a group existed, it would be small (see Chapter 22). The authors also did not find other commonly used treatments, such as physical therapy and medication, to be statistically more effective than spinal manipulation. Their conclusion was that spinal manipulation is more effective than placebo, and is one of several options of modest effectiveness for patients with low back pain. Traction. The literature in this area has been criticized because of disagreement as to whether studies done have used the appropriate weight of traction, frequency of treatment, and length of treatment session. Many studies have been of traction used once per week, and some practitioners believe traction should be done daily and that outcomes of studies with frequency less than this are invalid.85 Multiple randomized controlled trials using different doses of traction have been done, however, and most have not found traction to be effective for the treatment of back pain. No well-done study has shown that a specific weight or frequency of traction is effective over sham treatment.225,229 Lumbar Supports. Lumbar supports are used to both treat and prevent low back pain. Multiple types of lumbar support can be used. They vary from a simple elastic wrap to custom-molded plastic braces. High-quality studies comparing the effectiveness of different braces are generally lacking, although one study showed that patients who wore a lumbar support plus a rigid insert in the back had more subjective improvement than those who wore a brace without a rigid support.144 Several mechanisms of action have been proposed as to why lumbar supports would be effective. One hypothesis is that they prevent excessive spinal motion, either by physically blocking extremes of motion or by providing sensory feedback to remind the patient not to bend excessively. Another theory is that they increase intraabdominal pressure without increasing abdominal muscle activity, and therefore could reduce muscle force, fatigue, and compressive loading on the spine.222 A review of the literature regarding the mechanisms of action of lumbar supports showed that neither of these theories has been proven. In general, lumbar supports decrease ROM, but the results are not consistent. Decreases in ROM vary between subjects, with some subjects even showing increased range while wearing a brace. The plane of motion that is reduced also varies between subjects and the types of braces tested. Some types of brace reduce rotation, whereas others reduce flexion and extension. No evidence exists that lumbar supports actually increase intraabdominal pressure or decrease muscle forces and fatigue.222 Regarding the efficacy of lumbar supports, there is limited evidence that lumbar supports provide some pain relief for low back pain when compared with no treatment, but when compared with other treatments they are no more effective. Studies also have shown that generally there is poor compliance for subjects to consistently wear lumbar supports. No consistent evidence exists that lumbar supports prevent the occurrence of back pain (see Chapter 16).226

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Transcutaneous Electrical Nerve Stimulation. The development of transcutaneous electrical nerve stimulation (TENS) was based on the gate theory of pain of Melzack and Wall. In this theory, the stimulation of large afferent fibers inhibits small nociceptive fibers, causing the patient to feel less pain. Multiple types of TENS applications can be used, such as high frequency moderate intensity, low frequency high intensity, and burst frequency (see Chapter 21). Many patients find TENS helpful for temporary relief of low back pain. Evaluating the research in this area is difficult because of the difficulty of an equivalent placebo and the different types of TENS applications used between studies, and because most studies use patients’ memory of their pain (which is frequently inaccurate as an outcome measure).30 ­Metaanalyses of TENS outcomes show trends toward better pain reduction, better function, and satisfaction with treatment compared with placebo. These trends do not reach statistical significance, however, and, given the small changes, are of unclear clinical significance. Larger and methodologically sound studies are still needed to evaluate the efficacy of this treatment.145 Massage. Massage is one of the most commonly used complementary therapies for low back pain. The mechanism of action is thought to include relaxation, the therapeutic benefits of touch, and beneficial effects on the structure or function of tissues.68 Research that included massage has generally fallen into two categories: studies that measure the effect of massage and studies that assess the effectiveness of other interventions and use massage as a control with hands-on effects. In studies in which massage was used as the control, massage was not generally found to be more beneficial. This could be because of the effectiveness of both interventions, explaining why no differences were found, or it could have been due to publication bias. In studies in which massage was one of the main interventions, massage has been found to be effective for pain relief and in restoring function. For example, Cherkin et al.41 performed an interesting study that compared massage, acupuncture, and self-care education for chronic low back pain. After 10 weeks in which up to 10 treatments were allowed, the massage group showed improvements on disability scales, had decreased medication use, and had less time with restricted activity than the control group. After 1 year, many of these gains were maintained.41 Other high-quality studies have also found massage to be effective for improving symptoms and functions in those with subacute and chronic low back pain.68 High-quality studies on the effects of massage on acute low back pain have not yet been done. Complementary Movement Therapies. Many movement therapies are used in the treatment of low back pain. A few of the most commonly used therapies are listed below. These therapies have been found helpful in case series but have not been subjected to stringent randomized controlled trials. • Yoga: This is both an exercise system and philosophy that promotes relaxation, acceptance, and breathing techniques while various stretching and strengthening exercises are done. Multiple studies have found this to be as effective for low back pain as other group exercise programs.200,214

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• Pilates: This is a form of core-strengthening exercises that stress alignment and proper form. Positive results from small studies suggest that this might be an effective type of treatment for low back pain.183 • Alexander technique: This is an educational approach to posture and normalizing movement patterns. One recent randomized controlled trial of this technique showed short- and long-term effectiveness (up to 1 year) with this treatment.119 • Feldenkrais method: This is a combination of classes and hands-on work with therapeutic exercise to promote natural and comfortable movement patterns and improve body awareness. Multidisciplinary Pain Treatment Programs. Strong evidence exists that a multidisciplinary program with a goal of functional restoration is helpful for severe chronic pain.225 This is discussed further in Chapter 42 on chronic pain. Treatment of Comorbidities. Multiple comorbidities are often seen with back pain. Issues commonly associated with low back pain include depression, anxiety, and sleep disturbances. Treating these conditions often decreases pain and increases function. Those who suffer from low back pain often also have other illnesses associated with an unhealthy and sedentary lifestyle, such as obesity, non– insulin-dependent diabetes, and cardiovascular disease. These comorbidities must be taken into account when formulating a rehabilitation plan.

Prognosis of Low Back Pain Prognosis is difficult to fully ascertain for several reasons. One is that low back pain is a symptom caused by a vast spectrum of pathology with a variety of prognostic outcomes. Another is that the pain experience is individual, and treatment expectations vary. A huge body of medical literature highlights the complex cultural, psychologic, social support, and economic factors that influence pain and rehabilitation outcome.117 That being taken into account, the prognosis for low back pain is being better defined. The much quoted view that 90% of cases of acute low back pain will recover within 6 weeks does not include the entire story of low back pain, either in clinical practice or in reviews of the scientific literature. Most studies are performed with subjects who seek medical care for their low back pain, and this might be a select population not generalizable to all those who develop back pain. A recent metaanalysis of patients who sought medical care for back pain of less than 3 weeks’ duration was done. They included both those in treatment arms of studies and in the placebo arms, so that both the natural course and the clinical course of back pain could be evaluated. The study found that most patients rapidly improved within 1 month, and that most continued to have pain decrease, although more slowly, until about 3 months. From 3 months to 1 year, little change in pain was seen. The risk of a recurrence within 3 months varied between 19% and 34%, and the risk of a recurrence within 1 year was between 66% and 84%. This was a

heterogeneous diagnostic population, although the vast majority of patients fell under the diagnosis of mechanical low back pain.

Other Causes of Back Pain Greater Than Leg Pain Lumbar Spondylosis The degenerative cascade of Kirkaldy-Willis has already been described above. Because degenerative disease of the zygapophyseal joints generally coexists with degenerative disk disease, it is difficult to separate the two entities. Both can cause axial back pain. Both can also cause referred pain into the buttocks and legs. Mooney and Robertson146 and McCall et al.135 have studied the sclerotomal distribution of zygapophyseal joint pain in detail. Zygapophyseal joint pain has even been reported to refer below the knee in some cases. Delineating a degenerative zygapophyseal joint as the primary pain generator in axial low back pain, however, is difficult. Imaging studies are not particularly useful because many asymptomatic people have spondylotic changes in their spines. This diagnosis is also made more commonly in older patients. Older individuals have multiple findings in their history, in their physical examination, and on imaging studies that complicate arriving at specific diagnoses or specific pain generators as the cause of their complaints. Spondylotic zygapophyseal joints are seen commonly with other potential sources of low back pain, such as degenerative disks and lumbar stenosis. On physical examination, patients with these imaging findings commonly have postural abnormalities, poor pelvic girdle mechanics, and potentially multiple myofascial sources for pain. They typically have an accentuated lumbar lordosis, in part because of tight hip flexors, which exacerbates the problem by increasing stress on the posterior elements. From biomechanical studies and knowledge of anatomy, we know that lumbar extension and rotation increase forces placed on the posterior zygapophyseal joints. This specific maneuver, however, has not been shown to be diagnostic for zygapophyseal joint pain in clinical settings (by either history or examination). No unique identifying features are found in the history, physical examination, and radiologic imaging that are diagnostic for zygapophyseal joint pain. The only diagnostic maneuvers for zygapophyseal joint pain are fluoroscopically guided zygapophyseal joint injections with local anesthetic, and medial branch blocks (i.e., local anesthetic blocks of the medial branches of the dorsal primary rami that innervate the zygapophyseal joints).52,130 Using these injection techniques, the prevalence of facet-mediated pain in chronic low back pain sufferers has been estimated to be 15% in the younger population and 40% in older age groups.193,194 Schwarzer et al.’s 1994 study193 demonstrated that the vast majority of lumbar zygapophyseal joint pain originates from the L4–L5 and L5–S1 zygapophyseal joints. Consequently, if injections are used as treatment, most can be directed to those two lumbar levels. More conservative management options for the spondylotic spine and facet-mediated pain should be tried before resorting to invasive procedures such as intraarticular

CHAPTER 40  Low Back Pain

zygapophyseal joint corticosteroid injections or medial branch neurotomies. The conservative treatments are similar to treatments for osteoarthritic joints and can be categorized as lifestyle and activity modification, medications, and exercise. Lifestyle and activity modifications include weight control, relative rest, and initially limiting activities that result in increased pain (e.g., sleeping prone generally is to be avoided). Medications used include analgesics such as acetaminophen and NSAIDs. A role for glucosamine might exist because it has demonstrated a significant response for pain relief with knee osteoarthritis. Exercise programs are generally designed to decrease the forces acting on the zygapophyseal joints. This can include improving postural control by reducing any exaggerated lumbar lordosis. This is done through hip flexor stretching, pelvic tilts, and by developing the spine’s supportive musculature (including the deep abdominals, quadratus lumborum, and gluteal muscles) to stabilize the pelvis and lessen potential shearing forces in the lumbar spine. No single proven exercise program exists, however, for an exercise protocol for zygapophyseal joint-mediated pain. If land-based exercise is initially too aggravating, aquatic therapy can be the best starting place. Lumbar braces or corsets have not proven useful in the long term, but for an overweight patient with a protuberant abdomen or large pannus (which can certainly increase zygapophyseal joint stress by increasing the lordotic posture) one of these could be the best alternative. Interventional treatments for zygapophyseal joint pain have been briefly mentioned above. A more detailed discussion can be found in the chapter on interventional pain management chapter (see Chapter 25). Lumbar Disk Disease Diskogenic causes of low back pain generally fall into one of three categories: degenerative disk disease, internal disk disruption, and disk herniation. Diskogenic pain is classically described as bandlike and exacerbated by lumbar flexion, but this is not always the case. It can be unilateral, can radiate to the buttock, and can even be worsened by extension or side bending (depending on the site of disk pathology).

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described for disk herniation and radiculopathy; that is, chemical nociception from inflammatory mediators and mechanical stimulation. Disk Herniation The terminology used to describe disk material that extends beyond the intervertebral disk space is confusing. Herniated disk, herniated nucleus pulposus, disk protrusion, disk bulge, ruptured disk, and prolapsed disk are all commonly used terms, and sometimes are incorrectly used synonymously. Displaced disk material can be initially classified as a bulge (disk material is displaced >50% of its circumference) or as a herniation (> Axial Pain)

 

• Epidural steroid injections • Percutaneous disk decompression procedures • Chemonucleolysis � Ozone • Thermal � Laser • Mechanical � Automated devices � Radiofrequency nucleoplasty: coblation • Surgery • Microdiskectomy

BOX 40-5

Procedures for Diskogenic Low Back Pain (Internal Disk Disruption) (Axial Pain >> Leg Pain)

 

• Intradiskal steroids • Annuloplasty • Lumbar fusion • Disk arthroplasty

disk arthroplasty compared with fusion, only equal outcomes. The potential complications with disk arthroplasty are significantly more concerning, however, and it is currently unclear who would benefit from a disk arthroplasty over lumbar fusion.

Spondylolysis Spondylolysis is a defect of the pars interarticularis and is a common cause of back pain in children and adolescents. The most common hypothesized mechanism of injury is repetitive hyperextension loading in the immature spine, and is commonly reported in adolescent gymnasts and football linemen.60,94 Acute fracture from a severe hyperextension injury is also possible but less commonly reported.59 Pars defects have been reported in nonathletic individuals as well. In growing children, the defect is rarely seen before walking begins and most commonly occurs at age 7 to 8 years.153 An increase in incidence occurs during the adolescent growth spurt between ages 11 and 15 years. The pars defect appears to result from a combination of hereditary dysplasia of the pars and repetitive stressing of the spine by walking and extension loading.51 Unilateral or bilateral defects can occur, but bilateral involvement might result in spondylolisthesis. Ninety percent of these lesions occur at the L5–S1 level. Patients typically present with low back pain that is exacerbated by extension and alleviated by rest or activity limitation. Physical examination can demonstrate focal tenderness, pain with lumbar extension, and hamstring tightness (Figure 40-23). The neurologic examination is usually normal. If a spondylolisthesis is present, a palpable step-off with examination of the spinous processes might be evident.

CHAPTER 40  Low Back Pain

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BOX 40-6

Tokushima Classification for Grading Pars Defects • Acute (early): Hairline defect • Progressive: Moderately wide defect with round margins • Terminal (chronic): Wide effect with sclerotic margins

  Modified from Fujii K, Katoh S, Sairyo K, et al: Union of defects in the pars interarticularis of the lumbar, J Bone Joint Surg Br 86:225-231, 2004.

FIGURE 40-23 The standing one-leg hyperextension test.

The ideal radiographic assessment of a suspected pars injury is debated. Plain radiographs are of limited use in diagnosing a symptomatic spondylolysis. Oblique views can show a pars defect well; however, the sensitivity of detection on plain films does not increase much, and the radiation exposure is significantly greater.174 Standing anteroposterior and lateral radiographs can be obtained initially to identify a spondylolisthesis or any gross bony abnormalities.207 SPECT is more sensitive than plain radiography and planar bone scans. A positive bone scan or SPECT scan correlates with a painful pars lesion.86 In most retrospective analyses, however, increased uptake is present for approximately 1 year after the occurrence of the fracture.174 If the SPECT study is consistent with an active pars injury, a thin-slice CT through the abnormal level can be helpful to confirm the diagnosis and stage the lesion. Staging the lesion according to chronicity is helpful to predict healing. The Tokushima classification grades defects by CT as acute, progressive, or terminal (Box 40-6).66 A  recent metaanalysis demonstrated by using this classification system 68% of acute defects healed, 28% of progressive lesions healed, and no terminal lesions healed.109 Determining chronicity can help the clinician decide how quickly the athlete should progress through treatment. The use of MRI in diagnosing spondylolysis has garnered much attention in recent years. Standard magnetic resonance sequences identify only 80% of pars lesion seen on SPECT and should be used to look for other pathology.133 Campbell et al.,38 however, showed that nonstandard magnetic resonance sequences (oblique sagittal images) found 39 of 40 pars defects seen on CT and SPECT, but still MRI only correctly staged the lesion.29 A number of successful management strategies for spondylolysis have been used. Conservative management

is most common, typically beginning with relative rest and avoidance of activities that increase pain (especially repetitive extension). Patients typically are advised to rest for 3 months.207 This is the shortest amount of time over which healing of a pars lesion has been identified on serial imaging.253 Bracing, although a very commonly cited treatment, is not absolutely necessary. A recent metaanalysis demonstrated 84% of 665 patients with a spondylolysis treated nonoperatively were able to return to pain-free unrestricted activity by 1 year. No significant difference in clinical outcomes was seen between the braced and notbraced groups.109 A rigid brace might be considered after 2 weeks of rest if symptoms are not resolving.207 A radiographically stable bony union is the obvious goal but is not an absolute necessity, given many young athletes can become symptom-free in sports and everyday life even with a persistent pars defect. That same metaanalysis studied 847 defects and showed a 28% radiographic healing rate, with 71% of the unilateral defects healed and only 18% of the bilateral defects healed.109 In any event, braced or not, the young athlete is at risk for deconditioning. When pain allows, the patient should be encouraged to begin aerobic conditioning and eventually enter a spinal rehabilitation program before return to a sport. Once the athlete has mastered a basic core stabilization program, functional progression back to the specific sport is appropriate, with a focus on neuromuscular proprioceptive control and sport-specific drills before full return to play. For the patient with chronic low back pain and spondylolysis, O’Sullivan et al.158 demonstrated that a specific exercise program focused on training the lumbar multifidi and deep abdominals can be very effective. Surgical treatment is rarely indicated for the patient with spondylolysis alone but is more common in the setting of spondylolisthesis and/or radiculopathy. The natural history of spondylolysis and low-grade (